hyperion-health

Emotional Acceptance: How to Make Space for Difficult Feelings (Without Letting Them Run Your Life)

Mon, 16 Feb 2026 14:00:15 GMT

Emotional Acceptance

Some days, emotions hit hard. Stress, frustration, grief, anxiety, shame, irritability, overwhelm.

When that happens, many of us default to one of two strategies: fight the feeling (" I shouldn't feel this way ") or flee from it (scrolling, numbing, overworking, overeating, overtraining). Anything to make it go away.

The problem? The harder we try to shove emotions down, the louder they tend to get.

Emotional acceptance is a different approach: learning to acknowledge difficult feelings and accept them without judgment. It's not about enjoying " negative " emotions or pretending everything is fine. It's about understanding what you're experiencing and creating enough inner space to choose your next step on purpose.

What emotional acceptance actually means (and what it doesn't)

Emotional acceptance means:

Recognizing what you feel, as it is, in this moment
Allowing the feeling to be present without trying to " fix " it immediately
Not adding extra suffering through self-criticism or shame
Choosing actions that align with your values. Even when emotions are uncomfortable

Emotional acceptance does not mean:

Approving of what happened
Resigning yourself to feeling bad forever
"Letting emotions control you."
Ignoring problems that need to be solved

Acceptance is the middle path between denial and overwhelm. It's the skill of saying: " This is hard, and I can still respond in a way I respect. "

Why acceptance helps you feel safer inside your own body

A common fear is: " If I accept this feeling, it will get worse ". But acceptance isn't surrender, it's nervous system wisdom.

When you acknowledge emotions without judgment, you send your brain a powerful message:

" I can handle this ."

That sense of internal safety matters, especially if you're:

Managing persistent stress or burnout
Living with chronic pain or a long rehab process
Juggling work, family, school, and health changes
Trying to rebuild healthy habits after setbacks

Emotions are temporary and fluid; they move, shift, and change. The goal isn't to eliminate them, it's to stop treating them like emergencies.

The hidden cost of emotional "control."

Trying to control emotions often looks like:

Overthinking and rumination
Constant distraction
Perfectionism
People-pleasing
Emotional shutdown
Pushing harder in the gym to outrun stress
Skipping recovery because rest feels "lazy."

It can work in the short term, but in the long term, it drains your energy and creates friction in your life.

Acceptance gives you a better option: respond instead of react .

A practical framework: Accept ➡︎ Notice ➡︎ Choose

Here's a simple, repeatable process you can use in real life (in the middle of a tough day, not just in theory).

1) Name it (without judging it)

Try:

"I'm noticing anxiety."
"I'm feeling disappointed."
"I'm carrying a lot of tension."
"This is sadness."

Keep it factual. The goal is clarity, not commentary.

Why this works: Labelling emotions helps reduce the intensity and moves you out of autopilot.

2) Allow it (make space instead of fighting)

This step is subtle but powerful. It can be as simple as:

"This feeling is here right now."
"I don't like it, but I can allow it."
"I can feel this and still be okay."

If it helps, emotions like weather passing through, unpleasant sometimes, but not permanent.

3) Locate it in your body

Emotions are not just thoughts; they're physical sensations:

Tight chest
Heavy stomach
Jaw clenching
Restlessness
Lump in throat
Hot face

Try placing a hand where you feel it most and taking three slower breaths. You're not trying to erase the sensation; you're teaching your system that you can tolerate it safely.

4) Remember your goals (zoom out)

This is where emotional acceptance becomes empowering.

Ask:

"What matters to me here?"
"What kind of person do I want to be in this moment?"

This is values-based living: choosing behaviour that aligns with who you want ot be, even when feelings are messy.

5) Choose one small action in line with your values

Keep it small and specific:

Send the email you've been avoiding (kindly, clearly)
Take a 10-minute walk to reset
Do your rehab exercises at a sustainable pace
Eat a real meal instead of skipping
Ask for help or support
Set a boundary and log off

Acceptance doesn't remove discomfort; it makes good decisions possible while you're in discomfort.

Self-compassion: the "maintenance plan" for tough days

Acceptance works best when paired with self-compassion. That means treating yourself like someone you genuinely care about.

Try this three-part self-compassion script:

This is hard. (acknowledgement)
I'm not alone in this. (common humanity)
What do I need right now? (support)

A key mindset shift:

Your emotions don't define you. They're a temporary part of your experience. Commit to using self-compassion regardless of your life story.

What emotional acceptance looks like in health, rehab, and fitness

At Hyperion, we see this constantly: the emotional side of health is real, and it affects outcomes.

Emotional acceptance can help when:

Rehab feels slow: You can feel discouraged and still show up consistently
You're rebuilding your fitness, and you can feel self-conscious while still training appropriately.
Chronic pain is present. You can acknowledge it and reduce the extra suffering caused by fear and tension.
Motivation is low: You can act on values (health, function, independence) instead of waiting for the perfect mood.

This is often the difference between "all-or-nothing" cycles and sustainable progress.

A simple practice you can try today (2 minutes)

The 2-Minute Emotional Reset

Pause and name one feeling: "I'm noticing _______."
Take 5 slow breaths (longer exhale than inhale).
Ask: "What matters most in the next hour?"
Do one small action that supports that value.

That's it. Not dramatic. Not perfect. Just effective.

Closing thought

Emotional acceptance is a skill. And like any skill, it strengthens with repetition, not perfection.

You can acknowledge difficult feelings and still feel safe. You can be mindful of emotions and choose behaviours aligned with your values. You can build inner peace by remembering your goals and practicing self-compassion, again and again.

If you'd like support applying these principles alongside your training, rehab, lifestyle change, or stress management, Hyperion's team can help you build a practical plan that fits your real life.

What is a Kinesiologist?

j.oswald@hyperionhealth.ca (Jesse Oswald) — Wed, 29 Jan 2025 14:00:02 GMT

What is a Kinesiologist?

When you think of healthcare professionals, roles like doctors, nurses, and physiotherapists often come to mind. But behind the scenes, there’s another vital professional who plays an integral role in improving health, preventing injuries, and enhancing the quality of life: the Kinesiologist.

Whether you’re recovering from an injury, managing a chronic condition, or simply striving to live a healthier, more active life, Kinesiologists are movement specialists who can help you achieve your goals. Let’s dive deeper into what a Kinesiologist does, their education, and why they’re an essential part of the healthcare system.

What is Kinesiology?

At its core, Kinesiology is the scientific study of human movement . It’s a multidisciplinary field that examines how physical activity impacts the body’s structure, function, and overall health. By combining knowledge from anatomy, physiology, biomechanics, psychology, and exercise science, Kinesiologists develop evidence-based strategies to improve movement, promote recovery, and enhance performance.

Kinesiology focuses on movement as medicine —leveraging physical activity to prevent injuries, manage chronic diseases, and improve physical and mental well-being.

What Education and Qualifications Do Kinesiologists Have?

To become a Kinesiologist, individuals must earn a degree in Kinesiology or a closely related field, such as Human Kinetics or Exercise Science. This education includes rigorous coursework in:

Anatomy and Physiology : Understanding how the human body is structured and functions.
Biomechanics : Studying the mechanical principles behind movement.
Exercise Physiology : Exploring how the body responds and adapts to physical activity.
Psychology of Physical Activity : Understanding the mental and emotional aspects of exercise and rehabilitation.
Pathophysiology : Learning how diseases and injuries affect movement and health.

In provinces like Alberta and Ontario, Kinesiologists must also meet specific professional standards and may need to register with organizations like:

The Alberta Kinesiology Association (AKA)
The College of Kinesiologists of Ontario (CKO)

Certification ensures that Kinesiologists adhere to a strict code of ethics and provide safe, effective, and evidence-based care.

What Does a Kinesiologist Do?

Kinesiologists are highly versatile professionals who tailor their services to meet the unique needs of their clients. They often work with individuals across the lifespan, from children to older adults, addressing a wide range of health and wellness goals.

Here’s a closer look at what Kinesiologists do:

1. Injury Rehabilitation

Kinesiologists help individuals recover from injuries by:

Designing personalized exercise programs to restore mobility, strength, and function.
Teaching proper movement techniques to prevent re-injury.
Collaborating with physiotherapists, chiropractors, and other healthcare professionals for a holistic recovery plan.

2. Chronic Disease Management

For individuals living with chronic conditions such as diabetes, heart disease, or arthritis, Kinesiologists:

Develop safe, individualized exercise programs to manage symptoms and improve health.
Educate clients about the role of movement in disease prevention and progression.
Monitor progress and adapt plans as needed to ensure long-term success.

3. Performance Enhancement

Kinesiologists work with athletes and active individuals to:

Improve strength, endurance, flexibility, and overall performance.
Conduct movement assessments to identify areas for improvement.
Provide recovery strategies to optimize training and prevent burnout.

4. Workplace Health and Ergonomics

In corporate settings, Kinesiologists:

Analyze workspaces to improve ergonomics and reduce the risk of repetitive strain injuries.
Develop wellness programs to keep employees active and healthy.
Conduct Functional Capacity Evaluations (FCEs) to determine an individual’s ability to return to work after injury.

5. General Health and Fitness

For those looking to improve their overall health, Kinesiologists:

Provide fitness assessments and create customized exercise plans.
Help individuals set realistic goals for weight management, mobility, and strength.
Support long-term behavior change for sustainable health improvements.

Where Do Kinesiologists Work?

Kinesiologists work in a variety of settings, reflecting their adaptability and broad expertise. These include:

Rehabilitation Clinics: Assisting with recovery from surgeries, sports injuries, or chronic pain conditions.
Sports Performance Centers: Training athletes to achieve peak performance and minimize injuries.
Hospitals and Long-Term Care Facilities: Supporting mobility and functional independence in patients with chronic illnesses or disabilities.
Corporate Wellness Programs: Promoting employee health and reducing workplace injuries through ergonomic assessments and activity programs.
Community Health Organizations: Encouraging physical activity in populations at risk of chronic diseases.
Private Practice or Home Care Services: Delivering personalized care directly to clients.

Why Should You See a Kinesiologist?

You don’t need to be injured or an elite athlete to benefit from a Kinesiologist’s expertise. There are many reasons to work with one, including:

Injury Prevention: Learn how to move properly and reduce your risk of injuries at work, home, or during physical activity.
Chronic Disease Support: Manage conditions like diabetes, hypertension, and arthritis with safe and effective exercise programs.
Rehabilitation: Recover from injuries or surgeries with expert guidance to regain strength and function.
Sports Performance: Optimize your training, improve your skills, and prevent overuse injuries.
Health and Wellness Goals: Achieve sustainable weight loss, improved mobility, and better overall fitness with personalized plans.

What Sets Kinesiologists Apart?

Kinesiologists stand out because of their holistic approach to health. They:

Focus on the root causes of movement issues, not just the symptoms.
Use evidence-based strategies tailored to each individual’s unique needs.
Emphasize education and empowerment, teaching clients how to take control of their health.

Unlike many other healthcare professionals, Kinesiologists don’t just treat conditions—they aim to enhance the way people move, live, and thrive.

How to Find a Kinesiologist

If you’re ready to improve your health through movement, start by reaching out to a Kinesiologist near you. You can:

Search for registered professionals through organizations like the Alberta Kinesiology Association or the College of Kinesiologists of Ontario .
Ask for a referral from your doctor or physiotherapist.
Look for private clinics or community health programs offering Kinesiology services.

Move Better, Live Better with Kinesiology

Kinesiologists are movement experts who combine science and compassion to help people achieve their health and wellness goals. Whether you’re recovering from an injury, managing a chronic condition, or striving to enhance your performance, a Kinesiologist can provide the guidance and support you need to succeed.

Remember, better movement leads to better health—and better health leads to a better life. Discover the difference a Kinesiologist can make today!

Got questions about Kinesiology? Send us a message, and we’ll be happy to help!

Predicting Medical Costs with VO2max

j.oswald@hyperionhealth.ca (Jesse Oswald) — Mon, 20 Jan 2025 16:00:01 GMT

Highlights

Healthcare expenses are skyrocketing, with consumers and employers facing the significant brunt.
Identifying those likely to get sick is critical as our resource-strapped healthcare system should focus on those likely to become the most significant burden to the system.
VO2 max is a crucial longevity indicator that can also accurately predict healthcare expenses.

The rampant chronic disease epidemic and the resulting surge in medical expenses is one of the most dire problems of modern societies, probably only second to climate change. Healthcare inflation is on a meteoric rise, and for those with limited or no healthcare coverage, a medical emergency is the equivalent of personal bankruptcy.

A dire problem for employers

In the US, employers and consumers who face rising health insurance premiums and astronomical out-of-pocket medical expenses feel the brunt of rising healthcare costs. Such is the problem that even large, well-capitalized corporations choose to send employees overseas for specific medical procedures since the cost of traveling and treatment in a foreign country is lower than the cost of care in the US. Another startling example is the infamous "northern caravan," a term that describes people with diabetes in the northern states who travel to Canada to secure their insulin supply. According to McKinsey , a survey conducted among over 300 employers highlighted that the average increase in the cost of health benefits over the past three years has been within the range of 6 to 7 percent. This survey also indicated that any rate increases exceeding 4 to 5 percent were deemed unsustainable. Interestingly, 95 percent of the surveyed employers expressed willingness to contemplate reducing benefits if costs surged by 4 percent or more. The primary cost-control measures that these employers indicated they might explore included elevating the portion of premium costs covered by employees and a potential transition to high-deductible health plans.

Why is Breath Analysis relevant?

Vis-a-vis this problem, the early and accurate estimation of who will get sick and how much they will cost is as critical as the treatment itself. The reason is that no other method of accurately identifying at-risk populations exists; it helps focus our scarce prevention resources and attention on those most in need. Breath analysis, AKA VO2max or metabolic testing, is an assessment that reveals two key biomarkers that provide significant predictive value for one's likelihood of developing costly chronic conditions. These two biomarkers are VO2max and the Respiratory Exchange Ratio. In this article, we will dive into VO2max to understand why it's a critical reflection of our overall health and, consequently, a window into our future healthcare spend.

What is VO2max?

Let's start with the basics. What is VO2max? VO2 max is the maximum amount of oxygen the human body can absorb. It is measured in terms of milliliters of oxygen consumed per kilogram of body weight. The below formula below indicates how VO2max is calculated:

The numerator indicates the volume of oxygen your heart, lungs, and cells can absorb, expressed in milliliters per minute. The denominator indicates the weight of the individual represented in kilograms.

How is VO2max measured?

VO2 max is measured by analyzing the total amount of oxygen consumed by a person's body while exercising at maximal or near-maximal conditions. As our body begins to move, working muscles need to break down more nutrients (i.e., fats and carbohydrates) to cover the increased demand for energy. Since the oxidation (i.e., breakdown) of nutrients requires oxygen, our heart, lungs, and blood circulation will begin to work more intensely to deliver the necessary oxygen. As the intensity of exercise increases, so does the need for oxygen by the working muscles, and the more our cardio-respiratory system works harder. This is what we all experience when we start to exercise and continue increasing the intensity. Consequently, when we exercise at our peak, we consume the most significant amount of oxygen. This is our VO2max. A VO2max assessment is typically conducted on a stationary bicycle or treadmill.

The Oxygen Chain

Because of the fundamental nature of oxygen supply to our cells, a large part of our body specifically evolved to sustain this process. Our heart, lungs, and blood circulation's main task is to facilitate oxygen delivery clearance of carbon dioxide, in other words, to maintain the ongoing operation of aerobic metabolism. All these systems comprise the Oxygen Chain.

The oxygen chain is the bedrock of human longevity. This is manifested by the fact that nearly all chronic conditions likely to kill you or reduce your quality of life are either caused or displayed by a reduction in oxygen throughput in the respective system. For example, the reduced ability of the cells to absorb oxygen has been proven to be one of the most potent predictors of metabolic disorder and type II diabetes. A reduced ability of your heart to pump oxygen-rich blood is a reliable indicator of Coronary Artery Disease. The VO2max test is the only scientific assessment known to analyze the health of your oxygen chain and assess how effectively its parts operate individually and in unison in circulating oxygen and powering aerobic metabolism. VO2 max is the metric that summarizes the health of the oxygen chain most comprehensively. This is why decades-long longitudinal studies have established it as the most potent predictor of how long and well one will live. The range of scientific data supporting the power of VO2 max to predict mortality and morbidity led the American Heart Association to call for the institution of VO2 max testing as part of every person's annual physical examination.

Healthcare cost prediction

VO2max is a metric that has been extensively analyzed in its ability to predict the likelihood of mortality and morbidity and its ability to predict healthcare costs directly. Specifically, a landmark study published by The Mayo Clinic analyzes the correlation between healthcare expenses and Cardio-Respiratory Fitness (CRF), an alternate description of VO2 max. The study comprised 9,942 participants with a mean age of 59.11 years who underwent a maximal exercise test for clinical purposes from January 2005 to December 2012. Cardiorespiratory fitness was divided into four categories or quartiles, measured as a percentage of age-predicted peak metabolic equivalents (METs) attained. Data were obtained from the Veterans Administration Allocated Resource Center to analyze total and annualized healthcare expenses. Multiple regression techniques were employed to compare these costs while accounting for demographic and clinical factors.

An inverse relationship between cardiorespiratory fitness (CRF) and healthcare costs was observed. Those in the least-fit quartile had approximately $14,662 higher overall costs per patient per year compared to the fittest quartile, even after accounting for potential confounding variables (P<.001). Furthermore, for each 1-MET increase in fitness, there was a corresponding annual reduction of $1,592 in healthcare costs (equating to a 5.6% lower cost per MET). Additionally, moving up to a higher quartile of fitness resulted in a $4,163 annual reduction in costs per patient.

Interestingly, the impact of CRF on costs was more pronounced in subjects without cardiovascular disease (CVD), indicating that these findings were not driven by the possibility that less-fit individuals had a higher prevalence of CVD. The cost savings attributed to greater fitness were most significant in overweight and obese subjects, with lower savings observed among those with a body mass index of less than 25 kg/m². When considering historical, clinical, and exercise test data, heart failure emerged as the most influential predictor of healthcare costs, followed by CRF.

Conclusion

The vast amount of scientific evidence behind the relationship among VO2 max mortality, morbidity, and healthcare cost is a powerful tool to help providers and stakeholders in health and wellness contain the chronic disease pandemic. It's undeniable that our healthcare system is resource-strapped as providers face the most challenging time in modern times recruiting the necessary personnel. As such, targeting our limited resources where it matters most can make the difference between success and failure in mitigating healthcare costs.

Dietary Fat: An Essential Dietary Component Rather than the root of all Nutritional Health Issues

j.oswald@hyperionhealth.ca (Jesse Oswald) — Mon, 13 Jan 2025 16:00:01 GMT

Key points

A total fat intake between 20-35% ensures sufficient intake of essential fatty acids and fat-soluble vitamins
Omega-6 PUFAs are primarily found in vegetable oils, while omega-3 PUFAs are primarily found in fatty fish and fish oils
Both omega-3 PUFAs and MUFAs have established benefits for cardiovascular disease
TFAs are the only dietary lipids that have a strong positive relationship with cardiovascular disease
Omega-3 PUFA supplementation increases the beneficial bacteria of the human microbiome

Over the last three decades, there has been a great revolution against fat due to its suspected association with several nutritional health issues, especially cardiovascular disease. There was a tremendous amount of evidence that indicated dietary cholesterol and saturated fat as the main culprits of cardiovascular disease, thus morbidity and mortality. It was when all the low-fat and no-fat dairy products started to launch, promising even complete substitution of the cholesterol-lowering heart medication if these products were exclusively consumed.

Let’s start from the beginning. Dietary fat intake can vary significantly and still meet energy and nutrient needs. International guidelines suggest a total fat intake between 20% and 35% of the daily caloric consumption. This range ensures sufficient intake of essential fatty acids and fat-soluble vitamins. Not only does the quantity of the ingested fat matter, but most importantly, its quality. Some dietary fats have beneficial effects, with a significant role in maintaining good health, while others may threaten it.

Which are, after all, the dietary fats? Dietary fats is a rather heterogeneous group of organic compounds, including four main types of fat, which are elaborately described in the following sections of this article.

Polyunsaturated fatty acids (PUFAs)

Polyunsaturated fatty acids (PUFAs) have two or more carbon-carbon double bonds. Omega-6 PUFAs and omega-3 PUFAs are the main types of PUFAs and are classified according to the location of the first unsaturated bond (sixth and third carbon atom, respectively). Alpha-Linolenic acid (ALA), docosahexaenoic acid (DHA), docosapentaenoic acid (DPA), and eicosapentaenoic acid (EPA) are the most important omega-3 PUFAs. ALA is an essential fatty acid that can only be obtained from diet and can be converted into EPA and then to DHA, but the rate of this conversion is finite, approximately 7.0%–21% for EPA and 0.01%–1% for DHA. In the same way, the most important omega-6 PUFAs are linoleic acid (LA) and arachidonic acid (ARA). LA is an essential fatty acid that, in order to give rise to ARA, needs to be ingested through the diet as the human body cannot synthesize it. The recommended intake for total PUFA ranges between 5% and 10% of the total energy intake, while a total omega-3 PUFA intake of 0.5%–2% and a total omega-6 PUFA intake of 2.5%-5% is suggested. A dietary ratio of omega−6/omega−3 PUFA is recommended to be 1:1–2:1 to balance their competing roles and achieve health benefits.

Omega-6 and omega-3 PUFAs

Omega-6 PUFAs, in the form of LA, are plentiful in most crop seeds and vegetable oils, such as canola, soybean, corn, and sunflower oils. In contrast to omega-6 PUFAs, omega-3 PUFAs are obtained from a limited range of dietary sources. Flax, chia, and perilla seeds are rich in ALA, with significant amounts also detected in green leafy vegetables. The consumption of fatty fish, such as salmon, sardines, tuna, trout, and herring, provides high amounts of EPA and DHA. Besides fish and their oils, small amounts of omega-3 PUFAs are also detected in red meat like beef, lamb, and mutton. All the above dietary sources provide EPA, DPA, DHA, LA, and ARA in different amounts, and their intake is necessary for normal physiological function.

PUFAs play a critical role in many chronic diseases, affecting human cells by regulating inflammation, immune response, and angiogenesis. Omega-3 PUFAs’ role against hypertriglyceridemia has been clarified, and research indicates that systematically consuming oily fish can contribute to general heart protection. Supplementation with omega-3 PUFAs could potentially lower the risk of several cardiovascular outcomes, but the evidence is stronger for individuals with established coronary heart disease. Moreover, adequate EPA and DHA levels are necessary for brain anatomy, metabolism, and function. Although the mechanisms underlying omega-3 PUFAs' cardioprotective effects are still poorly understood, several studies have been conducted in this direction. Unfortunately, that does not hold true for their omega-6 counterparts, for which controversial emerging data tend to show anti-inflammatory behavior that needs to be further studied.

Monounsaturated fatty acids (MUFAs)

In contrast to PUFAs, monounsaturated fatty acids (MUFAs) are easily produced by the liver in response to the ingestion of carbohydrates. The main MUFA is oleic acid, found in plant sources, such as olive oil, olives, avocado, nuts, and seeds, while minimal amounts are also present in meat, eggs, and dairy products. Specific guidelines around MUFAs’ dietary consumption do not exist. Therefore, MUFAs are recommended to cover the remaining fat intake requirements to reach the total daily fat intake goal. A growing body of research shows that dietary MUFAs reduce or prevent the risk of metabolic syndrome, cardiovascular disease (CVD), and hypertension by positively affecting insulin sensitivity, blood lipid levels, and blood pressure, respectively.

Moreover, olive oil contains several bioactive substances, possessing anti-tumor, anti-inflammatory, and antioxidant qualities. According to a meta-analysis, consuming olive oil was linked to a lower risk of developing any sort of cancer, especially breast cancer and cancer of the digestive system. Another study found that an isocaloric replacement of 5% of the energy from saturated fatty acids (SFAs) with plant MUFAs led to an 11% drop in cancer mortality over a 16-year follow-up period. Therefore, including MUFAs in the everyday diet offers multifaceted benefits in chronic disease prevention and management, including cancer and general health promotion.

Saturated fatty acids (SFAs)

Saturated fatty acids (SFAs) form a heterogeneous group of fatty acids that contain only carbon-to-carbon single bonds. Whole-fat dairy, (unprocessed) red meat, milk chocolate, coconut, and palm kernel oil are all SFA-rich foods. These fatty acids have distinct physical and chemical profiles and varying effects on serum lipids and lipoproteins. Stearic, palmitic, myristic, and lauric acids are the principal SFAs found in most natural human diets. Dietary practice and guidelines recommend limiting SFA intake to <10% of the total energy (E%), while the American Heart Association suggests an even lower intake of <7 E% because total saturated fat consumption and LDL-C levels are positively correlated.

However, the role of SFAs in CVDs is quite complex, and the evidence is heterogeneous. In a recent study with a 10.6-year follow-up period, which included 195,658 participants, there was no proof that consuming SFAs was linked to developing CVD while replacing saturated fat with polyunsaturated fat was linked to an increased risk of CVD. Moreover, according to 6 systematic reviews and meta-analyses, cardiovascular outcomes and total mortality were not significantly impacted by substituting saturated fat with polyunsaturated fat. Even if these analyses were to be challenged, due to heterogenous evidence, the possible reduction in CVD risk associated with replacing SFAs with PUFAs in several studies may not necessarily be an outcome of SFAs’ negative effect but rather a potential positive benefit of PUFAs. Regarding SFAs' effect on different types of cancers, associations of their intake with an increased risk of prostate and breast cancer have been indicated. Conversely, a meta-analysis showed no link between SFA intake and a higher risk of colon cancer; similarly, consuming MUFAs, PUFAs, or total fat did not affect colon cancer risk. Hence, the role of SFA consumption in preventing, promoting, or having a neutral role in serious chronic diseases has not been fully elucidated yet.

Trans fatty acids (TFAs)

Trans fatty acids (TFAs) are created industrially by partially hydrogenating liquid plant oils or can be naturally derived from ruminant-based meat and dairy products. TFAs are highly found in commercial baked goods, biscuits, cakes, fried foods, etc. Guidelines regarding TFAs are stringent and limit TFA intake to <1% of energy or as low as possible. In 2015, the US Food and Drug Administration declared that industrial TFAs are no longer generally recognized as safe and should be eliminated from the food supply as their consumption is strongly linked to various CVD risk factors. Specifically, TFA intake raises triglycerides and increases inflammation, endothelial dysfunction, and hepatic fat synthesis, leading to a significantly increased risk of coronary heart disease (CHD). A meta-analysis suggested that increased TFA intake led to an increase in total and LDL-cholesterol and a decrease in HDL-cholesterol concentrations. Data also indicates that TFAs may influence carcinogenesis through inflammatory pathways, but the reported data are debatable. A recent study investigated the effects of all types of dietary fat intake on CVD risk. While PUFA, MUFA, and SFA intake were not linked to higher CVD risk, dietary TFA intake showed a strong association with CVD risk. Analysis indicated PUFA intake and CVD risk were inversely correlated, and the relative risk of CVD was reduced by 5% in studies with a 10-year follow-up.

Dietary lipids and the human microbiome

Dietary lipids also affect human microbiota composition. Studies have identified a close association between the human microbiome and metabolic diseases, including obesity and type 2 diabetes. Diets with a high omega-6 PUFA, SFA, and TFA intake increase the amount of many detrimental bacteria in the microbiome and reduce the amount of the beneficial ones, altering the microbiota composition and inducing inflammation via the secretion of pro-inflammatory cytokines. These bacteria may disrupt the gut barrier function, allowing lipopolysaccharides (LPS) translocation, which are bacterial toxins. This condition is linked to metabolic perturbations such as dyslipidemia, insulin resistance, non-alcoholic fatty liver disease (NAFLD), and CVD.

On the contrary, omega-3 PUFA (EPA and DHA) supplementation increases beneficial bacteria and limits harmful ones, enhancing intestinal barrier functioning and preventing LPS translocation and its implications. Omega-3 PUFA supplementation has also been studied as a means of mental health disorders management, but the evidence is still controversial. A possible protective impact of fish consumption on depression has been suggested by various studies, as well as a possible protective effect of dietary PUFAs on moderate cognitive impairment. A recent review of meta-analyses indicated that omega-3 PUFA supplementation might have potential value in mental health disorders, but data credibility is still weak.

Dietary lipids and obesity

Last but not least, obesity and its management is another field that dietary lipids intake seems to impact with their mechanisms. A diet high in PUFA has been shown to lower the total mass of subcutaneous white adipose tissue (the predominant fat type in human bodies), reduce blood lipid levels, and improve insulin sensitivity. In a study comparing PUFA and MUFA isocaloric intake, PUFA was more advantageous and lowered visceral adiposity in patients with central obesity. By stimulating brown adipose tissue, which aids energy expenditure through its elevated thermogenic activity, omega-3 PUFAs seem to elicit these positive effects in fat tissue, thus being useful in preventing and/or managing obesity. Another related study compared PUFA to SFA overfeeding in dietary surplus conditions that aimed to increase weight by 3%. While SFA overfeeding led to weight gain, primarily through the expansion of the visceral adipose tissue, PUFA overfeeding also led to weight gain, but because of a greater expansion of lean tissue mass.

To sum up, dietary fats are an essential part of the human diet with many important physiologic functions, including cell function, hormone production, energy, and nutrient absorption. Moreover, dietary fat consumption is associated with positive outcomes in regard to cardiovascular disease, metabolic syndrome, cancer, and depression. Therefore, there is no reason to demonize this valuable dietary component, incriminating it for irrelevant adverse health outcomes, primarily weight loss failure and obesity.

References

1. Astrup A, Magkos F, Bier DM, Brenna JT, de Oliveira Otto MC, Hill JO, King JC, Mente A, Ordovas JM, Volek JS, Yusuf S, Krauss RM. Saturated fats and health: A reassessment and proposal for food-based recommendations: JACC State-of-the-Art review. J Am Coll Cardiol. 2020;76(7):844-857. DOI: 10.1016/j.jacc.2020.05.077

2. Bojková B, Winklewski PJ, Wszedybyl-Winlewska M. Dietary fat and cancer-Which is good, which is bad, and the body of evidence. Int J Mol Sci. 2020;21(11):4114. DOI: 10.3390/ijms21114114

3. Custers, Emma EM, Kiliaan, Amanda J. Dietary lipids from body to brain. Prog Lipid Res. 2022;85:101144. DOI: 10.1016/j.plipres.2021.101144

4. de Souza RJ, Mente A, Maroleanu A, Cozma AI, Ha V, Kishibe T, Uleryk E, Budylowski P, Schünemann H, Beyene J, Anand SS. Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies. BMJ. 2015;351:h3978. DOI: 10.1136/bmj.h3978

5. Gao X, Su X, Han X, Wen X, Cheng C, Zhang S, Li W, Cai J, Zheng L, Ma J, Liao M, Ni W, Liu T, Liu D, Ma W, Han S, Zhu S, Ye Y, Zeng F-F. Unsaturated fatty acids in mental disorders: An umbrella review of meta-analyses. Adv Nutr. 2022;13(6):2217-2236. DOI: 10.1093/advances/nmac084

6. Liu AG, Ford NA, Hu FB, Zelman KM, Mozaffarian D, Kris-Etherton PM. A healthy approach to dietary fats: understanding the science and taking action to reduce consumer confusion. Nutr J. 2017;16(1):53. DOI: 10.1186/s12937-017-0271-4

7. Poli A, Agostoni C, Visioli F. Dietary fatty acids and inflammation: Focus on the n-6 series. Int J Mol Sci. 2023;24(5):4567. DOI: 10.3390/ijms24054567

8. Saini RK, Keum Y-S. Omega-3 and omega-6 polyunsaturated fatty acids: Dietary sources, metabolism, and significance-A review. Life Sci. 2018;203:255-267. DOI: 10.1016/j.lfs.2018.04.049

9. Saini RK, Prasad P, Sreedhar RV, Naidu KA, Shang X, Keum Y-S. Omega-3 polyunsaturated fatty acids (PUFAS): Emerging plant and microbial sources, oxidative stability, bioavailability, and health benefits-A review. Antioxidants (Basel). 2021;10(10):1627. DOI: 10.3390/antiox10101627

10. Zhao M, Chiriboga D, Olendzki B, Xie B, Li Y, McGonigal LJ, Maldonado-Contreras A, Ma Y. Substantial increase in compliance with saturated fatty acid intake recommendations after one year following the American Heart Association diet. Nutrients. 2018;10(10):1486. DOI: 10.3390/nu10101486

11. Zhu Y, Bo Y, Liu Y. Dietary total fat, fatty acids intake, and risk of cardiovascular disease: a dose-response meta-analysis of cohort studies. Lipids Health Dis. 2019;18:91. DOI: 10.1186/s12944-019-1035-2

Dietary Carbohydrates: Catalysts of Physical Performance and Regulators of Overall Health

j.oswald@hyperionhealth.ca (Jesse Oswald) — Mon, 06 Jan 2025 16:00:01 GMT

Key points

A recommended total carbohydrate intake ranges between 45-60% of the daily calories with a bottom value of 130 g/day to ensure the maintenance of adequate brain function
Metabolic disorders, such as obesity and diabetes, disrupt fat utilization at rest, promoting an increased reliance on carbohydrates for energy production
The phosphagen energy system, aerobic oxidative system, and anaerobic lactic system are the three energy systems activated during different types of exercise
Consuming a rich in complex carbohydrates meal 2-3 hours before engaging in endurance exercise lasting >60 minutes can help prevent hypoglycemia
Optimal post-workout recovery is achieved with co-ingestion of 1-2.2 g/kg carbohydrates and 0.3-5 g/kg proteins in a post-workout meal
Excessive consumption of simple carbohydrates found in processed foods, refined grains, and deserts poses considerable risks for metabolic and overall health
Complex carbohydrates, especially dietary fibers, found in whole grains, fruits, and vegetables, offer diverse health advantages

Over the years, social media has fostered a negative view towards carbohydrate (CHO) consumption, advocating that dietary patterns aiming at weight loss should limit or even exclude carbohydrates. These beliefs intensify the debate about the dietary intake of the three primary energy sources (carbohydrates, proteins, and fats) during rest and physical activity. Individuals derive about half of their daily energy requirements from carbohydrates on average. However, food abundance and easy accessibility have led to excess carbohydrate intake, particularly plain sugars, placing a significant metabolic burden on the body. Therefore, being mindful of carbohydrates' quantity, quality, and distribution throughout the day is essential for establishing a well-balanced approach to nutrition and maintaining overall health.

Carbohydrate classification

Carbohydrates are the primary energy source of the human diet. Particularly, each gram of any type of CHO renders four calories. They can be classified into simple and complex carbohydrates, depending on the amount of sugar they contain.

Simple carbohydrates

Simple carbohydrates are short-chain sugar molecules that can be quickly digested, inducing a sharp increase in blood glucose levels. This feature makes them an immediate source of energy. However, the blood glucose spikes are followed by an equally rapid drop in glucose levels, leading to feelings of hunger and fatigue. This type of carbohydrate is divided into two major categories, monosaccharides, and disaccharides, based on the sugar units they consist of.

Monosaccharides are composed of a single sugar unit and include glucose, fructose, and galactose. They are naturally present in honey and dried fruits but can also be found in elevated quantities in manufactured goods. Fructose, for example, particularly high-fructose corn syrup, is a constituent of many soft drinks and processed foods.

Disaccharides, on the other hand, consist of two sugar units, composing sucrose, lactose, and maltose. Sucrose is naturally derived from sugarcane, sugar beets, honey, and dates, while lactose is the sugar of dairy products. Maltose is predominantly found in beer, barley, and various cereals.

Complex carbohydrates

Complex carbohydrates are also divided into subgroups: oligosaccharides, polysaccharides, and dietary fiber. Oligosaccharide molecules constitute a chain of 3-10 sugar units, while polysaccharides comprise ≥ 10 sugar units. Fibers are a distinct category, including both oligo- and polysaccharide components. Contrary to simple carbohydrates, complex carbohydrates increase blood glucose progressively, providing prolonged feelings of satiety. As their digestion and absorption are gradual, quick energy depletion is averted.

Raffinose, stachyose, maltodextrin, and inulin are well-known representatives of the group of oligosaccharides. Various fruits, vegetables, legumes, and whole grains are rich in oligosaccharides.

Likewise, typical polysaccharides encompass glycogen and starch. Polysaccharides exist in high concentrations in plant-based food sources such as fruits, vegetables, legumes, whole grains, and nuts.

Several oligo- and polysaccharides belong to another special type of complex carbohydrates: dietary fiber. Examples of dietary fibers are pectins, beta-glucans, cellulose, and hemicellulose, all found in plant foods. Dietary fibers cannot be digested and absorbed by the small intestine; hence, they end up in the colon, where they are further metabolized by the gut microbiota or excreted. Based on their ability to be soluble in water, dietary fibers are further categorized into soluble and insoluble, exhibiting diverse physiological effects.

Carbohydrate intake recommendations

To clarify the recommended dietary carbohydrate intake, the Food and Nutrition Board of the Institute of Medicine released guidelines for dietary reference intakes (DRIs), encompassing recommendations for carbohydrate consumption. According to these guidelines, 45-60% of the daily calories should be obtained from carbohydrates, with added sugars not exceeding 10% of the total daily calorie intake. Based on the average glucose requirement for brain function, the minimum carbohydrate intake was set at 130 g/d for both adults and children, with adjusted values for pregnant and lactating women. Recommendations regarding fibers suggest an intake of 25-30 g/d for adults, while the target intake is lower in children.

Carbohydrate metabolism and stores

After a meal, carbohydrates are broken down to glucose, the primary fuel for energy needs. Once glucose has entered the circulation and uptaken by the body's tissues, it undergoes a series of complex enzymatic and biochemical reactions. This process finally facilitates the adenosine triphosphate (ATP) synthesis, the primary energy unit within the cells.

In case of a glucose surplus arising from ingested calories surpassing energy requirements, glucose is stored in the liver and muscles in the form of glycogen or converted into fat in the liver and adipose tissue. On the other hand, fasting periods, for example, during sleep or energy-demanding activities, may necessitate the mobilization of glycogen as the circulating glucose can shortly be depleted.

Carbohydrate utilization at rest and during exercise

Typically, during rest periods, the organism demands the necessary amounts of carbohydrates to sustain its proper functioning and homeostasis. Therefore, although energy expenditure is relatively low and the main energy substrate contributing to energy expenditure is fat, carbohydrates are still required for the optimal function of the brain, kidneys, reproductive system, and other vital systems. As already mentioned, under normal circumstances, the contribution of carbohydrates to energy production is minimal, as fats constitute the main energy substrate. The way the body utilizes energy substrates (fats and carbohydrates) at rest may be altered in case of metabolic disorders, such as obesity, diabetes, metabolic syndrome, etc., leading to an increased reliance on carbohydrates for energy production. This is due to impaired insulin action (hyperinsulinemia and insulin resistance) and glucose metabolism (hyperglycemia) related to such metabolic disturbances. As a result, fat oxidation is disrupted since a permanent surplus of glucose in the blood is ready to be oxidized for energy production. Thus, the body shifts towards an increased utilization of carbohydrates for energy production.

During physical activity, three major energy systems are activated in order to produce ATP, meaning the energy required to drive and support exercise: phosphocreatine (the phosphagen energy system), the aerobic oxidative system, and the anaerobic lactic (glycolytic) energy system.

The phosphocreatine energy system is immediately activated in the first 1-10 seconds of high-intensity exercise like sprints, track cycling, weightlifting, etc. This system utilizes the most readily available energy source, phosphocreatine (PCr). It is unable, though, to provide sufficient energy in the case of high-intensity exercise that lasts beyond 10 seconds (approximately 30 seconds-2 minutes). Therefore, the activation of the glycolytic system is necessary. The glycolytic energy system offers the required energy by oxidizing glucose and glycogen. Overall, the combination of the two systems is activated during resistance (high-intensity explosive exercises of decreased duration) and high-intensity interval (HIIT) exercise due to the elevated demand for immediate and sustained ATP production.

Conversely, the aerobic oxidative energy system is the long-term one activated in the case of low-to-moderate-intensity continuous endurance exercise, as the previous systems cannot provide the energy fuels needed for extended physical activity.

Exercise intensity is one of the primary parameters determining the utilization of carbohydrates as an energy substrate.

In low-to-moderate intensity endurance exercise, such as running, rowing, cycling, etc., where the intensity ranges between 50-75% of an individual’s VO2max or 60-80% of their heart rate peak, carbohydrates contribution in energy production is about 30-40%, meaning fat still remains the primary energy fuel. As the intensity of endurance exercise increases, meaning at exercise intensities >70% VO2max or > 80% of the heart rate peak, carbohydrates become the predominant energy fuel, accounting for up to 70% of the total energy expenditure.

Pre-workout carbohydrate recommendations

With glycogen stores representing only about 5% of the total energy storage, endogenous carbohydrates may not be adequate for prolonged moderate-to-high-intensity exercise. Therefore, consuming a pre-exercise meal rich in carbohydrates ensures both the accessibility of an immediate energy source (glucose) and optimizing glycogen stores. This aids in ensuring sufficient energy supply during physical activity, considering the carbohydrate oxidation rate, which typically ranges between 30-60 g/h. Studies have demonstrated a beneficial effect on exercise performance and prevention of hypoglycemia by consuming a meal rich in complex carbohydrates 2-3 hours before endurance exercise lasting more than 60 minutes.

The ingestion of low glycemic index carbohydrates, such as oats, quinoa, legumes, various fruits, and vegetables, is believed to contribute to preserving euglycemia during periods of exercise owing to the gradual release of glucose in the bloodstream and the steady insulin response.

Efficient glycogen replenishment

As already mentioned, physical activity, especially prolonged endurance exercise of moderate intensity, leads to depletion of glycogen stores, thus generating fatigue and exhaustion. Therefore, nutritional replenishment should be a cornerstone of all athletes’ recovery regimen.

