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wise athletes episodes

August 21#185 | GLP-1: Microdosing? | Vyvyane Loh MD
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Vyvyane Loh MD
Board certified in internal medicine and obesity medicine, with a long focus on immunometabolism.
Her book, The Architecture of Enough: Hunger, GLP-1, and the Immune Metabolic System, is available on Amazon (paperback: https://www.amazon.com/Architecture-Enough-Hunger-Immune-Metabolic/dp/B0H2R8HKS4 — and Kindle) and Barnes & Noble.
She also publishes an in-depth health e-zine at wellth-e.com (WELLTH-E — "wealth" as in money plus wellness); she points listeners to issue #3
Bottom line: For an otherwise healthy, fit person chasing a modest amount of weight, Dr. Loh's take is stay away if you can — the muscle and immune-metabolic costs outweigh the benefit, and these drugs are best reserved for clear medical need, used with a real clinician and a defined exit strategy.
*Note: Educational, not medical advice. Dr. Loh stresses these decisions should be made with a clinician genuinely involved in your care.*
Key learnings
Ask "where's the receptor?" to tell a direct drug effect from a general weight-loss effect.
Metabolism and immunity are inseparable — every metabolic change is an immune change.
Insulin resistance is an adaptive response; acute is healthy, chronic is the problem.
The drug delivers GLP-1 alone and supraphysiologically — missing the natural hormone "family" and overriding your own system.
GLP-1 curbs appetite partly by inducing a low-grade "sickness" state via IL-6.
IL-6 isn't just "bad"; suppressing it long-term may drive muscle loss and impair repair.
Biggest risk for fit people: trading fat for lost muscle (obesity+diabetes → sarcopenia+diabetes).
~75% regain most weight within a year of stopping, even while keeping good diet habits.
Beware catabolic states — surgery, illness, immobility — while on these drugs.
Skip no-follow-up, online platforms; pair any GLP-1 use with real lifestyle structure (meals, protein, hydration, sleep, lifting).
Summary
Two years after her last appearance, Dr. Vyvyane Loh returns to tackle the drugs everyone's asking about — the GLP-1s (Ozempic, Wegovy, semaglutide). Joe comes in tempted, like a lot of listeners: not a hundred pounds to lose, just a stubborn ten and the promise that these drugs are also good for your heart, kidneys, liver, and longevity. Dr. Loh's job in this episode is to separate what's real from what's hype — and to explain what these drugs may be costing that the marketing never mentions.
Her first tool for cutting through the noise is a simple question: "where is the GLP-1 receptor?" If a supposed benefit is happening in a tissue that has no GLP-1 receptor, it's probably just a general effect of losing weight (better sleep apnea, less inflammation) — not a direct, magical property of the drug. Much of the "good for everything" story, she argues, is really just "weight loss is good for people who were carrying excess fat."
The conceptual heart of the episode is her core thesis: metabolism and the immune system are the same conversation. Any metabolic intervention is also an immune intervention, and vice versa. She reframes insulin resistance not as a villain but as a natural, adaptive response — during infection, inflammation, or pregnancy, the body deliberately becomes insulin resistant so glucose spills into the bloodstream to fuel immune cells, the liver, and the brain. Acute insulin resistance is good design; it's *chronic* insulin resistance, driven by poor sleep, junk food, and constant stress, that turns destructive and can progress to diabetes.
On the mechanics: GLP-1 isn't just a "gut hormone." It's made in the gut, brain, and pancreas, and your own natural version has a half-life of about two and a half minutes. More importantly, your body makes GLP-1 by chopping up a big parent molecule (proglucagon) into a whole family of hormones — GLP-1, GLP-2, oxyntomodulin, glicentin — in balanced proportions that work together. The drugs "slam" just GLP-1 on board, in a modified form that resists breakdown and persists for weeks, at a bioavailable level Dr. Loh estimates is roughly 40–70× your natural peak. So the common "it's just natural GLP-1" pitch is, in her words, not really accurate — it's a supraphysiologic dose that overrides your own system.
Then the twist. GLP-1 is tightly linked to IL-6, an inflammatory cytokine, and to "sickness behavior." Inflammation raises GLP-1, and GLP-1 in turn drives IL-6 in immune cells — producing exactly the state you feel when you're sick: no appetite, low energy, low motivation. In a real sense, Dr. Loh explains, part of how GLP-1 curbs eating is by "making the body think it's mildly sick". And IL-6 isn't simply "bad" — it has multiple "voices," including a homeostatic one that's essential for muscle growth after exercise, brain development, and tissue repair after a stroke or concussion. Chronic GLP-1 use suppresses IL-6 overall, shifting your immune tone — one likely reason it's so hard to hold onto muscle on these drugs.
That muscle concern drives her caution for this audience. Her worry isn't the person with 100 pounds to lose; it's the fit, healthy person chasing eight to ten pounds and risking their muscle mass to do it. She paints the long-game picture: start at 55 with obesity and diabetes, and ten years of "stay on it forever" can leave you at 65 with sarcopenia and diabetes. A "microdose," she notes, is still supraphysiologic — and for small weight loss, not meaningfully different from a cheap old appetite suppressant like phentermine. Meanwhile, roughly "75% of people regain most of the weight within a year of stopping" — even those who kept their good habits — because the underlying biology reasserts itself.
She's careful not to be absolutist: some people genuinely benefit. But she insists on knowing *why* someone is on the drug, what success looks like, and what the exit strategy is. And she flags real risks around catabolic states — surgery, illness, injury, even long sedentary travel — where being on a GLP-1 can impair wound healing (surgeons and anesthesiologists are increasingly wary, also citing gastroparesis and aspiration risk).
If someone is still going to try, her practical guardrails: DO NOT use the click-a-button telehealth or gym platforms with no real follow-up (your poor primary care doctor ends up cleaning up the mess); work with a clinician actually involved in your care; and remember that "every pivotal trial paired the drug with intensive lifestyle support" — weekly dietitian and coaching visits for 72 weeks. Build the structure first: scheduled meals, adequate protein, hydration, sleep, and resistance training. The drug was never meant to replace the work, and "eat whatever you want" is marketing, not medicine.
Related Episodes & Links:
Episode 137 | The #1 Secret to Healthy Fat Loss | Vyvyane Loh MD
Episode 135 | What's Your Healthy Bodyfat %? | Vyvyane Loh MD
Episode 183 | VO2Max or What? | Mike T Nelson, PhD
Episode 182 | Leveraging Energy Stress | Jose Areta, PhD
Help the show:
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Leave a review (or share this episode)
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57 min
July 21#184 | Aging Athlete Heart Health | Guido Claessen PhD
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Guido Claessen, PhD
Guido Claessen is a Belgian sports cardiologist, physician-scientist (MD, PhD), and academic specializing in sports cardiology, exercise physiology, and advanced cardiovascular imaging. His research focuses on how intensive exercise affects the heart, distinguishing normal athletic adaptations from heart disease, and improving the diagnosis and treatment of cardiovascular conditions.
Summary
Sports cardiologist Guido Claessen — principal investigator on the Pro@Heart and Master@Heart studies out of KU Leuven and University of Hasselt — joins Joe to untangle one of the most uncomfortable questions in masters endurance sport: can you exercise too much for your heart? His answer is nuanced. The benefits of exercise are enormous and not in dispute: athletes live at least as long as the general population, probably longer, with far better quality of life. The benefit curve is steep early — the biggest gains come from going from sedentary to even an hour a week — and continues deepening to roughly three to six hours weekly before it plateaus. Past that point, Claessen argues, you're training for love of the sport, not for extra protection on the heart.
The harder material is what his own coronary-CT data revealed. Lifelong athletes in Master@Heart carried more coronary plaque than even very healthy active controls — the opposite of what his team expected. But the story doesn't end there: compared with a typical sedentary population, athletes' plaque skews toward the calcified, stable, rupture-resistant kind, which may be relatively protective. And the single most important caveat threaded through the whole conversation is that nobody yet knows whether that extra plaque actually translates into more heart attacks — the outcome data isn't in. Claessen closes with the practical throughline for older athletes: fitness is not a free pass. Screen the hidden risk factors — Lp(a), ApoB, home blood pressure — treat what needs treating, and don't fear the statin conversation, because the alternatives are now excellent. The takeaway isn't do less; it's do it with your eyes open.
Key learnings
Don't fear exercise — the longevity case is settled. Even very high training loads are associated with living at least as long as the general population, with major quality-of-life gains on top. There is no signal pointing toward becoming sedentary.
"Risk" is not one thing. Atrial fibrillation is more common in endurance athletes but it's a manageable nuisance, not sudden cardiac death. Disaggregating AFib from coronary disease from sudden death dissolves a lot of needless fear.
The benefit curve plateaus around 3–6 hours/week. The steepest gains come early; beyond the plateau, extra volume is a hobby choice, not added heart protection.
The athlete's heart is built by duration, not intensity. Counterintuitively, cumulative training volume — not how hard you go — drives cardiac enlargement. Tour-level pros trained less intensively than masters athletes yet had larger hearts.