The glycogen resynthesis process begins with physical activity termination and lasts 6 to 8 hours. The optimal carbohydrate intake is estimated at 1.2 g/kg/h. High glycemic index carbohydrates, meaning carbohydrates that cause a prompt spike in blood sugar, have been shown to accelerate the process of glycogen restoration, especially when only short-term recovery is available. This is due to the higher stimulation of insulin response triggered by ingesting high glycemic index carbohydrates, compared to low glycemic index carbohydrates. Despite the potential advantageous effects of high glycemic index carbohydrates in short-term recovery, their potency diminishes in prolonged recovery periods. Moreover, consuming a blend of dietary sources containing both glucose and fructose seems to be the most effective approach to glycogen restoration.

Lastly, evidence regarding post-workout nutrition suggests simultaneous adequate ingestion of both carbohydrate and protein amounts for muscle recovery and muscle gain purposes. Particularly, co-ingestion of about 1-2.2 g/kg carbohydrates, along with 0.3-5 g/kg proteins in a post-workout meal, is recommended as the optimal approach for post-exercise recovery.

Simple carbohydrates and overall health

Carbohydrates, in terms of quality and quantity, play a vital role not only in fueling exercise but in sustaining overall health as well. Increased consumption of foods containing simple carbohydrates, meaning high glycemic index carbohydrates, such as refined grains, sodas, desserts, etc., increases the risk for metabolic diseases, including obesity and type II diabetes.

The elevated glycemic index results in a rapid rise in blood glucose and, subsequently, an abrupt and uncontrolled secretion of insulin, causing a condition known as hyperinsulinemia. Chronic hyperinsulinemia can lead to insulin resistance, a condition where insulin’s ability to lower blood glucose levels is impaired, resulting in hyperglycemia and possibly type II diabetes. Type II diabetes is a medical condition characterized by insulin resistance due to both persistent hyperinsulinemia and the body's progressive decline in the body's ability to produce insulin. The excessive consumption of simple sugars is among the primary contributing factors to type II diabetes. Therefore, adjusting diet and modifying the quality of the ingested carbohydrates holds great significance in diabetes management.

Obesity is another clinical condition that can arise due to the excessive consumption of simple carbohydrates. The increased consumption of simple carbohydrates diminishes satiety signals by interfering with the regulation of dopaminergic and serotonergic systems in the hypothalamus that are responsible for appetite control. This leads to increased caloric intake and a glucose surplus, which is stored as fat, predominantly in the abdominal area (visceral fat). An increase in body fat, especially visceral fat, is associated with numerous health risks, including obesity, cardiovascular diseases, diabetes, etc.

Research has also focused on the relationship between CHO consumption and cancer, with several studies demonstrating that the elevated consumption of simple carbohydrates activates pathways that enhance cancer cell proliferation, resulting in tumor growth. However, the research is still ongoing, and no definite recommendations or conclusions can be made.

The health benefits of dietary fiber

Conversely to the detrimental effects of simple carbohydrates on metabolic, cardiovascular, and overall health, consuming complex carbohydrates, particularly dietary fibers, exerts significant health-promoting effects.

Studies have shown the efficiency of soluble dietary fibers, including beta-glucans, pectins, and inulin, in decreasing blood cholesterol, inhibiting atherosclerosis, and regulating blood glucose levels. Ingesting this type of fiber can also increase satiety and alleviate constipation. Moreover, water-soluble fibers are utilized by the gut microbiome, as they are highly fermentable by the gut bacteria. This process contributes to the production of short-chain fatty acids (SCFA), which serve as an energy substrate, regulate cholesterol synthesis, and exhibit anti-inflammatory and apoptotic properties. In other words, SCFA mediate part of the protective effect of soluble dietary fibers on cardiovascular, metabolic diseases, and cancer.

Another type of dietary fiber, resistant starch, is also fermented by gut bacteria, exerting the beneficial effects previously mentioned. It also contributes to regulating appetite while also exhibiting beneficial effects on blood glucose regulation and insulin sensitivity. Resistant starch is primarily formed in starchy food by cooling it after it is cooked. It also exists in raw starchy foods such as unripe bananas.

Lastly, insoluble fibers, such as cellulose and hemicellulose, effectively enhance fecal mass, decreasing the stool’s transit time in the intestine. Additionally, they induce satiety, thus contributing to weight loss, and also present anti-inflammatory effects.

Overall, carbohydrates are vital macronutrients that constitute major energy fuels, ensuring optimal brain and body function. During physical activity, their contribution shifts, with different energy systems being activated depending on the exercise intensity. Sufficient pre- and post-workout carbohydrate intake is crucial for achieving peak performance, improving strength, and supporting recovery. Furthermore, their impact on overall health has various dimensions. While simple carbohydrate consumption constitutes a central pathophysiologic mechanism for developing metabolic disorders such as obesity and diabetes, consuming complex carbohydrates, especially dietary fibers, provides multiple benefits to overall health.

REFERENCES

Alghannam AF, Gonzalez JT, Betts JA. Restoration of Muscle Glycogen and Functional Capacity: Role of Post-Exercise Carbohydrate and Protein Co-Ingestion. Nutrients. 2018 Feb 23;10(2):253. DOI: https://doi.org/10.3390/nu10020253
Clemente-Suárez VJ, Mielgo-Ayuso J, Martín-Rodríguez A, Ramos-Campo DJ, Redondo-Flórez L, Tornero-Aguilera JF. The Burden of Carbohydrates in Health and Disease. Nutrients. 2022 Sep 15;14(18):3809. DOI: https://doi.org/10.3390/nu14183809
DeMartino P, Cockburn DW. Resistant starch: impact on the gut microbiome and health. Curr Opin Biotechnol. 2020 Feb;61:66-71. DOI: https://doi.org/10.1016/j.copbio.2019.10.008
Jeukendrup A. A step towards personalized sports nutrition: carbohydrate intake during exercise. Sports Med. 2014 May;44 Suppl 1(Suppl 1):S25-33. DOI: https://doi.org/10.1007/s40279-014-0148-z
Ludwig DS, Ebbeling CB. The Carbohydrate-Insulin Model of Obesity: Beyond "Calories In, Calories Out". JAMA Intern Med. 2018 Aug 1;178(8):1098-1103. DOI: 10.1001/jamainternmed.2018.2933
Maino Vieytes CA, Taha HM, Burton-Obanla AA, Douglas KG, Arthur AE. Carbohydrate Nutrition and the Risk of Cancer. Curr Nutr Rep. 2019 Sep;8(3):230-239. DOI: 10.1007/s13668-019-0264-3
Margolis LM, Allen JT, Hatch-McChesney A, Pasiakos SM. Coingestion of Carbohydrate and Protein on Muscle Glycogen Synthesis after Exercise: A Meta-analysis. Med Sci Sports Exerc. 2021 Feb 1;53(2):384-393. DOI: 10.1249/MSS.0000000000002476
Mul JD, Stanford KI, Hirshman MF, Goodyear LJ. Exercise and Regulation of Carbohydrate Metabolism. Prog Mol Biol Transl Sci. 2015;135:17-37. DOI: https://doi.org/10.1016/bs.pmbts.2015.07.020
Ormsbee MJ, Bach CW, Baur DA. Pre-exercise nutrition: the role of macronutrients, modified starches and supplements on metabolism and endurance performance. Nutrients. 2014 Apr 29;6(5):1782-808. DOI: https://doi.org/10.3390/nu6051782
P NPV, Joye IJ. Dietary Fibre from Whole Grains and Their Benefits on Metabolic Health. Nutrients. 2020 Oct 5;12(10):3045. DOI: https://doi.org/10.3390/nu12103045
Soliman GA. Dietary Fiber, Atherosclerosis, and Cardiovascular Disease. Nutrients. 2019 May 23;11(5):1155. DOI: https://doi.org/10.3390/nu11051155
Trumbo P, Schlicker S, Yates AA, Poos M; Food and Nutrition Board of the Institute of Medicine, The National Academies. Dietary reference intakes for energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein and amino acids. J Am Diet Assoc. 2002 Nov;102(11):1621-30. DOI: https://doi.org/10.1016/S0002-8223(02)90346-9
Wu J, Yang K, Fan H, Wei M, Xiong Q. Targeting the gut microbiota and its metabolites for type 2 diabetes mellitus. Front Endocrinol (Lausanne). 2023 May 9;14:1114424. DOI: https://doi.org/10.3389/fendo.2023.1114424

The Place of Stimulants in the Field of Sports

j.oswald@hyperionhealth.ca (Jesse Oswald) — Mon, 30 Dec 2024 16:00:03 GMT

Key points

Stimulants belong to three distinct categories, each of which has a different mechanism of action: sympathomimetic amines, psychomotor stimulants, and central nervous system (CNS) stimulants
The World Anti-Doping Agency (WADA) has banned the use of some of the most known stimulants, such as amphetamines and ephedrine, by professional athletes
Stimulants are used by elite athletes for performance-enhancing purposes, to mitigate physical and mental fatigue as well as to lose weight ahead of competition in sports with weight classes
Long-term stimulant use can induce serious health complications related to major body systems, such as the heart and the brain

The number of athletes, especially at top levels of competition, as well as the general population reported to be using stimulants, has markedly increased in recent years. The term stimulants covers a broad class of substances directly affecting the central nervous system (CNS). Many individuals use these drugs for various reasons, including performance enhancement, medical benefits, and recreational purposes. They may be legal or illegal. Since one of the primary mechanisms through which stimulants exert their effects is increased blood flow and heart rate, cardiac dysfunction is one of the main concerns associated with their use, along with other adverse effects that will be discussed later. Therefore, in the following article, you will find information about the main stimulant classes and their way of action, the constitutional rules around their use, the negative effects regarding their use, contraindications, and finally, a short overview of the most popular ones.

Stimulants classification

According to the International Olympic Committee (IOC), stimulants are classified as sympathomimetic amines, psychomotor stimulants, and central nervous system (CNS) stimulants. Sympathomimetic amines mimic or potentiate the effects of the sympathetic nervous system (SNS) through the neurotransmitter norepinephrine. Psychomotor stimulants, such as amphetamines, cocaine, and caffeine, have several effects related to mental function and behaviour, including excitement and euphoria, motor activity increase, and fatigue mitigation. CNS stimulants increase the activity of the CNS's respiratory and vasomotor centres and reflexes.

Stimulant usage by athletes

Stimulants exert multiple effects pursued by elite and professional athletes. For example, athletes competing in aesthetic sports, such as artistic gymnastics, or in sports with specific weight classes, such as wrestling, may seek stimulant prescriptions for a weight loss advantage. Other athletes competing in team sports, like basketball and football, seek stimulants for increased alertness as well as reduced and delayed fatigue. Other athletes not only use stimulants for performance-enhancing but for recreational purposes as well.

Rules around stimulant use

The primary method of administration for stimulants is oral intake. Recreational administration of stimulants also occurs by intramuscular and/or intravascular injection, smoking, and intranasal administration. Stimulants can be found in their pure form or over-the-counter sports products, such as pre-workout supplements. In any case, since there is confusion around the rules and recommendations for stimulant use by athletes, the World Anti-Doping Agency (WADA) only permits athletes to take stimulants if deemed necessary by their physicians for therapeutic use. Therapeutic use of stimulants includes attention deficit hyperactivity disorder (ADHD), narcolepsy, asthma, and nasal and sinus congestion, among others. In this case, elite athletes who compete internationally and whose physicians feel they should continue stimulant use must obtain a Therapeutic Use Exemption (TUE) from WADA.

The adverse effects of stimulants

Given the harmful effects of stimulants, the existence of an organization like WADA is deemed necessary. Therefore, banned stimulants include amphetamines, methamphetamines, ephedrine, pseudoephedrine, cocaine, and other substances with similar chemical structures and biological effects. Regarding permitted stimulants, they can still induce a broad range of short-term and long-term adverse effects and may be physically dangerous when used by athletes who are pushing their bodies to extremes. Specifically, long-term stimulant use can result in decreased appetite and weight loss, headaches, anxiety, insomnia, and shortness of breath. More severe health effects include psychosis, paranoia, stroke, hypertension or hypotension, arrhythmias, myocardial infarction and sudden cardiac death, seizures, and coma. The major factors influencing these outcomes are the user’s body weight, the specific stimulant used, the dose of the agent taken, and tolerance.

There are also numerous relative contraindications to the use of stimulants, including individuals with established cardiovascular disease, severe hypertension, untreated hyperthyroidism, glaucoma, and cardiac arrhythmias. Younger athletes under the age of 12 and pregnant women should also avoid using stimulants.

The most known stimulants are shortly reviewed below.

Caffeine

It is the most commonly used stimulant in the world, employed for recreational as well as performance enhancement purposes. As the most commonly used stimulant, caffeine is found in various drinks and foods, such as tea, coffee, and chocolate. It is consumed habitually in many countries worldwide, given its mild to moderate stimulant effects, which promote alertness and increased energy levels. Caffeine is a relatively safe stimulant.

Amphetamines

They exert multiple effects, including general and cognitive performance enhancement along with euphoric effects. Their general mechanism of action is the stimulation of catecholamines, specifically norepinephrine and dopamine. These catecholamines lead to increased energy levels, euphoria, increased libido, and higher cognition. Athletes use many medications related to the amphetamine class of drugs for physical performance enhancement, including increased strength, acceleration, anaerobic capacity, time to exhaustion, and maximum heart rates. Still, all these drugs fall under bans by WADA. Methamphetamine, a kind of amphetamine, is a widely trafficked and illegal drug mainly used for recreational purposes.

Ephedrine and pseudoephedrine

They belong to the sympathomimetic amines class of stimulants whose primary mechanism is increased norepinephrine activity at the adrenergic receptors. They are both used as nasal and sinus decongestants caused by the common cold. Athletes may use over-the-counter formulations containing these substances to improve lung function and lower body strength and power before exercise.

Cocaine

It belongs to the psychomotor stimulants and acts through the blockade of the dopamine transporter protein, resulting in increased dopamine levels. It can temporarily increase energy levels, focus, alertness, and confidence, effects pursued by professional athletes who use it. However, in the long term, cocaine can only harm athletic performance since its use is associated with sleep disruptions, fatigue, anxiety, mood swings, reduced focus, arrhythmias, and hypertension, among others. Cocaine is also used for recreational purposes.

Overall, any performance enhancement that an athlete may receive from taking a stimulant raises an important ethical concern. An essential value in sports is fair competition. Athletes should play by the same rules and perform without external influences that may favour them. At high levels of competition, a performance advantage of even one hundred of a second can make a significant difference in first place, opportunities, and financial earnings. Applying this argument to the professional sports field, no use of performance-enhancing substances is fair and, therefore, should be prohibited.

References

1. Avois L, Robinson N, Saudan C, Baume N, Mangin P, Saugy M. Central nervous system stimulants and sport practice. Br J Sports Med. 2006;40(Suppl1):i16-i20. DOI: 10.1136/bjsm.2006.027557

2. Berezanskaya J, Cade W, Best TM, Paultre K, Kienstra C. ADHD prescription medications and their effect on athletic performance: A systematic review and meta-analysis. Sports Med-Open. 2022;8(1):5. DOI: 10.1186/s40798-021-00374-y

3. Farzam K, Faizy RM, Saadabadi A. Stimulants. In: StatPearls. StatPearls Publishing, Treasure Island (FL);2022. DOI: 30969718

4. Garner AA, Hansen AA, Baxley C, Ross MJ. The use of stimulant medication to treat Attention-Deficit/Hyperactivity Disorder in elite athletes: A performance and health perspective. Sports Med. 2018;48(3):507-512. DOI: 10.1007/s40279-017-0829-5

5. Reardon CL, Factor RM. Considerations in the use of stimulants in sport. Sports Med. 2016;46(5):611-617. DOI: 10.1007/s40279-015-0456-y

Linking Inflammation, Diabetes, and Breath Analysis

j.oswald@hyperionhealth.ca (Jesse Oswald) — Mon, 23 Dec 2024 16:00:11 GMT

Diabetes is as common as it is misunderstood. Perhaps the most common misconception is that

it’s a consequence of carbohydrate overconsumption. Perhaps the most straightforward proof that diabetes is not a result of carbohydrate consumption is the fact that humans consumed significantly more carbohydrates in previous centuries without triggering anything close to the diabetes epidemic our world faces today. Clearly, the fact that diabetes was practically nonexistent before the 1950s but has exponentially propagated in just a few decades indicates that it constitutes a much more complex metabolic dysfunction that is inextricably linked to our modern way of life. This article explains the pathophysiological origins of diabetes and its link to chronic inflammation and fat accumulation. A comprehensive 7-step overview explores how inflammation causes insulin resistance, leading to fat accumulation, low energy levels, and, ultimately, diabetes. Last, we discuss how the progression of this condition can be monitored reliably through breath analysis.

Step 1 - Onset of inflammation

Exogenous deleterious factors stimulate the production of inflammatory substances in our body’s response to mitigate the negative impact such factors may induce.

Inflammatory cytokines, such as tumour necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), can activate various signalling pathways that interfere with insulin signalling. This disruption often involves inhibiting insulin's ability to promote glucose uptake and utilization in cells, leading to insulin resistance. Some of the most prominent inflammatory factors include:

Excessive calorie consumption
Junk food
Lack of micronutrient intake
Lack of physical exercise
Lack of sleep

In our recent article about inflammation, we dive deeper into the exogenous stimuli that trigger our body’s inflammatory responses and the principal prevention mechanisms we can apply daily.

Step 2 - Inflammation neutralizes our cells’ insulin receptors (Insulin Resistance)

Inflammatory markers exert their detrimental effects on insulin receptors of cells through various molecular mechanisms. These markers initiate inflammatory pathways that interfere with insulin signalling cascades upon activation. This interference includes the increased phosphorylation of serine residues on insulin receptor substrate-1 (IRS-1), diminishing its ability to relay signals downstream in the insulin pathway. Additionally, inflammatory cytokines can directly hinder insulin receptor activity, possibly through receptor internalization or impaired autophosphorylation. Activation of stress-sensitive kinases, such as JNK and IKK, further exacerbates insulin resistance by phosphorylating IRS-1, impeding its interaction with downstream signalling molecules. Furthermore, inflammatory signals disrupt insulin-stimulated glucose transporter type 4 (GLUT4) translocation to the cell membrane, consequently reducing glucose uptake. These molecular disruptions culminate in insulin resistance, a pivotal factor in the pathogenesis of conditions like type 2 diabetes, where chronic low-grade inflammation plays a significant contributory role.

Step 3 - Insulin resistance causes fuel utilization dysfunction

When we consume food, our pancreas responds by secreting insulin, the hormone that enables glucose to enter cells and be oxidized. When cells, including muscle cells, become insulin resistant, there's an impaired ability to use glucose for energy efficiently. Cellular desensitization to insulin means that they no longer respond to insulin and are thus unable to absorb and utilize glucose. To compensate for this reduced glucose utilization, there is an increased reliance on alternative energy sources, such as fatty acids.

Step 4 - Fuel utilization dysfunction leads to fat accumulation and lower energy levels

In insulin-resistant states, cells, especially muscle cells, enhance their uptake of fatty acids and prioritize lipid storage over glucose utilization. This shift towards increased fatty acid uptake and storage contributes to the accumulation of intramyocellular lipids (i.e., the buildup of fat within our muscles and organs). Essentially, when cells become insulin resistant, they favour fat accumulation because their ability to respond to insulin's signals for glucose uptake properly is compromised. Since glucose is the primary energy source for cells, their inability to absorb it deprives them of the valuable fuel they need, leading them to develop feelings of fatigue and low energy levels.

Step 5 - Accumulated fat causes more inflammation and insulin resistance

Both visceral fat, found around internal organs in the abdominal cavity, and intramyocellular fat, which accumulates within muscle cells, are sources of inflammatory markers. Visceral fat is highly metabolically active and secretes pro-inflammatory cytokines and adipokines such as TNF-alpha, IL-6, and leptin. These substances contribute to chronic low-grade inflammation, a key factor in developing conditions like insulin resistance and cardiovascular diseases. Similarly, intramyocellular fat accumulation disrupts cellular processes and is associated with increased production of inflammatory markers. TNF-alpha, IL-6, and other cytokines released by intramyocellular fat can impair insulin signalling within muscle cells, further contributing to metabolic dysfunction and insulin resistance. Overall, both visceral and intramyocellular fat play roles in systemic inflammation through the secretion of inflammatory markers, which have significant implications for metabolic health and the development of chronic diseases.

Step 6 - Insulin resistance leads to elevated blood sugar (Pre-diabetes)

In insulin resistance, cells become less responsive to insulin signals, particularly muscle, fat, and liver cells. Typically, insulin facilitates glucose uptake into these cells by promoting the translocation of glucose transporter proteins, such as GLUT4, to the cell membrane. However, this process is impaired in insulin resistance, resulting in reduced glucose uptake by cells, particularly in muscle and fat tissues. Consequently, less glucose is taken from the bloodstream and sent into cells for energy use.

Step 7 - Pancreas goes on over-drive and ultimately fails (Diabetes)

Initially, the body attempts to compensate for insulin resistance by producing more insulin (hyperinsulinemia) to overcome the decreased responsiveness of cells. This compensatory mechanism helps maintain relatively normal blood sugar levels in the early stages of insulin resistance. However, over time, the pancreas may fail to sustain this increased insulin secretion, leading to a decline in insulin production and exacerbating hyperglycemia.

Breath analysis, an easy and reliable monitoring tool for metabolic function.

As described in the 7-step process above, the fundamental consequence that unilaterally describes metabolic dysfunction is the cells’ inability to metabolize glucose and instead favours nutrient storage overutilization for energy production. Simply put, when consuming food, metabolic impaired individuals store it instead of using it to power the body. Measuring the Respiratory Exchange Ratio (RER), the balance between carbon dioxide production over oxygen consumption during the post-prandial state (i.e., after a meal), is perhaps the easiest and most reliable method for understanding whether our cells can utilize the food we consume. In metabolically healthy individuals, the respiratory exchange ratio will rise precipitously after food consumption, indicating that cells absorb and use the nutrients ingested. Conversely, in metabolically compromised individuals, RER will exhibit a blunt increase, indicating that nutrients cannot enter cells, get oxidized, and produce carbon dioxide that would otherwise cause RER to rise. Breath analysis not only provides a direct measure of the fundamental mechanism defining metabolic dysfunction but also constitutes a non-invasive and easy assessment. This is in contrast to traditionally used methods such as the euglycemic insulin clamp, which requires trained medical professionals to perform blood analysis and be present at a medical facility.

Inflammation: A Tightly Regulated Biological Response that, if Uncontrolled, Can Turn out Fateful

j.oswald@hyperionhealth.ca (Jesse Oswald) — Mon, 16 Dec 2024 16:00:08 GMT

Key points

Inflammation is a physiological, tightly regulated, protective process in response to harmful stimuli, such as pathogens, trauma, chemicals, etc.
Chronic inflammation is associated with the development of severe chronic health issues, such as cardiovascular disease, type II diabetes, cancer, neurodegenerative and autoimmune diseases
The most important causative factors of chronic inflammation are obesity and specifically visceral fat, stress, sleep disturbances, environmental chemicals, and unhealthy dietary constituents and patterns
Regular exercise, adherence to healthy dietary patterns, and mind-body interventions have the potential to decrease or even reverse chronic inflammation

Over the last decade, there has been much discussion about inflammation and whether there is such a thing as chronic inflammation, as well as anti-inflammatory agents in terms of food and botanical constituents that could effectively battle it. It seems that it all adds up since chronic inflammation does exist and is at its peak rate, probably due to the contemporary lifestyle. In this post, topics such as what inflammation is as a biological process and what may cause it, its relation to lifestyle factors such as diet, exercise, and environmental chemicals, as well as its implication with chronic severe diseases such as obesity, type II diabetes, and cardiovascular disease will be discussed.

What really inflammation is and how is it caused

Inflammation is a physiological, tightly regulated, protective process in response to harmful stimuli. Insults that can trigger inflammation include:

Infection from pathogenic microorganisms like bacteria, viruses, or fungi
Tissue damage from trauma
Necrotic cells of human tissue remaining after fighting a harmful agent
External injuries like scrapes
Effects of irritants and toxic compounds like chemicals
Irradiation

The goal of inflammation is to destroy the harmful stimuli that initiated it and start the repair process, restoring the involved tissues to their pre-inflamed state and thus re-establishing homeostasis. Therefore, acute inflammation, which resolves in a few days after eradicating the inflammatory stimulus, is a beneficial, biologically appropriate process required for regaining tissue homeostasis after damage within the human body has occurred. Symptoms associated with signs of acute inflammation include redness, heat, swelling, pain, and temporary loss of function at the site of inflammation.

The acute inflammatory response involves the recruitment of immune system cells, known as leucocytes, such as neutrophils, macrophages, monocytes, etc. These cells release inflammatory mediators, including reactive oxygen species (ROS) and inflammatory cytokines, such as interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-a (TNF-a) to kill the harmful agent. Since the goal of the acute inflammatory response is threat removal, without specificity or selectivity, collateral tissue damage is the inevitable consequence of massive ROS and cytokine production from leucocytes. Nevertheless, the resolution and self-termination of inflammation and the return to baseline status in days to weeks following the eradication of the inflammatory stimulus ensures survival and is not a pathological response.

If this elegant coordination of immune system adaptations fails to resolve or resolves inadequately since the inflammatory stimuli persist or propagate, inflammation can become chronic, self-directed, and thus dangerous. Specifically, the chronicity of inflammation is associated with excessive human tissue damage and various severe disease states, including inflammatory bowel disease, cancer, type II diabetes, heart disease, and autoimmune disorders, such as rheumatoid arthritis, multiple sclerosis, and systemic lupus erythematosus.

Although this relationship is very complicated and has not yet been elucidated, possible mechanisms connecting chronic inflammation with multiple health conditions include its association with elevated blood glucose levels and insulin resistance, with sodium, fluid retention, and hypertension, as well as with persistently elevated levels of cytokines such as IL-6 and C-reactive protein (CRP).

As mentioned above, chronic low-grade inflammation is associated with the development of severe chronic health issues, some of them being among the top causes of death worldwide, such as cardiovascular disease, type II diabetes, obesity, cancer, and neurodegenerative diseases. It could be actually argued that inflammation is not only associated with the disease condition itself but could also be involved in its pathogenesis and progression.

The common feature in these disease states is a silent low-grade inflammatory process, reflected as an increase in systemic plasma concentrations of inflammatory markers, such as cytokines (IL-1, IL-6, TNF-a, CRP, etc.). For instance, higher concentrations of inflammatory markers such as IL-6, TNF-a, and CRP have been shown to be associated with higher cardiovascular risk.

So, how can this chronic silent inflammatory process be triggered? Lifestyle factors, including smoking, alcohol consumption, poor diet, low levels of physical activity, exposure to environmental chemicals, and increased stress, contribute to the development of low-grade inflammation. Hence, strategies to improve overall lifestyle, including adhering to a healthy diet, regular exercise, adequate sleep, and social support, may be an effective approach to prevent chronic inflammation by modifying risk factors for chronic diseases associated with it.

The most important causative factors of chronic inflammation are discussed below.

Obesity and its central role in chronic inflammation

The vast majority of human fat tissue is of the white type; this type of fat is mainly located beneath the skin (subcutaneous adipose tissue) and around internal organs (visceral adipose tissue). White adipose tissue is not only an energy storage place but is also metabolically active, regulating several metabolic pathways, including immunity and inflammation. Specifically, adipocytes secrete numerous hormones and cytokines, collectively called adipokines. Some of them are pro-inflammatory, such as the hormones leptin and resistin, and the cytokines IL-6, CRP, and TNF-a, and some of them are anti-inflammatory, such as the hormone adiponectin.

While research has shown an association between both central obesity (visceral fat) and total obesity and inflammation, increased visceral fat is the primary source of chronic systemic low-grade inflammation.

Although the association is not clear yet, it seems that the link between central obesity and inflammation is the oversecretion of pro-inflammatory adipokines and free fatty acids by the visceral fat of obese individuals.

More specifically, obesity is linked to the enlargement of adipocytes (hyperplasia), leading to hypoxic conditions within these cells. As a result, a local inflammatory response is triggered, with the recruitment of immune cells, such as macrophages, and the subsequent accumulation of the pro-inflammatory cytokines IL-6 and TNF-a. IL-6, in turn, stimulates CRP production in the liver and the employment of more immune cells. Simultaneously, since fat tissue has a limited capacity to store energy, once this is exceeded, like in hyperplastic fat cells, lipolysis occurs within the cells, causing a release of free fatty acids into the circulation. Free fatty acids reinforce the release of pro-inflammatory cytokines and also directly mediate the inflammatory process.

The association between visceral fat and inflammation is actually proportional, meaning the higher the body weight and the body fat, the higher the levels of the pro-inflammatory adipokines and, therefore, the higher the level of inflammation.

It’s thus becoming evident that obesity predisposes to a pro-inflammatory state. Inflammation results in the massive production of ROS, also leading to oxidative stress. Both oxidative stress and inflammation statuses are strongly associated with chronic severe health complications, including cardiovascular disease, insulin resistance, hypertension, type II diabetes, obstructive sleep apnea, rheumatoid arthritis, dementia, and cancer. Therefore, obesity, especially large visceral fat volumes (central obesity), through its chronic inflammatory components, is involved in the pathogenesis and progression of cardiometabolic, neurodegenerative, and autoimmune diseases.

Inflammation caused by dysregulated sleep patterns

Lifestyle behaviours like sleep have been linked to heightened inflammatory responses.

Moreover, sleep issues have been associated with an increased risk of multiple inflammatory disorders, including cardiovascular disease and neurodegenerative diseases.

So, could chronic inflammation be the link connecting sleep issues with adverse public health outcomes?

Indeed, sleep disturbances in terms of sleep deprivation, insomnia, sleep restriction (sleeping less than 5 hours per night), and sleep fragmentation (nocturnal waking for ≥ 90 minutes) lead to increased inflammation due to changes in the immune system that trigger inflammatory responses.

A possible mechanism is that sleep disturbances induce a shift in the temporal profile of inflammatory responses, with increased production of the pro-inflammatory cytokines IL-6 and TNF-a during the day rather than during the night, leading to excessive levels of inflammation. Due to the increased production of IL-6, there is also a subsequent overproduction of CRP, further propagating inflammation. If the sleep disturbance is persistent, it leads to sustained activation of the inflammatory response and, thus, chronic inflammation.

Inflammation caused by chronic stress

Chronic stress in major life domains (relationships, work, finances) stimulates chronic inflammation in both men and women, which is reflected in the elevated CRP levels.

Additionally, emerging research suggests that social support and network may have a role in mitigating the psychological impact of major life stressors, thus attenuating their potential to cause chronic inflammation.

Moreover, mind-body interventions such as tai chi and meditation are emerging as promising strategies to reduce stress and thus decrease or even reverse inflammation, with effects on the severity or even the prevention of pathologies related to chronic inflammation, such as neurodegenerative and autoimmune diseases.

Inflammation caused by environmental chemicals

Chemical exposure in the environment, including long-term exposure to polycyclic aromatic hydrocarbons (PAHs), perfuoroalkyl substances (PFAs), and metal exposure, is responsible for causing chronic inflammatory responses.

PFAs have significant bioaccumulation potential and are widely used in food packaging, household cleaning products, cosmetics, etc.

PAHs are a group of chemicals formed during the incomplete combustion of coal, oil, gas, and garbage, including vehicle exhaust, coal tar, wildfires, agricultural burning, etc.

Regarding metal exposure, arsenic is a toxic metal widely distributed in the environment and is present in soil, food, and water, leading to unavoidable human exposure. Cadmium is mainly released from nickel-cadmium batteries, plastic stabilizers, fossil fuel combustion, and garbage incineration. Mercury pollution primarily comes from burning coal, non-ferrous metals, and cement production.

All these environmental pollutants can enter the human body through the respiratory tract, digestive tract, and skin and interact with the immune system, inducing a chronic inflammatory response and, thus, the possibility of chronic inflammatory diseases, such as cancer and autoimmune disorders.

The implication of exercise with chronic inflammation

Physical inactivity is one of the most important lifestyle factors associated with persistent systemic low-grade inflammation and, thus, an increased likelihood of inflammatory diseases. On the other hand, regular exercise possesses anti-inflammatory effects, thereby reducing disease risk.

The anti-inflammatory effects of regular exercise are attributed to several mechanisms, the most critical of which are increased fat oxidation and reduced visceral body fat stores. Specifically, exercise results in an increased skeletal muscle capacity to burn fat, resulting in increased fat oxidation in mitochondria and decreased overall lipid storage inside cells. Consequently, exercise helps limit visceral fat accumulation and adipose tissue expansion. Since fat tissue and visceral fat, in particular, are metabolically active and release pro-inflammatory mediators, as stated before, exercise limits inflammation activation by downregulating these pro-inflammatory mediators, including cytokines. Specifically, it has been shown that regular exercise reduces the levels of IL-1 and IL-6.

Moreover, active skeletal muscles secrete molecules known as myokines, which help counterbalance the pro-inflammatory effects of cytokines.

Since the inflammatory effects of physical inactivity run mostly through its impact on visceral fat and obesity, it could be supported that a link between physical inactivity, visceral fat accumulation (central obesity), and inflammation likely exists. However, the association between chronic systemic inflammation and physical inactivity is independent of obesity status.

Collectively, regular physical activity and its associated fat loss may offer prevention and treatment for various chronic diseases associated with low-grade inflammation. It is inexpensive and without the side effects of many pharmacological therapies and could be viewed as a natural remedy for recovering part of the inflammatory burden caused by modern lifestyles.

The implication of diet with chronic inflammation

Primarily, nutrition serves as the source of essential nutrients, providing energy and substrates for numerous metabolic functions.

In cases of obesity and, thus, chronic inflammation, a dietary pattern encompassing caloric restriction has been proven effective in reducing inflammation and metabolic dysfunction related to obesity status.

Besides the caloric restriction that can reduce chronic inflammation by decreasing visceral fat, several studies demonstrate an inverse association between inflammatory markers and adherence to healthy dietary patterns. Specifically, nutritional factors such as dietary fiber, antioxidants, and omega-3 fatty acids have been associated with decreased concentrations of inflammatory markers. In contrast, dietary factors, such as trans and saturated fat, sugar, and sodium, have been associated with increased levels of inflammation.

Dietary fiber
Fiber-rich diets are often associated with a high intake of antioxidants and complex carbohydrates, both of which may reduce inflammation. Another anti-inflammatory mechanism of fiber is its conversion into immune-regulating substances, such as short-chain fatty acids, by the gut microbiota in the colon. These substances activate signaling pathways, eventually decreasing the inflammatory response by reducing the pro-inflammatory cytokines IL-6, TNF-a, and CRP production.
Polyphenols
Polyphenols are a heterogeneous group of bioactive substances found in plant-based foods. They are known to have potent antioxidant and anti-inflammatory effects, thanks to their ability to reduce ROS and the pro-inflammatory cytokines IL-6 and TNF-a, respectively.
Omega-3 fatty acids
Omega-3 fatty acids such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are found in fish and fish oils and are considered anti-inflammatory. They have been shown to improve markers of cardiovascular disease, rheumatoid arthritis, and cancer cachexia, all disease states associated with chronic inflammation.
Trans fatty acids
Trans fatty acids have predominantly pro-inflammatory properties by activating inflammatory pathways and increasing oxidative stress through increased ROS production. Their primary source is partially hydrogenated oils, usually the result of industrial food processing. They are also partly derived from ruminant animal products.
Saturated fat
Similarly to trans fatty acids, saturated fat also seems to exert pro-inflammatory effects due to increased production of ROS and activation of pro-inflammatory pathways.
Sugar
Food products with high levels of free-added sugar seem to have enhanced pro-inflammatory effects and may be linked to the development of chronic diseases associated with inflammatory processes, such as atherosclerosis, cancer, and Alzheimer’s disease. A possible explanation is a chronic and exaggerated increase in blood glucose caused by such foods, which can lead to the excessive formation of advanced glycation end products (AGEs). AGEs may cause oxidative stress and trigger inflammatory responses.
Dietary patterns
High adherence to the Mediterranean diet or the DASH (Dietary Approaches to Stop Hypertension) has been associated with decreased CRP, IL-6, and TNF-a levels, as well as oxidative stress biomarkers. The high content of anti-inflammatory nutrients such as omega-3 fatty acids, dietary fiber, complex carbohydrates, and polyphenols may explain the consistent anti-inflammatory effects of such diets, which are rich in fruits, vegetables, legumes, and whole grains.
Also, adherence to a Paleolithic diet, rich in plant-based and non-processed animal products but low in processed foods, added sugars, salt, and dairy, has also been linked to a decrease in inflammation markers, especially CRP and oxidative biomarkers. In contrast, the ‘’Western’’ dietary pattern rich in processed meats, refined grains, and sugary beverages is linked to increased inflammatory markers.

To sum up, the battlefronts of chronic inflammation are multiple, and if silently working chronically without us making lifestyle changes to decrease them or even completely eradicate them, they can lead to severe health issues that can compromise quality of life and reduce lifespan. However, the ability of inexpensive and undemanding remedies, such as diet, exercise, meditation, etc., to effectively combat chronic inflammation is in front of our eyes and the palm of our hands, so it should not be neglected.

References

1. Alexopoulos N, Katritsis D, Raggi P. Visceral adipose tissue as a source of inflammation and promoter of atherosclerosis. Atherosclerosis. 2014;233(1):104-112. DOI: 10.1016/j.atherosclerosis.2013.12.023

2. Bruckner F, Gruber JR, Ruf A, Thanarajah SE, Reif A, Matura S. Exploring the link between lifestyle, inflammation, and insulin resistance through an improved Healthy Living Index. Nutrients. 2024;16(3):388. DOI: 10.3390/nu16030388

3. Burini RC, Anderson E, Durstine JL, Carson JA. Inflammation, physical activity, and chronic disease: An evolutionary perspective. Sports Med Health Sci. 2020;2(1):1-6. DOI: 10.1016/j.smhs.2020.03.004

4. Ellulu MS, Patimah I, Khaza’ai H, Rahmat A, Abed Y. Obesity and inflammation: the linking mechanism and the complications. Arch Med Sci. 2017;13(4):851-863. DOI: 10.5114/aoms.2016.58928

5. Hess JM, Stephensen CB, Kratz M, Bolling BW. Exploring the links between diet and inflammation: Dairy foods as case studies. Adv Nutr. 2021;12(Suppl1):1S-13S. DOI: 10.1093/advances/nmab108

6. Irwin MR, Sleep and inflammation: partners in sickness and in health. Nat Rev Immunol. 2019;19(11):702-715. DOI: 10.1038/s41577-019-0190-z

7. Khanna D, Khanna S, Khanna P, Kahar P, Patel BM. Obesity: A chronic low-grade inflammation and its markers. Cureus. 2022;14(2):e22711. DOI: 10.7759/cureus.22711

8. Liu Y, Zhang Z, Han D, Zhao Y, Yan X, Cui S. Association between environmental chemicals co-exposure and peripheral blood immune-inflammatory indicators. Front Public Health. 2022;10:980987. DOI: 10.3389/fpubh.2022.980987

9. Oronsky B, Caroen S, Reid T. What exactly is inflammation (and what is it not?). Int J Mol Sci. 2022;23(23):14905. DOI: 10.3390/ijms232314905

10. Ricordi S, Garcia-Contreras M, Farnetti S. Diet and inflammation: Possible effects on immunity, chronic diseases, and life span. J Am Coll Nutr. 2015;34Suppl1:10-13. DOI: 10.1080/07315724.2015.1080101

11. Sotos-Prieto M, Bhupathiraju SN, Falcon LM, Gao X, Tucker KL, Mattei J. Association between a Healthy Lifestyle Score and inflammatory markers among Puerto Rican adults. Nutr Metab Cardiovasc Dis. 2016;26(3):178-184. DOI: 10.1016/j.numecd.2015.12.004

12. Stumpf F, Keller B, Gressies C, Schuetz P. Inflammation and nutrition: Friend or foe? Nutrients. 2023;15(5):1159. DOI: 10.3390/nu15051159

The Power of Sleep in Metabolic and Cardiovascular Health and the Profound Cost of its Deprivation

j.oswald@hyperionhealth.ca (Jesse Oswald) — Mon, 09 Dec 2024 16:00:04 GMT

Key Points

Sleep deprivation disrupts glucose metabolism and the typical secretion patterns of the appetite hormones, contributing to metabolic dysfunctions.
Sleep hygiene is a valuable tool for cardiovascular disease prevention.
Poor sleep quality shifts the autonomic nervous system balance towards sympathetic dominance, increasing the risk for cardiovascular disorders.
The circadian rhythms of cortisol, adrenaline, and melatonin influence cardiovascular parameters, with disruptions due to sleep deprivation compromising cardiovascular health.

Our previous article about sleep discussed basic sleep concepts, such as sleep quality and duration, and their impact on recovery and exercise performance. In closing the chapter about sleep and its broad influences on overall health and well-being, the impact of sleep on metabolic and cardiovascular health will be analyzed in the second part. Metabolic health aspects, such as glucose regulation, appetite hormones, and energy balance, as well as cardiovascular health aspects, such as autonomic nervous system regulation and hormones, will be considered.

Sleep and metabolic health

Glucose regulation

In healthy individuals, glucose regulation appears to be under circadian control. Particularly, insulin sensitivity and glucose tolerance, which are major regulating factors of glucose metabolism, tend to be elevated during mornings and decrease as the day progresses. Circadian misalignment induced by sleep deprivation, poor sleep quality, or irregular sleeping patterns can disrupt these abilities, resulting in elevated blood glucose levels and extended time to restore normal levels. Thus, the chronically elevated blood sugar levels associated with systematic sleep deprivation can result in insulin resistance, leading to a high risk of developing a plethora of metabolic disorders, such as type II diabetes, obesity, and metabolic syndrome. Indicatively, robust data from experimental sleep restriction indicated that individuals with short sleep durations (≤6–7 h/night) are at 30% greater risk for developing type II diabetes.