Lifelong athletes carry more coronary plaque — but more of the stable kind. More plaque than healthy controls (a surprise), yet compared with sedentary people it's more calcified and rupture-resistant.
The crucial unknown: more plaque ≠ proven more events. Whether higher plaque burden in high-volume athletes leads to more heart attacks is genuinely undetermined; longitudinal follow-up is ongoing. This is the load-bearing uncertainty of the whole episode.
Fitness doesn't excuse ignoring hidden risk factors. Check Lp(a), ApoB/LDL, and blood pressure — measure BP at home, not just in the office. Elevated Lp(a) tracked with higher plaque in his athlete cohort.
For plaque specifically, intensity does matter. The eTRIMP metric (duration × intensity-weighted load) was the best predictor of plaque burden — so remodeling is duration-driven, but plaque is sensitive to intensity too.
Consistent training buys down acute risk. The exercise paradox: a sudden vigorous effort raises acute heart-attack risk ~50-fold in the sedentary but only ~2-fold in the well-trained.
Statin intolerance is real but partly nocebo — and alternatives abound. The SAMSON trial showed placebo and statin produced similar symptoms (both above no-pill). If statins genuinely don't work for you, ezetimibe, bempedoic acid, and PCSK9 inhibitors/inclisiran are strong options.
https://www.masteratheart.be/
"Moderate-intensity aerobic exercise of at least 150 minutes per week has been shown to provide significant health effects with a 50% reduction in adverse cardiac events and reduced mortality...Endurance sports participation improves blood pressure control, lipid profiles and insulin sensitivity and therefore, not surprisingly, has been associated with a reduced incidence of myocardial infarction. This may explain the longer life expectancy of athletes as compared to the general population. On the other hand, there is increasing evidence suggesting that intense exercise, particularly intense endurance exercise, can be associated with adverse cardiac remodelling and an excess of arrhythmias. Thus, it is possible that it is healthy being an endurance athlete but not necessarily that the health benefit is derived from exercise itself, as opposed to all of the other favourable lifestyle factors."
50 min
June 24#183 | VO2Max or What? | Mike T Nelson, PhD
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Mike T Nelson, PhD
Dr. Mike blends deep academic knowledge with practical, field-tested insights to burn fat, build strength, and recover more effectively.PhD in Exercise Physiology from University of Minnesota
BA in Natural Science from St. Scholastica
MS in Biomechanics from Michigan Technological University
Adjunct Professor in Human Performance for Carrick Institute for Functional Neurology
Mike T Nelson website
Dr Mike's Newsletter signup link
There's a fight on the internet about VO₂max. One camp treats it as the single number that rules your healthspan — get it as high as humanly possible, no matter the cost. Another camp says it's overhyped, mismeasured, and not worth your attention at all. As usual, the loudest voices are the least useful.
So I brought the question to someone I actually trust: Dr. Mike T. Nelson, back on the show for his fourth conversation with me. Mike is the rare internet fitness voice with both the science and the scruples, and he's written about this exact controversy. My question for him was simple and a little selfish: I'm 64, I don't have unlimited time or unlimited recovery. How much should someone like me actually be chasing VO₂max — and once I've got "enough," where should my effort go instead?
His answer is what this episode is about, and it comes down to a sweet spot. Yes, VO₂max is one of the most powerful longevity predictors we've ever measured — climbing out of the bottom of the pack buys you more protection than almost anything else you can do. But the benefit curve flattens. There's a point where squeezing out another few percent costs enormous effort for very little return — effort that would do far more good aimed at whatever your real weak link is.
Along the way Mike takes apart some sacred cows. Why zone 2, for most of us, is not the magic everyone says it is. How to actually program intervals so you're building speed instead of just collecting misery. Why your fading max heart rate might be partly a use-it-or-lose-it problem. And how something as quiet as your breathing rate while you sleep can tell you whether you're sabotaging your own oxygen delivery.
If you've ever stared at the VO₂max number on your watch and wondered whether to celebrate it, panic about it, or ignore it — this one's for you.
Key learnings
VO2max predicts longevity — strongly, but with a caveat. The mortality benefit of moving from very unfit to fit appears larger than almost any other measured intervention, exceeding smoking cessation. But most of that effect comes from rescuing the bottom of the range, not pushing an already-good number higher. (Human observational data; reverse causality is a standing confounder.
The "VO2max is overblown" controversy is mostly noise. The complaint that studies use METs and submax estimates rather than gold-standard lab tests is technically correct — but the surrogates and the lab measures largely agree, so the distinction doesn't change the practical conclusion.