Appetite hormones and energy balance

Another aspect of metabolism associated with circadian misalignment due to sleep disturbances is the 24-hour variation of the appetite hormones leptin and ghrelin. Leptin and ghrelin are primary coordinators of energy intake and energy expenditure throughout the day. Leptin is the satiety hormone that maintains energy balance by reducing caloric intake through decreased appetite, deterring fat production, and increasing energy expenditure. On the other hand, ghrelin is considered an orexigenic hormone, secreted mainly by the stomach. Ghrelin also plays a fundamental role in energy balance regulation with an opposite to leptin function.

Their functions are synchronized with leptin levels, which typically rise during the early stages of sleep and reach their lowest early in the morning, while ghrelin follows an inverse pattern. Ghrelin declines during bedtime and reaches its peak early in the morning, remaining high before meals and typically returning to baseline postprandially.

Although further research is required to elucidate the exact mechanisms, existing studies suggest that poor sleep quality and sleep deprivation interfere with appetite hormones’ secretion by altering the timing of their secretion, thus leading to dysregulation. Particularly, sleep restriction and irregular sleeping patterns are associated with diminished secretion of leptin and increased secretion of ghrelin, promoting elevated caloric intake and subsequent weight gain. From the evidence obtained so far, there might be a link between short sleep duration, adiposity, and the development of metabolic disorders.

The primary mechanism proposed for the dysregulation of appetite hormones due to sleep abnormalities is that sleep deprivation acts as a chronic stressor, affecting the hypothalamic-pituitary-adrenal axis function. The hypothalamic–pituitary–adrenal axis is responsible for cortisol production and secretion, an aforementioned stress hormone with catabolic properties. Sleep deprivation-induced stress can lead to elevated cortisol secretion by the brain, interfering with the normal signaling of the appetite hormones. As a consequence, leptin’s sensitivity is diminished, and even when the body has adequate energy reserves, the individual does not experience satiety. Additionally, cortisol can stimulate ghrelin secretion, further boosting feelings of hunger and potentially leading to weight gain.

Overall, sleep deprivation can have adverse effects on various aspects of metabolic health by disrupting glucose regulation, inducing stress, and potentially altering appetite control, resulting in a heightened risk of metabolic disorders like diabetes, type II diabetes, obesity, and metabolic syndrome.

Sleep and cardiovascular health

Autonomic Nervous System’s adaptations during healthy sleep

Adequate and quality sleep is considered fundamental in preserving cardiovascular health, as underlined in the recent guidelines released by the American College of Cardiology/American Heart Association. These guidelines state that counseling on sleep and its hygiene is a valuable approach to cardiovascular disease (CVD) prevention.

This importance can be attributed to the vital rest period sleep offers the cardiovascular system. Particularly, during sleep, cardiovascular regulation is modified, and many biological functions slow down, allowing the heart to rest from the stress of waking hours and facilitating efficient restoration of the cardiovascular tissues. In this context, the autonomic nervous system (ANS), which controls physiological body processes that occur despite our control, plays a central role. Specifically, a suppression of the sympathetic nervous system and increased parasympathetic system activity occurs. In other words, our body transitions from an alert state, often called the «fight or flight» response, to a state of relaxation and rejuvenation. This shift is predominantly evident during stages N1, N2, and N3 of NREM sleep.

During NREM sleep, heart rate and arterial blood pressure tend to decrease. This is because a shift towards a more parasympathetic tone occurs, promoting vasodilation (widening of blood vessels), enhancing blood flow to peripheral tissues, and thus fostering relaxation and tissue repair. On the contrary, during REM sleep, which involves the transition from sleep to wakefulness, our nervous system is predominantly under sympathetic control, leading to elevated heart rate and arterial blood pressure values.

The interplay between the sympathetic and parasympathetic activities can be efficiently reflected by HRV, a marker that serves as an indicator of the fluctuations in the time intervals between consecutive heartbeats. HRV normal values differ between populations and depend on factors like age, gender, and fitness level. During sleep, higher HRV values, meaning broader time variation between heartbeats, are associated with balanced autonomic nervous system activity and resilience to stress. Conversely, lower HRV indicates autonomic dysregulation, diminished adaptivity between states of alertness and relaxation, and potential susceptibility to cardiovascular issues.

Autonomic Nervous System’s adaptations during sleep deprivation

It’s becoming clear that the interplay between the two major branches of the autonomic nervous system (the sympathetic and parasympathetic nervous systems) is of great importance in achieving restful sleep. Disruptions of sleep duration and quality appear to disrupt this interplay, resulting in considerable predominance of the sympathetic nervous system’s activity. This suggests that sleep deprivation impairs the nervous system’s ability to adapt to shifting toward relaxation mode, subjecting individuals to a prolonged state of alertness and stress. As a result, a cascade of events occurs, including lower HRV values, increased proinflammatory cytokine secretion, and vasoconstriction, increasing the risk of hypertension, coronary artery disease, endothelial dysfunction, and other cardiovascular disorders.

Circadian Hormonal Dynamics and Cardiovascular Health

The circadian rhythm has implications for the cardiovascular system, as well. Hormones like cortisol, melatonin, and adrenaline, which follow circadian patterns, play a critical role in cardiovascular regulation.

As mentioned before, cortisol is a stress hormone, and its levels typically rise in the morning and reach their lowest during the night, enabling the anabolic hormones to facilitate recovery. However, chronic sleep deprivation can alter this hormonal synchronization, leading to dysregulated cortisol levels, potentially contributing to increased blood pressure and consequent risk of cardiovascular diseases.

Likewise, adrenaline, another hormone typically released as a response to stress stimuli, peaks throughout the day when the individual is active and the sympathetic nervous system governs. Sleep deprivation and irregular sleeping patterns can result in circadian misalignment associated with dysregulation of adrenaline secretion. This dysregulation leads to sympathetic nervous system dominance and, thus, elevated heart rate and blood pressure, meaning an increased risk for cardiovascular disorders.

Finally, melatonin, a hormone released by the brain, typically rises during the night as sleeping time approaches. Melatonin is known to exert cardioprotective effects through its antioxidant, anti-inflammatory, antiatherogenic, and lipid-lowering properties. Moreover, melatonin regulates blood pressure and vascular tone by contributing to blood pressure reduction during sleep. Hence, disruptions in melatonin secretion, often originating from chronic insufficient or poor sleep, pose a non-negligent risk for cardiovascular diseases.

To sum up, adequate sleep quality is a good indicator of metabolic and cardiovascular health. Therefore, prioritizing sufficient and quality sleep for the optimal functioning of the cardiovascular and metabolic health system and thus for longevity is crucial and should not be ignored since sleep is, along with nutrition and exercise, amongst the main pillars of a healthy, long life.

REFERENCES

Baranwal N, Yu PK, Siegel NS. Sleep physiology, pathophysiology, and sleep hygiene. Prog Cardiovasc Dis. 2023 Mar-Apr;77:59-69. DOI: https://doi.org/10.1016/j.pcad.2023.02.005

Besedovsky L, Lange T, Born J. Sleep and immune function. Pflugers Arch. 2012 Jan;463(1):121-37. DOI: 10.1007/s00424-011-1044-0

Huang W, Ramsey KM, Marcheva B, Bass J. Circadian rhythms, sleep, and metabolism. J Clin Invest. 2011 Jun;121(6):2133-41. DOI: 10.1172/JCI46043

Korostovtseva L, Bochkarev M, Sviryaev Y. Sleep and Cardiovascular Risk. Sleep Med Clin. 2021 Sep;16(3):485-497. DOI: https://doi.org/10.1016/j.jsmc.2021.05.001

Lin J, Jiang Y, Wang G, Meng M, Zhu Q, Mei H, Liu S, Jiang F. Associations of short sleep duration with appetite-regulating hormones and adipokines: A systematic review and meta-analysis. Obes Rev. 2020 Nov;21(11):e13051. DOI: https://doi.org/10.1111/obr.13051

Liu S, Wang X, Zheng Q, Gao L, Sun Q. Sleep Deprivation and Central Appetite Regulation. Nutrients. 2022 Dec 7;14(24):5196. DOI: https://doi.org/10.3390/nu14245196

Morselli L, Leproult R, Balbo M, Spiegel K. Role of sleep duration in the regulation of glucose metabolism and appetite. Best Pract Res Clin Endocrinol Metab. 2010 Oct;24(5):687-702. DOI: https://doi.org/10.1016/j.beem.2010.07.005

Rogers EM, Banks NF, Jenkins NDM. The effects of sleep disruption on metabolism, hunger, and satiety, and the influence of psychosocial stress and exercise: A narrative review. Diabetes Metab Res Rev. 2024 Feb;40(2):e3667. DOI: https://doi.org/10.1002/dmrr.3667

Tobaldini E, Costantino G, Solbiati M, Cogliati C, Kara T, Nobili L, Montano N. Sleep, sleep deprivation, autonomic nervous system and cardiovascular diseases. Neurosci Biobehav Rev. 2017 Mar;74(Pt B):321-329. DOI: https://doi.org/10.1016/j.neubiorev.2016.07.004

Troynikov O, Watson CG, Nawaz N. Sleep environments and sleep physiology: A review. J Therm Biol. 2018 Dec;78:192-203. DOI: https://doi.org/10.1016/j.jtherbio.2018.09.012

The Power of Sleep in Recovery and Exercise Performance

j.oswald@hyperionhealth.ca (Jesse Oswald) — Mon, 02 Dec 2024 16:00:00 GMT

Key Points

Healthy adults typically require a minimum of 7 hours of sleep per night, while sleep requirements are increased during infancy, childhood, and adolescence.
Inconsistent sleep patterns are responsible for disrupting the circadian rhythm, promoting a vicious cycle of compromised sleep quality.
Sleep consists of four vital stages: N1, N2, and N3, which constitute NREM (Non-Rapid Eye Movement) sleep, and a fourth stage of rapid eye movement (REM) sleep.
During deep sleep, physiological processes such as the release of growth hormones occur, facilitating tissue recovery, muscle growth, and improving exercise performance

It would not be surprising to acknowledge that getting enough sleep is challenging for many people. The fast-paced modern way of living has led to the sacrifice of ensuring the appropriate amount of sleep in order to cope with daily responsibilities, making sleep deprivation a global public health matter. Poor sleep, referring to both quantity and quality, is associated with numerous detrimental health outcomes, compromising cognitive, heart, and metabolic well-being.

Yet, what defines poor sleeping status, and what is the ideal sleep regimen we should opt for? In the following article, there are going to be discussed the latest guidelines of sleep duration for all life stages, the different sleep stages and their importance regarding sleep quality, as well as the impact of sleep deprivation on recovery and exercise performance for all exercise modalities, including endurance, resistance, and HIIT training.

Sleep duration guidelines and other factors of sleep quality

Sleep duration recommendations vary across the lifespan. For healthy adults, the guidelines suggest 7 hours or more. Sleeping more than 9 hours appears to have substantial benefits only in younger adults or adults experiencing consistent sleep loss or illness. It is important to note that these recommendations do not apply to childhood, as children typically have higher sleep requirements to support growth and development. According to the National Sleep Foundation's latest guidelines, 14 to 17 hours is the goal set for newborns (0-3 months), 12 to 15 hours for infants, 9 to 12 hours for toddlers and preschoolers, and 8 to 10 hours for school-age children and adolescents.

Alongside sufficient sleep duration, a healthy sleep state is also defined by high sleep quality, meaning the effective utilization of the time spent in bed for sleeping. Many exogenous factors can affect sleep quality, such as stress, anxiety, caffeine and alcohol intake, and inconsistent sleep schedules, leading to difficulties in sleep, insomnia, and frequent awakenings during the nighttime.

Additionally, quality sleep suggests not only a regular sleep schedule but one that is also aligned with our internal clock-like regulation known as the circadian rhythm. The circadian rhythm regulates many aspects of the sleeping process and can be disrupted by many factors, including increased artificial light exposure and inconsistent sleep patterns. Hence, aligning our sleep schedule with our circadian rhythm is a principal way to ensure good quality sleep, as it ensures the optimal distribution of deep sleep and rapid eye movement (REM) sleep. The sleeping process consists of four stages: N1, N2, and N3, which constitute NREM (Non-Rapid Eye Movement) sleep, and a fourth stage of rapid eye movement (REM) sleep. NREM sleep reaches the deepest sleep state at stage N3, the most important stage of NREM sleep, determining sleep quality.

However, experiencing REM sleep is also a significant indicator of high-quality sleep. REM is a critical phase of the sleep cycle that individuals experience in the latter stages of their sleep, preparing the brain to return to consciousness. During REM sleep, brain activity resembles that of wakefulness, making it a vital sleep phase for the brain to process feelings, sort out information, dream, and undergo restorative processes.

Therefore, engaging in a healthy sleep regimen involves adherence to the recommended sleep duration guidelines according to age group as well as pursuing sleep quality in terms of optimal sleep timing and sleep stages duration.

Sleep impact on recovery

A robust body of evidence describes the restorative effect sleep exerts on the body's molecular and cellular processes, underlying the necessity of ensuring sufficient amounts of quality sleep. Sleep’s beneficial properties in cognitive function, immunity, and recovery from illness or injury have been attributed to the secretion of several growth hormones during different phases of the sleep period.

As mentioned before, sleep involves four main stages. While all sleep stages are necessary components of the sleep cycle, the N3 stage plays a crucial role in recovery. Growth hormones, such as growth hormone and prolactin, which are vital for recovery, are highly released during this phase of deep sleep. Their secretion fosters injury healing by promoting tissue repair, regeneration, and muscle growth. Additionally, they exert beneficial properties by suppressing inflammation and promoting immunity strengthening. This enhances the body’s ability to address illnesses and infections efficiently.

In addition, growth hormone release is associated with a significant decline in cortisol levels, the stress hormone. Cortisol typically exerts catabolic effects, and prolonged elevated cortisol levels are associated with increased tissue breakdown and immunity system suppression, thus delaying the process of healing and tissue repair. Cortisol levels, in alignment with the circadian rhythm, tend to peak during the day when the individual is awake and decrease at night as the body prepares for sleep. This decline in cortisol during nighttime allows growth hormones to facilitate tissue repair and healing effectively.

It is also worth noting the action of another type of substances, cytokines. Cytokines are proinflammatory molecules released when an individual experiences a lack of sleep. Cytokines, like IL-6 and CRP, negatively affect the immunity system, impede muscle recovery, promote pain, and disrupt the autonomic nervous system balance that regulates our automatic bodily functions, such as heart rate, respiratory rate, and digestion. Therefore, their release in case of sleep deprivation can hinder efficient recovery and also exert detrimental effects on numerous vital organs.

As a result, it’s clear that coordinated hormonal activity during sleep plays a crucial role in recovery.

Therefore, prioritizing sleep quantity and quality that guarantees the experience of all necessary sleep stages is paramount for optimal recovery.

Sleep impact on exercise performance

Numerous studies have documented the critical role of sleep in optimizing exercise performance. Their findings underline that sleep, alongside training and nutrition, hold equivalent importance as fundamental factors for peak performance.

For professional athletes, sleep requirements increase to 9 to 10 hours/day due to the increased physical and mental demands of their training sessions. While extended sleep duration is needed to ensure proper physical and cognitive recovery, most athletes find it difficult to attain sufficient sleep. This challenge stems from busy schedules, irregular sleep patterns, time-zone changes during competition periods, and the anxiety and stress they face, leading to severe sleep restriction or deprivation.

According to published data, sleep restriction or deprivation that both athletes and exercising individuals often experience seriously impacts athletic performance. This is associated with diminished ability to reach peak performance, injury susceptibility, and delayed recovery, emphasizing the significance of preserving optimal sleep patterns.

Endurance exercise

Low-to-moderate intensity endurance exercise that reaches 50-75% of an individual’s VO2max, such as running, rowing, cycling, etc., demands high cardiorespiratory activity and sustained effort for extended training periods. Sleep, alongside other critical factors, plays a fundamental role in achieving peak performance in this type of exercise as it contributes to efficient energy replenishment. Sleep, mainly NREM sleep, achieves that by facilitating glycogen synthesis and storage in muscles and the liver, which is a primary energy resource during endurance exercise.

Moreover, growth hormone that is extensively secreted during this sleep phase promotes muscle recovery and the storage of glucose as glycogen, contributing to efficient energy replenishment. Therefore, sleep restriction or deprivation contributes to decreased energy fuels and impaired muscle repair, ultimately diminishing the ability to maintain sustained effort during endurance activities.

Sleep deprivation has also significant impacts on cognitive function and mood. Many studies have demonstrated decreased strength, stamina, and motivation after overnight sleep loss or reduced sleep duration, leading to decreased athletic performance. Sleep deprivation also appears to increase the perception of the endurance athletes' effort, contributing to greater fatigue and exhaustion. This can elevate the risk of injuries as athletes push themselves trying to overcome the perceived strains. Lastly, feelings of frustration, anger, and confusion can also result from insufficient sleep, especially REM sleep, which is vital for cognitive restoration.

Resistance training

Resistance training imposes significant strain on the muscles, making sufficient sleep a priority to attain peak performance. As mentioned before, hormones are released during the nighttime, inducing muscle repair and growth, an essential metabolic procedure for gaining strength. While research data on the impact of sleep deprivation on resistance training performance is inconclusive, insufficient muscle repair and recovery seems to be the most likely underlying factor contributing to potential declines in performance.

In terms of cognitive function, sleep deprivation can alter the athletes’ psychomotor skills and affect their coordination, reaction time, and ability to make decisions, all parameters necessary for peak performance during resistance training.

High-Intensity Interval Training (HIIT)

Sleep is crucial in high-intensity interval training performance as well. Specifically, getting the adequate amount of sleep enhances the body’s ability to meet the increased HIIT demands by improving stamina and promoting muscle recovery through nighttime glycogen synthesis and hormonal regulation.

Similar to resistance training, HIIT requires proper cognitive function. Mental focus, coordination, and rapid reaction times are some of the parameters of cognitive function required during HIIT training, which appear to be threatened by sleep deprivation.

To sum up, sleep is frequently overlooked yet fundamentally crucial for overall health, with both quantity and quality holding great significance. Quality sleep assists in preserving good health by ensuring the accomplishment of the necessary sleeping stages and the optimal secretion of hormones responsible for growth and repair. Moreover, besides recovery and tissue repair, adequate sleep is crucial for performance optimization by enhancing physiological and cognitive performance abilities.

REFERENCES

Barbato G. REM Sleep: An Unknown Indicator of Sleep Quality. Int J Environ Res Public Health. 2021 Dec 9;18(24):12976. DOI: https://doi.org/10.3390/ijerph182412976

Charest J, Grandner MA. Sleep and Athletic Performance: Impacts on Physical Performance, Mental Performance, Injury Risk and Recovery, and Mental Health. Sleep Med Clin. 2020 Mar;15(1):41-57. DOI: https://doi.org/10.1016/j.jsmc.2019.11.005

Doherty R, Madigan SM, Nevill A, Warrington G, Ellis JG. The Sleep and Recovery Practices of Athletes. Nutrients. 2021 Apr 17;13(4):1330. DOI: 10.3390/nu13041330

Fullagar HH, Skorski S, Duffield R, Hammes D, Coutts AJ, Meyer T. Sleep and athletic performance: the effects of sleep loss on exercise performance, and physiological and cognitive responses to exercise. Sports Med. 2015 Feb;45(2):161-86. DOI: https://doi.org/10.1007/s40279-014-0260-0

Hirshkowitz M, Whiton K, Albert SM, Alessi C, Bruni O, DonCarlos L, Hazen N, Herman J, Adams Hillard PJ, Katz ES, Kheirandish-Gozal L, Neubauer DN, O'Donnell AE, Ohayon M, Peever J, Rawding R, Sachdeva RC, Setters B, Vitiello MV, Ware JC. National Sleep Foundation's updated sleep duration recommendations: final report. Sleep Health. 2015 Dec;1(4):233-243. DOI: https://doi.org/10.1016/j.sleh.2015.10.004

Vitale KC, Owens R, Hopkins SR, Malhotra A. Sleep Hygiene for Optimizing Recovery in Athletes: Review and Recommendations. Int J Sports Med. 2019 Aug;40(8):535-543. DOI: 10.1055/a-0905-3103

Watson AM. Sleep and Athletic Performance. Curr Sports Med Rep. 2017 Nov/Dec;16(6):413-418. DOI: 10.1249/JSR.0000000000000418

Watson NF, Badr MS, Belenky G, Bliwise DL, Buxton OM, Buysse D, Dinges DF, Gangwisch J, Grandner MA, Kushida C, Malhotra RK, Martin JL, Patel SR, Quan SF, Tasali E. Recommended Amount of Sleep for a Healthy Adult: A Joint Consensus Statement of the American Academy of Sleep Medicine and Sleep Research Society. Sleep. 2015 Jun 1;38(6):843-4. DOI: 10.5665/sleep.4716

The Role of Exercise in Weight Loss: A Comparative Look at Exercise vs. Diet

j.oswald@hyperionhealth.ca (Jesse Oswald) — Wed, 12 Jun 2024 14:00:01 GMT

The Role of Exercise in Weight Loss

When it comes to shedding those extra pounds, many of us wonder whether to focus on exercise or diet. Recent research, including a comprehensive study published in the British Journal of Sports Medicine , offers valuable insights into this debate. Let’s break down the findings and explore why exercise might be your best bet for sustainable weight loss, especially when it comes to reducing visceral fat.

The Power of Exercise

Exercise has long been championed for its numerous health benefits, including weight loss. The recent study compared the effects of exercise and caloric restriction (dieting) on reducing visceral fat, which is the harmful fat stored around internal organs. The study analyzed 40 randomized controlled trials involving 2,190 participants, focusing on overweight and obese adults.

Key Findings:

Visceral Fat Reduction: Exercise proved to be more effective than dieting alone in reducing visceral fat. While both interventions helped reduce this fat, exercise showed a significant dose-dependent effect. This means that the more you exercise, the greater the reduction in visceral fat.
Muscle Preservation: Unlike dieting, which can lead to the loss of both fat and muscle, exercise helps in maintaining muscle mass. This is crucial because muscle mass plays a vital role in regulating metabolism and overall energy expenditure.
Independent Fat Loss: Exercise can induce fat loss even without significant weight loss. This suggests that exercise improves body composition by reducing fat and preserving or even increasing muscle mass.

Why Not Just Diet?

While caloric restriction can lead to weight loss, it often comes with drawbacks:

Loss of Muscle Mass: Dieting can result in the loss of muscle along with fat, which can slow down your metabolism and make it harder to keep the weight off long-term.
Metabolic Adaptation: The body can adapt to low-calorie diets by becoming more efficient at storing fat, which can diminish the effects of dieting over time.

The Combined Approach

The study also highlighted that both exercise and caloric restriction together could reduce waist circumference, a good indicator of visceral fat reduction. However, exercise alone showed a stronger dose-response relationship with visceral fat reduction compared to dieting alone.

Real-Life Application

The implications of these findings are clear: incorporating regular exercise into your weight loss plan is crucial. It’s not just about the number on the scale but about improving body composition and overall health.

At Hyperion Exercise and Health , our exercise physiologists are dedicated to helping you develop a tailored exercise program to meet your weight loss goals. Whether you’re looking to reduce visceral fat, improve muscle mass, or enhance overall fitness, our experts can guide you on your journey to better health.

References

Recchia F, Leung CK, Yu AP, et al. Dose–response effects of exercise and caloric restriction on visceral fat in overweight and obese adults. Br J Sports Med 2023;57:1035–1041. doi:10.1136/bjsports-2022-106304.

For personalized exercise programs and expert guidance, visit Hyperion Exercise and Health .

This blog post highlights the importance of exercise over diet alone for effective and sustainable weight loss, particularly in reducing visceral fat, and encourages readers to seek professional advice from Hyperion Exercise and Health.

Metabolic Flexibility: A Valid Concept or a Catchy Term?

j.oswald@hyperionhealth.ca (Jesse Oswald) — Wed, 05 Jun 2024 19:00:00 GMT

Key Points

The body’s ability to rapidly and efficiently switch between oxidations of different energy substrates, namely fat and carbohydrates, depending on their availability, is known as metabolic flexibility.
Long-term caloric excess and ectopic fat accumulation are central mechanisms of impaired metabolic flexibility.
Insulin resistance is the link among a cluster of metabolic disturbances that are all characterized by impaired metabolic flexibility.
Mitochondrial dysfunction is a principal component of impaired metabolic flexibility.
Regular exercise and a healthy, low-calorie diet can significantly improve metabolic flexibility.
RER fluctuations measured through breath analysis when alternating between fasted and fed states can be used as an index of metabolic flexibility.

Human physiology has evolved during dramatic fluctuations in energy supply and demand. Coping with these challenges has enabled the human body to manage energy metabolism for optimal substrate storage and utilization during either food surplus or shortage and of either rest or increased calorie burn. This ability to efficiently adjust metabolism to fluctuations in energy demand by rapidly and efficiently switching between oxidations of different energy substrates, namely fat and carbohydrates, depending on their availability, is known as metabolic flexibility. More specifically, metabolic flexibility is our body’s ability to switch from high levels of fat oxidation during fasted states to increased carbohydrate utilization during feeding states. The greater our ability to burn the food we consume instead of storing it, the more metabolically flexible we are.

Humans constantly cycle from fasting to postprandial (post-meal) conditions and vice versa. The primary purpose of this substrate shift is to move from catabolic (the metabolic process of breaking down fuels for energy production) to anabolic (the metabolic process of synthesizing molecules such as glycogen and triglycerides for energy storage) activities in which energy can be effectively stored in skeletal muscle, fat, and liver tissues.

Metabolic flexibility is not an ‘’on-off’’ phenomenon. It involves constant, tightly regulated adaptive responses of human metabolism to maintain energy homeostasis by matching fuel availability and demand to various conditions such as periodic fasting, varying meal composition, physical activity, and environmental fluctuations. However, nowadays, when the food supply overflows and there is a plethora of calorically dense processed foods combined with low levels of physical activity, metabolic flexibility is directly obstructed.

In this article, we will review the principle mechanisms that control metabolic flexibility, its implications for health, and the prominent role diet and exercise play in maintaining it.

Physiologic Mechanisms Leading to Metabolic Inflexibility

Healthy cells of metabolically active organs such as the liver, skeletal muscle, and fat tissue are metabolically flexible and communicate to organize the utilization of available fuels best. The inability to adapt to fuel availability may result in an abnormal mobilization and utilization of fat and glucose, leading to increased fatty acids and glucose concentration. After fat cells reach a threshold of calorie and lipid capacity, lipids accumulate in locations other than fat tissue, including skeletal muscle and the liver. This process, known as ectopic fat deposition, leads to lipotoxicity and, eventually, metabolic abnormalities and disrupts metabolic flexibility. Therefore, the previously healthy cells have now turned into dysfunctional cells.

Metabolic inflexibility is characterized by reduced skeletal muscle glucose transport, increased suppression of fat tissue lipolysis, reduced suppression of hepatic glucose production, and skeletal muscle mitochondrial dysfunction. All these defects result in increased glucose production by the liver, reduced glucose utilization for energy by the muscles, and decreased fat burn. At the core of these processes lies long-term caloric excess and ectopic fat accumulation. As a result, metabolic inflexibility and ectopic fat accumulation reinforce each other in a vicious cycle, causing and further cultivating metabolic dysfunction.

Metabolic Flexibility and its Association with Insulin Resistance

Impaired metabolic flexibility is associated with an increased risk of obesity and obesity-related pathologies, such as metabolic syndrome, type 2 diabetes, systemic inflammation, cardiovascular disease, and cancer. Simultaneously, obesity, especially central obesity, where fat accumulates around the abdomen, is the leading cause of insulin resistance. Insulin resistance is the inability of muscle, liver, and fat cells to respond to insulin, thus taking up and utilizing ingested carbohydrates for energy.

Insulin resistance is a vital component of the metabolically inflexible state, which is typically characterized by decreased fat oxidation during fasting and a reduced ability to upregulate carbohydrate oxidation during feeding. Therefore, the ingested carbohydrates are stored as fat in the fat tissues and other organs (ectopic fat).

Insulin resistance is also the predominant factor leading to type 2 diabetes and the link among a constellation of cardiometabolic risk factors known as metabolic syndrome, linking obesity, type 2 diabetes, and cardiovascular disease. Consequently, it’s becoming clear that not only Impaired metabolic flexibility is associated with an increased risk of insulin resistance but that insulin resistance itself deteriorates metabolic flexibility as well; hence why most individuals with obesity and/or type 2 diabetes are metabolically inflexible.

Metabolic syndrome is defined as having at least three components: visceral obesity in terms of elevated waist circumference, insulin resistance in terms of elevated fasting glucose, high blood pressure, elevated triglycerides, and/or low HDL-cholesterol. One of the hallmarks of metabolic syndrome is chronic systemic inflammation. Along with obesity and insulin resistance, systemic inflammation can trigger and propagate metabolic inflexibility. Thus, metabolic inflexibility, inflammation, obesity, and insulin resistance are part of a vicious cycle where the one trigger and reinforces the other. While impaired metabolic flexibility is strongly associated with insulin resistance, which of the two precedes is still unresolved.

Overall, metabolic health is defined as a comprehensive state of well-being, and metabolic flexibility is essential for metabolic health and the absence of metabolic diseases, such as the metabolic syndrome.

Mitochondrial Dysfunction: The Cause or the Consequence of Metabolic Inflexibility?

Mitochondria are dynamic intracellular organelles that play a foundational role in energy metabolism. When energy supply exceeds energy demand across the mitochondria (chronic caloric surplus), their oxidative capacity is reduced, predisposing to adverse health outcomes, such as the development of type 2 diabetes and obesity.

The concept of metabolic flexibility has particularly been associated with the mitochondria's function and places mitochondrial function at its core. Mitochondria are crucial in determining whole-body metabolic flexibility, and the deregulation of mitochondrial function underlies the onset of metabolic inflexibility. More specifically, mitochondrial dysfunction, in terms oflow skeletal muscle mitochondrial capacity, function, and/or density, is associated with reduced resting lipid oxidation and, therefore, increased muscle lipid accumulation (ectopic fat) and insulin resistance.

Although the hypothesis that such mitochondrial abnormalities may be a primary cause of metabolic inflexibility has been raised, definite conclusions regarding the causal relationship cannot be drawn based on current evidence. However, a substantial body of evidence supports impaired mitochondrial adaptation as a principal component of systemic metabolic inflexibility, particularly in conditions related to insulin resistance, such as metabolic syndrome. Therefore, the relationship between insulin resistance and altered mitochondrial function seems to be bidirectional and mutually amplifying.

Metabolic Flexibility and its Relation to Physical Activity and Diet

Several studies have highlighted the positive relationship between sedentary behaviours, such as time spent sitting, and the risk of developing obesity, type 2 diabetes, and cardiovascular disease. Indeed, regular physical exercise is a key determinant of metabolic flexibility, favouring metabolic and cardiovascular health while preventing weight gain and its related metabolic abnormalities. Exercise training increases metabolic flexibility by reducing insulin resistance and increasing muscle lipid oxidation.

Therefore, it’s becoming clear that exercise profoundly affects metabolic flexibility. This effect is also mediated by the impact of exercise on the mitochondria. Current evidence shows that exercise-trained skeletal muscles, especially of endurance athletes, present increased skeletal muscle mitochondrial biogenesis and have higher mitochondrial content, capacity, and function. In other words, exercise-enhanced mitochondrial performance is related to better metabolic flexibility. In contrast, skeletal muscle from individuals with obesity and insulin resistance is metabolically inflexible compared with skeletal muscle from healthy individuals.

Besides physical activity, a chronic caloric surplus is another major factor impairing mitochondrial function and inducing metabolic flexibility. Therefore, weight loss through a suitably applied caloric deficit is crucial in restoring metabolic flexibility and is the most common intervention for obesity and obesity-related metabolic comorbidities.

Physical activity, especially aerobic exercise, is an effective way to improve metabolic flexibility. Combined with a proper nutrition regime that will not be characterized by overconsumption of calories and nutrients from highly processed caloric-dense foods that promote weight gain, thus dysregulation of metabolic health,it can comprise the best strategy to restore metabolic flexibility.

Can breath Analysis be Utilized as an Index of Metabolic Flexibility?

Metabolic flexibility as individuals alternate between feeding and fasting can be assessed through changes in the respiratory exchange ratio (RER), calculated from the VCO ₂ -to-VO ₂ ratio measured by breath analysis (AKA indirect calorimetry). RER is an index of the proportion of carbohydrates and fat being oxidized for energy.

RER typically fluctuates between 0.7 and 1.0 in humans, depending on the fuel being oxidized. When fat or glucose is the unique energy source, the RER is 0.7 or 1.00, respectively. In fasted conditions, typically, RER is about 0.80 in subjects fed with mixed diets, while values lower than 0.75 are observed in individuals fed with low-carbohydrate diets (<30% of energy from carbohydrates). Individuals with negative energy balance or fed high-fat diets (>50% of energy from fat) tend to have even lower fasting RER values. However,in a state of increased visceral fat (central obesity) and insulin resistance, there is a higher preference for glucose relative to fat as an energy source in the fasting state (high fasting RER).

The extent to which RER increases from fasting to feeding conditions has been considered an index of metabolic flexibility. An impaired drop in RER during an overnight fast (high fasting RER→glucose oxidation predominance and inability to switch to fat oxidation), as well as an impaired rise in RER in response to feeding (baseline RER of ≈0.85, which fails to increase further), indicates a metabolically inflexible state. Several studies suggestthis is the case for obese insulin-resistant and type 2 diabetic subjects.

However, indirect calorimetry should be used with caution and critical thinking to measure metabolic flexibility. Someone should always consider a subject’s energy balance and dietary macronutrient composition while interpreting the results since those factors affect the RER.

In summary, metabolic flexibility is not only a valid term regarding metabolic health. Still, it may actually underlie the epidemic changes in metabolic disease that affect all demographic groups and burden healthcare systems. It may also be an early condition that, if timely detected and appropriately handled, could prevent the onset of several serious metabolic disturbances, such as type 2 diabetes and cardiovascular disease.

Exercise Capacity and Biological Age: A Powerful Relationship

j.oswald@hyperionhealth.ca (Jesse Oswald) — Wed, 29 May 2024 14:00:01 GMT

Key Points

Chronological age should not be used to accurately predict morbidity and mortality since biological age is a more reliable lifespan indicator.
VO ₂ max is the gold standard method to determine exercise capacity during graded exercise testing and one of the best indicators of biological age.
VO ₂ max is the strongest independent predictor of health and longevity, and VO ₂ max-derived biological age allows for better risk stratification and management of individuals undertaking exercise testing.

Regular physical activity at both the recreational and competitive levels contributes substantially to healthy aging and health-enhancing physiological adaptations by helping to prevent or control many health problems that often reduce individuals' quality and length of life.

However, increasing age is associated with declining physical activity and changes in several physiological parameters, such as the aerobic and anaerobic energy systems.

While anaerobic power and capacity decline at similar rates at about 6-8% per decade , peak aerobic power declines much slower with age.

In keeping with the unprecedented growth rate of the world’s aging population, there is a clear need for a better understanding of the aging process and the determinants of healthy aging.

Biological Age vs. Chronological Age

Aging is a complicated process in which molecular and cellular damage accumulates, resulting in a gradual functional and structural decline, increased susceptibility to disease, and, ultimately, death. Although the prevalence of functional impairment with age is inevitable and biologically inherited, there is a tremendous individual variation in the rate and degree of physiological decline. Environmental conditions like stress, physical inactivity, and nutrition may modify these time-related deteriorations. As a result, individuals with the same chronological age vary widely in health and function. They may be younger or older than their birth date or have a different life span, the so-called biological age . This heterogeneity may be attributed to diversity in genotypes, living habits, and environments.

Consequently, when measured chronologically, age is not a reliable indicator of the rate of a physiological breakdown associated with the aging process. It should not be used to predict morbidity and mortality accurately. Therefore, to better assess an individual’s degree of aging, and thus residual life span or disease susceptibility, new approaches that provide predictive power beyond that from measuring chronological age alone need to be developed.

Biological age, which is one of them, represents the degree to which an individual has aged and may be able to provide a surrogate measure to determine an individual’s level of damage accumulation as well as the extension of a healthy lifespan. It has gained ground over chronological age since it holistically encapsulates the state of an individual’s health and accounts for some of the variations in morbidity, mortality, and other health outcomes among individuals of the same chronological age.

When measured longitudinally, biological age can be used to track the trajectory of mortality and health damage, such as myocardial infarction (ΜΙ) , over time.

Studies have demonstrated that the combination of diet and exercise, in terms of both aerobic and resistance training, cannot only prevent aging but also reverse it, thereby improving biological age and increasing a healthy lifespan.

Advanced biological age, on the other hand, has been associated with disability, worse cognitive function, and mortality in older individuals.

Health Benefits of Physical Activity

While physical inactivity has been associated with greater mortality, regular aerobic exercise can slow or reverse functional deterioration, reducing an individual’s biological age by ten or more years . Regular exercise training increases a variety of physiological parameters, including elevated cardiac output, augmented blood volume, skeletal muscle angiogenesis, increased skeletal muscle mitochondrial density as well as maximal oxygen uptake (VO ₂ max).

VO ₂ max indicates the body’s ability to deliver oxygen to the working muscles, which rely on adequate oxygen supply to meet their metabolic demands.

The cardiovascular system represents the primary limitation of VO ₂ max, which is negatively affected by aging but can dramatically improve through exercise.

At least 30 minutes of moderate-intensity exercise training on most days of the week can increase VO ₂ max by more than 20% . Although high-intensity exercise is more effective for improving VO ₂ max in healthy individuals, lower-intensity physical activity can also enhance VO ₂ max in high-risk individuals. Therefore, the level of physical activity sufficient to improve VO ₂ max depends on the initial fitness status and health, the training history, and the exercise's duration, frequency, and intensity.

Whereas resistance training can improve VO ₂ max, endurance training represents the preferred intervention to improve cardiorespiratory fitness (CRF). Endurance exercise training, especially when combined with specific respiratory muscle training, can preserve and improve VO ₂ max.

Besides cardiovascular fitness, exercise training can also develop and maintain strength, flexibility, bone health, coordination, and balance , all essential aspects of independent living in old age. Moreover, exercise delays the age-associated change in body composition, namely the loss of muscle mass and the increase in fat mass.

The Clinical Prognostic Value of VO2 Max

Physical fitness is typically expressed as cardiorespiratory fitness (CRF) and/or exercise capacity, and VO ₂ max is an objective measure. Specifically, VO ₂ max is the gold standard for assessing the amount of oxygen consumption in a maximal effort, beyond which no increase in workload can further raise it. VO ₂ max during exercise represents cardiac, circulatory, respiratory function, and muscle oxygen use under physiological stress conditions.

As a reasonable, direct, and objective measure of CRF, VO ₂ max can provide a quantifiable measurement of the level of physical activity. Physical inactivity and poor physical fitness have been estimated to account for 12% of all deaths in the US. Indeed, Individuals with low VO ₂ max have a substantially higher risk of all-cause mortality and cardiovascular disease (CVD) compared to those with intermediate and high VO ₂ max.

Therefore, VO ₂ max is a strong predictor and independent risk factor for CVD-related and overall mortality and premature death and can be considered equally important as other conventional modifiable risk factors such as smoking, hypertension, hypercholesterolemia, obesity, and diabetes. Specifically, increased VO ₂ max may offset the harmful consequences of excess body fatness, hypertension, and hyperglycemia, namely major CVD risk factors, thereby allowing individuals to be ‘’fat but fit’’ , meaning to have a lower risk of CVD outcomes, regardless of body mass index (BMI) levels.

Proposed Biological Age Biomarkers

During the past decades, various specific aging biomarkers have come into play in an effort to identify biological age better. They can be separated into genetic, molecular, and phenotypic biomarkers.

Genetic factors, such as telomere length, decrease progressively with aging; hence, it has been proposed as a potential marker of biological aging. Genetic factors cause approximately 20-50% of the biological variations. Recent reports have shown an association between shortened telomere length and increased risk of age-related pathologies, such as CVD and all-cause mortality. Telomeres are located at the end of human chromosomes and consist of highly repetitive DNA sequences, which shorten every time cells divide.

The results of a study demonstrated that vigorous habitual aerobic exercise and maximal aerobic exercise capacity preserve telomere length among healthy older adults. Thus, their cellular and physiologic function with aging is compared with a sedentary lifestyle or short-term exercise training. Besides telomere length, molecular indicators used as biological age biomarkers are T-cell DNA rearrangement and DNA methylation , also known as the epigenetic clock. However, the association of the above biomarkers with aging is inconsistent. Some studies show positive and other negative correlations; hence, more research is needed before they are used as established biomarkers for biological age.

VO2 Max as a Biomarker of Health and Longevity

VO ₂ max is a commonly used biomarker of biological age. Based on a scientific statement from the American Heart Association (AHA) , it is the strongest independent predictor of future life expectancy in healthy and cardiorespiratory-diseased individuals. Age, sex, duration, intensity, frequency, type of physical activity, genetic factors, and clinical or subclinical disease determine VO2 max.

VO ₂ max typically decreases by about 7% (women) to 10% (men) per decade from around 25 years, and the physical activity level is directly related to the rate of this decline. For each 1ml/min/kg decrease , the risk of functional dependency increases by 14%, suggesting a need to maintain, if not improve, cardiovascular fitness.

Although genetic factors determine around 50% of VO2 max, regular endurance training can significantly improve it in 8-52 weeks by 13-20% or around 0.5L/min, depending on exercise intensity.

VO ₂ max, determined through cardiopulmonary exercise testing (CPET), has an inverse, graded, and independent association with all-cause mortality risk, supporting the value of exercise testing as a clinical tool ; it is non-invasive, relatively inexpensive, and provides clinically relevant diagnostic and prognostic information.

Notably, among established risk factors such as hypertension, smoking, and diabetes, VO ₂ max achieved during a graded exercise test has the strongest inverse association with all-cause mortality and cardiac events in both a clinically referred population and among asymptomatic people of both sexes without existing cardiovascular disease.

Deriving biological age from VO ₂ max has great clinical utility since it may enable a more accurate risk stratification in those individuals undergoing exercise testing. For example, a trained 70-year-old can exhibit the same biological age as an untrained 50-year-old based on their VO ₂ max. Indeed, in a recent study , VO ₂ max-associated biological age demonstrated better discrimination for mortality and MI than chronological age.

Therefore, biological age may help identify those most benefit from pharmacologic and more aggressive lifestyle interventions. Furthermore, utilizing biological age provides an intuitive understanding of fitness-mediated risk and may prompt greater compliance with important lifestyle changes.

The Numbers Behind the Strong Link Between VO2 Max and Longevity

A proportionally high VO ₂ max is a strong clinical vital sign of health and longevity. Probably, no other biological variable has as much relevance to health and longevity as VO ₂ max, to an extent where a high VO ₂ max attenuates the negative impact of the presence of other known cardiovascular risk factors, such as hypertension, hypercholesterolemia, and diabetes.

The greatest rates of mortality are found at levels of VO ₂ max lower than 27.6 ml/min/kg.

Every 3.5ml/min/kg VO ₂ max increase corresponds to a 12% gain in life expectancy.

Furthermore, each 3.5ml/min/kg VO ₂ max increment in peak treadmill workload is associated with a 14% reduction in cardiac events and a 7ml/min/kg VO ₂ max increase in treadmill performance is related to a 30% reduction in mortality.

Among patients who have had an MI, every 3.5ml/min/kg VO ₂ max increase is associated with a reduction in mortality from any cause that ranges from 8-14% over 19 years of follow-up.

In a 20-year follow-up study, mortality risk was 61% lower in physically fit individuals compared with their unfit counterparts. The mortality risk was also 34% lower in participants defined as unfit during the initial exercise test, who became physically fit by the follow-up test though. Lastly, fit participants who drifted into the unfit category by the second test maintained 41% lower risk than those who were unfit in both tests.

A recent follow-up studysuggested that 1ml/min/kg higher VO ₂ max re-examination at 11 years was associated with a 9% relative risk reduction in all-cause mortality. This study even set the threshold in the elderly at 17.5 ml/min/kg for an independent lifestyle and a higher survival rate.

Key Takeaways

Overall, fitness-related health benefits, such as the reversion of biological age, can be achieved regardless of age or fitness status. According to the AHA guidelines, the addition of VO ₂ max as a measure of exercise capacity for risk classification can help improve patient management and reinforce lifestyle-based strategies to improve overall health. Therefore, health professionals should encourage individuals to initiate and maintain a physically active lifestyle to improve their exercise capacity and thus lower the risk of morbidity and mortality.

How Breathing & Physical Health Interact

j.oswald@hyperionhealth.ca (Jesse Oswald) — Wed, 22 May 2024 19:00:00 GMT

Highlights:

Breathing affects physical health through 3 fundamental mechanisms. The excitation of the central nervous system, the mechanical movement of the diaphragm, and the regulation of our blood’s chemistry.
These three pathways can become the source or a significant contributor to several conditions, from lower back pain to allergic reactions, inflammation, and cardiovascular disease.
Breathing correctly is thus a fundamental mechanism for maintaining healthy blood chemistry, nervous system balance, and abdominal function.

Humans have widely leveraged the connection between breathing and physical health throughout millennia as a healing tool for the disorders of our body and the soul. Our previous article, “Breathing & Psychological Stress: A two-way street,” described the physiological processes that connect the brain and breathing, enabling us to control stress levels and emotions by deliberately changing our breathing. However, a set of similar functions can also heavily influence other core physiological processes that can impact our physical health.

The scientific community’s renewed interest in the mechanics and biology of breathing has shed light on the fundamental mechanisms connecting respiration and the mind and those connecting respiration and physical health. By analyzing them, we can begin to understand how chronic inflammation and over-excitation of our immune system lead to auto-immune disorders, lower back pain, digestion disorders, and more.

As a first step, let’s understand the fundamental biomarkers that characterize how healthy our breathing process is. These include:

End-tidal CO2: The amount of carbon dioxide we exhale.
Tidal volume: The volume of air we exhale.
Breathing frequency: The number of breaths we take per minute.

These biomarkers reflect our breathing health because they constitute the basic mechanisms by which breathing affects nearly everybody process, including digestion, immune response, mitochondrial function, cardiovascular health, and hormonal balance. To understand how all these systems are affected by our breathing, let’s examine, step by step, the sequence of events occurring when the three fundamental breathing variables are perturbed from their average values.

How Breathing Affects The Nervous System

Breathing and the autonomic nervous system (ANS) are inextricably linked through various mechanisms. ANS is divided into two parts: the Sympathetic Nervous System (SNS) and the Parasympathetic Nervous System (PNS) . SNS causes us to go into “fight-or-flight” mode by engaging all the mechanisms required for movement, preservation, and fast reaction. Conversely, PNS causes feelings of relaxation and enables us to recover, digest, and heal. The link between ANS and breathing is made possible through how the neurons connect to the different lung parts. Specifically, SNS is connected to the upper part, whereas PNS is connected to the lower lungs. Due to the anatomy of the connection between lungs, SNS, and PNS, we engage SNS and partially deactivate PNS when we breathe faster and shallower. On the contrary, when we deliberately breathe deeper and slower, we can activate PNS thanks to its connection to the lower part of our lungs and thus enable feelings of relaxation.

Breathing continuously faster and shallower, a condition called Chronic Hyperventilation Syndrome (CHS), causes a chronic hyper-activation of SNS, setting our body in a perpetual state of increased stress. Engagement of SNS signals to our body the presence of danger and thus triggers a chain of reactions to prime us for facing it. Although these processes have been developed over thousands of years of evolution and can be lifesaving given their effect of setting us ready to respond to threats, their constant activation causes a cascade of negative repercussions. Here are the main mechanisms and physiological systems affected:

Digestive System: The engagement of SNS causes blood to leave the stomach and core and is channelled to the brain and muscles to render our body ready to think and react fast. Stomach ischemia (lack or absence of blood) causes digestion to slow or halt, leading to chronic digestion and gastrointestinal issues.
Cardiovascular System: Engagement of the SNS increases blood pressure to render our muscles better able to reach fast and respond to threats. However, a chronic increase in blood pressure leads to hypertension, eventually leading to life-threatening cardiovascular conditions such as coronary artery disease. Moreover, irregular breathing patterns can lead to diaphragmatic atrophy, in which the diaphragm moves less, adding additional strain to the heart.
Immune System: Engagement of the SNS also engages our immune system through the Hypothalamic-Pituitary-Adrenal (HPA) axis. The HPA axis is the conglomeration of three critical physiological systems, namely the Hypothalamus, the Pituitary, and the Adrenal gland, that cooperate to convert brain signals and stimuli into physiological responses necessary to elicit the appropriate bodily reaction. When stress stimulus occurs
Endocrine regulation: Engagement of the SNS also impacts our hormones critical to the endocrine balance through the Hypothalamic-Pituitary-Adrenal (HPA) axis. The HPA axis is the conglomeration of three crucial physiological systems, namely the Hypothalamus, the Pituitary, and the Adrenal gland, that cooperate to convert brain signals and stimuli into physiological responses necessary to elicit the appropriate bodily reaction. When a stress stimulus is perceived through the hypothalamus, it sends an alert to the pituitary gland through the corticotropin-releasing hormone (CRH). In addition to stimulating the sympathetic nervous system, CRH will stimulate the pituitary gland and cause it to release adrenocorticotropic hormone (ACTH). ACTH travels through the body and targets the adrenal gland causing them to release cortisol. When stress is constantly elevated, cortisol levels will remain high and induce a cascade of adverse effects, including:
Suppression of reproductive function
Increase in insulin resistance, a precursor to diabetes
Suppression of growth and thyroid hormone release impedes development, physical recovery, and thyroid function.
Immune system hyperactivation: Our central nervous system is also interconnected with our immune system through a molecule called Cytokines. Cytokines are a general category of small proteins that play an essential role in cell signalling. They control the growth and activity of immune blood cells, enabling them to trigger inflammation and respond to pathogens. Overactivation of the sympathetic nervous system can, therefore, result in constant activation of the immune system, leading to chronic inflammation and auto-immune disorders.

How Mechanics Of Breathing Affect Our Body

In addition to the nervous-based interaction between breathing and several key sectors of our physiology, breathing also affects our health through the mechanics of respiration.

Cardiovascular Strain: One of the most critical systems in our breathing apparatus is the diaphragm, a dome-shaped muscle between the lungs and the abdominal area. The diaphragm moves down and up, and we inhale and exhale. Our abdomen contains 25-30% of our body’s total blood volume, making it one of the most blood-dense areas of our body. Rapid and shallow breathing reduces the engagement of the diaphragm and can, over time, lead to diaphragmatic atrophy, the state where the diaphragm weakens and moves less during respiration. The movement of the diaphragm aids in abdominal blood circulation, representing a significant part of the overall blood circulation in our body. This is why the diaphragm is also referred to as the second heart . As a result, diaphragmatic atrophy leads to a minor contribution of the diaphragm on blood circulation and thus increases the load our heart has to support whole-body circulation.

Posture and skeletal muscular disorders: The diaphragm is a critical component of our breathing apparatus. Strong diaphragmatic engagement increases abdominal pressure, engages the abdominal muscles, and thus provides support to our core and lower back. On the contrary, weak diaphragmatic movement caused by shallow breathing weakens our core stability and is a key factor for developing lower back pain and other skeletal muscle disorders.

Brain oxygenation: Breathing and hyperventilation is the primary regulator of the blood's balance between oxygen and carbon dioxide. As breathing becomes faster, the air exhaled increases along with the amount of carbon dioxide (CO2) expelled through the body. As more CO2 leaves the body, CO2 circulating in the blood declines, causing a cascade of adverse effects as it is responsible for two critical biological functions. First, CO2 enables oxygen molecules to detach from hemoglobin (the substance in our blood responsible for transporting oxygen from our lungs across the body) and enter the cells that need them to produce energy. Second, CO2 regulates how narrow or wide our arteries are and the amount of blood delivered across the body. As a result, reducing, making it harder for oxygen to enter cells and narrowing the arteries, diminishing blood delivery to the brain and across the body.

The following graph provides a summary of how these mechanisms interact with each other:

Conclusion

Breathing is a crucial regulator of several critical functions, including blood chemistry, nervous system balance, and abdominal pressure. Learning how to breathe in accordance with your metabolic needs can become a healing factor for many psychosomatic disorders and prevent the onset of chronic conditions. As a result, breathing is the most influential physiological function that’s in your control.

Exercise and Mental Health

j.oswald@hyperionhealth.ca (Jesse Oswald) — Wed, 15 May 2024 19:00:03 GMT

Highlights

Exercise has been shown to be a powerful drug against mental disorders
Physical exercise induces its beneficiary effect through several mechanisms that involve growth factor production, mitochondrial biogenesis, and angiogenesis
According to one of the most significant meta-analysis studies on mental health, exercise should be a primary tool for mental health preservation.

In our previous article, “Nutrition & Mental Health,” we looked into the transformative nature nutrition can have on brain metabolism and, by implication, mental health. According to the decades-old theory correlating metabolism and mental health disorders, abnormalities in cellular brain metabolism, specifically mitochondria function, result in abnormal behaviour in several physiological mechanisms that control our mood, including neurotransmitter release, hormone release, hormonal resistance, and premature brain cell death. The quality, timing, and amount of food we consume have been shown to either promote or deter these deleterious mechanisms and, as a result, cause our mental health to deteriorate or improve respectively. Food is, consequently, a significant driver of mental health. Exercise has also been shown to be an equally, if not more significant, contributor to mental health. In this article, we explore the mechanisms through which physical exercise can support brain metabolism and thus play a significant role in helping one overcome psychiatric disorders.

How Exercise Impacts Brain Function

Exercise impacts brain metabolism through various mechanisms. Here are the main ones involved:

Blood delivery: Physical activity increases blood flow and oxygen delivery to the brain, which enhances the brain's energy metabolism. This increased blood flow also promotes the release of growth factors and neurotrophins, which support the growth and survival of neurons.
Neurotransmitter production: Exercise also stimulates the production of neurotransmitters, such as dopamine and serotonin, which play a role in mood regulation and cognitive function. These neurotransmitters can improve mood, reduce stress, and enhance cognitive abilities.
Growth factors: Furthermore, exercise has been shown to increase the production of brain-derived neurotrophic factor (BDNF), a protein that supports the growth and maintenance of neurons. BDNF promotes neuroplasticity, which is the brain's ability to adapt and change in response to new experiences and learning.
Angiogenesis: Regular exercise has also been linked to forming new blood vessels in the brain, a process called angiogenesis. This increased vascularization improves blood flow and nutrient delivery to brain cells, supporting their overall function.
Mitochondrial biogenesis: During exercise, the increased demand for energy triggers a process called mitochondrial biogenesis, which involves the creation of new mitochondria. This increase in mitochondrial density enhances the brain's ability to produce ATP, the energy currency of cells.
Protein synthesis: Exercise also stimulates the production of proteins involved in mitochondrial function and maintenance. These proteins help optimize the efficiency of mitochondrial respiration and the electron transport chain, which are essential for generating ATP.

The Unique Role of Zone 2 Training

Out of all types of exercise, Zone 2 training holds a special place in brain metabolism and, thus, mental health. Before diving into why, let’s first closely examine the different types of exercise. The three main types of training include endurance base training (also known as Zone 2 training which involves continuous exercise at Zone 2), resistance training (lifting weights or using other means to apply muscle resistance), and interval training (alternating between different exercise intensities while doing some sort of cardio like running or cycling). Here’s how each type affects our brain function and emotional state:

Improved mitochondrial function: Zone 2 training specifically targets and improves mitochondrial function. Mitochondria are the powerhouses of our cells and are responsible for producing energy. Enhancing mitochondrial function through Zone 2 training gives the brain a more efficient and sustained energy supply, improving cognitive function and overall brain health.
Enhanced fat-burning efficiency: Zone 2 training promotes the utilization of fat as a fuel source during exercise. This can be beneficial for brain health as it helps maintain stable blood sugar levels and prevents spikes in insulin. Consistent fat-burning during exercise can also support healthy brain metabolism and reduce the risk of metabolic disorders that can negatively impact brain function.
Increased secretion of growth factors: Zone 2 training stimulates the secretion of growth factors in the brain. These growth factors promote the growth of new blood vessels and cells in the brain, leading to improved memory, cognition, and overall brain health.
Improved recovery capacity: Zone 2 training helps enhance the body's recovery capacity, allowing for faster recovery after intense bouts of exercise. This is important for brain health as it reduces the risk of overtraining and supports optimal cognitive function.

A Widely Studied Intervention

The mechanisms through which exercise affects brain metabolism and its benefits for mental health are widely recognized and substantiated by an incredible breadth of scientific research. The scientific validation covers various psychiatric disorders through large-scale epidemiological studies.

Depression: Numerous studies have shown that exercise can effectively treat depression. For instance, a meta-analysis of 25 randomized controlled trials found that exercise significantly reduced depressive symptoms in individuals with major depressive disorder.
Anxiety disorders: Exercise has been shown to reduce symptoms of anxiety disorders, such as generalized anxiety disorder and panic disorder. A systematic review and meta-analysis of 49 studies found that exercise interventions were associated with a significant reduction in anxiety symptoms.
Post-traumatic stress disorder (PTSD): Exercise benefits individuals with PTSD. Research suggests that exercise can help reduce symptoms of PTSD, such as intrusive thoughts and hyperarousal, and improve overall well-being.
Attention deficit hyperactivity disorder (ADHD): Exercise has been shown to affect individuals with ADHD positively. Studies have indicated that exercise can improve attention, executive function, and behavioural symptoms in children and adults with ADHD.
Substance use disorders: Exercise can be a helpful adjunct to treatment for substance use disorders. Research suggests that exercise can reduce cravings, improve mood, and support overall recovery in individuals with substance use disorders.

The effectiveness of exercise on psychiatric disorders was also recently validated through a large-scale meta-analysis study encompassing an enormous amount of data points from 97 meta-reviews of 1,039 randomized controlled trials involving 128,119 participants.

Conclusion

In conclusion, the relationship between nutrition, exercise, and mental health is becoming increasingly evident as scientific research sheds light on these lifestyle factors' transformative impact on brain metabolism and overall well-being. Nutrition significantly influences brain function by affecting cellular metabolism, neurotransmitter release, and hormonal balance. Similarly, exercise exerts powerful effects on brain metabolism through increased blood flow, neurotransmitter production, growth factors, angiogenesis, mitochondrial biogenesis, and protein synthesis.

Among various exercise modalities, Zone 2 training is particularly beneficial for brain health due to its targeted improvement of mitochondrial function, enhanced fat-burning efficiency, increased secretion of growth factors, and improved recovery capacity. The substantial body of scientific research supporting the positive effects of exercise on mental health covers a wide range of psychiatric disorders, including depression, anxiety disorders, PTSD, ADHD, and substance use disorders.

Incorporating regular exercise and a balanced diet into our daily lives can significantly benefit mental health and cognitive function. These lifestyle choices can act as powerful tools to help individuals overcome psychiatric disorders and improve their overall well-being. As we continue to deepen our understanding of the intricate relationship between nutrition, exercise, and mental health, it becomes increasingly clear that promoting a healthy lifestyle benefits our physical health and is essential for nurturing a resilient and vibrant mind.

Respiratory Training: A Neglected but Significant Training Modality

j.oswald@hyperionhealth.ca (Jesse Oswald) — Wed, 08 May 2024 19:00:00 GMT

Respiratory Training

Respiratory training is the deliberate modification of how we usually breathe throughout the day by implementing specific exercises and techniques to eventually improve oxygen uptake, lung function, and overall well-being and enhance athletic performance. Respiratory training aims to strengthen the diaphragm, which is the primary muscle of respiration, as well as the inspiratory rib cage muscles. This will eventually increase lung capacity and optimize oxygen delivery to the body’s tissues, including muscles, at rest and during exercise.

Respiratory training can be applied through various techniques based on the ultimate goal and what best suits the individual. The most popular type of respiratory training is diaphragmatic breathing. It can be performed in a supine position, sitting or standing, based on the practice level of the individual. When you first learn the diaphragmatic breathing technique, you should practice it lying on your back. Bend your knees and support your head using a pillow or a folded towel to relax your neck and shoulder muscles. Place one hand on your upper chest and the other on your belly below your ribcage to feel your diaphragm moving up and down. Breathe slowly through your nose so your stomach pushes out, causing your hand to rise. The hand that lies on your chest should remain as still as possible. To exhale, pursue your lips as if you are going to whistle or gently blow on a hot drink. Exhale slowly and gently through your pursed lips by tightening your abdominals so that your stomach moves in.

Two other common forms of respiratory training include inspiratory muscle training (IMT) and yogic breathing. IMT involves breathing exercises using a pressure threshold device to strengthen the inspiratory muscles, such as the external intercostals. It’s a form of resistance training for these muscles since it strengthens them, improving stamina and reducing breathing fatigue. It is performed sitting or standing, where the individual puts on a nose clip, holds the IMT device by the handle grip, and places the mouthpiece in the mouth. They breathe out as far as they can and take a fast, forceful breath through their mouth, trying to breathe as much air as they can while expanding their chest. They then breathe out slowly with minimal effort while letting their shoulders relax. Yogic breathing, also referred to as pranayama, is mainly practiced through the guidance of a certified yoga instructor. It involves breath control via patterns and variations in respiration rate, with specific instructions regarding the number of breaths over a certain period of time. Some variations of yogic breathing include alternate nostril, paced, and box breathing.

Respiratory training is mainly used by people suffering from breathing problems such as asthma and chronic obstructive pulmonary disease (COPD). COPD is a group of respiratory diseases that cause airflow obstruction and breathing-related problems, such as dyspnea. It includes emphysema and chronic bronchitis and is the fourth leading cause of death in the US. However, respiratory training is also regularly used by athletes who wish to improve their sports performance by strengthening their breathing muscles, thus improving breathing stamina and strength, and eventually endurance during aerobic exercise.

The benefits of respiratory training are due to a combination of physiological mechanisms. Two of the main mechanisms are increased oxygen delivery and improved tissue oxygenation. Respiratory training allows increased amounts of oxygen to enter the bloodstream through the lungs, enhancing oxygen delivery to the body’s tissues and organs, such as the working muscles. The improved tissue oxygenation is crucial for the proper functioning of cells. It promotes metabolic processes which require oxygen to be attained and produce energy, which is valuable for accomplishing vital cellular functions. The increased cellular energy produced is in the form of adenosine triphosphate (ATP). ATP is the primary energy source for cells and derives from this increased metabolic function attained through respiratory training. Another vital mechanism through which respiratory training works is wound healing. Adequate oxygen levels are necessary for tissue repair and regeneration as well as angiogenesis (the growth of new blood vessels) in the injured area.

Regarding mechanisms around lung mechanics per se, respiratory training alleviates the strain on the respiratory system by strengthening inspiratory muscles, better controlling breath, and eventually making breathing easier. Therefore, it reduces the effort required to breathe (work of breathing) and improves oxygen exchange in the lungs. This is particularly helpful when oxygen demand increases, as happens in pulmonary diseases and/or during exercise. Especially when the intensity of exercise increases, the breathing volume or ventilation must also rise to cope with the oxygen demand. The inspiratory muscles must contract more forcefully and rapidly to keep pace with the substantial increase in metabolism, and this process can be attained through respiratory training.

Each proposed mechanism above can lead to several benefits that respiratory training may offer an individual who regularly practices it. One of the most important benefits associated with the first two mechanisms described above is the reduction of lung disease symptoms, such as shortness of breath (at rest and during exercise), whizzing, chest tightness, and lack of energy. Therefore, people suffering from pulmonary diseases can have a much better quality of life by participating and enjoying all aspects of life. By improving lung health-related symptoms, respiratory training can vastly enhance sleep quality. Many people with compromised lung function face sleeping-related breathing disorders, with sleep apnea being the most common. Engaging in respiratory training techniques can significantly decrease these symptoms, resulting in better sleep and reduced daytime fatigue.

Nevertheless, as already mentioned, respiratory training can also lead to improved physical performance, which most athletes long for. Elevated oxygen uptake can increase the amount of lung capacity a person is able to use per breath (tidal volume) as well as the oxygen delivered to the working muscles during exercise, thus improving cardiovascular endurance during exercise or sports activities, such as running and cycling. Lung capacity and cardiovascular endurance are also assessed through the active test performed by the PNOĒ metabolic analyzer. Their respective metrics in the PNOĒ active reports are expressed as aerobic health and respiratory capability, respectively. Respiratory training can further enhance athletic performance by contributing to the recovery process after exercise. It helps reduce muscle soreness, accelerate tissue repair, and promote faster recovery between workouts. This increased recovery capacity is also assessed and depicted in the PNOĒ active reports.

Respiratory training also strengthens the inspiratory muscles and improves breath control at rest and during exercise. Therefore, it helps improve breathing and posture as well as breathing and stability, metrics provided in the PNOĒ resting and active metabolic reports, respectively. As a result, musculoskeletal problems, especially in the spine, arising from not breathing properly, thus not properly activating the deep core muscles, especially during exercise, can be avoided. Lastly, respiratory training can improve brain oxygenation, enhancing cognitive performance, improved concentration, and mental clarity at rest and during exercise. These are also metrics assessed through the PNOĒ metabolic analyzer (the breathing & cognition metrics in both the resting and active metabolic reports).

Respiratory training is the deliberate modification of how we usually breathe by implementing specific exercises and techniques. Its benefits are due to a combination of mechanisms, including increased oxygen delivery, improved tissue oxygenation, increased energy (ATP) levels, and enhanced respiratory muscle strength. These mechanisms work together to reduce lung disease symptoms and improve sleep quality, sports performance, recovery, and brain function.

References

Ambrosino N. Inspiratory muscle training in stable COPD patients: enough is enough? Eur Respir J. 2018;51(1):1702285
Basso-Vanelli RP, Di Lorenzo VAP, Labadessa IG, Regueiro EMG, Jamami M, Gomes ELFD, Costa D. Effects of inspiratory muscle training and calisthenics-and-breathing exercises in COPD with and without respiratory muscle weakness. Respir Care. 2016;61(1):50-60
Bostanci O, Mayda H, Yilmaz C, Kabadayi M, Yilmaz AK, Ӧzdal M. Inspiratory muscle training improves pulmonary functions and respiratory muscle strength in healthy male smokers. Respir Physiol Neurobiol. 2019;264:28-32
de Medeiros AIC, Fuzari HKB, Rattesa C, Brandão DC, de Melo Marinho PÉ. Inspiratory muscle training improves respiratory muscle strength, functional capacity and quality of life in patients with chronic kidney disease: a systematic review. J Physiother. 2017;63(2):76-83
HajGhanbari B, Yamabayashi G, Buna TR, Coelho JD, Freedman KD, Morton TA, Palmer SA, Toy MA, Walsh C, Sheel AW, Reid DW. Effects of respiratory muscle training on performance in athletes: a systematic review with meta-analyses. J Strength Cond Res. 2013;27(6):1643-1663
Illi SK, Held U, Frank I, Spengler CM. Effect of respiratory muscle training on exercise performance in healthy individuals: a systematic review and meta-analysis. Sports Med. 2012;42(8):707-724
Walterspracher S, Pietsch F, Walker DJ, Röcker K, Kabitz H-J. Activation of respiratory muscles during respiratory muscle training. Respir Physiol Neurobiol. 2018;247:126-132

The Role of Exercise and Kinesiologists in Preventing Chronic Disease and Alleviating Healthcare Burden in Alberta, Canada

j.oswald@hyperionhealth.ca (Jesse Oswald) — Wed, 01 May 2024 19:00:00 GMT

Introduction:

Chronic diseases impose a substantial burden on healthcare systems globally, with sedentary lifestyles contributing significantly to their prevalence. In Alberta, Canada, sedentary behaviours have become alarmingly common, leading to a surge in chronic disease incidence and healthcare costs. This report delves into the importance of exercise and physical activity in preventing chronic diseases, the challenges physicians face in promoting physical activity, and the potential role of kinesiologists and clinical exercise physiologists in mitigating these challenges.

Importance of Exercise and Physical Activity in Preventing Chronic Disease:

Physical activity is essential for maintaining overall health and preventing chronic diseases. According to statistics from Alberta Health Services, sedentary behaviour is a significant risk factor for chronic diseases, with approximately 36% of Albertans reporting low physical activity levels. This places a substantial burden on the healthcare system, contributing to increased healthcare costs associated with managing chronic conditions.

The Canadian Physical Activity Guidelines recommend that adults aim for at least 150 minutes of moderate to vigorous physical activity weekly to achieve health benefits. However, Canadian Community Health Survey data indicates that approximately 66% of adults and 28% of youth do not meet the recommended physical activity guidelines. Insufficient physical activity is a proven risk factor for the development of chronic diseases, including obesity, type 2 diabetes, hypertension, and coronary artery disease.

Statistics on Sedentary Behaviours and Healthcare Burden in Alberta:

In Alberta, sedentary lifestyles are pervasive, contributing to the high incidence of chronic diseases. According to the Alberta Health Services, approximately 62% of adults in Alberta are considered overweight or obese, and only 55% meet the recommended levels of physical activity. This sedentary behaviour contributes to the increasing burden on the healthcare system, with chronic diseases accounting for approximately 80% of healthcare expenditures in the province.

Impact of Physical Activity on Chronic Disease Incidence:

Regular physical activity has been shown to significantly reduce the risk of developing chronic diseases. For instance, a meta-analysis published in the British Medical Journal found that physically active individuals have a 30-40% lower risk of developing type 2 diabetes compared to sedentary individuals. Similar reductions in the incidence of cardiovascular diseases and certain cancers have been observed among physically active individuals.

Challenges Faced by Physicians in Promoting Physical Activity:

Physicians are critical in promoting physical activity and lifestyle interventions to manage chronic conditions. However, time constraints and competing priorities often limit their ability to provide comprehensive exercise and physical activity counselling. Many physicians report needing to be more adequately trained in exercise prescription and lifestyle interventions, further hindering their effectiveness in promoting physical activity among patients.

Role of Kinesiologists and Clinical Exercise Physiologists:

Kinesiologists and clinical exercise physiologists are allied healthcare professionals specialized in exercise prescription and rehabilitation. In Alberta, Certified Exercise Physiologists (CEPs) certified by the Canadian Society for Exercise Physiology (CSEP) and Professional Kinesiologists (PKs) certified by the Alberta Kinesiology Association play a crucial role in promoting physical activity and managing chronic conditions.

Education and Scope of Practice of CSEP-CEP and Professional Kinesiologists in Alberta:

CSEP-CEPs undergo rigorous education and training, including a bachelor's degree in kinesiology or related fields, followed by certification through the CSEP. They are trained to assess individuals' health status, develop personalized exercise prescriptions, and provide ongoing support and monitoring to enhance physical activity adherence and health outcomes. PKs also possess similar education and training, focusing on exercise science and kinesiology principles, and are equipped to work with individuals of all ages and levels of complexity in their disease process.

Integration of Kinesiologists and Clinical Exercise Physiologists in the Healthcare System:

Kinesiologists and clinical exercise physiologists support the work of physicians by offering customized exercise programs tailored to individual needs and abilities. They can be found in various healthcare settings, such as primary care clinics, rehabilitation centers, and community health programs, where they collaborate closely with physicians to provide comprehensive care to patients with chronic conditions. The exercise specialists at Hyperion Exercise and Health have master's training and hold dual certifications, including the Alberta Kinesiology Association - Professional Kinesiologist designation and the Canadian Society for Exercise Physiology - Clinical Exercise Physiologist designation. Our practitioners are particularly well-informed and experienced in managing the care of patients with one or more stable chronic medical conditions, as well as prescribing exercise for musculoskeletal injury rehabilitation and chronic pain management.

Hyperion Exercise and Health's Role in Facilitating Physical Activity:

Hyperion Exercise and Health understands the challenges patients face in promptly accessing exercise interventions. We aim to help patients avoid long wait times to consult an exercise specialist within the Primary Care Network (PCN). Patients often lose motivation or urgency to get active when faced with several weeks to month-long wait times for consultation within the PCN, especially those in the pre-contemplation, contemplation, or preparation stages of behaviour change. By reducing wait times, we ensure that the motivation or urgency to get active is preserved. Our secure tele-health system provides direct and immediate access to our team of master's trained professional kinesiologists and clinical exercise physiologists. Our team offers personalized exercise and lifestyle programming, ensuring safe and effective interventions to help patients become physically active and manage chronic conditions at a low cost. Some extended health benefits providers may also cover kinesiology or exercise physiology services. By bridging the gap between patients and exercise professionals, we aim to empower individuals to lead healthier lives and alleviate the burden on the healthcare system.

Conclusion:

Exercise and physical activity are paramount in preventing chronic diseases and reducing healthcare burden in Alberta, Canada. Despite physicians' challenges in promoting physical activity, kinesiologists and clinical exercise physiologists offer a viable solution by providing specialized exercise interventions and support to individuals with chronic conditions. By leveraging the expertise of exercise professionals and innovative approaches such as telehealth services, we can enhance access to exercise interventions and improve health outcomes for individuals across the province.

References:

Alberta Health Services. (2020). Physical Activity in Alberta: A snapshot of current behaviours. Retrieved from https://www.albertahealthservices.ca/assets/info/public/health-res-prov-physical-activity-in-alberta.pdf
Alberta Health Services. (n.d.). Alberta's Obesity Strategy. Retrieved from https://www.albertahealthservices.ca/strategicdirections/priorities/obesity.aspx
American College of Sports Medicine. (2020). ACSM's Guidelines for Exercise Testing and Prescription. Wolters Kluwer.
Canadian Physical Activity Guidelines. (2020). Retrieved from https://csepguidelines.ca/
Canadian Society for Exercise Physiology. (n.d.). CSEP-CEP Certification. Retrieved from https://www.csep.ca/education/certification/csep-cep-certification
Colberg, S. R., Sigal, R. J., Fernhall, B., Regensteiner, J. G., Blissmer, B. J., Rubin, R. R., ... & Braun, B. (2010). Exercise and type 2 diabetes: the American College of Sports Medicine and the American Diabetes Association: joint position statement executive summary. Diabetes care, 33(12), 2692-2696.
Statistics Canada. (2020). Physical activity during the COVID-19 pandemic. Retrieved from https://www150.statcan.gc.ca/n1/pub/11-627-m/11-627-m2020038-eng.htm
Warburton, D. E., Nicol, C. W., & Bredin, S. S. (2006). Health benefits of physical activity: the evidence. Canadian medical association journal, 174(6), 801-809.

Habit Formation and its Application to Lifestyle Patterns such as Diet and Exercise

j.oswald@hyperionhealth.ca (Jesse Oswald) — Wed, 24 Apr 2024 19:00:00 GMT

Key Points

Habit formation is encouraged by attitudes, goals, and motivation to attain desired outcomes.
Habit maintenance is governed by the coexistence of salient environmental cues in a friction-minimizing context and with adequate reward mechanisms, which will make the habit easy and enjoyable to repeat.
Habit slips can normally happen under stressful and other unfavourable conditions, but applying effective strategies can create concrete habit change towards adopting good habits.

We, as humans, are all creatures of habit. From drinking coffee in the morning to brushing our teeth before bed, much of our lives are driven by habits. Habits are thus these default responses, or more articulately, a specific behaviour's sufficiently frequent or consistent performance in a stable context. Some habits persist for longer periods in the natural course of life, whereas others are not maintained. Habits are essential in regulating desirable everyday behaviour or consolidating long-term behaviour change. However, habits may decay when they are no longer activated or are replaced by other actions.

Habit Formation

Behavioural scientists who study habit formation say that most of us try to establish healthy habits incorrectly. For instance, we make bold resolutions to start exercising or lose weight without taking the steps needed to set ourselves up for success .

To begin with, positive, strong, and stable attitudes can be an important starting point for behaviour change, especially if the behaviour is something a person really wishes to form. If successful, such change may be consolidated by turning the newly formed behaviour into a habit (habit formation). Therefore, when we do something new, and it works, or we like it, this behaviour will likely be repeated and ultimately become habitual.

Furthermore, goals influence habit formation by energizing and directing action toward a desired end state. For example, if we decide to start eating one fruit every morning, we can actively manage our context accordingly by placing it on the nightstand before bed. Since everyday habits develop as people pursue life goals, habit formation is a product of repeated behaviours in the service of goal pursuit.

Although attitudes and goals play an essential role in habit formation, once habits are established, they get automatically activated by context cues independent of attitudes or motivation. Various cues, including locations, particular people, visual cues, and existing good habits, might trigger habit performance . For example, existing good habits, such as having breakfast, can be utilized to more easily stack new habits, such as by supplementing this breakfast with fruits.

Apart from cues, habit formation also strengthens through reward-learning mechanisms. Using rewards (extrinsic or intrinsic motivation) can also promote habit formation . Extrinsic rewards, especially when uncertain or unexpected, encourage habit formation by engaging dopamine systems. More specifically, dopamine signals promote habit learning as people repeat responses to extrinsic rewards, such as praise from a friend for going to the gym.

Furthermore, adopting a new habit may be rewarding (intrinsic motivation) because it makes life easier by eliminating the need for new learning or decision-making (reduced mental effort). Intrinsic rewards are generally superior to external rewards for habit formation.

Overall, habit formation is crucial since it accumulates specific features, such as frequency, thus speed, and fluency, as well as the simplicity of the behaviour, that are more likely to favour the habit over other alternatives.

Habit Maintenance

For good and constructive behaviours that serve desired goals, such as adhering to a diet or taking up regular exercise, the longevity of the behaviour is desirable, and habit formation is crucial. Once established, habits are not easily influenced by the distraction caused by tempting alternative courses of action, stress, fatigue, or lack of motivation. They are characterized by automaticity and a lack of awareness ; they directly happen due to recurring environmental cues without being consciously guided by goals, rewards, intentions, and attitudes anymore.

Therefore, individuals who form and maintain good habits can pursue desired outcomes with minimal effort. In other words, habit maintenance makes life work better for the individual and protects goal accomplishment, particularly under depleted mental resources when good habits might otherwise be derailed. So, if, for whatever reason, an individual is less capable of exerting willpower to accomplish desired outcomes, habits become the default behaviour; thus, procrastination and rationalization can be avoided.

If, on the other hand, those behaviours have not been turned into habits, they are vulnerable to attitudinal fluctuations, temptations, or rationalizations, hence the possibility of falling back on bad or undesirable habits.

Habit Slips

Everyone tends to fall back on existing bad habits when they lack the capacity or motivation to make decisions that align with their goals. Habit slips do not happen due to unfavourable attitudes or lack of motivation. They are especially likely to occur when various factors reduce the motivation or ability to deliberately pursue desired goals and thus tip the balance towards relying on bad habits. Such factors include distractions, time pressure, stress, addictions, limited task ability, and limited willpower .

Although an ideal scenario would be to keep your good habits one hundred percent of the time, this is highly unlikely to be the case since recurring environmental cues of the bad old habits continue to be activated automatically. However, habit slips are not always bad and should not disappoint the individual, let alone when people can quickly and consciously get back on track.

To more efficiently manipulate possible habit slips, the individual should be able to recognize and troubleshoot the reasons that triggered them, as well as move away from the obstacles that disrupted the routine around this habit.

Habit Change

Bad habits may change or be overcome with sufficient motivation, strong attitudes, and opportunities. Therefore, unless we are distracted, stressed, or fatigued, we can effortfully discontinue a bad habit and think about better alternatives. For example, when existing habits conflict with our current goals, we can use these goals to inhibit the bad habit. This process is cognitively demanding, though, and requires awareness and motivation to deliberately inhibit the bad habit.

Habit change depends on three core processes : a) disrupting cues associated with bad habits, b) structuring the environment to make it easy to repeat beneficial habits in stable contexts, and c) linking desired habits to rewards (extrinsic, such as praise from a friend and/or intrinsic, such as the sense of self-esteem and confidence for adopting a good habit).

We are more likely to change a bad habit, such as eating a lot of fast food or sitting too much with a good one, such as eating fruits and vegetables or exercising, if we apply appropriate strategies toward that goal. More specifically, if we restructure our environment to make the good habit easily repeatable in a stable context devoid of temptations and to disrupt antagonistic habits and their cues and make the good habit rewarding, we have exploited the core mechanisms for long-term habit change.

Therefore, breaking bad habits is less about how much one intends to change behaviour and more about whether one eliminates or disrupts the specific cues associated with the undesired habit. For example, we can modify our environment to make it easy and convenient to eat fruit instead of a sweet by eliminating sweets from our drawers and fridge and leaving fruits on a very visible site in our home (e.g., counter). We can also establish a consistent time and location for exercise each day or some days per week. Lastly, we can find ways to reward ourselves for eating healthy and exercising by emphasizing aspects of the habit that are immediately and unexpectedly rewarding (e.g., a sense of accomplishment or stress relief from constantly looking for food to order).

Strategies to Avoid Bad Habits

The most straightforward strategy to avoid or change an unwanted habit is to monitor the behaviour and the circumstances of its occurrence and effortfully try to inhibit the performance of the habit. This process, known as vigilant monitoring , is the most effective strategy to inhibit unwanted habits. For example, if you go out for dinner and mostly eat junk food, you can hinder this bad habit by having cooked and eating at home before going out. Also, if you return home after work and do not have the willpower to go to the gym, you can have the training bag with you so that you go straight after work instead of crashing out on the sofa watching Netflix.

Another critical tool to diminish the likelihood of a bad habit is reducing friction for a more desired course of action by making it simpler, i.e., breaking it into small, achievable, more readily available steps. In other words, to manipulate the environment to increase the likelihood of frequent and consistent execution of the desired habit and minimize the possibility of the antagonistic habit. For example, people are more likely to grab food items nearer to them, even if preferred items are available further away. This arrangement promotes healthier eating habits if the nearby items constitute good-quality food and the less proximate low-quality food.

Overall, the creation of new habits which may ultimately lead to lasting behaviour change requires consistent repetition in a stable, friction-minimizing context with solid environmental cues and adequate reward mechanisms.

Habits are crucial in terms of valued long-term goals related to diet, exercise, and overall well-being, and they can support or hinder their achievement. By understanding habit mechanisms and building interventions to change such lifestyle behaviours, we may successfully disrupt unwanted habits, such as poor diet and limited exercise, and help people to form better ones that meet their goals for healthy, productive lives.

An Ancient Finnish Tradition That May Hold Significant Benefits for Health

j.oswald@hyperionhealth.ca (Jesse Oswald) — Wed, 17 Apr 2024 19:00:00 GMT

The Healing Power of Saunas

Sauna is a traditional Finnish practice and has been a part of Finnish culture for centuries, considered a social activity. It is also becoming increasingly popular around the fitness world, with many gyms and wellness centers offering sauna as a way to promote relaxation and improve health. The process involves sitting in a sealed wooden room, heated with a stove or heater, creating a temperature of 70-100℃. Sauna sessions typically last between ten and thirty minutes, during which the individual sweats profusely, which is said to have several health benefits. Afterward, there is usually a cooldown period, where the subject takes a cold shower or jumps into a cold pool or lake.

The health benefits of sauna are likely to result from a combination of several physiological mechanisms. Firstly, due to the high-temperature exposure during sauna, the body’s core temperature rises above normal levels, a process known as heat stress. Heat stress can lead to adaptations in the body, including increased sweating, vasodilation, and increased blood flow, hence improved tissue circulation and oxygenation. The vasodilation occurring through heat stress can cause a drop in blood pressure and a subsequent compensatory increase in the heart rate. As a result, regular sauna use may lead to improvements in cardiovascular health and function. However, people with certain heart conditions or on medication where an increase in the heart rate may not be safe should avoid it. Increased sweating is a separate mechanism by itself since it helps the body eliminate toxins, such as chemicals and heavy metals, through the skin, reduce inflammation, and also regulate body temperature (thermoregulation).