VO2max is limited by your weakest link — either oxygen delivery (heart, blood flow) or oxygen utilization(muscle, mitochondria). Train the limiter. Note Mike's own caveat: the limiter may not even be stable week to week in the same person.
A higher ceiling makes everything easier. Like a bigger 1RM makes submaximal lifts feel light, a higher VO2max makes all sub-threshold work more sustainable.
For raising VO2max: accumulate time at goal pace. Use 2–6 minute intervals at (or slightly above) target pace, and add volume only if you can hold the pace. Most people tolerate this only 1–2× per week.
Short anaerobic intervals work — but quality over fatigue. 30–180 second repeats build power and lactate handling, but stop the set once output drops off meaningfully. Grinding through massive drop-offs just trains fatigue.
Zone 2 is overrated for most non-elites. Mike argues ~90–95% of people get more cardiac-development return from Zone 3 touching Zone 4 (e.g., 6-minute progressives) than from the 2–3 weekly hours Zone 2 demands. (This is his most contested claim and runs against the polarized-training consensus he acknowledges holds for elite endurance athletes.)
Defend your max heart rate as you age. Falling max HR drives much of age-related VO2max decline — and some of that may be disuse, not pure aging. "Reach and touch" ~90–95% of max HR about once a week. (Anecdotal; max HR decline is largely age-intrinsic in the literature, so treat the disuse angle as a hypothesis.)
Strength training helps VO2max indirectly by making each stride, stroke, or pedal more submaximal. For most older athletes, added muscle is not a performance penalty.
CO2 tolerance matters more than people think. Over-breathing blows off the CO2 you need (via the Bohr effect) to actually offload oxygen into muscle. Longer exhales, nasal breathing, and lower resting respiratory rate can help — though part of the benefit is likely neuroplastic stress-inoculation rather than pure gas exchange.
Know the sweet spot. ~50 mL/kg/min is a strong general target. Below the 75th percentile, gains come relatively fast and are worth chasing. Above it, returns flatten — at that point, only pursue more if VO2max is a genuine competitive priority.
The three most longevity-protective trainable traits: VO2max, lower-body strength/muscle mass, and grip strength.
Summary
VO2max gets called the single best predictor of longevity — and then, predictably, the internet declared it overblown. In this episode, Dr. Mike T. Nelson cuts through both extremes. He explains what VO2max actually measures (the lesser of two capacities: your ability to deliver oxygen via heart and blood flow, and your ability to use it at the mitochondria), why the "it's just METs, not real VO2max" controversy is technically true but practically useless, and why a higher ceiling makes everything below it easier — the same way a bigger deadlift makes submaximal loads feel light.
The heart of the conversation is what to actually do. Mike walks through a complete training hierarchy for the older athlete: accumulate time at goal pace in 2–6 minute intervals, use short anaerobic repeats only while you can hold your output, and — controversially — spend far less time in Zone 2 than the internet insists, favoring Zone 3 touching Zone 4 for most non-elites. He covers the role of strength training, the underrated importance of CO2 tolerance and breathing mechanics, and the "reach and touch" approach to defending your max heart rate as you age.
Most importantly for Wise Athletes, Mike defines the sweet spot. Past roughly the 75th percentile (or about 50 mL/kg/min as a strong general target), the returns on chasing a bigger VO2max flatten hard. For the older athlete with finite time and energy, that's the asymmetric-risk insight: get to "good," then redirect effort toward whatever's actually weakest — because beyond that point, ten percent more VO2max may cost what a fifty percent gain elsewhere would.
Related Episodes & Links:
Episode 178 | Athletic Longevity Isn't Easy | Brenden Egan PhD
Episode 154 Adaptive Range Expansion for Peak Performance | Mike T Nelson PhD
Episode 144 | Muscle for Athletic Performance | Mark Tarnopolsky MD PhD
Episode 143 | Chronic Overbreathing | George Dallam PhD
Help the show:
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Leave a review (or share this episode)
Check out our Fullscript site to save big on high quality supplements. Thank you!