Another proposed mechanism of sauna is its potential to improve immune function. More specifically, it can stimulate the production of white blood cells and antibodies, which are important in fighting off infections and diseases. Last but not least, the heat from the sauna stimulates the release of endorphins, hormones that are natural painkillers and mood boosters. Along with the decrease in the levels of the stress hormone cortisol, it can help promote relaxation and reduce stress and anxiety.

Due to the fact that saunas have been used for centuries and are also becoming increasingly popular, especially with athletes, there is a lot of research surrounding their benefits. Among the most engaging benefits pertain to cardiovascular health since sauna can potentially lower blood pressure, increase heart rate variability and overall improve cardiovascular function, hence cardiovascular fitness. Another significant benefit of sauna is related to its potential to enhance and accelerate recovery, either in terms of pain relief or tissue repair and growth. In particular, regular sauna use can provide pain relief for chronic conditions such as arthritis, fibromyalgia, and exercise-related muscle soreness, as well as promote enhanced recovery from exercise-induced muscle damage and fatigue through improved circulation, reduced inflammation, and increased production of heat shock proteins. In response to heat stress, the body produces heat shock proteins that have anti-inflammatory and antioxidant properties, protecting against exercise-induced muscle damage.

One of the most widely known benefits of saunas, and why many people are so keen on them, is their relaxation and stress relief properties, as well as the improved skin health attributed to the skin’s pore opening and removal of toxins. Conversely, one of the least ubiquitous potential benefits of sauna is its effect on metabolism. Some evidence suggests that sauna use may increase resting metabolic rate (RMR) in the short term. During a sauna session, the body temperature rises, increasing heart rate, blood flow, and sweating. These physiological responses require energy, hence the increase in metabolic rate. The magnitude and the duration of this effect seem to be modest, with an average increase of 3,5% and an average time of up to two hours. Lastly, regular sauna use may help the human body more effectively combat or recover from infections and illnesses, thanks to its potential to reduce inflammation and enhance the immune function on the whole.

Overall, sauna has been shown to have many potential benefits for both the body and mind, including improved circulation, increased sweating, decreased blood pressure, more effective combat of infections, reduced symptoms of chronic pain, accelerated recovery from exercise, and stress reduction. These benefits result from several physiological mechanisms, including heat stress, increased blood flow, increased heart rate, activation of the immune system, and reduced cortisol levels. However, the benefits of sauna use may vary depending on individual factors, such as certain diseases and medications, so it is essential to speak with a healthcare professional before beginning a new health regimen.

References

Crinnion WJ. Sauna as a valuable clinical tool for cardiovascular, autoimmune, toxicant-induced and other chronic health problems. Altern Med Rev. 2011;16(3):215-225.
Hannuksela M L, Ellahham S. Benefits and risks of sauna bathing. Am J Med. 2001;110(2):118-126.
Laukkanen T, Kunutsor S, Kauhanen J, Laukkanen JA. Sauna bathing is inversely associated with dementia and Alzheimer's disease in middle-aged Finnish men. Age Ageing. 2017;46(2):245-249.
Leppäluoto, J, Huttunen P, Hirvonen J, Väänänen A, Tuominen M, Vuori J. Endocrine effects of repeated sauna bathing. Acta Physiol Scand. 1986;128(3):467-470.

The Effect of Cryotherapy on Recovery and Other Parameters of Human Health

j.oswald@hyperionhealth.ca (Jesse Oswald) — Wed, 10 Apr 2024 19:00:00 GMT

The Science Behind Cryotherapy

Post-exercise cooling is a widely accepted recovery modality. It is believed to improve subjective (e.g., ratings of muscle soreness) and objective (e.g., measurements of muscle swelling, maximum voluntary contraction (MVC), and functional performance) recovery characteristics. This process, widely known as cryotherapy, is a therapeutic technique that involves exposing the body to extremely low temperatures for a short period. It is commonly employed in the fields of sports, medicine, and physiotherapy. It can be done in a variety of ways, including whole-body cryotherapy (WBC), cold-water immersion (CWI), and local cryotherapy, such as with ice packs.

WBC involves exposing the entire body to very low temperatures, usually around -110℃ to -140℃ between two to four minutes. During this process, the subject enters a special chamber cooled by liquid nitrogen or refrigerated cold air. On the other hand, CWI involves immersing the body or parts of the body in cold water, typically at temperatures ranging from 5℃ to -15℃ for five to twenty minutes. Finally, local cryotherapy can be easily done by applying a cold compress or ice pack to a specific body part.

Cryotherapy is widely used to relieve symptoms of various diseases, including inflammation, pain, muscle spasms, swelling, injuries, and overuse symptoms. The idea behind cryotherapy is that cold temperatures work by triggering a physiological response in the body. Specifically, it is believed to activate the body's natural healing mechanisms and stimulate circulation, resulting in the health benefits mentioned above. Apart from its recovery-related benefits, there is evidence that it may boost the immune system, increase energy levels and strength, and even help with weight loss.

The benefits of cryotherapy are due to a combination of physiological mechanisms that occur in response to exposure to cold temperatures. One of the main mechanisms proposed for cryotherapy is vasoconstriction. Exposure to cold temperatures causes the blood vessels in the body to constrict, reducing blood flow to the affected area. This response can help to reduce inflammation and swelling and may relieve pain. After the initial vasoconstriction, the body responds to the cold by increasing blood flow to the affected area, a process known as vasodilation. As a result, increased oxygen and nutrients help accelerate healing and recovery. Another proposed mechanism of cryotherapy is the endorphins and collagen augmented release occurring during exposure to cold temperatures. Endorphins are bodily hormones that act as natural painkillers, reducing pain and improving mood. At the same time, collagen is the most abundant protein in the body, which works by promoting tissue repair and regeneration.

Exposure to cold temperatures is also thought to activate two other critical body systems that may be implicated in the benefits of cryotherapy: the immune system and the mitochondria. Specifically, cryotherapy may stimulate the production of white blood cells, including neutrophils, lymphocytes, and natural killer (NK) cells, which play a crucial role in the immune system’s response to inflammation. It may also help modulate the body’s inflammatory response, reducing the production of pro-inflammatory cytokines while increasing the production of anti-inflammatory cytokines. Regarding mitochondrial function, some studies have shown that cryotherapy can activate and even increase the amount of brown fat adipose tissue, a type of adipose tissue rich in mitochondria. Due to its high content in mitochondria, brown fat is highly metabolically active and is involved in regulating energy expenditure, making it a potential target for weight loss. However, the relationship between brown fat and cryotherapy is still an active area of research with equivocal evidence. Therefore, cryotherapy should not be used as a standalone treatment for weight loss, and applying an adequate calorie deficit through a combination of diet and exercise should always be the priority.

Each of the proposed mechanisms above can lead to several benefits that cryotherapy may offer an individual who opts to undertake one of its modalities. The most solid benefits of cryotherapy are recovery related. Specifically, it may help better cope with fatigue and delayed-onset muscle soreness (DOMS), relieve pain, and improve recovery after exercise by reducing inflammation, increasing circulation, and promoting healing and repair. Through attenuating the inflammatory process, cryotherapy can also be beneficial for various chronic inflammatory diseases, such as arthritis and rheumatoid arthritis. Moreover, the release of endorphins during cryotherapy can help better combat stress, thus increasing mood and energy levels during the day. The possible effect of cryotherapy on brown adipose tissue and mitochondria function can improve cellular health and increase cellular energy production, thus enhancing fat-burning efficiency and boosting metabolism. Lastly, cryotherapy may have a positive impact on athletic performance, including muscle endurance as well as explosive strength. However, research on the specific effects of cryotherapy on athletic performance is mainly related to its potential for accelerated recovery. In contrast, its effect on particular aspects of performance has yet to be distinctly established.

To sum up, cryotherapy involves exposing the body to extremely cold temperatures for a short period. The benefits of cryotherapy are due to a combination of physiological responses, including vasoconstriction, decreased vasodilation, increased endorphins and collagen production, increased circulation, reduced inflammation, increased mitochondrial activity, enhanced tissue repair, and improved immune function. These mechanisms reduce pain and inflammation, promote healing and recovery, and improve immune and cellular health and function.

References

Bleakley C, McDonough S, Gardner E, Baxter GD, Hopkins JT, Davison GW. Cold water immersion (cryotherapy) for preventing and treating muscle soreness after exercise. Cochrane Database Syst Rev. 2012;(2):CD008262.
Costello JT, Baker PRA, Minett GM, Bieuzen F, Stewart IB, Bleakley C. Whole-body cryotherapy (extreme cold air exposure) for preventing and treating muscle soreness after exercise in adults. Cochrane Database Syst Rev. 2015;(9):CD010789.
Guillot X, Tordi N, Mourot L, Demougeot C, Dugué B, Prati C, Wendling D. Cryotherapy in inflammatory rheumatic diseases: a systematic review. Expert Rev Clin Immunol. 2014;10(2):281-294.
Rose C, Edwards KM, Siegler J, Graham K, Caillaud C. Whole-body cryotherapy as a recovery technique after exercise: A review of the literature. Int J Sports Med. 2017;38(14):1049-1060.
Vaile J, Halson S, Gill N, Dawson B. Effect of hydrotherapy on recovery from fatigue. Int J Sports Med. 2008;29(7):539-44.
Ziemann E, Olek RA, Grzywacz T, Kaczor JJ, Antosiewicz J, Skrobot W, Kujach S, Laskowski R. Whole-body cryostimulation as an effective way of reducing exercise-induced inflammation and blood cholesterol in young men. Eur Cytokine Netw. 2014;25(1):14-23.

Advocating for the Inclusion of Kinesiology in Extended Health Insurance Plans in Alberta

j.oswald@hyperionhealth.ca (Jesse Oswald) — Thu, 04 Apr 2024 21:51:27 GMT

Introduction:

In Alberta, Canada, the landscape of healthcare coverage often prioritizes certain services over others, leaving valuable resources under-utilized. One such service is kinesiology or exercise physiology, which plays a crucial role in promoting preventive healthcare and aiding in injury rehabilitation. Despite its proven benefits, kinesiology remains overlooked in extended health insurance plans, while services like massage therapy receive widespread coverage. This blog post aims to advocate for the inclusion of kinesiology as a primary service on extended health insurance plans in Alberta, with direct billing privileges, highlighting its importance in preventive healthcare and injury recovery.

1. Massage Therapy vs. Kinesiology: The Disparity in Coverage:

Massage therapy is commonly included in extended health benefits and health insurance plans across Canada, including Alberta. While massage therapy offers therapeutic benefits, it primarily falls under the category of wellness services rather than healthcare interventions. Unlike kinesiology and exercise physiology, which focus on promoting physical activity and functional movement, massage therapy typically targets muscle tension, relaxation, and stress relief. While valuable for managing acute musculoskeletal complaints, massage therapy alone may not address the underlying causes of chronic conditions or provide the long-term health benefits associated with regular exercise. On the other hand, kinesiology and exercise physiology offer evidence-based interventions for preventing chronic diseases and facilitating recovery from injury and pain.

Despite this distinction, massage therapy is widely covered by extended health insurance plans in Canada, often at a higher reimbursement rate than kinesiology and exercise physiology services. This discrepancy underscores the need for a reassessment of healthcare priorities, with a greater emphasis on preventive measures and evidence-based interventions that promote long-term health outcomes. Moreover, it's noteworthy that massage therapy is not a regulated health profession in Alberta as defined by the Alberta Health Professions Act (HPA), yet it continues to receive coverage under health insurance plans. Conversely, while kinesiology is not currently regulated in the province, it operates under professional associations that uphold high standards of education and professional practice. Therefore, the argument for its exclusion based on regulation lacks merit.

2. The Importance of Kinesiology in Healthcare:

Kinesiology and exercise physiology play a pivotal role in preventive healthcare by promoting physical activity and healthy lifestyle choices. Numerous studies have shown that regular exercise significantly reduces the risk of chronic diseases such as cardiovascular disease, diabetes, and obesity [1]. Additionally, kinesiologists and exercise physiologists specialize in developing personalized exercise and lifestyle programs tailored to individual needs, aiding in chronic disease prevention, injury rehabilitation, and pain management [2]. By integrating kinesiology services into extended health insurance plans, individuals can access evidence-based interventions that enhance their overall well-being and quality of life. Kinesiology and exercise physiology also take a holistic approach to health, addressing not only physical fitness but also mental well-being and quality of life. Regular exercise has been shown to alleviate symptoms of anxiety, depression, and stress, while promoting cognitive function and overall mental wellness [3]. By integrating these services into extended health insurance plans, insurers can support a comprehensive approach to healthcare that prioritizes both physical and mental health outcomes.

3. Proposed Solution: Requiring Physician Referral for Kinesiology Services:

To ensure appropriate utilization of kinesiology services and optimize healthcare resources, one potential solution is to require a physician referral for coverage. Similar to other allied health services, such as physiotherapy and chiropractic care, requiring a physician referral can ensure that kinesiology services are utilized for medically necessary purposes. This approach would not only promote collaboration between healthcare providers but also streamline the process for patients to access kinesiology services under their insurance coverage.

Conclusion:

In conclusion, the inclusion of kinesiology as a primary service on extended health insurance plans in Alberta is imperative for promoting preventive healthcare and supporting injury rehabilitation. By addressing the disparity in coverage between massage therapy and kinesiology, insurers can prioritize evidence-based interventions that contribute to better health outcomes for Albertans. Additionally, implementing measures such as requiring physician referral for kinesiology services can ensure appropriate utilization and maximize the effectiveness of healthcare resources. It's time to recognize the value of kinesiology in promoting a healthier Alberta.

Ready to Make a Difference?

Are you tired of seeing essential healthcare services overlooked in Alberta's health insurance plans? Do you believe in the power of preventive healthcare and evidence-based interventions? If so, we invite you to join us at Hyperion Exercise and Health and the Alberta Kinesiology Association in advocating for change.

We're on a mission to elevate the status of kinesiology and exercise physiology in Alberta by having them added as direct billable primary services on all health insurance plans. These services are vital for preventive healthcare, injury rehabilitation, and overall well-being, yet they are often under-utilized due to limited coverage.

By signing our petition, you'll be adding your voice to the call for action. Together, we can urge policymakers and insurance providers to recognize the importance of kinesiology and exercise physiology in promoting healthier communities.

Here's how you can make a difference:

Sign the Petition: Visit our website or our Change.org petition page and sign our petition calling for the inclusion of kinesiology as a direct billable primary service on all health insurance plans in Alberta.
Spread the Word: Share our petition with your friends, family, and colleagues, and patients. The more signatures we gather, the stronger our message becomes.
Get Involved: Join us at Hyperion Exercise and Health or become a member of the Alberta Kinesiology Association to stay updated on our advocacy efforts and participate in upcoming initiatives.

Together, we can create positive change and ensure that Albertans have access to the healthcare services they need and deserve. Join us today and let's make a difference together!

Sign the Petition Now:

Hyperion Exercise and Health & Alberta Kinesiology Association

Empowering Albertans for a Healthier Future

References:

Warburton, D. E., Nicol, C. W., & Bredin, S. S. (2006). Health benefits of physical activity: the evidence. Canadian Medical Association Journal, 174(6), 801-809.
Barker, T., & Martins, T. (2020). Kinesiology interventions for individuals with chronic disease or disability: a scoping review. Disability and Rehabilitation, 1-16.
Mammen, G., Faulkner, G., & Rhodes, R. (2013). The use of theory in studies of factors affecting the adoption of physical activity behavior change in adults with chronic disease: a systematic review. Health Education Research, 28(4), 673-688.

The Role of Nutrient Timing in Performance and Recovery

j.oswald@hyperionhealth.ca (Jesse Oswald) — Wed, 03 Apr 2024 19:00:00 GMT

Key Points

Nutrient timing is the strategic consumption of energy, macronutrients, fluids, and micronutrients in the hours before, during, and after exercise to optimize performance, enhance the adaptations to exercise, and accelerate recovery.
The recommended intake of carbohydrates for most endurance athletes typically ranges from 5-12 g/kg/d, with the upper ends reserved for those engaging in ≥8 hours/week of ≥70% VO ₂ max exercise.
Most exercising individuals should consume approximately 1.2-2.0 g/kg/d of protein to optimize training-induced adaptations. The exact amount depends on the mode and intensity of exercise, protein quality, as well as the caloric intake of the individual.
Athletes should follow appropriate rehydration strategies during exercise to limit the total body fluid losses to <2% of body weight and thus avoid adverse outcomes in exercise performance and recovery.

Nutrient timing , or peri-workout nutrition, is the consumption of nutrients pre-, during, and post-exercise. The primary goal of peri-workout nutrition is to provide nutritional support to allow the athlete to stay injury-free while maximizing performance and the functional and metabolic adaptations to their exercise program. Thus, the strategic consumption of energy in the form of carbohydrates, protein and/or fats, fluids, and micronutrients in the hours before, during, and after exercise can maximize muscle repair, improve body composition, optimize performance, and enhance muscular-related adaptations, such as strength and hypertrophy.

Nutrient needs and the practical strategies for meeting them pre-, during, and post-exercise depend on various factors , including the exercise per se (mode, intensity, duration), the environment, carryover effects from previous activity, appetite, and individual preferences.

Strategies implemented in pre-, during, and post-exercise periods should address various nutrition-related factors that can cause fatigue and deterioration in performance outputs (e.g., power, strength, agility, skill, and concentration). These factors include dehydration, electrolyte imbalances, glycogen depletion, hypoglycemia, and gastrointestinal (GI) discomfort.

Overall, nutrient timing when it comes to a workout, let alone a competition or event, can influence performance, recovery, training stimuli, and adaptations to exercise.

Energy Requirements

An appropriate energy intake is the cornerstone of an athlete’s diet since it supports optimal body function, determines the intake levels of macronutrients and micronutrients, and assists in manipulating body composition when required.

Athletes must consume adequate energy in terms of both the amount and timing, especially during high-intensity and/or long-duration training, to maintain health and maximize training outcomes.

An athlete’s energy requirements depend on the periodized training and competition cycle and may significantly vary throughout the yearly training plan relative to training volume and intensity changes.

Moreover, energy requirements are influenced by biological and environmental factors. Namely, energy needs are increased during training in cold and/or hot environmental conditions, high altitude exposure, physical injuries, and by increases in fat-free mass. Conversely, energy requirements are lowered by aging, decreases in fat-free mass, and possibly during the follicular phase of the menstrual cycle.

Although there are demonstrated advantages to achieving a certain body composition and body weight, low energy intake can result in unwanted loss of muscle mass, hormonal disturbances, sub-optimal bone density, increased fatigue, injury risk, impaired training adaptation, and an extended recovery process.

This especially applies in sports such as weightlifting, combat sports, distance running, etc., where athletes may feel pressure to attain unrealistically low weight/body fat targets or to reach them in an unrealistic time frame.

Under such circumstances, extreme weight loss behaviours or continuous dieting may result in poor nutrient support and compromised health and performance.

Consequently, when loss of body weight is required, it should be programmed to occur well out from the competition phase to minimize loss of performance. It should be achieved with techniques that maximize body fat loss while preserving muscle mass and other health goals.

The first step is determining energy requirements through indirect calorimetry rather than predictive equations and/or energy intake formulas. Afterward, a slight energy deficit should be applied to achieve a slow rather than rapid weight loss rate. In this energy-restricted framework, the provision of a higher protein intake, up to 2.3 g/kg/d , will retain muscle mass while losing body fat.

For most, decreasing energy intake by ~ 250-500 kcal/d from their periodized energy needs while either maintaining or slightly increasing energy expenditure can achieve progress towards short-term (3-6 weeks) body composition goals.

Athletes who frequently restrict their energy intake for the above reasons, probably eliminating one or more food groups, may consume sub-optimal micronutrients. Therefore, they should perform frequent blood tests. In case of deficiencies, they should adequately supplement, especially with calcium, vitamin D, iron, and some antioxidants.

Carbohydrate Intake

Carbohydrates have a vital role in performance and adaptation to exercise. There is evidence that exercise performance is enhanced by strategies that maintain high carbohydrate availability , namely, matching glycogen stores and blood glucose to the fuel demands of exercise. In contrast, depletion of these stores is associated with muscle fatigue, impaired skill and concentration, and increased perception of effort.

General guidelines for the suggested intake of carbohydrates can be provided according to the athlete’s body weight and the characteristics of the workout. The timing of carbohydrate ingestion over the day and in relation to training can also be manipulated to promote optimal carbohydrate reserve.

Endurance training

Manipulating nutrition and exercise in the hours and days leading up to a critical endurance workout, competition, or event, a highly prioritized feeding period, allows an athlete to maximize endogenous (muscle and liver) glycogen stores.

The delivery of carbohydrates, thus the appropriate glycogen filling, is a priority around this time since prolonged (>60-90 minutes) and moderate-to-high-intensity (65-80% VO ₂ max) endurance activities rely extensively upon carbohydrates as a fuel source.

Therefore, carbohydrate feedings maximize endogenous glycogen stores during this time while also helping maintain blood glucose levels, improve performance, and facilitate recovery. Strategies to attain these goals should first follow a brief period of reduced training volume in conjunction with a high daily intake of 5-12 g/kg/d carbohydrates. The upper end of this range (8-12 g/kg/d) should be reserved for those athletes completing high volumes (≥8 hours/week) of moderate-to-high intensity (≥70% VO ₂ max) exercise and subsequently requiring rapid continuous endogenous glycogen replenishment.

Overall, if the diet contains ≥8 g/kg/d carbohydrates, maximal glycogen levels are restored within 24 hours, and only moderate levels of muscle damage are present.

Individuals who engage in low-intensity/skill-based activities or moderate-intensity exercise programs for around one hour per day should consume 3-5 g/kg/d and 5-7 g/kg/d carbohydrates, respectively.

Recommended pre-exercise carbohydrate ingestion

Pre-exercise fueling is necessary only in the hours leading up to a high-intensity (≥70% VO ₂ max), long duration (>90 minutes) competition or workout, where glycogen levels are best maintained or increased by consuming snacks or meals high in carbohydrates (1-4 g/kg/d) for several hours before. Solid (bars, gels) or liquid (energy drinks, clear fruit juices) carbohydrates, deriving from everyday dietary choices or sports products, based on the athlete’s preference, tolerance, and experience, similarly promote glycogen resynthesis, allowing more flexibility.

Acute fueling strategies to promote high carbohydrate availability in cases of competition and/or key training sessions can also be categorized as pre-exercise nutrition. In < 90 minutes duration exercise cases, the athlete may consume their usual daily intake of 5-12 g/kg/d carbohydrates, with ≥8 g/kg/d carbohydrates, 24 hours before. In cases of >90 minutes of sustained intermittent exercise, the athlete may consume 10-12 g/kg/d carbohydrates 36-48 hours before.

Recommended during-exercise carbohydrate ingestion

As glycogen levels decline during exercise, the ability of an athlete to maintain exercise intensity and work output also decreases while rates of muscle breakdown increase. Therefore, during extended (>70 minutes) bouts of high-intensity (>70% VO ₂ max) workouts, carbohydrates should be ingested at a rate of ~ 30-60 g/h (i.e., 230-350 ml of a 6-8% carbohydrate solution) every 10-15 minutes throughout, to spare glycogen, thus optimize performance and maintain blood glucose levels.

During ultra-endurance exercise lasting more than 2.5-3 hours, where glycogen stores are substantially depleted, carbohydrate ingestion may increase to 90 g/h .

Athletes may choose well-trialed carbohydrate-rich sources low in fat, fiber, and low-to-moderate protein to avoid GI issues and promote gastric emptying. Carbohydrate feedings during exercise are especially crucial when pre-exercise carbohydrate consumption is neglected since they may help offset the potential for performance decrement.

Mouth rinsing with carbohydrate solutions, such as sports drinks, is recommended during sustained high-intensity exercise lasting 45-75 minutes. The frequent exposure of the oral cavity to small amounts of carbohydrates can still enhance performance via stimulation of the brain and central nervous system.

Lastly, during brief exercises lasting less than 45 minutes, carbohydrates are not necessary.

Resistance training

Resistance exercise , especially resistance-based workouts of 3-6 sets of 8-20 RM, using multiple exercises targeting all major muscle groups, can also significantly decrease muscle glycogen concentration. Even though these decreases are modest compared to endurance exercise, carbohydrate ingestion during such workouts still promotes euglycemia, increases muscle glycogen stores, mitigates muscle damage, and facilitates greater acute and chronic training adaptations.

Post-workout carbohydrate supplementation offers a small contribution from a muscle development standpoint, provided adequate protein is consumed. So, benefits derived from carbohydrate administration more favorably impact aspects of muscle glycogen recovery instead of stimulating muscle mass accretion.

The Importance of Hydration

To preserve homeostasis, optimal body function, and exercise performance, athletes should consume appropriate fluids before, during, and after exercise. Fluid deficits of >2% body weight result in hypohydration and, if not corrected, eventually dehydration, severely compromising exercise performance and recovery and increasing the perception of effort and well-being. For example, skeletal muscle cramps, although typically caused by muscle fatigue, may also be associated with dehydration and electrolyte imbalances, particularly when the athlete is not acclimatized to environmental conditions, such as heat.

It is not uncommon that athletes begin to exercise in a hypo-hydrated state and finish exercising with a fluid deficit.

Regarding pre-workout hydration guidelines, athletes may achieve euhydration by consuming a fluid volume equivalent to 5-10 ml/kg body weight 2-4 hours before exercise .

After exercise, the athlete should restore fluid balance by drinking a volume equivalent to ~ 125-150% of the remaining fluid deficit (e.g., 1.25-1.5 L of fluid for every 1 kg body weight lost through sweat). Hence, post-exercise rehydration strategies should essentially strive to replace as much sweat loss as possible.

In addition to water, sweat contains substantial amounts of sodium, with less potassium, calcium, and magnesium. Sodium should be ingested during exercise when large sweat losses occur. Scenarios include athletes with high sweat rates (>1.2 L/h), ‘’salty sweat’’, or prolonged exercise exceeding two hours.

Sweat rates vary during exercise from 0.3-2.4 L/h , dependent on exercise intensity, duration, fitness level, heat acclimatization, altitude, and other environmental conditions (e.g., humidity, etc.). Ideally, athletes should drink sufficient fluids during exercise to limit the total body fluid deficit to <2% of body weight. Rehydration strategies should primarily involve consuming water and sodium at a modest rate that minimizes urinary losses.

The fluid rehydration plan that suits most athletes during exercise is an intake of 0.4-0.8 L/h . Otherwise, the routine measurement of pre- and post-exercise body weight can help athletes estimate sweat losses during sporting activities to customize their fluid replacement strategies. Without other factors that alter body mass during exercise, a 1kg body weight loss represents approximately 1 L sweat loss.

Protein Intake

Proteins are the building blocks of all bodily tissues, including muscles, bones, and organs. They comprise twenty amino acids, nine essential (EAAs) and eleven non-essential (NEAAs). EAAs cannot be produced in the body thus, must be consumed in the diet.

Protein sources containing higher levels of EAAs are higher quality sources of protein.

Protein quality is defined as how effectively a protein stimulates muscle protein synthesis (MPS) and promotes muscle hypertrophy. Products containing animal and dairy-based proteins contain the highest percentage of EAAs, resulting in greater hypertrophy and protein synthesis following training compared to a vegetarian protein-matched protein source, which typically lacks one or more EAAs.

For example, a standard serving of 113.4g of lean beef provides 10g of the EAAs (3.5g of leucine) and 30g of total amino acids. Among the EAAs, leucine has been shown to independently stimulate increases in MPS, with 1-3g of leucine per meal being a sufficient dose for this process. However, the most crucial factor for increasing MPS is a balanced consumption of EAAs, with an approximate dose of 10g per mea l stimulating maximal MPS.

Endurance training

Very few studies have investigated the effects of prolonged periods (one week or more) of dietary protein manipulation on endurance performance. Protein does not appear to improve endurance performance and/or recovery when given for several days, weeks, or immediately before, during, and after endurance exercise.

In any case, endurance athletes should consume sufficient amounts of protein to repair and rebuild skeletal muscle following intense training bouts or athletic events.

Although the current recommended dietary intake for protein is 0.8 g/kg/d, evidence systematically indicates that this amount is insufficient for an exercising individual. Daily intakes of 1.2-2.0 g/kg/d are recommended, while greater intakes may be suitable for people attempting to restrict their energy intake while maintaining their muscle mass (refer to the energy requirements section).

Resistance training

It has been widely reported that protein consumption directly after resistance exercise (45 minutes to one hour maximum) is an effective way to promote a positive muscle protein balance, hence a net gain or hypertrophy of muscle. Specifically, during the post-prandial phase (1-4 hours after a meal), MPS is elevated by 30-100%, resulting in a positive muscle protein balance. In contrast, MPS rates are lower in a fasted state, and muscle protein balance is negative, meaning muscle mass accretion only occurs in the fed state.

However, the extent to which protein intake, either through protein food sources alone or through the combination of food and protein supplementation in conjunction with resistance training, enhances maximal strength and hypertrophy is contingent upon many factors, including

Resistance-training program variables, such as intensity, volume, and progression
Duration of the resistance-training program
Training status of the athlete
Total energy intake
Quality and quantity of protein intake
Co-ingestion of additional dietary elements that may favourably impact strength, such as creatine.

Therefore, it is becoming evident that protein timing does not play such a significant role in strength and hypertrophy. This is especially true for people who already consume increased amounts of protein (e.g., ≥1.6 g/kg/d), where the alleged benefits of protein timing are attenuated anyway.

Since skeletal muscle is sensitized to the effects of dietary protein for at least up to 24 hours after resistance exercise, general recommendations for maximal MPS rates and muscle hypertrophy are 0.25-0.40 g/kg or 20-40g of protein rich in EAAs and leucine (10-12g of EAAs and 1-3g of leucine) per meal. Spreading these protein doses approximately three hours apart has been consistently reported to promote the greatest increase in MPS, muscle hypertrophy, and performance benefits.

Recommended pre-exercise protein ingestion

As stated above, total protein intake is the strongest predictor of positive adaptations to resistance training, while protein timing influences MPS and hypertrophy to a much lesser degree. Besides sufficient protein intake, the body also needs adequate energy consumption to accumulate muscle mass since amino acids are spared for protein synthesis and are not oxidized.

Although protein timing may minimally contribute to performance and recovery benefits, especially in non-athletic populations, a professional athlete for whom every single detail plays a role should consider the concept of pre-workout and post-workout protein meals.

It has been demonstrated that when enough protein ( 0.4-0.5 g/kg of lean body mass ) is consumed less than five hours before the anticipated completion of a workout, in terms of a pre-workout meal, the need for immediate post-exercise protein ingestion is minimal. Specifically, the closer a protein pre-workout meal is consumed prior to resistance exercise, the larger the post-workout anabolic window, thus the smaller the need for a post-workout meal.

Recommended during-exercise protein ingestion

Potential benefits of ingesting protein during resistance training have not been identified, provided there is sufficient daily protein intake (20-40g per meal) evenly spaced throughout the day (every 3-4 hours).

Pre-sleep protein intake and protein safety

Pre-sleep protein consumption, namely 30 minutes before sleep and two hours after the last meal, may benefit MPS rates and muscle recovery. Several studies indicate that the pre-sleep consumption of 30-40g of casein protein increases overnight MPS, improves strength and muscle hypertrophy, and may also increase metabolic rate without influencing overnight lipolysis or fat oxidation.

Chronic protein intakes of up to 2.5-3.3g/kg/d in healthy resistance-trained individuals exert no harmful effects on blood lipids or kidney and liver function markers.

Combination of protein + carbohydrate intake in the peri-workout period

The simultaneous ingestion of carbohydrates and protein close to or throughout both endurance and resistance exercise may operate as an effective strategy to enhance performance of a subsequent exercise bout or event as well as specific exercise-induced adaptations.

Furthermore, for athletes combining resistance training sessions with sport-specific training, providing carbohydrate + protein close to each session guarantees optimal recovery for subsequent bouts and adaptation.

Eventually, if rapid restoration of glycogen is required (<4h of recovery time), the combination of carbohydrate sources (0.8 g/kg/h) with protein sources (0.2-0.4 g/kg/h) increases the rate of glycogen synthesis.

However, adding protein to carbohydrates is useful in performance enhancements, muscle damage amelioration, and muscle glycogen recovery only when carbohydrate ingestion during the peri-workout period is suboptimal (<1.2 g/kg/h) .

Therefore, when optimal carbohydrate intake is met, adding protein offers little to no additional benefit on endurance or resistance exercise performance and recovery.

It seems prudent for athletes who prefer combining carbohydrates and protein in their peri-workout period rather than just consuming carbohydrates since both methods similarly affect glycogen repletion rates, protein balance, performance, recovery, and muscle repair.

Fat Intake

Fat is a necessary component of a healthy diet, providing energy, structural elements of cell membranes, and facilitating the absorption of fat-soluble vitamins (A, D, E, and K).

The recommended fat intake for athletes is in accordance with public health guidelines, meaning 20-35% of total energy intake , with saturated fats limited to less than 10% and trans fats to less than 1%.

There are no specific guidelines regarding fat timing in relation to exercise. As stated above, athletes should avoid consuming fatty meals and/or snacks before and during exercise, especially concerning competition, to prevent any GI disturbances.

Some athletes may excessively restrict their fat intake below 20% of energy intake to lose body weight or improve body composition. The reduction in dietary variety often associated with such restrictions is likely to reduce the intake of various nutrients, such as fat-soluble vitamins and essential fatty acids, especially omega-3 fatty acids.

Therefore, athletes should be aware that not only consuming <20% of energy intake from fat does not benefit health and performance; in contrast, it is very likely to compromise them, especially if applied chronically.

Micronutrient intake

Athletes should consume diets that provide at least the Recommended Dietary Allowance (RDA) for all micronutrients.

Therefore, vitamin and mineral supplements are unnecessary for athletes with a balanced diet, providing high-energy availability from various nutrient-dense foods.

However, athletes who restrict energy intake or use severe weight-loss practices are very likely to eliminate food groups from their diet and thus are at greater risk of micronutrient deficiencies. In such cases, a multivitamin/mineral supplement may be appropriate, always considering the specific micronutrient deficiency that ought to be treated or prevented (e.g., iron, vitamin D, etc.).

Key Takeaways

Nutrition goals and requirements are not static. Nutrition support, in terms of both the peri-workout nutrition as well as athletes’ nutrition as a whole, should be periodized, taking into account the periodization of the exercise regime (a range of ‘’easy’’ workouts to highly demanding sessions or competitions).

Nutrition must also be personalized to the individual athlete, considering the specificity of their sport, performance goals, competition, food preferences, and recovery.

Especially during competition, nutrition strategies should focus on improving substrate stores to meet the fuel demands of the exercise while striving to enhance performance, minimize psychological stress and safeguard physical health.

Supplements can be of great value when used as an addition to a well-crafted nutrition plan but are rarely effective outside these conditions, especially for young, growing athletes.

Plant-Based Eating Patterns and their Association with Exercise Performance and Chronic Disease. Are there any Nutritional Risks?

j.oswald@hyperionhealth.ca (Jesse Oswald) — Wed, 27 Mar 2024 19:00:00 GMT

Key Points

Plant-based diets are dietary patterns emphasizing higher intakes of plant foods and are low or completely void of animal foods.
Plant-based diets have been linked to lower risk for chronic diseases, including cardiovascular disease, type 2 diabetes, obesity, and some cancers.
If appropriately planned, plant-based diets can be nutritionally adequate and safe for athletes and specific population groups, such as pregnant and breastfeeding women and the elderly.

As their name reveals, plant-based diets (PB) mainly or only comprise plant foods, such as grains, legumes, nuts, seeds, vegetables, and fruits, excluding foods from animals, including dairy, meat, poultry, fish, and seafood. They vary in restrictiveness, from avoiding only red meat to avoiding animal products entirely. For example, a strict vegan will not consume anything from an animal, including honey and gelatin.

The proportion of the population reporting following a PB diet continues to increase, with approximately 5-10% in developed countries reporting following some PB.

Whether to include animal-derived protein in the diet may relate to concerns about physical health, environmental sustainability, socioeconomic considerations, ethics related to the worker or animal welfare, or religious convictions, among other motivations.

There are many subcategories under the plant-based umbrella term, including the following:

Lacto-ovo-vegetarian is primarily plant-based, including dairy products and eggs, excluding animal flesh (meat, poultry, fish).
Vegan is strictly plant-based, excluding all animal products, from red meat and eggs to honey and gelatin.
Pescatarian allows fish and seafood consumption, excluding red meat, chicken, dairy, and eggs.
Flexitarian is primarily plant-based, occasionally including red meat, poultry, dairy, or fish.

These subcategories are the main directions of PB diets. Still, they are not exhaustive since each ramifies to additional subcategories, such as Lacto-vegetarians, ovo-vegetarians, vegans who follow a raw or fruit diet, and people who abide by a macrobiotic diet.

The Environmental Benefits of PB Diets

There is a considerable variation in the ecological footprint of animal-based products, with beef being especially detrimental to the environment compared to other products such as pork, chicken, or eggs. An increasing body of evidence suggests that the production of plant foods tends to be less resource-intensive and environmentally destructive for several reasons, mainly due to lower levels of greenhouse gas emissions (GHGs) compared to raising animals for human consumption.

The Academy of Nutrition and Dietetics advocated that ‘’PB diets are more environmentally sustainable than diets rich in animal products because they use fewer natural resources and are associated with much less environmental damage.’’ Following a PB diet is often considered the most effective strategy for systemically reducing GHGs and agricultural land use related to food production and consumption, thus decreasing environmental impact.

A review study concluded that adopting lacto-ovo-vegetarian diets could reduce GHG emissions by 35%, land use by 42%, and freshwater use by 28%. Furthermore, a 25% reduction in meat consumption and a transition to a PB diet would minimize the impact of agricultural land expansion on the ecosystem's biodiversity and carbon dioxide emissions. Altogether, embracing a PB eating pattern, especially in developed countries, could be an effective strategy for reducing the food system’s environmental degradation and our use of the earth’s resources.

The Role of PB Diets in Health and Disease

PB diets are considered nutritionally upgraded , compared to omnivorous diets, since they contain less saturated fat and cholesterol and more folate dietary fibre, antioxidants, phytochemicals, and carotenoids.

Several studies have shown that plant-based dietary patterns are linked to a lower risk of cardiovascular disease (CVD) and cardiovascular disease mortality. Specifically, vegetarians are 32% less likely to develop coronary heart disease (CHD) than meat eaters. Moreover, PB diets have been shown to reverse atherosclerosis in individuals with established CVD. They also reduce systolic and diastolic blood pressure and enhance insulin sensitivity, thus reducing the risk of type 2 diabetes and improving glycemic control in individuals with diabetes. Based on systematic reviews of randomized clinical trials, vegetarians tend to have a lower body mass index (BMI) and waist circumference, hence decreased obesity risk, reduced incidence of specific cancers, and lower all-cause mortality.

One study showed that adopting a low-fat vegan diet in post-menopausal women resulted in a mean weight loss of 5.8kg in 14 weeks, significantly greater than the control diet.

PB diets might act through multiple pathways in terms of their proposed health effects , including improvements in the lipid profile of vegetarians/vegans, including decreases in total cholesterol, LDL cholesterol, and triglycerides, reduced visceral fat, enhanced oxidative stress and inflammation markers, and reduced glycosylated hemoglobin (HbA1c).

However, these positive health outcomes stem from healthful plant food sources rich in dietary fibre, such as whole grains, fruits, vegetables, legumes, nuts, and plant protein, such as soy. PB diets can also be unhealthful, containing high amounts of refined carbohydrates, sugar, and highly processed mock meats. Therefore, an unhealthy PB diet may be equally compounding to an omnivorous diet in terms of their risk in health outcomes.

Besides the metabolic benefits of healthful PB diets, there is evidence that they may be associated with a lower risk of chronic kidney disease (CKD). Specifically, a recent study found that when one serving of red and/or processed meat was replaced with plant proteins, the risk of CKD was significantly lower. It was also demonstrated that a healthful PB diet, emphasizing fruits, vegetables, whole grains, nuts, legumes, coffee, and tea, was associated with a slower GFR, the optimal marker to measure kidney function decline. However, the protective effect was lost when healthy plant foods were replaced with poor plant-based food choices, such as commercial fruit juice, refined grains, and sweets.

Considerations for Athletes Consuming a PB Diet

PB diets can meet the needs of athletes at all levels, from recreational to elite athletes. However, if not appropriately planned, a PB diet may provide insufficient amounts of certain macro- and micro-nutrients. Thus, depending on food preferences, athletes need to ensure adequate intake of nutrients found less abundantly in PB diets or less well absorbed from plants than animal sources. Nutrition recommendations should consider each athlete’s training volume (intensity and frequency), sport, season, performance goals, and food preferences.

➢ Energy intake

Dietary fibre, abundant in PB diets, slows digestion, increases feelings of satiety, and decreases total daily energy intake. While such characteristics benefit overall health, they could make meeting the energy requirements of elite sports challenging. Especially endurance running athletes should be conscious not to overconsume dietary fibre during competition since they have been correlated with gastrointestinal disturbances. To ensure adequate energy is consumed, athletes should monitor their weight and be aware of involuntary or sizeable degrees of weight loss. Some strategies for PB athletes to ensure adequate intake include eating five to eight meals and snacks daily, decreasing high-fibre foods, and choosing energy-dense food choices, such as nuts and seeds, nut and seed butter, avocados, dried fruits, hummus, and granola.

➢ Protein intake

Branched-chain amino acids (BCAAs), leucine, isoleucine, and valine, are particularly important for promoting muscle protein synthesis (MPS). Although they are more concentrated in animal-based protein than plant-based protein, intervention studies utilizing either a whey protein or a soy protein supplement in conjunction with resistance training yield negligible differences between groups regarding muscle gain.

Nevertheless, some athletes may struggle to meet their protein needs from PB foods if their caloric requirements are exceptionally high. As mentioned before, a PB diet tends to be very filling due to the high fibre content. Therefore, athletes may find it challenging to consume enough protein from plant food sources to support optimal muscle protein synthesis. Some studies suggest increasing the amount of protein consumed at each meal and consuming it evenly throughout the day. It is also recommended to mix plant-based protein sources , including soy foods, legumes, nuts, seeds, quinoa, and other grains, to ensure a more balanced amino acid profile of all essential amino acids and support most training needs.

Recent work has also shown that distributing protein consumption throughout the day and including a pre-sleep protein feeding promotes MPS overnight, especially when preceded by resistance training.

The American College of Sports Medicine recommends that athletes consume 1.2-1.7g/kg/day and, during times of energy restriction, to promote muscle mass retention, to consume up to 2.0g/kg/day. If an athlete still struggles to meet protein recommendations, a soy protein supplement may be particularly adjuvant due to its high leucine content.

➢ Omega-3 fatty acids

Most studies indicate that plasma levels of EPA and DHA are lower in PB athletes than omnivores. Hence, athletes looking to optimize their performance may need to ensure they achieve optimal intake levels from the omega-3 fatty acids , EPA, and DHA, primarily found in fatty fish, hence may be lacking in such diets. As a result, supplementation with an algal DHA supplement may improve muscle adaptation, energy metabolism, muscle recovery, and injury prevention.

➢ Iron

Although iron is found abundantly in a PB diet, the bioavailability of iron in plant food sources (non-heme iron) is less than that found in animal sources (heme iron). In combination with the increased iron needs in athletes, especially females and endurance, this may result in lower ferritin levels and iron deficiency, which needs to be treated with an iron supplement so that exercise performance will not be compromised. To maximize their body’s non-heme iron absorption , individuals are suggested to pair plants' iron food sources, such as whole grains, legumes, nuts, seeds, dried fruits, green leafy vegetables, and iron-fortified cereals, with a vitamin C source, such as lemon, citrus fruits, peppers, tomatoes, and strawberries. They are also recommended to cook acidic foods, such as tomatoes in cast-iron skillets, avoid the simultaneous consumption of iron-rich foods with calcium supplements and beverages rich in tannins, such as coffee, tea, and cocoa, as well as avoid exercise within two hours of consumption.

➢ Zinc

Research has shown that athletes with insufficient dietary zinc intake may negatively impact exercise performance regarding strength and endurance. However, PB athletes tend to have normal Zinc levels; hence supplementation is unnecessary. Vegetarian food sources for zinc include whole grains, legumes, tofu, tempeh, nuts, and seeds. However, the high phytate content of these foods decreases zinc absorption. Some practical food preparation techniques to increase zinc bioavailability include soaking and sprouting beans, grains, nuts, seeds, and leavening bread.

➢ Calcium

A well-planned PB diet provides sufficient calcium for the athlete to meet the recommended daily intakes. However, vegans especially consume substantially less calcium than other vegetarians and omnivores. Therefore, athletes with inadequate calcium intake should consistently use calcium-fortified foods, such as fortified breakfast cereals, fortified fruit juices, and fortified plant-based milk, or at least take a calcium supplement. Moreover, phytic and oxalic acids in plant-based calcium food sources inhibit calcium absorption. Hence, food choices with good absorption calcium rates include beans, almonds, tahini, dried figs, soy products, and low-oxalate vegetables such as kale, broccoli, Chinese cabbage, and bok choy. Boiling can also reduce oxalate content in high-oxalate vegetables like spinach and Swiss chard.

➢ Vitamin D

Athletes following a PB diet may be at greater risk for inadequate vitamin D levels due to limited PB sources of vitamin D (fatty fish, fish oils, and egg yolk are the richest nutritional sources), particularly if they do not achieve sufficient sun exposure (10-30 minutes between 10 a.m. and 3 p.m.) and/or have darker skin. Since vitamin D is vital for athletes due to its role in immune function, inflammatory modulation, and exercise performance, plausible deficiencies should be addressed. Fortified plant-based milk, fortified orange juice, fortified margarine, and fortified breakfast cereals provide modest amounts of vitamin D for PB athletes. Therefore, supplementation may be needed to achieve an adequate vitamin D status, depending on dietary intake and sunlight exposure, hence a healthy bone mineral density.

➢ Vitamin B ₁₂

Vitamin B ₁₂ is solely found in animal products and, therefore, requires supplementation. Notably, the mean dietary intake of vitamin B ₁₂ for vegan athletes falls well below the recommended allowance; hence, supplementation is obligatory. Lacto-ovo-vegetarians, on the other hand, may be marginally normal, depending on the use of dairy products. Marginal amounts may also be available through nutritional yeast, fortified cereals, fortified vegan meat analogs, and plant-based milk, such as soy, almond, oat, etc., but such sources will not provide sufficient intake. In addition to detrimental health effects, such as megaloblastic anemia and fatigue, vitamin B ₁₂ deficiency is associated with lower creatine biosynthesis, which, along with the low creatine intake through plant-based foods, may eventually impair exercise performance. Therefore, all vegans should check their B ₁₂ status annually as a good preventative measure.

➢ Creatine

Creatine supplementation may optimize short-duration, high-intensity, and resistance exercise performance in athletes following a PB diet. Creatine supplementation may also benefit cognitive function and concussion recovery, especially for athletes in team skill-based sports.

PB Diets and Exercise Performance

Carbohydrates are the primary energy source during moderate and high-intensity aerobic exercise. Compared to other dietary patterns, the high concentration of carbohydrates typically found in a PB diet has been reported to increase muscle glycogen concentration, improving endurance performance .

Although regular exercise reduces the risks for many chronic diseases, such as obesity, type 2 diabetes, and CVD, intense exercise performed by elite athletes can elicit an inflammatory response and increase oxidative stress, leading to muscle fatigue and delayed-onset muscle soreness syndrome (DOMS). Since muscle glycogen levels are directly correlated with time to fatigue in moderate (60-80% VO ₂ max) intensity exercise, optimizing glycogen levels may delay fatigue in endurance and team sports. Furthermore, since phytochemicals such as polyphenols and antioxidants reduce inflammation and oxidative stress, PB diets abundant in these compounds have been considered superior for performance than animal-based dietary patterns.

Nevertheless, the limited evidence available suggests that PB diets neither hinder nor aid exercise performance in terms of strength, aerobic power (VO ₂ max), or power performance. Additional research is needed to determine whether such diets improve exercise performance and/or accelerate recovery.

Potential Nutritional Risks Associated with PB Diets

Although PB diets can have many health benefits, as described above, a major criticism is the risk of nutrient deficiencies related to long-term use, particularly the more strict forms of PB diets, such as veganism. This notion is intensified for sensitive life cycle stages, such as childhood and adolescence, pregnancy, lactation, and older adulthood.

Pregnant women who adhere to vegan diets are at higher risk of protein deficiency, especially in the second and third trimesters of pregnancy. Hence, 25g of additional protein is recommended, including 2 ½ cups of soy milk and 1 ½ cups of lentils daily. So, if protein consumption is adequate, PB dietary patterns have no difference regarding infant birth weight compared with omnivorous mothers.

PB dietary patterns are associated with a reduced risk of excessive weight gain, gestational diabetes mellitus, hypertensive disorders during pregnancy, and preterm birth. Pregnant and lactating vegetarians who are well-supplemented with vitamin B ₁₂ and the omega-3 fatty acid DHA derived from microalgae and also have sufficient sun exposure (see above) and a well-balanced diet by consuming a variety of nutrient-dense and fortified plant foods can effectively meet their energy and nutrient needs.

Vegetarian children and adolescents generally meet their protein needs when their diets contain adequate energy and a variety of plant protein sources. Other than vitamin B ₁₂ , which needs to be consumed through fortified foods and/or supplement, especially in vegans, deficiencies of other micronutrients are rarely seen when well-balanced PB diets are consumed.

The same applies to older adults consuming PB diets, with extra attention for possible vitamin D and calcium deficiencies, which, when present, should be corrected through the reinforced consumption of fortified foods and/or supplements.

A systematic review involving 37,134 subjects found vegetarians and vegans had lower bone mineral density at the femoral neck and lumbar spine than omnivores. The effect was greater in vegans, who also had higher fracture rates. Another review concluded that the balance between protective factors in PB diets and potential nutrient shortfalls might leave vegetarians, especially vegans, at increased risk of bone loss and fractures.

A meta-analysis found that vitamin B ₁₂ deficiency was associated with stroke, Alzheimer’s disease, vascular dementia, and Parkinson’s disease. Similar health damages may arise from iron insufficiency, another commonly assumed risk for plant-based dieters.

Although protein is abundant in PB diets, the amino acid profile in plants is often suboptimal compared to animal-based sources, particularly in BCAAs. However, the Academy of Nutrition and Dietetics has reported that consuming a wide variety of PB protein sources and adequate energy intake is sufficient to meet the required intakes of all essential amino acids.

Like any diet, the nutrition quality of a PB diet lies on the spectrum from a minimally nutritious diet based on nutrient-poor, processed foods to a maximally healthy diet rich in whole food sources. Therefore, when appropriately planned, a PB diet consisting of minimally processed and fortified foods can be nutritionally adequate and safe for all age groups and physiological conditions, including childhood, adolescence, pregnancy, lactation, and older adulthood. Particular attention should be given to calcium, iron, omega-3 fatty acids, vitamin D, and especially vitamin B ₁₂ , the only micronutrient that may be missing entirely from a vegan diet unless supplemented.

Key Takeaways

Plant-based diets are eating patterns that more or less, depending on the subcategory, encompass the consumption of plant foods, such as fruits, vegetables, grains, legumes, nuts, and seeds, while avoiding the inclusion of animal or animal-derived products, such as dairy, eggs, and honey.

Well-planned and nutrient-dense PB diets, especially the pescatarian and lacto-ovo-vegetarian subcategories, can be adopted by individuals who seek to improve their overall health, particularly in terms of body weight, blood pressure, lipid, and metabolic profile, and cancer risk.

Plant-based diets are potentially nutritionally adequate and safe for all population groups, from athletes to lactating women and children, provided they are appropriately planned and well-balanced.

Anyone following a plant-based diet who thinks they cannot meet their macro- and/or micro-nutrient needs or have already established nutritional deficiencies should work with a registered dietitian to assist them, let alone athletes whose exercise performance strongly relies on that.

Maximizing Injury Recovery: The Synergy of Manual Therapy and Exercise

j.oswald@hyperionhealth.ca (Jesse Oswald) — Wed, 20 Mar 2024 14:00:01 GMT

Introduction:

Injuries are not just physical setbacks; they can disrupt daily life, hinder athletic performance, and lead to long-term complications if not managed effectively. When it comes to rehabilitation, the combination of manual therapy and exercise often emerges as a popular choice. In this comprehensive exploration, we delve into the nuanced roles of manual therapy and exercise in injury recovery, backed by evidence from scientific literature. Moreover, we'll highlight the distinctive advantages of exercise-based interventions over reliance solely on manual therapy, emphasizing the active engagement and long-term benefits they offer.

Understanding the Short-Term Benefits of Manual Therapy:

Manual therapy encompasses various hands-on techniques aimed at alleviating pain, improving joint mobility, and enhancing tissue flexibility. From massage therapy to joint manipulation, these interventions can provide immediate relief by reducing muscle tension, improving circulation, and modulating pain perception. Many individuals find solace in the immediate effects of manual therapy, experiencing temporary relief from discomfort and improved range of motion.

Research supports the short-term efficacy of manual therapy in pain management and functional improvement. A study by Bialosky et al. [1] proposed a comprehensive model elucidating the mechanisms underlying manual therapy's effects on musculoskeletal pain. According to the model, manual therapy techniques exert their influence through neurophysiological, biomechanical, and psychological mechanisms, leading to short-term pain reduction and improved functional outcomes. However, it's crucial to recognize that while manual therapy may offer transient relief, its long-term effectiveness in promoting sustained recovery remains debated.

Unveiling the Limitations of Manual Therapy:

Despite its immediate benefits, manual therapy alone may not suffice for achieving long-term recovery or preventing injury recurrence. One of the primary limitations lies in the transient nature of its effects. Unlike exercise, which fosters adaptive changes in musculoskeletal tissues and neuromuscular control, manual therapy provides temporary relief without addressing the underlying factors contributing to the injury.

Moreover, sustaining the frequency of manual therapy sessions required for lasting improvement may not be feasible for everyone. Accessibility, cost, and time constraints often limit individuals' ability to undergo frequent manual therapy sessions. Consequently, relying solely on manual therapy may result in dependency and neglect of essential components of rehabilitation, such as strengthening, proprioceptive training, and functional movement restoration.

Evidential Emphasis on Exercise-Based Interventions:

In contrast to the transient effects of manual therapy, exercise-based interventions offer a holistic and sustainable approach to injury recovery. Exercise therapy encompasses a diverse range of interventions, including strengthening exercises, flexibility training, neuromuscular re-education, and functional movement patterns. By engaging individuals in active participation, exercise promotes tissue adaptation, enhances motor control, and addresses underlying biomechanical imbalances.

Numerous studies have underscored the effectiveness of exercise therapy in promoting long-term recovery and reducing the risk of injury recurrence. Hayden et al. [2] conducted a systematic review highlighting the robust evidence supporting exercise therapy for non-specific low back pain. The review concluded that exercise interventions, particularly those targeting core stabilization, flexibility, and endurance, yielded significant improvements in pain relief and functional outcomes compared to passive interventions or control groups.

Similarly, Page et al. [3] conducted a meta-analysis examining the efficacy of manual therapy and exercise for rotator cuff disease. The findings revealed that while manual therapy provided short-term pain relief, exercise-based interventions were associated with sustained improvements in pain, function, and shoulder range of motion. These results underscore the pivotal role of exercise in achieving long-term recovery and functional restoration following musculoskeletal injuries.

Hyperion Exercise and Health: Pioneering Active Rehabilitation Solutions:

At Hyperion Exercise and Health, we champion an active approach to injury rehabilitation, emphasizing the integration of manual therapy and exercise within a comprehensive treatment framework. Our team of expert exercise physiologists is dedicated to empowering individuals with the knowledge, skills, and tools necessary for long-term recovery and injury prevention.

Through personalized assessment and tailored exercise programming, we strive to address the root causes of injury, enhance functional capacity, and optimize performance potential. From self-mobilization techniques and targeted strengthening exercises to progressive loading protocols, our evidence-based interventions are designed to foster sustainable improvements in pain management, mobility, and overall quality of life.

Conclusion:

Injury recovery is a multifaceted journey that demands a comprehensive and proactive approach. While manual therapy can offer immediate relief, its transient effects may fall short of achieving lasting recovery. In contrast, exercise-based interventions provide the foundation for sustainable improvements in pain, function, and overall well-being. By embracing an active rehabilitation paradigm that integrates manual therapy with evidence-based exercise programming, individuals can reclaim their vitality and resilience in the face of injury.

References:

Bialosky JE, Bishop MD, Price DD, Robinson ME, George SZ. The mechanisms of manual therapy in the treatment of musculoskeletal pain: a comprehensive model. J Orthop Sports Phys Ther. 2009;39(1):1-18. doi:10.2519/jospt.2009.2796

Hayden JA, van Tulder MW, Malmivaara AV, Koes BW. Exercise therapy for treatment of non-specific low back pain. Cochrane Database Syst Rev. 2005;(3):CD000335. doi:10.1002/14651858.CD000335.pub2

Page MJ, Green S, McBain B, et al. Manual therapy and exercise for rotator cuff disease. Cochrane Database Syst Rev. 2016;(6):CD012224. doi:10.1002/14651858.CD012224.pub2

Heart Rate Variability: A Valuable Biomarker with A Major Impact on Physiological and Psychological Health

j.oswald@hyperionhealth.ca (Jesse Oswald) — Wed, 13 Mar 2024 19:00:00 GMT

Key Points

Heart rate variability is a noninvasive, easy-to-measure, and reliable physiological and psychological health biomarker.
Heart rate variability can be a great tool to monitor exercise performance and progress as well as the prognosis of various clinical conditions, such as cardiovascular disease and depression.
HRV isn’t just one metric; it actually comprises different sub-metrics, with each one generally representing a different physiological system (e.g. metabolism, neurological activation, etc.)
The Mediterranean diet, frequent exercise as well as certain lifestyle habits are the most effective ways of improving HRV.

Heart rate is the number of heartbeats per minute, and heart rate variability (HRV) quantifies the heart rate variability. Although the heart rate may be reasonably stable, the time between two successive heart contractions (R-R intervals) can vary considerably at rest; hence, HRV is the beat-to-beat variation in the time intervals between adjacent or consecutive heartbeats, called the inter-beat intervals (IBIs). The oscillations of a healthy heart are complex and constantly changing, which allows the cardiovascular system to adjust rapidly to sudden physical and psychological challenges to homeostasis.

HRV is considered a noninvasive, practical, and reproducible biomarker of autonomic nervous system function since the oscillations between consecutive heartbeats mainly result from the dynamic interaction between the parasympathetic (PNS) and sympathetic nervous system (SNS) inputs to the heart. Specifically, increased sympathetic input decreases HRV , whereas increased parasympathetic input increases HRV. While the SNS activity increases during stress, physical threat, or exercise, the PNS relaxes your body after periods of stress or danger and makes you feel safe and relaxed. The PNS and SNS constitute branches of the autonomic nervous system, which, along with the somatic nervous system, comprise the peripheral nervous system.

In a healthy human heart, there is a dynamic relationship between the PNS and SNS. PNS activity predominates at rest, resulting in an average heart rate of ~ 75 beats per minute.

HRV represents the heart's ability to respond to physiological and environmental stimuli. Therefore, the ability of the autonomic nervous system to respond dynamically to environmental changes results in increased HRV and generally indicates a healthy heart. Conversely, a low HRV is associated with impaired regulatory and homeostatic autonomic nervous system functions, which reduce the body’s ability to cope with internal and external stressors.

Many physical conditions and lifestyle habits can affect HRV, including physiological factors (e.g., breathing, circadian rhythms, and posture), non-modifiable factors (e.g., age, sex, and genetic factors), modifiable lifestyle factors (e.g., physical activity, body mass index, smoking, drinking, and stress), and other factors (e.g., medication such as anticholinergics, stimulants, and beta-blockers)

Altogether, a high level of HRV is associated with overall health, self-regulatory capacity, adaptability, and physiological and psychological resilience.

HRV Metrics

HRV can be analyzed via a) time-domain measures, b) frequency-domain measures, and c) non-linear measures.

Time-domain indices of HRV quantify the variability in measurements of the inter-beat interval (IBI), which, as previously mentioned, is the time between successive heartbeats. The two most common measures are the standard deviation of R-R intervals (SDRR), a measure of overall variability, and the root mean square of successive differences of R-R intervals (RMSSD), a measure of beat-to-beat variability.

While time-domain measurements display a parameter versus time, frequency-domain measurements display a parameter versus frequency. A given measure can be converted between the time and frequency domains with a pair of mathematical operators called transforms. Frequency-domain indices estimate the absolute or relative power distribution into four frequency bands or rhythms that operate within different frequency ranges. Therefore, heart rate oscillations are divided into ultra-low-frequency (ULF), very-low-frequency (VLF), low-frequency (LF), and high-frequency (HF) bands.

The ULF band (≤0.003Hz) requires a recording period of at least 24 hours. It reflects circadian oscillations, body temperature, metabolism, and activity of the renin-angiotensin system.
The VLF band (0.0033-0.04Hz) requires a recording period of at least 5 minutes but may be best monitored over 24 hours. It represents long-term regulation mechanisms, thermoregulation, and hormonal mechanisms.
The LF band (0.04-0.15Hz) is typically recorded over a minimum two-minute period and comprises rhythms with periods between 7 and 25 seconds. It reflects a combination of sympathetic and parasympathetic influences.
The HF band (0.15-0.40Hz) is conventionally recorded over 1 minute and reflects parasympathetic activity. It is also called the respiratory band because it corresponds to the heart rate variations related to the respiratory cycle (heart rate increases during inhalation and decreases during exhalation).

Different respiratory rhythms affect different frequency bands. Particularly, the LF band is affected by breathing from ~ 3-9 breaths per minute, whereas the HF band is influenced by breathing from ~ 9-25 breaths per minute.

Lastly, the LF to HF power ( LF/HF ratio ) reflects the balance between the SNS and PNS activity under controlled conditions. A low LF/HF ratio reflects parasympathetic dominance. In contrast, a high LF/HF ratio indicates sympathetic dominance, which occurs when we engage in fight-or-flight behaviours. In addition to time and frequency domain HRV, there are other HRV measures based on non-linear dynamics , such as power-law analysis, approximate entropy (ApEn), dimensionality, and detrended fluctuation analysis (DFA).

The Effect of Exercise Training on HRV

Exercise training has increased HRV in healthy individuals, with exercise intensity being the strongest determinant of HRV.

The limited body of evidence suggests that prolonged exercise duration can decrease HRV during exercise.

As for the exercise mode, during moderate steady-state exercise, upper body exercise elicits greater HRV compared to lower body and body weight exercise at the same submaximal heart rate and the same absolute/relative % VO2 max work rates.

More importantly, regular physical activity reduces the risk of morbidity and mortality from various clinical conditions, including cardiovascular disease (CVD) and diabetes.

It is strongly recommended for CVD patients, including those who have experienced a myocardial infarction (MI) and patients with chronic heart failure (CHF).

Several studies have documented improvements in HRV via participation in exercise training programs among MI patients.

One study found that following an eight-week cardiac rehabilitation program, participants significantly increased HRV parameters compared to those not participating in the training program.

In another study , researchers reported a 30% reduction in LF/HF ratio after MI patients completed an eight-week endurance rehabilitation program. These improvements continued for one year following participation in the program.

Improvements in HRV may also be achieved through unsupervised low intensity walking programs and anaerobic threshold exercise training.

Physical activity has also been found to benefit HRV in patients with CHF. CHF is characterized by impaired cardiac function and is associated with reduced exercise tolerance and HRV. Improvements in HRV among CHF patients have been observed in supervised aerobic exercise programs, supervised resistance training programs, and home-based training programs.

Nevertheless, the exact mechanisms underlying the beneficial modification of HRV by exercise training in these conditions are unknown. One hypothesis suggests that physical exercise increases cardiac parasympathetic tone and reduces sympathetic cardiac influences. However, more research is required to substantiate these claims. Further research is also needed to identify the exercise regimen, in terms of intensity and duration, that produces optimal improvements in HRV.

HRV as a Tool for Optimization of Exercise Training

HRV, apart from being a tool for assessing autonomic nervous system function, has also been investigated for monitoring training load, individual adaptations to training regimens, and recovery, as well as the early detection of overtraining phenomena .

HRV-guided training elicits greater improvements in maximal training load (+6-8%). Also, it allows significant performance improvements with a lower training load, not only in trained athletes but in untrained individuals. HRV should be measured regularly throughout the year in competitive sports to control the athlete’s response to different training stimuli. Yet, when training adaptations are monitored via HRV, it is necessary to consider the athlete’s training phase. Therefore, more frequent HRV measurements are recommended in the transition and competitive phases, whereas a few weekly ones may be sufficient during the preparatory phase.

What about recovery, though? A subtle balance between exercise stress and recovery is necessary to elicit optimal adaptations and performance improvements. High-performance athletes are constantly exposed to intensive training stimuli in a way that training-induced fatigue, and insufficient recovery may occur. If training is continued without recovery, there is a high possibility of developing overtraining syndrome, which requires several weeks or even months for an athlete to overcome and successfully return to their training.

Since chronic training overload decreases HRV, the use of HRV measurements offers great potential for the early detection and prevention of overtraining.

HRV and Cognitive Function

Participants with high HF-HRV perform better in cognitive tasks than participants with low HF-HRV. More specifically, high HF-HRV was associated with better verbal reasoning ability. In contrast, low HF-HRV had weaker performance in global cognitive functions, such as verbal reasoning abilities, memory responses, and executive functions.

Some studies have also reported a link between low HF-HRV and the risk of developing cognitive impairment, such as Alzheimer’s disease. Moreover, lower LF-HRV is linked to worse cognitive performance, particularly memory, language, and global cognitive scores. Overall, HRV appears to correlate with verbal but not visual cognitive facets.

Diet and Its Implication With HRV and Mental Health

Various aspects of diet have been associated with HRV. For example, dietary consumption of fatty fish and omega-3 fatty acids is independently associated with HRV. Specifically, greater consumption of tuna or other boiled or baked fatty fish such as salmon and mackerel was associated with improved HRV indices, thus a lower risk of arrhythmic outcomes, including sudden death, arrhythmic coronary heart disease (CHD), and atrial fibrillation.

Furthermore, a Mediterranean dietary pattern , sufficient vitamin and mineral intake, and caffeine consumption have all been associated with increased HRV.

On the other hand, aspects of an unhealthy dietary pattern, such as a high-saturated or trans-fat diet, reduce HRV.

Lastly, although smoking cigarettes and drinking alcohol have negatively been associated with HRV, wine intake , in particular, is positively and independently associated with HRV.

Therefore, the consistent relationship between HRV and diet supports the view that HRV may act as a biomarker of the influence of food and diet on health.

Even though it is clear that diet influences HRV, the pathways underlying such effects are multifactorial and rather complex. It is plausible that the impact of diet on HRV operates indirectly through changes in mental health.

Traditionally, heart rate has been considered a product of emotional response or stress.

Furthermore, many studies have found an association between mental health and HRV . Thus, demanding situations may give rise to an increase or a decrease in HRV. The former might arise when an individual successfully self-regulates the demands of the situation, and the latter may occur when the situation is perceived as threatening. On the other hand, diet influences brain functioning, cognition, and mood, which are then reflected in changes in HRV.

Notably, the link between HRV and eating disorders points toward the possibility of mutual causation. Most studies investigating HRV in those with anorexia nervosa have found parasympathetic dominance.

Similarly, those with bulimia nervosa are characterized by higher parasympathetic activity, particularly HF-HRV. Another study found reduced HRV in those with a propensity towards disinhibited eating, which is a tendency to overeat in the presence of palatable foods or other disinhibiting stimuli, such as emotional stress. Lastly, a low resting HRV has been associated with adopting maladaptive emotion regulation strategies and poor impulse control problems in identifying emotions.

Altogether, it appears that individuals who have difficulty regulating their emotions and are generally depressed are predisposed to adopting emotion regulation strategies such as the consumption of ‘’comfort’’ foods, with a resulting decrease in the quality of their diet. In turn, a poor-quality diet could further exacerbate the reduction in HRV. These data suggest that dietary behaviour and diet quality at least partially mediate the association between depressed mood and HRV. Nevertheless, future research will guarantee more solid evidence on the metabolic pathways linking mood, diet, and HRV. A wide range of diseases is associated with decreased HRV, including CVD, diabetes, obesity, and psychiatric disorders.

The Connection Between HRV and Heart-Related Pathologies

The primary interest in HRV relates to its potential prognostic value in CVD and sudden cardiac death. Indeed, HRV independently predicts sudden death in coronary patients, and a lower HRV is associated with a subsequent 40% increase in the risk of suffering a first cardiovascular event. Overall, reduced HRV, reflecting increased SNS or reduced PNS activity, has been associated with the development of many cardiovascular conditions , including coronary artery disease, hypertension, CHF, and MI, as well as poor cardiovascular outcomes in those who already ail. Specifically, decreased HRV has been found to be an independent predictor of morbidity and mortality following MI.

LF/HF ratio has also been found to be inversely associated with a lifetime risk of CVD . Particularly, healthy men with decreased HRV have approximately 4% higher lifetime risk of CVD, whereas healthy women have an 8% higher lifetime risk. In addition, the rate at which CHF and arrhythmias occur has been related to a reduced HRV. Moreover, HRV may be an independent prognostic determinant for individuals with unstable angina. Hence, reduced HRV is associated with a worse prognosis in several heart-related medical conditions. Since HRV measures are simple and non-invasive, they may greatly contribute to CVD prevention.

A possible mechanism through which HRV influences cardiovascular health is the C-reactive protein (CRP) . CRP is a protein produced by the liver as a response to inflammation. Higher CRP levels are associated with a greater risk of CVD. Whether by influencing inflammation or other mechanisms, HRV may be used as a biomarker of cardiac morbidity and mortality as well as CVD progression and future risk complications.

HRV and Diabetes

Studies suggest that an impairment of the functioning of the autonomic nervous system functioning, reflected in HRV, occurs during the early stages of diabetes and becomes progressively worse. In one study, HF-HRV, which indicates PNS activity, was lower in diabetics than in controls. It was concluded that frequency-domain measures of HRV are useful when evaluating diabetic autonomic and peripheral neuropathies. In another study, HF-HRV in non-diabetics was greater in those with lower fasting insulin levels. Thus, a relationship between insulin resistance, as indicated by higher fasting insulin levels, and lower HRV was implied. In addition, after a 9-year follow-up, there was a general decline in HRV . Overall, HRV appears to be associated inversely with plasma glucose levels.

How HRV is Related to Weight-Related Issues

It seems that obesity can alter HRV. Indeed, several studies have demonstrated an inverse association between weight gain and HRV. Notably, visceral adiposity may have a stronger association with HRV than total body fatness. In a study, an average weight loss of 3.9kg in overweight postmenopausal women was associated with an increased HRV. Also, in subjects who had undergone caloric restriction for an average of seven years, several measures of HRV metrics were significantly higher. Low cardiorespiratory fitness and higher body fatness are associated with lower HRV , with the former being the stronger determinant. Although adiposity adversely influences HRV, this effect may be reversible with weight loss and/or caloric restriction.

HRV and Psychiatric Illnesses

A dysfunctional autonomic nervous system, with an associated reduction in HRV, has been found in a wide range of psychiatric disorders, including bipolar disorder, anxiety disorders, post-traumatic stress disorder, and schizophrenia. There is also evidence that HRV indices are reduced in conditions characterized by emotional dysregulation, such as depression. When depressed patients and healthy controls were compared, the former had a lower HRV; it was particularly lower in those with more severe symptoms. Importantly, HRV can predict the onset of psychological illness ten years later. Given the links between HRV, emotion regulation, and executive functioning, it has been proposed that HRV is a biomarker of mental illness .

Key Takeaways

Research suggests HRV as a biomarker in individuals with various clinical conditions, particularly of cardiac etiology, an indicator of health in the general community and a non-invasive tool of autonomic heart rate control during physical and mental challenges. Many modifiable lifestyle factors can beneficially modulate HRV, including physical exercise and diet. Applications and devices measuring HRV are increasingly popular, particularly among athletes, to monitor different aspects of their training, including exercise performance, training adaptations, and recovery.

Breathing & Psychological Stress: A Two-Way Street

j.oswald@hyperionhealth.ca (Jesse Oswald) — Wed, 06 Mar 2024 19:00:00 GMT

Highlights:

Breath is one of the most powerful regulators of our emotions and stress levels. Through intricate pathways, the way we breathe impacts how we feel and vice versa.
The principal physiological elements defining the health of our breathing are Carbon Dioxide, Tidal Volume, and Breathing Rate. Perturbing them away from their normal values can cause a cascade of negative consequences.
Discover, step-by-step, how the lungs, brain, and nervous system are intertwined and how breathwork can provide a viable path to mental health.

Humans have leveraged the power of breathing to improve their bodies and minds for millennia. Cultures and societies in all corners of the world understood and appreciated to some extent the beneficial effects of breathing in regulating our emotional and physical well-being. Despite being separated by continents and oceans, the ancient Greeks, Chinese, Indians, and other important cultures of humanity revered breath as the ultimate manifestation of life and regarded it as the foundational mechanism for healing the mind and body.

Despite thousands of years of exploring the effects of breathing and using its powers to improve mental and physical health, the art of breathing was largely lost in modern times. This resulted from the general marginalization of nearly every natural healing process by Western medicine’s obsession with pharmacological intervention.

However, the renewed interest in alternative medicine coupled with a re-orientation of the scientific community’s focus on breathing has increased our understanding of breathing and allowed us to appreciate its pivotal role in regulating nearly every core aspect of human physiology. One of them is mental health and our emotional state. This article aims to explore the intricate relationship between breathing and mental health and dissect the biological mechanism through which our mind, nervous system, and lungs are connected.

As a first step, let’s understand the fundamental biomarkers that characterize how healthy our breathing process is. These include

End-tidal CO2: The amount of carbon dioxide we exhale,
Tidal volume: The volume of air we exhale
Breathing frequency: The number of breaths we take per minute.

These biomarkers reflect our breathing health because they constitute the basic mechanisms by which breathing affects nearly every process in our body, including our mental and emotional state. To understand this process, let’s examine, step by step, the sequence of events occurring when we experience stress.

How The Lung-Brain Connection Works

Step 1. Stress is perceived through our brain after one or more of our sensory systems (e.g., our eyesight) is triggered.

Step 2. The excitation of our brain engages our Autonomic Nervous System (ANS). ANS is divided into two parts: the Sympathetic Nervous System (SNS) and the Parasympathetic Nervous System (PNS) . SNS causes us to go into “fight-or-flight” mode by engaging all the mechanisms required for movement, preservation, and fast reaction. PNS, on the other hand, causes feelings of relaxation and enables us to recover, digest, and heal. Experiencing psychological stress will almost immediately engage SNS and partially deactivate PNS.

Step 3. Our brain is connected to our lungs and other critical organs through the vagus nerve, a principal conduit responsible for many of the psychosomatic processes in our body or the interaction between emotions and physical symptoms. The vagus nerve helps form the brain-lung axis. Specifically, SNS is connected to the upper part, whereas PNS is connected to the lower lungs. Due to the anatomy of the connection among lungs, SNS, and PNS, we breathe faster and shallower when psychological stress occurs, thus engaging SNS and partially deactivating PNS. On the contrary, when we deliberately breathe deeper and slower, we can activate PNS thanks to its connection to the lower part of our lungs and thus enable feelings of relaxation.

Step 4. Due to the rise in breathing rate, the amount of air exhaled increases along with the amount of carbon dioxide (CO2) expelled through the body. As more CO2 leaves the body, CO2 circulating in the blood declines, causing a cascade of adverse effects as it is responsible for two critical biological functions. First, CO2 enables oxygen molecules to detach from hemoglobin (the substance in our blood responsible for transporting oxygen from our lungs across the body) and enter the cells that need it in order to produce energy. Second, CO2 regulates how narrow or wide our arteries are and the amount of blood delivered across the body. As a result, a reduction of CO2 levels in the blood will cause a tighter connection between oxygen molecules and hemoglobin , making it harder for oxygen to enter cells and narrowing the arteries, diminishing blood delivery to the brain and across the body.

Step 5. Our brain understands the critical nature of CO2 for our physiology and will try to compensate for its changes. To achieve this, our brain is equipped with a sensory system that detects variations in CO2 concentrations and sends signals to our lungs to change the breathing rate accordingly.

Step 6. When stress becomes constant, steps 1-5 become almost permanent, thus causing breathing to be faster and CO2 levels to be lower constantly. After years of exposure to this state, our brain’s CO2 sensory system becomes accustomed to lower blood CO2 levels and faster breathing, a condition also known as Chronic Hyperventilation Syndrome (CHS). As described above, lower blood CO2 levels reduce oxygen delivery to every cell and the brain. Insufficient brain oxygenation reduces cognitive capacity and mental clarity and increases the likelihood of mental disorders.

Step 7. A constant state of rapid and shallow breathing (i.e., chest breathing) will engage SNS, the “fight-or-flight” part of our nervous system because SNS is connected to the upper part of our lungs.

The infographic below provides a visual representation of these steps.

Breathwork: A Way Out Of Chronic Stress

As described in steps 1-7, our stress response mechanism, nervous system, brain, and lungs are highly interconnected, and chronic stress can set them into a vicious self-fueling cycle. Simply put, stress causes our breathing to become unhealthy, whereas unhealthy breathing can cause or further promote psychological anxiety or mental disorders.

Based on steps 1-7, it becomes evident that breathing sits at the core of our brain and nervous system regulation. Luckily, breathing is the only core physiological function under our control. Breathing changes can change how our brain and nervous system work, thanks to the bilateral brain-lung connection. In other words, deliberate changes in our breathing patterns, a process also referred to by many as breathwork, can induce positive effects in our brain and nervous system and thus provide a viable solution to chronic stress.

Breathwork has many forms; each one targets a different part of our breathing apparatus. The graph below provides an overview of the most popular breathwork techniques categorized based on the element of our breathing system they affect most.

Conclusion

Our brain, nervous system, and lungs are connected in an intricate relationship that can bring about a virtuous or vicious cycle for our mental health. In other words, breath can be the obstacle or the enabler of mental health. Understanding whether your breathing is positively or negatively affecting your stress levels and psychosomatic state is the first step toward leveraging the power of breathing to achieve a better quality of life. No matter the quality of your breathing, breathwork and the deliberate manipulation of your breathing can improve your mental state and habits that can improve your life.

Managing Chronic Pain: An Active Approach Through Exercise and Pacing Strategies

j.oswald@hyperionhealth.ca (Jesse Oswald) — Wed, 28 Feb 2024 19:00:01 GMT

What is pain? Where does it come from?

Pain is a complex and subjective experience that is produced in the brain. While pain is often associated with tissue damage or injury, the sensation of pain itself is not produced in the damaged tissue, but rather in the brain as a protective mechanism. Understanding how pain is produced in the brain can help us to better manage and treat chronic pain.

The sensation of pain is produced by a complex network of neurons in the brain. When we experience an injury or tissue damage, specialized nerve cells called nociceptors are activated in the affected area. These nociceptors transmit signals to the spinal cord, which in turn sends signals to the brain.

Once these signals reach the brain, they are processed in a complex network of neurons in the somatosensory cortex, which is responsible for processing sensory information from the body. The brain also takes into account other factors, such as emotions, memories, and expectations, when processing pain signals.

The brain also has a complex system for modulating pain signals, which involves the release of neurotransmitters such as endorphins and serotonin. These neurotransmitters can help to reduce the intensity of pain signals, and can also produce feelings of pleasure and well-being.

While acute pain is a normal and important response to injury or tissue damage, chronic pain is a maladaptive response that persists long after the original injury or tissue damage has healed. Chronic pain is associated with changes in the nervous system that can lead to increased sensitivity to pain signals and a decreased ability to modulate pain signals.

Chronic pain is a complex condition that affects millions of people worldwide. It is defined as pain that lasts for more than 12 weeks, even after the original injury or underlying cause has healed. Chronic pain can have a significant impact on a person's daily life, making it difficult to carry out simple tasks and participate in activities they used to enjoy.

While medication and other passive treatments can provide temporary relief, an active approach to managing chronic pain can be particularly beneficial in the long run. This involves taking an active role in your own pain management, through the use of exercise and pacing strategies, rather than relying solely on medication or other passive treatments.

The solution?

Chronic pain is a complex and debilitating condition that affects millions of people worldwide. It can have a significant impact on a person's daily life, making it difficult to carry out simple tasks and participate in activities they used to enjoy. While medication and other passive treatments can provide temporary relief, an active approach to pain management through the use of exercise and patient education can be particularly beneficial in the long run.

Exercise is a key component of an active approach to pain management, as it can help to improve strength and flexibility, reduce inflammation, and release endorphins - the body's natural painkillers. Exercise can also help to improve overall mood and well-being, which is important for managing the emotional impact of chronic pain. Studies have shown that exercise can be effective in reducing pain and improving physical function in people with chronic pain.

However, it is important to approach exercise in a safe and gradual manner, especially if you have been inactive due to pain. Pacing strategies can be helpful in this regard, as they involve breaking down activities into manageable chunks and gradually increasing the duration and intensity of exercise over time. This can help to avoid exacerbating pain and prevent setbacks in recovery.

In addition to exercise, patient education is also an important component of an active approach to pain management. Education can help people with chronic pain to better understand their condition, manage their symptoms, and improve their overall quality of life. Education can also help to reduce fear and anxiety, which can contribute to the experience of chronic pain.

At Hyperion Exercise and Health, we offer evidence-based Active Chronic Pain management services aimed at helping individuals manage their pain effectively and improve their overall quality of life. Our services include specialized exercise therapy, pacing strategies, and patient education. Our team of experienced kinesiologists and exercise physiologists work with individuals to create a personalized pain management plan that incorporates safe and effective exercise and pacing strategies. We also provide support and guidance throughout the recovery process, helping individuals to achieve long-term relief and improve their overall quality of life.

In conclusion, an active approach to pain management through the use of exercise and patient education can be particularly beneficial in the long run for people with chronic pain. At Hyperion Exercise and Health, we offer evidence-based Active Chronic Pain management services aimed at helping individuals manage their pain effectively and improve their overall quality of life. Our team of experienced professionals can provide the support and guidance necessary for individuals to achieve long-term relief and improve their overall quality of life.

References

American Physical Therapy Association. (2021). Physical Therapy Guide to Chronic Pain Management. https://www.choosept.com/symptomsconditionsdetail/physical-therapy-guide-to-chronic-pain-management
Apkarian, A. V., Bushnell, M. C., Treede, R. D., & Zubieta, J. K. (2005). Human brain mechanisms of pain perception and regulation in health and disease. European Journal of Pain, 9(4), 463-484.
Eccleston, C., Crombez, G., & Worry, E. (2019). Pain psychology: A global needs assessment and national call to action. Pain, 160(10), 2059-2071.
Geneen, L. J., Moore, R. A., Clarke, C., Martin, D., Colvin, L. A., & Smith, B. H. (2017). Physical activity and exercise for chronic pain in adults: an overview of Cochrane Reviews. Cochrane database of systematic reviews, (4).
Melzack, R., & Wall, P. D. (1996). The challenge of pain (2nd ed.). New York: Basic Books.
Moseley, G. L. (2007). Reconceptualising pain according to modern pain science. Physical therapy reviews, 12(3), 169-178.
Nijs, J., Loggia, M. L., Polli, A., Moens, M., Huysmans, E., Goudman, L., ... & Malfliet, A. (2018). Sleep disturbances and severe stress as glial activators: key targets for treating central sensitization in chronic pain patients?. Expert opinion on therapeutic targets, 22(9), 821-830.
Woolf, C. J. (2011). Central sensitization: Implications for the diagnosis and treatment of pain. Pain, 152(3 Suppl), S2-S15.