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1 hr 14 min
June 14#182 | Leveraging Energy Stress | Jose Areta, PhD
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Jose Areta, PhD
Dr. José Areta is an Associate Professor in Exercise Metabolism and Nutrition at the School of Sport and Exercise Sciences, Liverpool John Moores University (UK). Originally from Argentina and trained first as a biologist (with a minor in zoology), he completed his PhD in exercise physiology and nutrition at RMIT University in Melbourne, then spent roughly three years as a postdoctoral researcher at the Norwegian School of Sport Sciences before moving to Liverpool. His research centers on training–nutrition interactions in humans — how manipulating carbohydrate, protein, fat, and overall energy availability shapes adaptation to training and physical performance. In recent years his work has focused on the endocrine, metabolic, and physiological effects of energy deficiency, including the first dynamic proteomic profiling of how human skeletal muscle responds to a short-term energy deficit combined with exercise. He is also a practicing athlete, coach, and practitioner, and has roughly 60 peer-reviewed publications.
Jose Areta, PhD profile
Most of us treat an energy deficit as a problem to be corrected — a state where you've fallen below a known requirement, risking lost muscle and blunted performance. Areta's reframe: think of it as energy stress. Like exercise stress, it's a signal the body is built to adapt to, and — at least as a working hypothesis — one you may get better at handling with repeated, progressive exposure. We (probably) evolved under intermittent scarcity, and a body that responded to hunger by becoming weak and slow wouldn't have survived to find its next meal. The practical hook for the older athlete: if you're always in a calorie surplus to recover and build, you're adding fat alongside muscle. Energy stress, used deliberately, becomes the tool for managing body (low) fatness without sacrificing the performance and muscle you've worked for.
Key learnings
You can get stronger in a deficit without getting bigger. Energy deficit plus resistance training yields the same strength gains as energy-balanced training — but without the same hypertrophy. The gains come from neuromuscular adaptation, not added mass. (Function over form.)
Protein is the lever that makes a deficit safe. Requirements rise to roughly 2.2 g/kg/day to preserve lean mass during a deficit. The threshold that matters: deficits beyond about 500 kcal/day impair muscle-building even with training; below that, recomposition (muscle gain + fat loss) stays achievable.
Fat is the fuel; contractile muscle is largely spared. In Areta's short-term deficit study, energy came predominantly from fat oxidation, and most of the apparent "lean loss" was water — the contractile machinery was preserved.
The deficit upregulates mitochondrial machinery. Deficit-plus-exercise increased mitochondrial protein synthesis and quality-control proteins — the stress acted as an adaptive signal, not just depletion. Meanwhile the collagen "scaffolding" proteins that rise with aging were reduced — though whether that's net-beneficial isn't yet settled.
The body has no fixed metabolic rate. It adjusts expenditure and efficiency to energy availability (the Hadza/Pontzer finding: lots of activity, not many extra calories burned). Caveat: this is bounded, not unlimited, and the interpretation is debated.
Performance testing at the bottom of a deficit will mislead you. Low muscle glycogen impairs high-intensity output, so refeed before anything that matters — don't judge your true capacity, or the strategy, by how you feel mid-deficit.
The load-bearing question — "functionally superior muscle." The most exciting idea (that energy stress yields muscle that's stronger per unit mass) is also where human outcome data is thinnest. Treat it as a promising hypothesis, not an established finding.
Discussion outline
The reframe — why "energy stress" beats "energy deficit," and the exercise-stress / progressive-overload analogy
The evolutionary lens — why locomotion and physical capacity are protected under scarcity
Macronutrients first — carbohydrate, fat, and protein around training, and what too much / too little looks like
Strength without size — neuromuscular adaptation vs. hypertrophy in a deficit
Protein as the safety lever — the ~2.2 g/kg/day target and the ~500 kcal/day deficit threshold
Inside the muscle — the proteomics study: mitochondrial upregulation, ECM/collagen reduction, preserved contractile protein
Is there a basal metabolic rate? — adaptive efficiency, the Hadza data, and what it means for "calories in/out"
The glycogen catch — why deficit impairs high-intensity performance and when to refeed
The REDs debate — Areta's critique of single-cause framing, and the allostatic-load alternative
The open protocol question — cycle energy stress vs. find a sustained minimum floor; is calories or protein the bigger driver?
Practical takeaways for the older athlete — using deficit to manage body fat while protecting muscle and performance
Studies & further reading
Areta, J.L. (2023). Physical performance during energy deficiency in humans: an evolutionary perspective.Comparative Biochemistry and Physiology Part A, 284, 111473. doi:10.1016/j.cbpa.2023.111473 — the core "energy stress" / evolutionary argument. Open-access PDF: researchonline.ljmu.ac.uk/id/eprint/23006/
Areta et al. (2021). Low energy availability: history, definition and evidence of its endocrine, metabolic and physiological effects in prospective studies in females and males. (Review of the LEA evidence base.)
The proteomics intervention study — short-term pronounced energy deficit + aerobic training and its effect on skeletal-muscle proteomic, metabolic, and endocrine adaptation (the mitochondrial-up / ECM-down finding). Discussed in depth on Sigma Nutrition Radio #594 (Feb 2026): sigmanutrition.com/episode594/
Murphy, C. & Koehler, K. (2022). Energy deficiency impairs resistance training gains in lean mass but not strength: a meta-analysis and meta-regression. Scand J Med Sci Sports, 32:125–137 — the basis for "strength preserved, size not."
Areta et al. Reduced resting skeletal muscle protein synthesis is rescued by resistance exercise and protein ingestion following short-term energy deficit. Am J Physiol Endocrinol Metab — the MPS-rescue finding.
Melin et al. (2023). Direct and indirect impact of low energy availability on sports performance.
Areta lab, world-tour female cyclist case study (Tour de France Femmes, 2023) — a real-world example of extreme energy expenditure and the limits of performance as a marker of fueling.
Guest links: LJMU research profile and ResearchGate (full publication list); Areta on Sigma Nutrition Radio #508 and #594, and That Triathlon Show #378, for prior long-form discussions.
Summary
Most of us treat an energy deficit as a problem to be corrected — a state where you've fallen below a known requirement, risking lost muscle and blunted performance. Areta's reframe: think of it as energy stress. Like exercise stress, it's a signal the body is built to adapt to, and — at least as a working hypothesis — one you may get better at handling with repeated, progressive exposure. We evolved under intermittent scarcity, and a body that responded to hunger by becoming weak and slow wouldn't have survived to find its next meal. The practical hook for the older athlete: if you're always in a calorie surplus to recover and build, you're adding fat alongside muscle. Energy stress, used deliberately, becomes the tool for managing body fatness without sacrificing the performance and muscle you've worked for.
Related Episodes & Links:
Episode 178 | Athletic Longevity isn't Easy | Brendan Egan PhD/
Episode 154 Adaptive Range Expansion for Peak Performance | Mike T Nelson PhD
Episode 144 | Muscle for Athletic Performance | Mark Tarnopolsky MD PhD
Episode 71 | Framework for Durability | Dr Nick Dinubile
Episode 65 | Optimizing Aging Muscle | Brendan Egan PhD
Help the show:
3 ways to support our show:
Leave a review (or share this episode)
Check out our Fullscript site to save big on high quality supplements. Thank you!
Email us your questions at [email protected].
1 hr 7 min
May 17#181 | No Time for Pain | Rick Olderman MSPT
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Rick Olderman, MSPT
Author of "Fixing You" series
Author of Pain Patterns
www.rickolderman.com
This episode focuses on addressing chronic pain in older athletes using a comprehensive "systems thinking" approach to physical therapy. Rather than treating pain as an isolated symptom with a checklist of generic exercises, the discussion highlights the importance of diagnosing the underlying root causes through a simplified series of diagnostic tests. The conversation digs into how systemic bodily compensations hide underlying structural issues, how dysfunctional walking patterns directly trigger chronic lower body pain, and how most chronic back pain is mistreated by conventional physical therapy methods.
Key Discussion Points
Immediate Pain Feedback: Effective physical therapy should yield almost immediate feedback and pain relief during testing if the correct underlying trigger is successfully targeted and adjusted.
The "Spaghetti Against the Wall" Approach: Conventional physical therapy often hands patients a long list of general exercises without meaningful, personalized testing to determine the specific cause of pain.
The Deception of Painless Damage: Our bodies are masterful "compensation machines," meaning structural degradation (visible on MRIs) can silently accumulate completely under the radar long before rising to the level of actual pain.
Walking as a Keystone: Chronic pain tracking from the lower back all the way down to the feet is heavily tied to dysfunctional walking patterns; fixing the gait is fundamental to resolving this pain.
The Over-Striding Error: A highly common walking issue involves throwing the foot too far out in front of the body with a heavy heel strike, which locks the knee and shuts off the gluteus maximus.
Activating the Glutes: To properly engage the glutes and control pelvic/hip mechanics, walkers must focus on moving their entire body forward with the advancing foot, ensuring the knee stays automatically softened.
The Three Body Systems and Patterns: The human frame operates on three distinct systems (movement, fascial, and reflex neurological) that get trapped in three fundamental problematic patterns: extension (too arched), flexion (too flat), or side-bending (uneven pelvis).
The Back Crease Photo Test: A simple diagnostic test for a side-bending problem is having a photo taken of your bare back; a larger crease at the waist on one side indicates an uneven pelvis and rib cage, which typically aligns with the side of sciatic or SI joint pain.