Semaglutide, the Magic Pill Against Obesity: Truth or Fallacy?

j.oswald@hyperionhealth.ca (Jesse Oswald) — Sun, 25 Feb 2024 00:54:24 GMT

Key Points

Pharmacological treatments for adults with a body mass index (BMI) ≥ 30kg/m ² or ≥ 27kg/m ² in those with an obesity-related comorbidity can provide a valuable adjunct to diet and exercise.
Semaglutide is a GLP-1 agonist recently approved for obesity treatment and is the most effective among the other FDA-approved anti-obesity medications.
The main side effects of semaglutide administration are transient and mild-to-moderate gastrointestinal (GI) symptoms.
Semaglutide administration can lead to significant losses of muscle mass and considerable loss of total and visceral fat mass.

Obesity is a highly prevalent, multifactorial, chronic, relapsing disease that affects 650 million adults globally, translating into approximately 30% of men and 35% of women. Obesity requires long-term management and is associated with several physical and mental health complications. Specifically, it can lead to insulin resistance and type-2 diabetes, hypertension, dyslipidemia, cardiovascular disease, obstructive sleep apnea, and nonalcoholic fatty liver disease (NAFLD). It is also associated with reduced life expectancy, mainly due to cardiovascular morbidity and mortality.

Although lifestyle intervention (diet and exercise) represents the cornerstone of obesity management, sustaining weight loss over the long term is challenging. Most overweight or obese people typically achieve only modest weight loss that is often regained, thus going through countless weight loss failures. Notably, it has been demonstrated that weight loss through lifestyle modification usually plateaus at a level of 5%-10% and is associated with a high risk of relapse, which may be related to metabolic adaptation. Although weight loss of 5%-10% is linked to improvements in cardiovascular risk factors, type-2 diabetes, and quality of life, weight losses beyond 10% produce even greater health benefits, including remission of type-2 diabetes and reductions in cardiovascular (CVD) events. As such, weight loss of ≥ 10%-15% is recommended in people with complications of overweight and obesity, such as cardiovascular disease, osteoarthritis, obstructive sleep apnea, NAFLD, and type-2 diabetes.

Therefore, pharmacological treatments for people unable to achieve such weight loss goals only with a comprehensive weight loss program provide a valuable adjunct to lifestyle interventions. Clinical guidelines suggest adjunctive pharmacotherapy (anti-obesity medications) with a reduced calorie diet and increased physical activity for adults with a body mass index (BMI) ≥ 30kg/m ² or ≥ 27kg/m ² in those with an obesity-related comorbidity such as type-2 diabetes, hypertension, or dyslipidemia.

The current medications approved for chronic weight management in the US or Europe are orlistat, phentermine-topiramate, naltrexone-bupropion, liraglutide 3.0 mg, and semaglutide 2.4 mg. While the first four generally produce an average of 4%-8% greater weight loss than lifestyle interventions alone (2.6 kg to 8.8 kg in one year), semaglutide appears to increase this value to 15%, translating into a mean weight loss of 12.5kg from baseline weight after 68 weeks. Semaglutide given for two years resulted in substantial and sustained changes in body weight versus lifestyle interventions alone (-15.2% vs. -2.6%), encouraging long-term weight loss maintenance. Taken together, results show semaglutide to be the most effective currently approved for weight loss in adults with overweight or obesity.

Both liraglutide and semaglutide are glucagon-like peptide-1 (GLP-1) agonists. GLP-1 is a gut hormone released in response to food intake, acting as a satiety signal in the brain, thus regulating energy homeostasis. Moreover, it controls glucose metabolism by stimulating insulin release and inhibiting glucagon secretion. For chronic weight management, liraglutide is administered subcutaneously at a dose of 3.0 mg daily. In comparison, semaglutide has a more long-acting effect and is administered subcutaneously at a dose of 2.4 mg weekly. Although both have been shown to reduce energy intake, decrease hunger and food cravings as well as increase feelings of satiety, semaglutide has the most potent effect.

Liraglutide was the first GLP-1 agonist approved by the Food and Drug Administration (FDA) for chronic weight management after demonstrating weight losses of 4%-6% over that achieved with lifestyle intervention alone after 20-56 weeks. Semaglutide, on the other hand, was initially approved by the FDA in 2017 under the brand name Ozempic for the treatment of type-2 diabetes and for reducing classical cardiovascular risk factors (e.g., blood pressure, lipid levels), thus the risk of cardiovascular events in persons with type-2 diabetes and cardiovascular disease. Moreover, a once-daily oral version of the medication, at a maximum dose of 14 mg, was approved for treating type-2 diabetes in the US in 2019 and in Europe in 2020. Semaglutide lowers blood glucose and improves HbA1c via stimulating insulin and suppressing glucagon secretion in a glucose-dependent manner, leading to lower blood glucose levels with a low risk for hypoglycemia.

In June 2021, the FDA approved semaglutide as an adjunct to reduced calorie intake and increased physical activity for chronic weight management since scientific evidence demonstrated an extra 12.4% weight loss compared with other anti-obesity medications. Weight loss with semaglutide was also accompanied by greater improvements with respect to cardiometabolic risk factors, including reductions in waist circumference, blood pressure, glycated hemoglobin levels (HbA1c), and lipid levels as well as a greater decrease in C-reactive protein (CRP), a marker of inflammation. Therefore, it is becoming evident that semaglutide can be very useful for people with overweight and obesity complications (e.g., prediabetes, hypertension, and obstructive sleep apnea) who require weight losses of 10% to 15% or more to alleviate these complications.

Currently, once-weekly subcutaneous semaglutide 2.4 mg is approved for use in Canada, Europe, the UK, and the USA under the brand name Wigovy as an adjunct to a reduced calorie diet and increased physical activity for chronic weight management in adults with obesity (BMI ≥30kg/m ² ) or overweight (initial BMI ≥27kg/m ² ) with at least one weight-related comorbidity.

Growing data has demonstrated the efficacy and tolerability of once-weekly subcutaneous semaglutide 2.4 mg in individuals who are overweight or obese. The main side effect is the possibility of GI symptoms, which are typically transient and mild-to-moderate in severity. The chief safety issues with drugs of this class are the rare occurrence of pancreatitis and a prohibition of use in patients with a personal or family history of multiple endocrine neoplasia type 2 or medullary thyroid carcinoma.

Another safety issue that has emerged and deserves discussion is the quality of weight loss with semaglutide. The usual proportion of lean mass loss in total weight loss is 25%. In the semaglutide-treated participants, a mean loss of 8.36 kg of total body fat mass and 5.26 kg of total body lean mass was observed, meaning that lean mass accounted for approximately 39% of total weight, substantially higher than ideal. Intriguingly, this average proportion was also applicable to even less total weight loss, meaning that in cases of <15% weight loss, muscle mass loss may be even equal to fat mass loss. This is concerning since a decrease in muscle mass is associated with an increased risk of sarcopenia and frailty, especially in older patients, with a higher likelihood of weight regain after weight loss as well as with an increased risk for elevated blood glucose levels, thus type-2 diabetes. Therefore, it is preferable to predominantly reduce body fat without significant loss of muscle mass when losing weight. The fact that semaglutide results in increased losses in muscle mass also does not take away the significant decreases in total fat mass (-19.3% from baseline) and visceral fat mass (-27.4% from baseline). It just highlights the importance of diet and physical activity, which should always be the first line of treatment for obesity, and even in cases where the criteria of pharmacological interventions are met, to complement the medical prescription closely.

Overall, semaglutide and other anti-obesity medications are not a panacea and should only be used by obese adults with a body mass index (BMI) ≥ 30kg/m ² or overweight adults with a BMI ≥ 27kg/m ² with at least one obesity-related comorbidity. Moreover, the importance of combining lifestyle modifications such as dietary and physical activity should not be ignored in obesity treatment. Dietary modification and physical activity of at least 150-250 minutes/week are fundamental for the long-term management of obesity and should always be prioritized or at least be utilized adjunctively to pharmacotherapy.

References

Bergmann NC, Davies MJ, Lingvay I, Knop FK. Semaglutide for the treatment of overweight and obesity: A review. Diabetes Obes Metab. 2023;25(1):18-35. DOI: 10.1111/dom.14863
Chao AM, Tronieri JS, Amaro A, Wadden TA. Semaglutide for the treatment of obesity. Trends Cardiovasc Med. 2023;33(3):159-166. DOI: 10.1016/j.tcm.2021.12.008
Deng Y, Park A, Zhu L, Xie W, Pan CQ. Effect of semaglutide and liraglutide in individuals with obesity or overweight without diabetes: a systematic review. Ther Adv Chronic Dis. 2022;13:20406223221108064. DOI: 10.1177/20406223221108064
Lingvay I, Brown-Frandsen K, Colhoun HM, Deanfield J, Emerson SS, Esbjerg S, Hardt-Lindberg S, Hovingh GK, Kahn SE, Kushner RF, Lincoff AM, Marso SP, Fries TM, Plutzky J, Ryan DH. Semaglutide for cardiovascular event reduction in people with overweight or obesity: SELECT Study baseline characteristics. Obesity (Silver Spring).2023;31(1):111-122. DOI: 10.1002/oby.23621
Ryan DH. Next generation antiobesity medications: Setmelanotide, Semaglutide, Tirzepatide and Bimagrumab: What do they mean for clinical practice? J Obes Metab Syndr. 2021;30(3):196-208. DOI: 10.7570/jomes21033
Ryan DH, Lingvay I, Colhoun HM, Deanfield J, Emerson SS, Kahn SE, Kushner RF, Marso S, Plutzky J, Brown-Frandsen K, Gronning MOL, Hovingh JK, Holst AG, Ravn H, Lincoff AM. Semaglutide effects on cardiovascular outcomes in people with overweight or obesity (SELECT) rationale and design. Am Heart J. 2020;229:61-69. DOI: 10.1016/j.ahj.2020.07.008
Uchiyama S, Sada Y, Mihara S, Sasaki Y, Sone M, Tanaka Y. Oral semaglutide induces loss of body fat mass without affecting muscle mass in patients with type 2 diabetes. J Clin Med Res. 2023;15(7):377-383. DOI: 10.14740/jocmr4987
Wilding JPH, Batterham RL, Calanna S, Davies M, Van Gaal LF, Lingvay I, McGowan BM, Rosenstock J, Tran MTD, Wadden TA, Wharton S, Yokote K. Once-weekly semaglutide in adults with overweight or obesity. N Engl J Med. 2021;384:989-1002. DOI: 10.1056/NEJMoa2032183
Wilding JPH, Batterham RL, Calanna S, Davies M, Van Gaal LF, McGowan BM, Rosenstock J, Tran MTD, Wharton S, Yokote K, Zeuthen N, Kushner RF. Impact of semaglutide on body composition in adults with overweight or obesity: Explanatory Analysis of the STEP 1 Study. J Endrocr Soc. 2021;5(Suppl1):A16-A17. DOI: 10.1210/jendso/bvab048.030

The Concept of Energy Balance and Its Implication in Health and Disease

j.oswald@hyperionhealth.ca (Jesse Oswald) — Sun, 25 Feb 2024 00:45:05 GMT

Key Points

Energy balance implies weight balance (weight maintenance), positive energy balance, weight gain, and negative energy balance weight loss.
Energy balance comprises two components: energy intake (the food we consume) and energy expenditure (the calories we burn at rest, through exercise, and food digestion)
Breath analysis, through measuring the volume of oxygen consumption (VO ₂ ) and carbon dioxide production (VCO ₂ ), is the gold standard method for determining energy balance.

Energy balance is based on the fundamental thermodynamic principle that energy cannot be destroyed and can only be gained, lost, or stored by an organism. It is defined as the state achieved when energy intake equals energy expenditure. When the body is in energy balance, body weight is stable; when the body is in positive energy balance, body weight increases; and when the body is in negative energy balance, body weight decreases. In other words, energy balance practically means weight balance, positive energy balance means weight gain and negative energy balance implies weight loss. This is also known as the calories in/calories out (CICO) rule, where weight loss occurs when the calories consumed are lower than the calories burnt, and weight gain occurs when the calories consumed are higher than the calories burnt. Weight maintenance occurs when the calories consumed are equal to the calories burnt.

To better understand energy balance, let’s delve into its two components: intake and expenditure. Energy intake refers to the calories humans ingest from protein, carbohydrates, fat, and alcohol through consuming foods and drinks. On the other hand, energy expenditure refers to the calories humans expend through the resting metabolic rate (RMR), the thermic effect of food (TEF), and physical activity. RMR is the energy required to fuel the body at rest to maintain vital body functions and homeostasis. RMR accounts for 60-75% of total daily energy expenditure and is proportional to muscle mass, meaning the greater the muscles somebody has, the higher their RMR. TEF refers to the energy required to absorb, digest, and metabolize the food consumed and typically accounts for 8-10% of total daily energy expenditure. Lastly, the energy expended through physical activity, the most variable component of total daily energy expenditure, involves the calories expended through voluntary and non-voluntary exercise, such as postural control and shivering. This is also known as non-exercise activity thermogenesis (NEAT).

Energy intake and energy expenditure are primarily controlled by the central nervous system (CNS). Upon food consumption, smell, taste, and texture inputs are sent to the cognitive and emotional brain, regulating eating behaviour. While food enters the gastrointestinal (GI) tract, physical distension of the stomach creates a satiation signal that is transmitted to the brain to stop eating. Moreover, digested food components such as fatty acids further promote satiation by stimulating short-term satiety hormones, such as cholecystokinin, from GI endocrine cells. Finally, after food consumption has terminated, hormones from the fat tissue (leptin) and the pancreas (insulin) are secreted, further suppressing appetite. The energy balance regulation is not only a short-term but, most importantly, a long-term process. The hypothalamus, a particular brain region, regulates long-term energy balance, thus body weight, by encoding information about total energy availability and reserve in the body.

A chronic positive energy balance caused by a combination of genetic (obesity genes) and environmental (food abundance, low cost of high fat and sugar palatable foods, lack of infrastructure, and motives for physical activity) factors leads to fat accumulation and eventually obesity. Conversely, energy expenditure must exceed energy intake (negative energy balance) to lose weight. However, the magnitude of this negative energy balance is highly debatable, and many theories have been developed over the years. One of the most popular ones is the ‘’3,500 kcal per pound’’ rule used to predict the weight-change time course of a dietary intervention. Specifically, this rule states that it takes a 3,500kcal calorie deficit for someone to lose 1 pound. This rule has been confirmed since it is generally acknowledged that compensatory changes occur with weight change in energy expenditure, rendering this balance more complex than a simple mathematical equation.

The shift of the energy balance towards a lower energy intake relative to the total energy expenditure has a host of distinct biological adaptations, including decreased RMR, reduced NEAT, and altered levels of circulating hormones that regulate appetite (increased levels of orexigenic or hunger hormones such as ghrelin and reduced levels of anorexigenic or satiating hormones such as leptin), known to influence weight loss but even more importantly long-term weight maintenance. The most powerful biological adaptations that occur during weight loss and operate against its continuum are the decrease in RMR and the increase in skeletal muscle activity efficiency, especially during low levels of exercise (previously referred to as NEAT). These adaptations are collectively referred to as adaptive thermogenesis (AT), where the cells in your body, and especially your skeletal muscle cells, burn fewer calories for their activities (mainly NEAT-type activities) per unit of weight compared to what they would normally do, given the hypocaloric environment did not exist. The abovementioned changes are the principal causes of weight loss plateau and complete or partial weight regain. Therefore, since the energy balance constitutes a susceptible mechanism that can easily be disrupted, especially through extreme and improper dietetic practices such as the very-low-calorie diets (VLCD), dieters should always refer to professional dietitians to guide them through this process.

Overweight and obesity arising from a chronic positive energy balance are major risk factors for serious chronic diseases, especially cancer, cardiovascular disease, and type II diabetes. Obesity is a causal factor for many types of cancer, including colorectum, endometrium, kidney, esophagus, pancreas, thyroid, breast, and prostate, among others. Adipose tissue is a metabolically active tissue producing hormones and inflammatory cytokines contributing to increased risk for certain cancers. Moreover, insulin resistance, a hallmark of obesity and a precursor of type II diabetes, causes hyperinsulinemia, which stimulates the production of insulin-like growth factor -1 (IGF-1), resulting in increased cancer risk. Obesity is also a strong risk factor for the development of cardiovascular disease, causing hypertension, hyperlipidemia, and endothelial dysfunction. Weight loss through adopting a healthy, balanced dietary pattern, such as the Mediterranean diet, diminishes the harmful effects of a long-term positive energy balance on the heart and the circulatory system in general.

A positive energy balance is not always unfortunate. Creating an adequate energy surplus is often a prerequisite, especially for lean athletes who attempt to gain muscle mass. The magnitude of this surplus so that the athlete can build 1 kg of skeletal muscle mass has not yet been defined due to inestimable variables such as genetics, age, sex, body composition, and training status. However, since muscle mass accretion through a positive energy balance is also associated with increased fat mass, the general recommendation is a surplus of 350-500kcal per day for an efficient anabolic context. A positive energy balance is insufficient, provided there is no adequate prescription for a resistance training program and adequate protein intake, the most critical macronutrient in skeletal muscle hypertrophy.

RMR, consequently, energy balance can be accurately measured through respiratory indirect calorimetry, which is the gold standard test for measuring energy expenditure. Breath analysis monitors gas exchange, namely the volume of oxygen consumption (VO ₂ ) and carbon dioxide production (VCO ₂ ) at rest and during exercise. The ratio of CO ₂ production to O ₂ consumption is known as the respiratory exchange ratio (RER) and represents fuel oxidation, specifically carbohydrate and fat relative contribution to energy expenditure. During pure carbohydrate oxidation, the amount of CO ₂ produced equals the amount of O ₂ consumed (RER=1.0), while during pure fat oxidation, RER equals 0.7. A greater ability to oxidize fat at rest is important for metabolic health, weight management, and body composition, while obese individuals with insulin resistance have impaired fat-burning efficiency. In addition, a high resting RER is predictive of fat mass regain after diet-induced reductions in body weight.

Overall, energy balance is a complex equilibrium with many components that may vary significantly among individuals. This equilibrium implicates complex biological mechanisms such as hormones and neural circuits, the disruption of which can have adverse long-term effects on metabolic health. While a chronic positive energy balance is related to obesity and other severe chronic health issues, it can also be desirable for athletes who strive to gain muscle mass. All people seeking a valid energy balance measurement should undertake breath analysis testing, the gold standard method for measuring energy expenditure, thus determining energy intake and, eventually, energy balance.

References

Cooney C, Daly E, McDonagh M, Ryan L. Evaluation of measured resting metabolic rate for dietary prescription in ageing adults with overweight and adiposity-based chronic disease. Nutrients. 2021;13(4):1229. DOI: 10.3390/nu13041229
Hall KD, Heymsfield SB, Kemnitz JW, Klein S, Schoeller DA, Speakman JR. Energy balance and its components: implications for body weight regulation. Am J Clin Nutr. 2012;95(4):989-994. DOI: 10.3945/ajcn.112.036350
Hill JO, Wyatt HR, Peters JC. The importance of energy balance. Eur Endocrinol. 2013;9(2):111-115. DOI: 10.17925/EE.2013.09.02.111
Hill JO, Wyatt HR, Peters JC. Energy balance and obesity. Circulation. 2012;126(1):126-132. DOI: https://doi.org/10.1161/CIRCULATIONAHA.111.087213
Pati S, Irfan W, Jameel A, Ahmed S, Shahid RK. Obesity and cancer: A current overview of epidemiology, pathogenesis, outcomes, and management. Cancers. 2023;15(2):485. DOI: https://doi.org/10.3390/cancers15020485
Powell-Wiley TM, Poirier P, Burke LE, Després J-P, Gordon-Larsen P, Lavie CJ, Lear SA, Ndumele CE, Neeland IJ, Sanders P, St-Onge M-P. Obesity and cardiovascular disease: A scientific statement from the American Heart Association. Circulation. 2021;143(21):e984-e1010. DOI: https://doi.org/10.1161/CIR.0000000000000973
Romieu I, Dossus L, Barquera S, Blottiére HM, Franks PW, Gunter M, Hwalla N, Hursting SD, Leitzmann M, Margetts B, Nishida C, Potischman N, Seidell J, Stepien M, Wang Y, Westerterp K, Winichagoon P, Wiseman M, Willett WC. Energy balance and obesity: what are the main drivers? Cancer Causes Control. 2017;28(3):247-258. DOI: 10.1007/s10552-017-0869-z
Rui L. Brain regulation of energy balance and body weights. Rev Endocr Metab Disord. 2013;14(4). DOI: 10.1007/s11154-013-9261-9
Slater GJ, Dieter BP, Marsh DJ, Helms ER, Shaw G, Iraki J. Is an energy surplus required to maximize skeletal muscle hypertrophy associated with resistance training? Front Nutr. 2019;6:131. DOI: 10.3389/fnut.2019.00131

Metabolism & Mental Health Part 1

j.oswald@hyperionhealth.ca (Jesse Oswald) — Sun, 25 Feb 2024 00:28:45 GMT

Highlights

Our current understanding of mental disorders is very limited as we have no widely accepted biological measurements for diagnosing them, whereas our treatment focuses on mitigating symptoms.
Metabolism holds great promise for providing a universal model for explaining the occurrence and progression of mental disorders.
The metabolic-based model for mental health opens up the possibility for diet and exercise being powerful cures against the mental health epidemic.

Introduction

Mental health is considered by many medical experts the most dire epidemic of today's society. Its distractive nature is rooted in both the psychological impairment it causes and the physiological co-morbidities it triggers. Nearly every debilitating physiological chronic disease, including metabolic, cardiovascular, and neurodegenerative disease, strongly correlates with mental health disorders. Despite its prevalence, mental health is arguably the least well-understood condition, making consensus around its diagnosis and treatment challenging. A decades-old theory correlating metabolism and mental health disorders has recently come to light, acquiring renewed attention and holding the promise of deterministic diagnosis and treatment. In this three-article series, we explore the link between mental health disorders and metabolism, review the shortcomings of our current understanding of mental health, and discuss the potentially transformative role diet and exercise may have.

Syndrome or Condition? A Difference That Reveals our Limited Understanding of Mental Health

Despite its prevalence and exploding propagation, mental disorders are poorly understood. Modern medicine's poor understanding of mental disorders is reflected in the fact that they are diagnosed and treated as syndromes, not as conditions. The difference between the two is critical, so let's understand it.

In medicine, a condition refers to any health problem or abnormality that can be identified and diagnosed through specific biomarkers, also known as signs (e.g., VO2 max below a certain threshold or fasting blood glucose above a particular level). For example, diabetes is when fasting blood glucose remains elevated above 120 mg/dL. On the other hand, a syndrome is described as a set of symptoms that often occur together and suggest a specific underlying cause or disease but do not have a particular set of biomarkers or observations that will deterministically define its presence. A specific medical condition, genetic mutation, or environmental exposure can cause a syndrome.

In psychiatry, mental disorders are typically diagnosed and treated as syndromes based on the presence of a specific collection of symptoms, not signs. A sign is an objective indicator of an illness that someone else can observe or measure, such as a seizure, a blood pressure measurement, a laboratory value, or an abnormality seen on a brain scan. On the other hand, a symptom is a subjective experience that a patient must report, such as moods, thoughts, experiences of pain or numbness, or sleep disturbances. In psychiatry, most diagnoses are based on symptoms rather than signs. Most mental disorders are diagnosed based on a cluster of symptoms commonly occurring together, referred to as a syndrome. There are currently no laboratory tests, brain scans, or other objective measures that can accurately diagnose any mental disorder.

Our single-faceted focus on symptoms and lack of understanding of the underlying pathology of mental health is also highlighted in how we approach pharmacological treatment for mental disorders. Most common psychiatric disorders, such as depression, major depression, anxiety, and bipolar disorder, are usually treated with the same class of medication. Ultimately, the above highlights the fact that our approach towards psychiatric disorders focuses exclusively on symptoms and implies our ignorance of their actual cause.

Metabolism and Mental Health

Metabolism may offer a way out of our lack of understanding of the underlying pathology of mental disorders. The proposed mechanism linking metabolism and mental health is complex and interconnected but can be boiled down to the fact that mental disorders are metabolic disorders of the brain. Metabolic problems, which can stem from factors such as diet, exercise, sleep, stress, and genetic predisposition, can directly affect neurotransmitter and hormone levels, oxidative stress, inflammation, and immune system function in the brain. This can lead to various mental health conditions such as anxiety, depression, bipolar disorder, schizophrenia, etc. To treat these conditions, interventions that target metabolisms, such as diet and lifestyle changes, medications, and therapy, can effectively restore balance to the brain's metabolic processes.

To understand, however, what metabolic disorders are and their link with brain dysfunctions, we must first understand the fundamental organelle playing the most critical role in our metabolic activity, the mitochondria. Mitochondria are organelles found in eukaryotic cells, including in humans. They are often called the "powerhouses" of the cell because they produce energy in the form of adenosine triphosphate (ATP) through oxidative phosphorylation. In addition to producing energy, mitochondria play other vital roles in cell function, including regulating calcium signalling, producing reactive oxygen species (ROS), and serving as the site of specific biosynthetic pathways. Mitochondria also have their DNA (mtDNA) separate from the cell's nuclear DNA and encode genes essential for mitochondrial function.

Mitochondrial dysfunction can lead to various problems in brain function, including decreased energy production, increased oxidative stress, and impaired neurotransmitter signalling. Specific mitochondrial dysfunctions that have been linked to brain disorders include:

Impaired mitochondrial respiratory function: This can lead to decreased ATP production and impaired energy metabolism, contributing to neurological and psychiatric disorders.
Mitochondrial DNA mutations: Mutations in mitochondrial DNA can impair mitochondrial function, leading to decreased energy production and oxidative stress.
Abnormal mitochondrial morphology: Disrupted mitochondrial shape and distribution can impair mitochondrial function and contribute to neurodegenerative diseases.
Dysregulated mitochondrial quality control: Disruptions in the processes that maintain mitochondrial health, such as mitophagy and autophagy, can contribute to mitochondrial dysfunction and neurological disorders.

Overall, mitochondrial dysfunction is found at the center of metabolic brain dysregulation and can significantly contribute to a range of mental health conditions. Identifying and addressing these dysfunctions through targeted interventions may be essential to improving brain health.

What are the causes of mitochondrial dysfunction in the brain?

Various factors, including genetic mutations, aging, toxic exposures, nutrient deficiencies, hormonal imbalances, oxidative stress, inflammation, and lifestyle factors such as poor diet, lack of exercise, and chronic stress, can cause mitochondrial dysfunction in the brain. As mentioned, mitochondrial dysregulation from external factors such as alcohol, inflammatory signals, neurotransmitters, and hormones can also contribute to brain mitochondrial dysfunction. Moreover, certain medications can cause mitochondrial dysfunction as an adverse effect. These factors can impair the function of the mitochondria, leading to deficits in energy production, increased oxidative stress, and impaired cellular signalling. Over time, this can lead to cellular damage and death, contributing to disease states such as neurodegeneration, metabolic disorders, and mental health conditions. By identifying and addressing the causes of mitochondrial dysfunction, it may be possible to prevent or treat these diseases and improve overall brain health.

Summary

Mental health is arguably the most rampant but misunderstood chronic condition battering modern societies. Understanding the physiological adaptations that lead to mental disorders is the first step towards understanding them and devising effective long-term plans against them. The proposed mechanism linking mental health to mitochondrial health holds great promise not only because it ecumenically explains the complexity of psychiatric disorders but also because it opens up the exciting potential for diet and exercise, the two most potent and accessible drugs known to humanity, as a cure. In the following two articles of this series, we dive into the transformative role diet and exercise can play in overcoming mental health problems.

The work of Chris Palmer, MD has inspired this article. For further information about metabolism and mental health, readers can refer to his book, Brain Energy . New Paragraph

Meal Timing: Recommendations For Weight Loss, Appetite Control, And Athletic Performance

j.oswald@hyperionhealth.ca (Jesse Oswald) — Sat, 24 Feb 2024 01:29:49 GMT

Meal Timing Key Points:

Meal timing is the strategic scheduling of eating whole foods, fortified foods, and dietary supplements.
Meal timing helps you create an eating routine that keeps you energized, focused, and productive throughout the day.
Correctly timing your meals can help with weight loss and appetite control, stabilize blood glucose, and improve exercise performance and recovery.
Some challenges of appropriately timing meals include hormonal fluctuations, sleep schedules when an individual has time to exercise and work schedules.
Re-evaluate your meal timing routine as necessary as lifestyle and exercise goals change.

What Do I Need To Know About Meal Timing?

Meal or nutrient timing is the strategic scheduling of eating whole foods, fortified foods, and dietary supplements. More specifically, a person may eat a specific nutrient in a particular amount at an exact time for a specific reason.

If that sounds like a mouthful…well…it is. To simplify things, let's create an example.

If I’m a person looking to lose weight, I would :

Focus on eating a healthy balance of carbs, fats, and proteins.
With a daily macronutrient breakdown of 45-65% carbs, 10-25% protein, and 20-35% fat.
Eat 50-70% of my calories in the morning.
Eat 20% of my calories in the afternoon
Eat 10% of my calories in the evening.
Timing meals and snacks in this fashion has led to weight loss.

That, in essence, is what meal timing is all about. In addition to using meal timing for exercise benefits, it can also be used for appetite control, blood sugar regulation, weight loss, muscle strength, size, and recovery.

So far, meal timing sounds swell! Next, let’s discuss why it matters.

Why Meal Timing Matters

Meal timing matters for a lot of different reasons. One of the significant reasons is it helps you maintain a better routine. This is key when trying to stick to a diet, as when dialled in, meal timing can take a lot of the guesswork out of an eating schedule.

Proper meal timing also matters because of it:

It keeps you energized throughout the day.
It helps you avoid blood sugar crashes to stay focused and productive.
Regulates mood swings.
It enables you to feel your best before exercise.
Promotes a great night's sleep.
Optimizes muscle and whole-body recovery.

If you’re still not convinced that hopping on the meal timing train is a good idea, let’s briefly look at the health and performance benefits before diving into the research. This is the juicy stuff you’re going to want to know!

Meal Timing Benefits

Correctly timing your meals and snacks can benefit overall health and exercise/athletic performance. These include:

Weight Loss
Appetite Control
Blood Sugar Regulation
Energy For Cardio And Endurance Exercise
Increased Muscle Strength, Size, And Recovery

Let’s look at these benefits and see what the research recommends.

What The Research Says On Meal Timing

Fortunately for us, there isn’t a shortage of evidence regarding research on meal timing. Hundreds of clinical trials have been performed on thousands of subjects that have examined how meal timing can affect health, performance, and other variables in sedentary, obese, and athletic populations.

After reading this section, you’ll practically have your Ph.D. in meal timing.

Weight Loss

If one of your main goals is weight loss, the evidence suggests there is an ideal time to eat.

A landmark study conducted in 1997 required subjects to complete two six-week diet periods that delivered similar calories (~ 1950 kcals) and similar macronutrient composition.

In one group, the participants consumed 70% of their total daily calories during breakfast, while in the other study group, participants consumed 70% of their total daily calories during dinner.

The researchers discovered more significant weight loss in the group that ate most of their daily calories at breakfast.

More recently, a study conducted by Jakubowicz et al. had overweight and obese women consume 1400 calories each day for 12 weeks.

One group ate 50% of their daily calories (700 kcals) during breakfast, 35% during lunch (500 kcals), and 15% during dinner (200 kcals), while the other group ate the exact opposite distribution, 15% for breakfast (200 kcals), 35% for lunch (500 kcals) and 50% for dinner (700 kcals).

Approximately 2.5 times more weight was lost, and significantly greater changes in waist circumference and body mass index values were observed when most calories were consumed at breakfast.

Also, triglyceride levels decreased by 34%, more significant improvements in glucose and insulin were observed, and feelings of satiety were improved in the group that consumed most of their calories at breakfast.

The key point from these two studies indicates that if weight loss is your goal, eat more in the morning and less in the evening.

Appetite Control

Just as eating more in the morning and less in the evening helps with weight loss, the same can be said about appetite control and suppression.

A 2019 study published in the Obesity Journal demonstrates this.

For this study, researchers compared two groups of people (early eating and the control group) who ate the same three meals per day for four days but at different times. The early eating group ate the majority of their calories during the morning. The control group consumed the majority of their calories in the evening.

On the fourth day of the study, both groups had their metabolism measured…specifically calories burned and the amount of fat, carbs, and proteins burned. Both groups also rated various measures of appetite, like hunger, desire to eat, and fullness.

The researcher also measured levels of hunger hormones in each group.

The results are fascinating. The early eating group burned more calories and fat while having lower levels of the hunger hormone ghrelin. The group also reported less hunger and desire to eat than the control group.

If appetite control is ever an issue for you, eating most of your calories at breakfast and lunch is suggested.

Blood Sugar Regulation

Blood sugar spikes are no joke. Too high, and they can cause you to feel anxious and jittery. Too low can cause hypoglycemia, that horrible lightheaded and tired feeling.

It should also be noted that eating a large amount of carbs, such as a bowl of pasta, at 10 pm compared to 10 am will cause a higher blood glucose spike due to fluctuations in your circadian rhythm. Individuals should eat more carbs in the morning and less in the evening/night.

Meal timing can play a big part in helping to avoid the lows and highs of blood sugar levels and help keep it steady so you remain energized and focused.

The strategy here is to never go too long between meals and snacks and eat every 3-4 hours. This schedule will help stabilize blood glucose levels and avoid blood sugar spikes.

It also helps people avoid overeating when hungry and consume fat-laden, calorie-dense foods to satisfy their appetite.

Energy For Cardio And Endurance Exercise

Carbs are king when fueling endurance exercise, especially as intensity increases. Therefore, people can strategically time their meals/carbs when they want to run, bike, or do other endurance exercises for optimal performance. Here are the guidelines that also include a note on post-workout meal timing for recovery.

Pre Workout Meal Timing

Eat carbs three to four hours before your planned exercise time to saturate muscle glycogen stores and elevate blood glucose. The amount you eat/need will depend on your gender, exercise levels, and goals. Getting a metabolic test done to determine your specific carb needs is recommended.
Sixty minutes before exercise, eat a small number of carbs if needed. Focus on eating simple sugars from foods like bananas or sports drinks.
Fifteen minutes before training, another 20-50 grams of carbohydrates can be consumed if needed and won’t cause gastrointestinal distress.

Post Workout Meal Timing

Eat 1.2 grams of carbs per kilogram of body weight per hour for 3-4 hours to restore muscle glycogen.
Combine the carbs with 25-30 grams of a high-quality protein like whey. This will kickstart muscle recovery and help with glycogen resynthesis.

Muscle Strength, Size, And Recovery

If you want to get stronger or put on size, meal timing for strength training differs from endurance training. The difference is that your pre and post-meal macronutrient profile will include fewer carbohydrates and more protein and amino acids.

Before and after strength training sessions, meal timing maximizes muscle protein synthesis, minimizes exercise-induced muscle damage, and facilitates short and long-term training adaptations (strength, size, power, endurance).

Pre Workout Meal Timing

Twenty-five grams of high-quality protein or 5 grams of branched-chain amino acids and a small number of carbs. Protein can come from whole food sources or a high-quality whey protein. The BCAAs should contain at least 3 grams of leucine. 50-75 grams of carbs should be consumed. Combining protein or amino acids plus carbs will stimulate muscle protein synthesis while elevating blood glucose.

Post Workout Meal Timing

Like the pre-workout meal, one should consume another 25 grams of protein with more carbs (100-150 grams) to help muscle recovery and replenish glycogen.

Sample Meal Timing & Exercise Schedule

6 am: Wake Up
6:30am - 7am: Breakfast
9 am - 10am: Exercise
Post-workout snack immediately after exercise
12 pm -12:30 pm: Lunch
4 pm: Snack
5 pm - 6 pm: Afternoon exercise if no morning exercise was performed
6:30 pm - 7:00 pm: Dinner
10 pm: Bedtime

The Bottom Line On Meal Timing

When and what you eat can affect your health and exercise performance. Therefore, following the advice above and developing a meal plan that works for you is recommended. To recap:

Eat most of your calories in the morning for weight loss and appetite control. As the famous saying goes, eat breakfast like a king, lunch like a prince, and dinner like a pauper.
To keep blood glucose steady, eat every 3-4 hours. This will help you avoid blood sugar spikes while keeping you energized and focused.
Eat carbs leading up to endurance exercise to top off muscle glycogen and elevate blood glucose.
Eat prote in or amino acids with a small number of carbs before and after strength training. This will maximize muscle protein synthesis, minimize exercise-induced muscle damage, and facilitate short and long-term training adaptations.

Your meal timing plan should be re-evaluated as necessary, depending on your lifestyle and athletic goals.

References:

Kerksick, C. M., Arent, S., Schoenfeld, B. J., Stout, J. R., Campbell, B., Wilborn, C. D., ... & Antonio, J. (2017). International Society of Sports Nutrition position stand nutrient timing. Journal of the international society of sports nutrition, 14(1), 1-21.
Xiao, Q., Garaulet, M., & Scheer, F. A. (2019). Meal timing and obesity: Interactions with macronutrient intake and chronotype. International journal of obesity, 43(9), 1701-1711.
Paoli, A., Tinsley, G., Bianco, A., & Moro, T. (2019). The influence of meal frequency and timing on human health: the role of fasting. Nutrients, 11(4), 719.
Thomas, E. A., Zaman, A., Cornier, M. A., Catenacci, V. A., Tussey, E. J., Grau, L., ... & Rynders, C. A. (2020). Later meal and sleep timing predicts higher percent body fat. Nutrients, 13(1), 73.
Moran-Ramos, S., Baez-Ruiz, A., Buijs, R. M., & Escobar, C. (2016). When to eat? The influence of circadian rhythms on metabolic health: are animal studies providing the evidence?. Nutrition research reviews, 29(2), 180-193.
Wang, C., Almoosawi, S., & Palla, L. (2021). Relationships Between Food Groups and Eating Time Slots According to Diabetes Status in Adults From the UK National Diet and Nutrition Survey (2008–2017). Frontiers in nutrition, 8.
Lopez-Minguez, J., Gómez-Abellán, P., & Garaulet, M. (2019). Timing of breakfast, lunch, and dinner. Effects on obesity and metabolic risk. Nutrients, 11(11), 2624.
Ravussin, E., Beyl, R. A., Poggiogalle, E., Hsia, D. S., & Peterson, C. M. (2019). Early time-restricted feeding reduces appetite and increases fat oxidation but does not affect energy expenditure in humans. Obesity, 27(8), 1244-1254.
Richter, J., Herzog, N., Janka, S., Baumann, T., Kistenmacher, A., & Oltmanns, K. M. (2020). Twice as high diet-induced thermogenesis after breakfast vs dinner on high-calorie as well as low-calorie meals. The Journal of Clinical Endocrinology & Metabolism, 105(3), e211-e221.

Does The Menstrual Cycle Affect Exercise Performance?

j.oswald@hyperionhealth.ca (Jesse Oswald) — Sat, 24 Feb 2024 00:48:41 GMT

Menstrual Cycle And Exercise Key Points:

The menstrual cycle is a biological process that supports reproduction.
The three main phases of the cycle are the follicular, ovulatory, and luteal phases.
During each phase, the fluctuations of two primary sex hormones, estrogen and progesterone, might impact exercise performance in women.
However, any detrimental effects of menstruation on exercise are trivial at best during the different phases.
Instead, it is recommended that women track their cycles and training and combine them to develop an individualized approach to exercise and nutrition.

Over the last 30 years, there has been a significant rise in the number of women participating in exercise. However, research on female athletes and those interested in general fitness has yet to keep pace with this exponential rise in participation.

One area of research on women that has been neglected is the effects of the menstrual cycle on exercise performance, specifically, how menstruation might affect strength, aerobic and anaerobic capabilities, and muscle recovery.

Before we discuss how the menstrual cycle might affect exercise performance, we first need to understand:

What is the menstrual cycle?
The phases of the menstrual cycle.
The main hormones found in each cycle and their fluctuations.

Let’s Dive in!

What Is The Menstrual Cycle?

You can think of the menstrual cycle as an essential biological process with significant changes in a woman’s sex hormones. The primary purpose of these fluctuations is to support reproduction, BUT they also might exert various effects on the cardiovascular, respiratory, metabolic, and neuromuscular systems. These effects might affect exercise performance.

What Are The Different Phases?

The menstrual cycle can be divided into six separate phases. In order, these are:

Early follicular - Days 1-5.
Late follicular - Days 6-12.
Ovulation - Days 13-15.
Early luteal - Days 16-19.
Mid-luteal - Days 20-23.
Late luteal - Days 24-28.

Next, let’s discuss the two primary hormones found in each phase and how their levels fluctuate.

Hormonal Changes During The Different Phases Of Menstruation

Estrogen and progesterone are essential hormones that fluctuate during the menstrual cycle. Let’s briefly discuss each before moving on to how they rise and fall during each menstruation phase.

What Is Estrogen, And What Does It Do?

Estrogen plays various roles in the body, but one of its primary functions is to help develop and maintain both the reproductive system and female characteristics. Furthermore, estrogen can be broken down into three different types.

Estrone is present in the body after menopause. It is a weaker form of estrogen that can be converted to other forms as necessary.
Estradiol is the most common type of estrogen during a female's reproductive years. This type of estrogen might have the most significant effect on exercise performance.
Estriol levels rise during pregnancy and peak just before birth. It functions to help the uterus grow.