The Prevalence of Extension Problems: Roughly 99% of patients with chronic back pain suffer from an extension problem (an over-arched back), which is easily identified if back pain worsens when laying flat with straight legs or standing.
The Flaw in Standard Back Care: Most traditional physical therapy methods treat chronic back pain by prescribing back-arching and prone press-up exercises, which actually worsen pain for 99% of chronic patients because it reinforces their existing extension problem.
1 hr 4 min
April 18#180 | The Art of Avoiding Injury | Jeremy Bettle, PhD
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Jeremy Bettle, PhD
Award-winning coach and VITALITY expert
UCSB – Director of Sports Performance
Brooklyn Nets Basketball – Head of Strength & Conditioning, Director of Nutrition
Toronto Maple Leafs Hockey – Director of Sports Science & Performance
Anaheim Ducks Hockey – Director of High Performance
New York City Football Club – Director of High Performance
Vitality Collective – Co-Founder
Bettle earned a Ph.D in human performance and a master’s degree in exercise science
from Middle Tennessee State University. He also holds earned his bachelor’s degree in sport and exercise science from
Leeds Metropolitan University (England).
Vitality-Collective.com
Discussion Points
The Core Injury Framework Injuries happen when the demands of an activity exceed the capacity of the tissue being asked to perform. Demands come in three forms: force (how hard the impact), velocity (how fast the contraction must happen), and direction (planes of movement the tissue hasn't been trained for). Training is the process of systematically raising capacity to match and just slightly exceed demands — not avoiding demands.
"The Sport Is Not Enough" Principle Playing your sport builds sport-specific fitness but does not prepare the tissues for the worst-case demands of that sport. The athlete who only cycles or only lifts has gaps in planes of movement that become injury sites the moment life — or a new activity like pickleball — demands something different. Training must prepare the body for more than the sport itself.
The Range of Training That Matters Four modalities, all necessary:
Strength training — high effort to near-failure, 8–12 reps; equivalent stimulus to heavy singles but dramatically lower injury risk
Cardiovascular training — continuous aerobic work
High-intensity intervals — critical for performance and longevity
Power training / plyometrics — massively underrated, but inherently risky; must be earned through the progression below
The Progression — Sequence Matters This cannot be rushed or reordered:
Phase 1 — Foundation (weeks 1–8+): Core and hip training first. The core transfers force between upper and lower body — without it, every compound movement is a liability. Start with wall sits, hip work, fundamental movement patterns at 12–15 reps.
Phase 2 — Strength: Progress to squat (goblet squat) and hinge patterns. Move from 12–15 reps down to 6–12 reps with heavier absolute load. This is where strength, muscle mass, body composition, and bone density gains accumulate.
Phase 3 — Power (only after Phase 2 is established): Power = strength × speed. Sequence within this phase:
Slow eccentric loading first (3–4 second descent on squats, pause, fast up)
Fall-prevention drills: tip-toe fall-forward-and-catch, snap-downs
Vertical jumps in place (no box required for masters athletes)
Jump for distance, skater jumps side to side, single-leg jumps
Box jumps: Bettle explicitly recommends against them for masters athletes — trip-and-fall risk outweighs benefit; ground-based jumps achieve the same stimulus more safely
Sprinting Progression — Velocity Before Distance Joe's mistake: went from jogging straight to 20-yard sprints. Correct sequence:
Start at 70–80% maximum sprint velocity for 20 yards, multiple reps
Build velocity over weeks to 85–90%, then 95–100%
Only after full velocity is achieved do you extend distance
Longer distance = more hamstring involvement = new injury site that must be built separately
Tempo runs (60–70% effort, longer distance) condition the hamstrings before adding sprint distance
Isometrics for Tendon Health Tendons have poor blood flow — nutrient delivery is slow, which is why tendinopathy lingers. Isometrics address this directly:
Wall sits, 30–45 seconds, 3 sets — load the tendon, stimulate remodeling
Tendon fibers become disordered with injury; only load through range realigns them
Isometrics before a run can quiet Achilles pain enough to train
Pain tolerance during isometrics: up to 3/10 is acceptable; sharp/pinching/stabbing pain = stop and see a physio
PRP and collagen alone without load will not fix tendinopathy — the load is irreplaceable
Jump Rope Bettle's Achilles injury prevention tool in the NBA: daily jump rope warm-ups, no Achilles tears in four seasons. For masters athletes: primes tendon elasticity, builds ankle stiffness, low impact. Highly underrated.