It’s also important to know that estrogen is a very anabolic (muscle-building) hormone and may help increase glycogen storage while increasing fat utilization. All of which could have important implications for exercise performance.

Next, let’s discuss estrogen’s counterpart, progesterone.

What Is Progesterone?

Progesterone is the other primary hormone involved in the menstrual cycle. Its purpose is to prevent the fertilization of more than one egg and strengthen the pelvic muscle walls in preparation for labour.

Progesterone can also be thought of as the ying to estrogens yang. Meaning as progesterone levels rise during menstruation, estrogen levels fall.

This is important to remember as we move on to the next section of this article. How this rise and fall of estrogen and progesterone during each menstrual cycle phase might positively or negatively affect exercise.

The Follicular Phase And Exercise

Early Follicular

During this phase, concentrations of both estrogen and progesterone are low.

As mentioned earlier, estrogen is a potent anabolic hormone that helps protect against exercise-induced muscle damage while reducing inflammatory responses. When levels are low, there is a possibility of adverse effects on muscular performance or maximal and submaximal intensity exercise performance.

On the flip side, during the follicular phase (and due to low estrogen), the body might be able to utilize more glucose/glycogen. This can be highly advantageous for exercise, especially for longer duration/higher intensity training and events. It can also benefit those who strength train as working muscles use creatine phosphate and muscle glycogen as primary fuel sources.

In sum, even though muscle performance and performance might be slightly reduced during the early follicular phase due to low estrogen, the increased utilization of glycogen by the body might help offset it.

Late Follicular

Estrogen concentrations (anabolic hormone) rise during the late follicular phase while progesterone levels remain low. Compared to the early follicular phase, this may be ideal for focusing on strength training where the environment is primed.

High weight (75-85% of 1 repetition max), medium reps, and medium rest periods should be emphasized during this period. This may lead to more significant gains in strength and quicker recovery times when combined with the higher estrogen levels.

For example, one could perform four sets of 8 reps of compound exercises (bench press, deadlift, shoulder press, squat) with 75 seconds of rest between sets and 2 minutes of rest between exercises.

Cardio-wise, high-intensity interval training would improve cardiorespiratory fitness during the late follicular phase.

However, it must be stressed that more research is needed to verify this theory.

The Ovulation Phase And Exercise

Estrogen will continue to rise (progesterone remains low) and hit its highest level during this phase. This has the potential to impact substrate metabolism. More specifically, your body can store and use carbohydrates as energy.

Carbohydrates act as the primary fuel source when exercise intensity increases and moves from more aerobic to anaerobic. Anaerobic metabolism (think strength training, intervals, or HIIT) can only be fueled by carbohydrates. Without carbs, high-intensity exercise cannot be maintained.

During this phase, it may be recommended to focus on lower intensity exercise as your body utilizes more fat as an energy source during this phase.

The Luteal Phase And Exercise

During the luteal phase, both estrogen and progesterone levels are high. A 2019 study suggests that bloating and fatigue are common symptoms that make exercise uncomfortable during this phase.

Heart rate and core body temperature may also increase during the luteal phase, which may alter performance when exercising in the heat and humidity.

Lastly, central nervous system fatigue is higher in this phase, and the increased progesterone levels can contribute to sodium loss.

Considering all the above, it may be advisable to adjust training schedule to include more lower-intensity exercise during this phase while minimizing exercise in hot conditions.

The Bottom Line On Menstruation And Exercise

From the available research, knowing menstruation's effects (positive and negative) on exercise might help a woman develop a training program where certain performance variables are focused on during each phase.

For example:

During the early follicular phase, the focus should be on higher intensity, more prolonged duration cardio activities due to the body utilizing glycogen more efficiently. Strength training can also be done but should be conducted at a medium intensity as muscle recovery may be affected by the lower circulating estrogen levels.
Due to higher estrogen levels, the body is primed for intense strength and high-intensity interval training during the late follicular phase.
During the ovulatory phase, estrogen levels peak and may affect the body’s ability to utilize muscle glycogen. Therefore, low-intensity training like long, slow cardio is recommended as the body uses more fat as fuel.
During the luteal phase, estrogen and progesterone levels increase. Exercise in hot, humid environments should be avoided. Low-intensity cardio and strength training should be the primary focus.

In addition to the above information, It is also recommended that women track their cycles and training and combine them to develop an individualized approach to exercise and nutrition. Certain apps like FitrWoman may help with this.

References:

McNulty, K. L., Elliott-Sale, K. J., Dolan, E., Swinton, P. A., Ansdell, P., Goodall, S., ... & Hicks, K. M. (2020). The effects of menstrual cycle phase on exercise performance in eumenorrheic women: a systematic review and meta-analysis. Sports Medicine, 50(10), 1813-1827.
Dasa, M. S., Kristoffersen, M., Ersvær, E., Bovim, L. P., Bjørkhaug, L., Moe-Nilssen, R., ... & Haukenes, I. (2021). The female menstrual cycles’ effect on strength and power parameters in high-level female team athletes. Frontiers in Physiology, 12, 164.
de Jonge, X. A. (2003). Effects of the menstrual cycle on exercise performance. Sports medicine, 33(11), 833-851.
Thompson, B., & Han, A. (2019). Methodological recommendations for menstrual cycle research in sports and exercise. Medicine and science in sports and exercise, 51(12).

Oxygen, The Ultimate Measure of Longevity

j.oswald@hyperionhealth.ca (Jesse Oswald) — Sat, 24 Feb 2024 00:21:24 GMT

The Vital Role of Oxygen in Sustaining Life and Promoting Longevity

Oxygen is the molecule of life. It’s involved in every reaction in our body necessary to sustain life and movement. It’s also the foundational element for a long and high-quality life.

Without oxygen, death is inevitable. Luckily, our body houses a unique computer system that allows us to breathe without thinking about inhaling and exhaling. Our brain and neurons ensure that oxygen exchange and transport of oxygenated blood across every cell in our body happens seamlessly in the background.

In this article, we will do a deep dive into the mechanisms through which oxygen is the cornerstone of longevity, the research that stands behind this statement, and how its absorption by our body can be measured to provide a clear assessment of longevity and health.

The Oxygen Chain

To better understand the statement “Oxygen is the molecule of life,” we should first understand how and why our bodies use oxygen. Oxygen is the catalyst for energy release in every cell, a process necessary to sustain life and power movement. This mechanism involves using oxygen to oxidize or, in other words, “burn” nutrients we consume. These nutrients consist primarily of fats and carbohydrates. This burning process is similar to what happens in your fireplace when you set a piece of wood aflame, and oxygen interacts with wood in a chemical reaction to release energy, in this case, heat. The oxidation of nutrients releases our cells' energy to stay alive, move, and power other vital functions. Although this process may sound simple, it involves several systems in our body and employs most of the core organs. Here’s how this process works:

First, oxygen molecules enter the lungs through inhalation.
The lungs then absorb oxygen molecules through specialized alveoli membranes and transfer them into the bloodstream. Their transfer into the bloodstream occurs through a specialized hormone called hemoglobin, which can attract and retain oxygen molecules onto its surface and thus act as a transport mechanism. As hemoglobin draws oxygen molecules, the blood becomes rich in oxygen that can be transferred around the body.
Oxygenated, or oxygen-rich blood, is pumped with the help of the heart across the body, helping oxygen molecules reach every cell.
Once oxygen molecules reach their destination, they detach from hemoglobin and enter the cell. Inside the cell are dedicated systems called mitochondria responsible for using the newly delivered oxygen to oxidize and break down the fats and carbohydrates we have consumed.
The breakdown of fats and carbohydrates releases energy used to maintain the proper temperature across our body and move (e.g., movement of muscles).
The oxidation of fats and carbohydrates releases carbon dioxide (CO2), which must be cleared from our bodies. Consequently, CO2 is expelled from the cell and released into the bloodstream, where it’s carried back to the lungs. CO2-carrying blood is then pumped back into the lungs. There, through the opposite mechanism of oxygen used to enter the bloodstream, CO2 exists in blood circulation into the inner cavity of the lungs. Lastly, through exhalation, this CO2 is expelled into the environment.

This process is also known as Aerobic Metabolic or Cellular Respiration. Aerobic comes from the Greek word “Aερας” (aˈe.ɾas), which means air and refers to the presence of oxygen in the energy release process. Aerobic metabolism accounts for more than 95% of our overall energy generation. It is distinct from the secondary energy release mechanism called Anaerobic Metabolism, which will be covered in a separate post.

What’s important to keep in mind from the process described above is that:

Oxygen is a hard requirement for our body to release the energy it needs to stay alive, regulate its temperature, and move.
Four significant systems are involved for oxygen to be absorbed, delivered, and utilized in the “burning” of fats and carbohydrates: lungs, heart, blood, and cells.
Metabolism is the collective function of all these systems. A “broken” metabolism may mean that any part of this chain may be problematic and hampering the most fundamental process in the human body, the oxygen chain.

Chronic disease & Oxygen Chain

To understand how oxygen plays a crucial role in regulating the quality and length of one’s life, one should examine the relationship between the ability to utilize oxygen and the primary factors hampering longevity, namely chronic diseases.

Chronic diseases are typically conditions caused by lifestyle factors such as poor nutrition, lack of exercise, or tobacco use and inflict an ongoing reduction in quality and duration of life. The four most common, deadly, and costly chronic conditions are heart disease, lung disease, cancer, and diabetes.

Besides cancer, the scientific community now openly acknowledges that heart disease, lung disease, and diabetes are highly interlinked in terms of their underlying lifestyle drivers and their high degree of comorbidity (i.e., one leads to the other). The term used to characterize this collective disorder is “Cardio-metabolic Syndrome.”

Cardio-metabolic syndrome is driven primarily by lifestyle factors, which, for the most part, can be traced to poor nutrition and lack of exercise. No matter the contribution of exercise or nutrition to the cardiometabolic syndrome, its advent can always be traced to the oxygen chain. Specifically, a disruption of the oxygen chain in any of the three fundamental components, namely heart, lungs, and cells, is directly related to the rise of the equivalent cardio-metabolic syndrome’s facet, namely heart disease, lung disease, and diabetes.

The implications of this phenomenon are significant for the early detection and prevention of these conditions. In short, analyzing and monitoring the oxygen chain can help early detect a predisposition for heart disease, lung disease, or diabetes. Here’s a brief description of how oxygen denotes deterioration in each system.

Heart Disease

The heart is our body’s blood pump and helps push oxygen-rich blood from the lungs to every cell. It also moves carbon dioxide-rich blood from the cells back to the lungs. Nearly every form of heart disease, including Ischemic Heart Disease and Heart Failure, causes the heart to be less effective in pumping oxygen-rich blood into your body. This manifests through reducing the amount of oxygen your body consumes per heartbeat. This is measured during a graded breath analysis test through a variable called O2pulse. A separate blog post covers a detailed review of how breath analysis can help detect heart conditions.

Lung Disease

Nearly every form of lung disease will cause the lungs to be less effective in absorbing oxygen. Whether it’s Asthma, Chronic Pulmonary Obstructive Disorder (i.e., COPD), or Pulmonary Embolism, the effects are a reduced ability to absorb oxygen and deliver it to the bloodstream. The main breath variables used to detect this deficiency include the maximum amount of air lungs can exchange with the environment (i.e., MVV or maximum voluntary ventilation), the amount of oxygen transferred into the blood (i.e., SpO2 or blood oxygen saturation), and the maximum amount of air one can exhale during exercise (i.e., Peak VT or maximum tidal volume). A separate blog post covers a detailed review of how breath analysis can help detect lung conditions.

Diabetes

Diabetes is a condition in which cells cannot metabolize carbohydrates, thus leaving them in the bloodstream. The presence of carbohydrates in the bloodstream is toxic as it causes gradual degradation of every tissue in the body. The onset of diabetes can also be traced back to the oxygen chain, but this time on a cellular basis. When cells become less able to absorb and utilize oxygen, they become less able to oxidize fat as a fuel source. This leads to increased intramyocellular lipids levels (i.e., fat within muscles and tissue) and a higher blood concentration of free fatty acids. This, in turn, stimulates higher glucose release in the liver and further insulin secretion by the pancreas. Exposing your body to a constant state of increased insulin concentration in the blood makes your cells less “sensitive” to insulin, leading to insulin resistance and, consequently, diabetes. A separate blog post covers a detailed review of how breath analysis can help detect a predisposition to diabetes.

Quantifying Longevity Through Oxygen

The importance of oxygen for long-term health has been established through studies examining the function of individual elements found in the oxygen chain (i.e., heart, lungs, cells) and its global function (i.e., overall oxygen consumption). The latter has been scrutinized through epidemiological studies that have examined the correlation between mortality risk and the total amount of oxygen one’s body can absorb. After decades of rigorous scientific research measuring peak oxygen consumption among individuals of various backgrounds, ethnicities, and ages and subsequently tracking their fatality rates over several decades, the scientific community concluded that cardio-respiratory fitness, AKA VO2peak or peak oxygen consumption, is the strongest predictor of how well and long someone will live. Although a low VO2 peak can’t reveal the exact sub-system (e.g., heart, lungs, or cells) causing its deterioration, it can certainly indicate that at least one is facing an underlying problem and is thus a strong indicator of chronic disease onset. This immediately translates into a reduction in expected lifespan and quality of life. The findings of these studies were summarized in a landmark scientific statement published by the American Heart Association in 2016, which elevated VO2peak into a critical vital sign that provides the most substantial evidence about life expectancy and quality. Specifically, for every unit increase in VO2peak, measured in Metabolic Equivalent (i.e., METs), one’s likelihood of death and onset of chronic disease declines by ~15%. Such is its predictive power that the American Heart Association openly called for implementing VO2peak in annual physical examinations.

Conclusion

Most people train for life, meaning that a longer and better life is the motivation behind picking up a workout routine or cleaning up their diets. Therefore, assessing how effective a wellness routine is for one’s longevity goals is essential to success. Breath analysis provides the gold standard in determining how the oxygen chain and its components work globally, thus indicating whether a wellness routine leads to a longer and better life. It does so while also pinpointing the sub-systems of the oxygen chain, namely lungs, heart, and cells that may have been impacted by age, lifestyle, or other factors requiring a closer medical examination. Ultimately, oxygen is the molecule of life. How it flows through the body is the best picture of one’s health, and breath analysis is its most reliable measurement tool.

The Steps to Longevity

j.oswald@hyperionhealth.ca (Jesse Oswald) — Fri, 23 Feb 2024 23:56:07 GMT

Key Points:

Chronic disease and deterioration of health don’t happen overnight. Poor nutrition, exercise, and a recovery program ensure long-term health.
Nutrition, training, and exercise all support the pillars of health and longevity, including Cellular, Heart, Lung, Gut, Mental, and Skeletal Muscle Health.
Understand how each type of training, nutrition, and recovery elements impact each pillar of health and longevity.

Living a long, healthy life can be one of the most complicated goals. Most of us don’t know where to start, can’t establish a correlation between lifestyle choices and health benefits, and thus spend years experimenting based on empirical knowledge from health professionals, friends, and the media. It doesn’t have to be this way, though. Any significant and daunting endeavour can be turned into an achievable objective if you break it down into small, understandable, and actionable steps. This article discusses the pillars of longevity and the fundamental lifestyle choices influencing them. In simple terms, we aim to explain the focus areas and what you can do about them by leveraging nutrition, exercise, and recovery.

What is longevity made of?

Living a long and healthy life stems from ensuring that specific elements of our biology remain healthy. These include cardiovascular, pulmonary, cellular, skeletal muscle, mental, and gut health.

Heart health: Our cardiovascular system includes our heart, arteries, and veins and gives rise to the most common and costly chronic conditions, including heart failure, coronary artery disease, and hypertension. It’s the most common cause of death in the developed world; consequently, high cardiovascular health is a prerequisite for longevity.

Lung health: The American Lung Association elevated lung disease as the leading cause of death this year. Unlike popular belief, the degradation of lung health can be caused by several factors, including air pollution, infectious diseases (e.g., COVID-19), and chronic syndromes (e.g., COPD). Although pulmonary conditions may likely not be the immediate cause of death, their comorbidity with other more dangerous conditions, such as heart disease, threatens one’s life span. Moreover, their ability to hamper physical activity renders them a depreciation factor of life’s quality.

Cellular health: Cellular health is the third puzzle against chronic disease. Metabolic syndrome and obesity directly relate to how our cells utilize oxygen to burn nutrients and sustain life and power movement. Studies have now linked diabetes to our cells' inability to use oxygen effectively. Moreover, studies have shown that metabolic slowdown , where our cells use less oxygen and burn fewer calories than predicted, is the primary factor leading to weight loss failure. Obesity and diabetes consequently become the cause of life-threatening conditions such as heart disease and thus become the root cause of premature and, in most cases, expensive fatalities.

Skeletal & muscle health: Skeletal and muscle deficiencies such as lower back pain and hip displacement are the primary factors depreciating quality of life. Moreover, due to their debilitating effect on physical activity, they become the root cause of obesity and metabolic syndrome, leading to cardiovascular and pulmonary conditions. These will, in turn, lead to lower quality and span of life.

Mental health: Depression, stress, and anxiety can bring about physiological and life-threatening conditions through several pathways. First, they can be the root cause of physical activity and unhealthy eating habits. Moreover, as our blog post “The effects of chronic stress on energy balance” states, chronic stress can lead to several hormonal perturbations that promote visceral fat accumulation and increase the likelihood of metabolic syndrome independently of weight gain. The combination of these factors leads many to develop one or more common chronic conditions (i.e., cardiovascular, pulmonary, metabolic), leading to lower quality and span of life.

Gut health: Our gut is a complex “superorganism” that can positively or negatively affect our health in countless ways. An impaired gut microbiome can impair fat metabolism and energy absorption and affect our immune system, giving rise to a host of diseases, including pulmonary and metabolic syndrome . Moreover, our brain and gut are inextricably connected, which renders the gut microbiome a potent modulator of our mental health. Consequently, a healthy gut safeguards against metabolic, lung, cardiovascular, and cognitive disorders.

What can I do to live longer and better?

The short answer is to ensure all the systems mentioned above work correctly. To achieve this, however, one needs to employ different tools for each one of these systems. The table below summarizes the influence training, nutrition, supplementation, and recovery have on the other areas of our health.

Cellular health

Resistance training: Resistance training elevates your metabolism and prevents it from slowing down. This is of paramount importance as the metabolic slowdown is proven to be the most potent contributor to weight gain.

Interval training: Interval training increases growth hormone levels, essential for burning fat and maintaining and maintaining muscle mass.

Endurance training: Interval training increases growth hormone levels, essential for burning fat and maintaining muscle mass.

Micronutrient balance: Micronutrients have a central role in human metabolism. They are required for the appropriate functioning of energy production in the cells by metabolizing carbohydrates, proteins, and fats. A shortfall in any of them will be rate-limiting for energy production, with potential metabolic complications.

Macronutrient balance: Macronutrients are the nutritional components of food that the human body needs in large amounts for energy production (metabolism) and maintaining physiological functions. They include carbohydrates, fat, and protein. The diet macronutrient ratio doesn't directly influence weight. To optimally manage your weight, find a ratio you can stick with, whether a low-fat diet or a low-carb diet, etc., focus on healthy food choices across all food groups, and eat fewer calories than you burn.

Energy balance: Energy balance is the state achieved when energy intake from food equals energy expenditure from everyday activities and calories burnt at rest to perform essential functions such as breathing, heart beating, etc. (RMR). When the human body is in energy balance, body weight is stable. Body weight will decrease when the energy intake is lower than the energy expenditure, otherwise known as a caloric deficit. Irrespective of the type of diet (keto, vegetarian, Mediterranean, etc.) through which this caloric deficit will be accomplished, the most essential weight loss driver is the caloric deficit per se. With a sufficient caloric deficit, weight loss will be feasible. Body weight will increase when the energy intake is higher than the energy expenditure, otherwise known as caloric surplus.

Meal-timing: Meal timing may be crucial in obesity and weight loss treatment. In particular, it may affect 24-hour body cycles (circadian rhythm) that can predict weight loss. For example, night shift workers have an increased risk for obesity and may experience an increased appetite for energy-dense foods. More specifically, for people with the highest caloric intake until 2 hours before bedtime, the so-called evening chronotypes, the probability of being obese increases five times compared to people who eat the most significant proportion of their daily calories two hours after waketime, the so-called morning chronotypes. Moreover, it has been shown that eating your lunch late (after 3 p.m.) predicts difficulty in weight loss. However, meal timing can only be a potential tool to combat obesity since a sufficient caloric deficit will always be the most crucial determinant.

Adequate sleep: Maintaining a consistent sleep schedule with sufficient sleep time is vital for maintaining normal hormonal function, regulating hunger, and preventing stressed eating. It's also critical for recovering effectively and thus maintaining muscle mass and high metabolism.

Mental Health

Resistance/Interval/Endurance training: Every form of physical exercise significantly reduces stress, depression, and anxiety.

Micronutrient balance: Inadequate intake of micronutrients, which are particularly important for mental health, has been associated with inflammation in the central and peripheral nervous system (neuroinflammation); hence, mental disorders such as depression, sleep disorders, stress, and anxiety. Vitamin E, B12, folate, and magnesium are the most important micronutrients for mental health.

Macronutrient balance: A healthy dietary pattern affects not only the brain composition, structure, and function but also hormones, neuropeptides, and neurotransmitters, which play a crucial role in mental health. Fat is the most essential macronutrient for mental health, especially the omega-3 polyunsaturated fatty acids EPA and DHA. They are found primarily in fatty fish, such as salmon, sardines, and fish oil. They can help alleviate mood disorders such as depression symptoms and decrease antidepressant medication dosages.

Energy balance: Obesity is positively associated with various mental health issues, including depression, anxiety, and eating disorders. Obesity also impacts the quality of life, with many obese people experiencing increased stigma and discrimination because of their weight.

Meal timing: Irregular meal timing has been associated with higher productivity loss through more significant problems with sleep and stress. It has also been correlated with higher neuroticism and lower subjective overall well-being scores and perceived mental health.

Adequate sleep: Maintaining a healthy schedule is critical for regulating anxiety and mental health. Sleep and mental health are undeniably connected bi-directionally, with sleep deprivation or sleep schedule distortion being fundamental drivers of all mental health issues ranging from anxiety to depression and panic attacks.

Muscle and Skeletal Health

Resistance/Interval/Endurance training: Resistance training is critical for maintaining bone density, joint strength, and proper posture. High bone density is essential for averting osteoporosis with aging, whereas joint strength and correct posture are essential for avoiding common injuries like lower back pain.

Micronutrient balance: Inadequate intake of micronutrients that contribute to the antioxidative capacity of the cells, such as vitamins A, B6, B12, and E, folate, selenium, and zinc, may be related to increased muscle fatigue and frailty. On the other hand, the micronutrients of most significant importance for bone health and, hence, osteoporosis prevention are calcium and vitamin D.

Macronutrient balance: An increased dietary protein intake is recommended to prevent bone loss. A higher percentage of carbohydrate energy intake is associated with a higher risk of low bone mineral density. Therefore, the isocaloric substitution between carbohydrates and protein is significantly associated with bone health. Similarly, protein is the essential macronutrient for gaining and maintaining muscle strength and size. However, all three macronutrients through a healthy, balanced diet are crucial to developing and maintaining muscle mass.

Energy balance: Increased body fat typically accompanies a concomitant increase in fat deposition within skeletal muscle, leading to sarcopenia (progressive loss of muscle mass and strength) and physical disability. The increase in fat mass is also frequently associated with a simultaneous decrease in muscle mass and, therefore, a reduced metabolic rate. Hence, sarcopenic obese individuals burn fewer calories at rest, and their progressive muscle weakness leads them to chronic inactivity and, thus, even lower energy expenditure. On the other hand, obesity may increase bone density because it is associated with higher mechanical loads, which may protect bones. However, overly obese people (BMI>35) are more likely to fall and break bones; hence, over a certain BMI, obesity does not protect against fractures and may even increase their risk.

Meal timing: Although meal timing does not somehow affect muscle and skeletal health, nutrient timing, i.e., when relative to exercise, someone ingests their macronutrients, carbohydrates, and protein, in particular, seems to maximize the muscle stimuli of the exercise that has been preceded. Protein is vital to supporting muscle growth and muscle recovery. Consuming 20g of protein within 30 minutes to 2 hours after exercise, particularly resistance training, will help the muscle tissue recover and aid skeletal muscle growth. This amount of protein is recommended to be complemented by a sufficient amount of carbohydrates in a ratio of 1:3 or 1:4.

Adequate sleep: A healthy sleep schedule is equivalent to adequate physical recovery. Too short or too long a sleeping schedule has been linked to skeletal muscle problems like lower back pain.

Gut Health

Resistance/Interval/Endurance training: All forms of exercise have been shown to elicit positive effects on the gut microbiome. Specifically, exercise:

Reduces intestinal permeability (the degree to which the surface of the digestive system is permeable to substances), thus blocking pathogens that may be found in the gut from entering the bloodstream.
Increases the diversity of beneficial gut bacteria that aid digestion.

Micronutrient balance: Micronutrients can modulate the diversity and composition of the gut microbiome, leading to the prevalence of beneficial bacteria and gut health or harmful bacteria and gut and overall health complications. This relationship is bidirectional since gut bacteria synthesize essential micronutrients, considerably impacting the micronutrient balance.

Macronutrient balance: Macronutrients have various effects on gut health, both positive and negative. Specifically, non-digestible plant-derived carbohydrates, named dietary fibre, can improve gut microbial diversity and promote gut health. Dietary fibre increases the population of health-beneficial bacteria, such as Bifidobacterium and Lactobacillus. On the other hand, diets rich in saturated fat mainly derived from full-fat dairy products and animal-based foods such as beef and lamb harm the richness and diversity of gut microbiota.

Energy balance: The microorganisms that live in our gut (gut microbiota) could play a significant role in whether or not we become obese. Also, obesity per se seems to be able to change the composition of our gut microbiota by reducing its diversity and favouring a higher proportion of gut Firmicutes species compared to the Bacteroidetes species. These changes are associated with more marked overall fat accumulation and metabolic complications such as increased blood lipids (cholesterol) and glucose. Therefore, obesity and gut health share a bi-directional relationship where one determines the state of the other.

Meal timing: Meal timing does not seem to affect gut health in any other way other than increasing the possibility of experiencing heartburn and gut distress symptoms such as abdominal pain, bloating, etc., in general when having your large meal close to bedtime.

Adequate sleep: A healthy sleep schedule is critical for maintaining a healthy gut. Low sleep efficiency, sleep disturbances, and irregular sleeping windows have been proven to negatively affect the gut microbiome in several ways. A compromised gut microbiome leads to digestive, metabolic, and mental disorders.

Heart Health

Resistance/Interval/Endurance training: Interval and endurance training are heart health's most potent positive factors. They positively affect all areas of the cardiovascular system, including the heart and blood, arteries, and veins. Specifically, they:

Strengthen the heart muscle
Prevent arterial clogging
Improve hemoglobin content in the blood

Micronutrient balance: A diet that prioritizes the consumption of a range of heart-healthy nutrients, including magnesium, potassium, B vitamins, vitamin D, and selenium, through the consumption of a variety of fruits and vegetables at every meal can lower the risk of coronary heart disease, stroke, and the overall incidence of cardiovascular diseases.

Macronutrient balance: Macronutrient balance has been linked to cardiovascular disease and related risk factors (high LDL and low HDL cholesterol). Specifically, increasing the consumption of monounsaturated fat (olive oil), omega-3 polyunsaturated fatty acids (fatty fish), and good-quality carbohydrates (whole grains, fruits, vegetables) while decreasing the amount of saturated fat (full-fat dairy products, animal-based foods) and refined grains (sweets, white carbs) can reduce the risk of cardiovascular disease.

Energy balance: Obesity accelerates the risk of developing cardiovascular disease by increasing circulating lipids (blood cholesterol and triglycerides) and blood pressure. Obesity is also associated with chronic inflammation and progressive physical activity decline and thus cardiorespiratory fitness, compromising heart health even more. This association is powerful when the excess fat deposition is in the abdominal area. This fat is called visceral fat and accumulates around vital organs, progressively leading to heart health issues.

Meal timing: Nighttime eating, defined as consuming food after bed, has been associated with a 55% greater risk of cardiovascular disease than non-nighttime eating. Although eating your largest meal late in the day could pose a greater risk for heart health issues, most results arise from observational studies and not from clinical studies, which would address the causality between meal timing and cardiovascular disease. Such studies have failed to demonstrate a direct link between meal timing and heart health. Therefore, based on current scientific evidence, meal timing is not a strong determinant of heart health.

Adequate sleep: A healthy sleep schedule is essential for preserving cardiovascular health. During sleep, blood pressure is reduced, and consequently, lack of sleep inevitably means that your blood pressure will remain higher for longer during the day. Elevated blood pressure is the most prominent risk factor for developing life-threatening heart conditions.

Lung Health

Interval/Endurance training: Interval and endurance training are the most potent positive factors of lung health. They positively affect all areas of the respiratory system, including the lungs and respiratory muscles. Specifically, they:

Strengthen the respiratory muscles
Improve oxygen transfer efficiency in the alveoli
Increase vital lung capacity

Micronutrient balance: Certain micronutrients have anti-inflammatory and anti-oxidative properties, which can directly target the pathogenesis of lung function decline, such as chronic obstructive pulmonary disease, and thus promote lung health. These are vitamin A, vitamin E, vitamin C, and selenium.

Macronutrient balance: Carbohydrate metabolism acutely increases CO2 production and may deteriorate lung function in the long term, especially in older adults. Indeed, a carbohydrate-rich diet has been negatively associated with health markers of lung function, such as the FEV1, whereas protein and fat intake are inversely associated with lung function decline. This relationship is more powerful when carbohydrates derive from food sources rich in refined carbohydrates (sweets, refined grains) with low dietary fibre content.

Energy balance: Obesity is a significant risk factor for asthma, obstructive sleep apnea, and obstructive pulmonary disease. It also increases susceptibility to respiratory infections, and hospitalization rates are higher in obese patients with respiratory disease than in healthy-weight individuals. Fat accumulation in the abdominal area (visceral fat) is especially linked to asthma and impaired lung function, changing the normal physiology and part of the lungs.

Adequate sleep: Sleep deprivation has been shown to elicit the loss of breathing control, a risk factor for developing respiratory disorders such as asthma and COPD.

Breath Analysis & Diabetes

Fri, 23 Feb 2024 23:11:50 GMT

Key takeaways:

Diabetes begins with a condition called insulin resistance, which is caused by elevated free fatty acids and intramyocellular lipids.
The accumulation of free fatty acids and intramyocellular fat results from impaired fat-burn efficiency by our cells and/or weight gain.
Breath examination provides an excellent tool for tracking fat-burning efficiency and the likelihood of obesity.

Unfortunately, diabetes is as common as it is misunderstood. Although pre-diabetes and diabetes are among the most common conditions, many of us, including doctors and health professionals, are unsure of their origin. As a result, we may claim that diabetes is a lifestyle disease, but we just cannot put our fingers on what exactly in our lifestyle causes it. This article explains the biological process of diabetes and how breath analysis provides an excellent tool for predicting its onset.

What is diabetes?

Metabolism is the process by which our bodies transform the nutrients we eat into the energy we need to maintain essential functions (i.e., heartbeat, brain function, etc.), regulate temperature, and perform physical activities (e.g., move and exercise). Fat and carbohydrate are the two most commonly used nutrients in our metabolic process and thus supply more than 90% of our body's energy daily.

Although both macronutrients are used in significant amounts throughout the day, the process by which they are being treated varies vastly. This difference stems from the way they are stored. On the one hand, our body can store practically unlimited amounts of fat in adipose tissue (e.g., the fat accumulated around our abdomen, back, and other areas). Still, on the other hand, we can store only a minimal amount of carbohydrates. To put things into perspective, the average person may store up to 30,000 kcal worth of fat, which can increase tremendously by becoming overweight or obese, but can only store approximately 2,000 kcal of carbohydrates. The limited ability of our body to store carbohydrates ultimately means that whenever ingested, they need to be used immediately, stored in our small carbohydrate reserves (in case there is room), or converted into fat through a process called de-novo lipogenesis. Since the second pathway is unlikely and the third one energetically costly, our bodies will resort to the immediate burn of carbohydrates when ingesting them.

Let’s now look into the process by which our body burns carbohydrates. Much like fats, carbohydrates must reach the inner part of our cells to be processed by the mitochondria, our body’s energy factory that converts fats or carbohydrates into the calories we use to survive and move. To achieve this, the following process takes place . Initially, carbohydrates need to be converted into glucose, which begins in our mouth but primarily in our small intestine. The intestine membranes absorb glucose, enter the bloodstream, and transfer it to the liver, where it is used, stored, or directed to other body parts. When it enters our muscle mass to be stored for future use, it is converted into glycogen.

As glucose levels rise in the blood, our body reacts through the secretion of insulin, a hormone required for managing glucose across our organs. Specifically, insulin is a substance that “latches” onto glucose molecules and enables them to enter cells, thus clearing them from the bloodstream. This is necessary because although glucose is a valuable nutrient that provides useful energy, it can be toxic for our organs if it remains in the bloodstream for too long. The toxic effects of lingering glucose in the blood slowly degrade all forms of tissue and can cause heart disease, neurodegenerative diseases such as Alzheimer's disease, and, in advanced cases, even require amputation of one’s leg. As a result, once glucose enters the bloodstream from the membranes of our small intestine, it needs to be stored in the liver or used by the working muscles immediately. Our body uses the hormone insulin , secreted from our pancreas, to enable glucose to enter our liver and muscle cells. This is where the route of diabetes lies. Specifically, diabetes occurs if our pancreas doesn’t produce enough insulin or our cells are not responsive enough to it, a condition also known as insulin resistance

What causes diabetes?

As described above, diabetes is a confluence of two conditions: cells becoming unresponsive to insulin and the pancreas not producing enough insulin. The combined effect of the two phenomena is that insulin production cannot clear glucose from the bloodstream. The lingering glucose thus causes widespread deterioration of all tissues across our body. Although both conditions need to coexist for diabetes to occur, their onset is not simultaneous but sequential.

The first of the two conditions is insulin resistance caused by excessive accumulation of intramyocellular lipids (IMCL) and plasma-freefatty acids (FFAs). Intramyocellular lipids are fat stores within muscles, whereas free fatty acids are fat molecules circulating in our bloodstream. The common denominator between the two is that they cause cells to become less responsive to insulin and thus cause insulin resistance. These two conditions occur when overall fat accumulation across the body increases, or in other words, when one starts to transition from average weight to an obese or overweight state.

To compensate for the fact that cells are now less responsive to insulin, the pancreas of an individual with early stages of insulin resistance starts to secret more insulin. This sets the person’s pancreas in a constant state of “overdrive,” meaning it constantly operates above its normal capacity. It is important to note, however, that this doesn’t always lead to pancreatic failure and insulin secretion shutdown. Nearly 80% of obese and overweight individuals live in a state where their pancreas is secreting excessive insulin to compensate for their varying degrees of insulin resistance. This state is also known as hyperinsulinemia.

However, in case hyperinsulinemia leads to partial or complete pancreatic failure. Insulin levels drop sharply, circulating blood glucose cannot penetrate cells, and ultimately, lingering blood glucose starts to cause its deleterious effects. This is when the onset of Type II Diabetes (T2D).

Given the above mechanism, it is evident that fat accumulation is the underlying driver of T2D. This is corroborated by every piece of longitudinal data about the disease and its correlation with obesity levels. Specifically, T2D started to become a health concern and subsequently a dire epidemic at the same time that people began gaining weight. Given that obesity is founded on our unhealthy nutrition habits and lack of physical activity, it is an undeniable fact that T2D is largely a disease of our modern lifestyle.

The myth of carbs causing diabetes and fat treating it

The above mechanism elucidates the nature of T2D and how it is routed in weight gain and fat accumulation. However, it also sheds light on the fact that the macronutrient composition of one’s diet is irrelevant. In other words, following a low carb high, fat or low-fat high, carb diet can’t cause or cure diabetes. Besides, we describe in another one of our blogs, “Obesity Explained,” that through millennia, humans have followed all kinds of diets ranging from almost exclusively fat and animal protein-based to almost solely carb-based ones. Despite the wide range of diets followed by our ancestors, diabetes never became a health concern until obesity came along. As a result, weight loss and re-ignition of the cells’ insulin sensitivity through physical exercise to insulin are the only ways to mitigate the effects of T2D or, in some cases, even cure it.

How breath analysis provides an early warning for diabetes

Diabetes begins when insulin resistance occurs due to toxins secreted by free fatty acids (FFAs) and intramyocellular lipid (IMCL) accumulation. These toxins affect the cells’ ability to respond to insulin and thus prevent them from being able to absorb glucose that is circulating in the blood. In simple words, insulin becomes less effective when insulin resistance occurs as the “key” for glucose to enter cells. Therefore, we must first understand the root cause of fat accumulation to uncover the origins of insulin resistance. Specifically, the build-up of FFAs and IMCL can be traced back to two factors:

Reduced ability to burn fat: Fat is a fuel source that requires oxygen and higher mitochondrial density compared to carbohydrates. Simply put, it requires “well-training” mitochondria as it’s a more complex fuel to process. Lack of exercise or constant consumption of high glycemic index carbs will gradually reduce mitochondrial density, making your cells less able to burn fat as a fuel source. Less fat oxidation means higher intramyocellular lipids and free fatty acids in the blood.
Obesity and visceral fat: Adipose tissue, in other words, accumulated body fat, impacts metabolism by releasing hormones and other substances, including leptin, cytokines, adiponectin, and proinflammatory substances. Another essential substance released in the process is FFAs. Individuals who are obese or overweight, therefore, have higher than average FFAs circulating in their blood. Out of the substances that adipose tissue releases that affect insulin sensitivity, the most are FFAs. The higher the level of circulating FFAs, the higher the insulin resistance and, thus, the likelihood of T2D.

Both phenomena can be traced or predicted through breath analysis. Specifically, the ability to utilize oxygen and burn fat at rest is assessed most accurately by analyzing the balance between oxygen and carbon dioxide in the breath, also known as the Respiratory Exchange Ratio. Studies have also proven this concept by showing that reduced fat oxidation at rest is a risk factor for diabetes even before the onset of elevated blood sugar levels during a fasted state (a condition also known as pre-diabetes).

Moreover, the likelihood of obesity can be accurately assessed by determining the metabolic level of an individual, in other words, whether one’s metabolism is faster or slower than expected based on age, gender, and body size. The gold standard for analyzing a person’s metabolism is also breath analysis.

Conclusion

Diabetes is undeniably a lifestyle disease that stems from physical inactivity and poor nutrition habits. Combined, they lead to impaired cellular oxygen uptake ability and fat accumulation, leading to insulin resistance. As a result, addressing diabetes through nutrition and exercise should be a priority for everyone looking to avoid it or overcome it.

hyperion-health

Emotional Acceptance: How to Make Space for Difficult Feelings (Without Letting Them Run Your Life)

Emotional Acceptance

A practical framework: Accept ➡︎ Notice ➡︎ Choose

What is a Kinesiologist?

What is a Kinesiologist?

What is Kinesiology?

What Education and Qualifications Do Kinesiologists Have?

What Does a Kinesiologist Do?

1. Injury Rehabilitation

2. Chronic Disease Management

3. Performance Enhancement

4. Workplace Health and Ergonomics

5. General Health and Fitness

Where Do Kinesiologists Work?

Why Should You See a Kinesiologist?

What Sets Kinesiologists Apart?

How to Find a Kinesiologist

Move Better, Live Better with Kinesiology

Predicting Medical Costs with VO2max

Highlights

A dire problem for employers

Why is Breath Analysis relevant?

What is VO2max?

How is VO2max measured?

The Oxygen Chain

Healthcare cost prediction

Conclusion

Dietary Fat: An Essential Dietary Component Rather than the root of all Nutritional Health Issues

Key points

Polyunsaturated fatty acids (PUFAs)

Omega-6 and omega-3 PUFAs

Monounsaturated fatty acids (MUFAs)

﻿

Saturated fatty acids (SFAs)

Trans fatty acids (TFAs)

Dietary lipids and the human microbiome

Dietary lipids and obesity

References

Dietary Carbohydrates: Catalysts of Physical Performance and Regulators of Overall Health

Key points

Carbohydrate classification

Simple carbohydrates

Complex carbohydrates

Carbohydrate intake recommendations

Carbohydrate metabolism and stores

Carbohydrate utilization at rest and during exercise

Pre-workout carbohydrate recommendations

Efficient glycogen replenishment

Simple carbohydrates and overall health

The health benefits of dietary fiber

REFERENCES

The Place of Stimulants in the Field of Sports

Key points

Stimulants classification

Stimulant usage by athletes

Rules around stimulant use

The adverse effects of stimulants

Caffeine

Amphetamines

Ephedrine and pseudoephedrine

Cocaine

References

Linking Inflammation, Diabetes, and Breath Analysis

Step 1 - Onset of inflammation

Step 2 - Inflammation neutralizes our cells’ insulin receptors (Insulin Resistance)

Step 3 - Insulin resistance causes fuel utilization dysfunction

Step 4 - Fuel utilization dysfunction leads to fat accumulation and lower energy levels

Step 5 - Accumulated fat causes more inflammation and insulin resistance

Step 6 - Insulin resistance leads to elevated blood sugar (Pre-diabetes)

Step 7 - Pancreas goes on over-drive and ultimately fails (Diabetes)

Breath analysis, an easy and reliable monitoring tool for metabolic function.

Inflammation: A Tightly Regulated Biological Response that, if Uncontrolled, Can Turn out Fateful

Key points

What really inflammation is and how is it caused

Obesity and its central role in chronic inflammation

Inflammation caused by dysregulated sleep patterns

Inflammation caused by chronic stress

Inflammation caused by environmental chemicals

The implication of exercise with chronic inflammation