Collagen + Vitamin C Take 30–40 minutes before tendon-specific training. Exercising the tendon increases local blood flow, which delivers the nutrients already in the system. Bettle's position: not a replacement for loading, but adds benefit with minimal downside.
The Injury Cascade — Why Consistency Is the Only Metric That Matters Injury → detraining → all systems downregulate → athlete tries to return at prior level → exceeds now-reduced capacity → re-injury → greater detraining → frailty → withdrawal from sport and social community → metabolic and cognitive decline. The cascade is real and compounding. One bad injury is not a setback — it is the beginning of a sequence that leads somewhere much worse. This is why Bettle kept the Maple Leafs injury-free for 3.5 years — not by training less, but by training intelligently enough to never trigger the cascade.
Timeframe 6 to 9 to 12 months depending on starting point. Eight weeks to begin adapting to any given phase. Six to nine months to complete the full progression. The social contract with the client: "Around eight weeks in, you're going to be irritated with me because I won't let you do the fun stuff yet."
Related Episodes & Links:
Episode 178 | Athletic Longevity isn't Easy | Brendan Egan PhD/
Episode 154 Adaptive Range Expansion for Peak Performance | Mike T Nelson PhD
Episode 144 | Muscle for Athletic Performance | Mark Tarnopolsky MD PhD
Episode 71 | Framework for Durability | Dr Nick Dinubile
Episode 65 | Optimizing Aging Muscle | Brendan Egan PhD
Help the show:
3 ways to support our show:
Leave a review (or share this episode)
Check out our Fullscript site to save big on high quality supplements. Thank you!
Email us your questions at [email protected].
55 min
March 01#179 | TRT: Less is More | Nayan Patel PharmD
Professional Supplements for Wise Athletes (click to see the "always on" discount)
Nayan Patel, PharmD
Doctor of Pharmacy (PharmD) degree from the University of Southern California School of Pharmacy and serves as adjunct faculty there.
Hormone health influences everything from energy and sleep to mood, metabolism, and libido—yet mainstream treatments are often driven by generic protocols and limited lab interpretations. Dr. Patel has helped thousands of patients find clarity and results by looking beyond “normal” hormone levels and building therapy around how people actually feel and function. He offers a practical view into what personalized hormone care should look like—and where most systems are getting it wrong.
He is globally regarded as an expert on glutathione, a molecule often referred to as the “master antioxidant,” and is recognized for research into its absorbable forms. He has authored a book titled The Glutathione Revolution: Fight Disease, Slow Aging & Increase Energy with the Master Antioxidant.
Find Dr Patel here: centraldrugsrx.com and here: aurowellness.com
Discussion Points
The hard truth is that you cannot inject your way out of a broken lifestyle
Sex hormone optimization is a necessary but small piece of the puzzle.
Extra (more than the minimum) TRT is a poor solution to overcome poor lifestyle for stress and diet, and it comes with extra negative side effects.
Find the least effective dose for your physiology; use bio-identical hormones (have to use every 1-3 days)
How to “feel” like the young you. The solution pyramid is:
Sex hormones— 10% (necessary for older athletes but not sufficient)
Thyroid mgmt — 20% (pollution, autoimmune)
Diet / insulin - 30% (over eating, visceral fat)
Adrenals / Stress mgmt - 40% (lifestyle; sleep)
Also have to address oxidative stress issues (glutathione).
Related Episodes & Links:
Episode 178 | Athletic Longevity isn't Easy | Brenden Egan PhD
Episode 155 | Hormonal Triple Whammy | Kyle Gillett MD
Episode 144 | Muscle for Athletic Performance | Mark Tarnopolsky MD PhD
Episode 115 | Winning Athletic Longevity | Rick Cohen MD & Daniel Tawfik, Healthspan
Episode 102 | Maximizing Performance Health | Jim Lavalle R.Ph.
Help the show:
3 ways to support our show:
Leave a review (or share this episode)
Check out our Fullscript site to save big on high quality supplements. Thank you!
Email us your questions at [email protected].
1 hr 9 min
February 15#178 | Athletic Longevity isn’t Easy | Brendan Egan, PhD
Professional Supplements for Wise Athletes (click to see the "always on" discount)
Brendan Egan, PhD
Associate Professor of Sport & Exercise Physiology at Dublin City University
Associate Dean for Research (Faculty of Science & Health)
Current research investigates skeletal muscle function and adaptation across the life course, with special interest in the synergy between nutrition and exercise interventions ranging from athletes to older adults.
Nutrients investigated include caffeine, creatine, omega-3 fatty acids, resveratrol, leucine, protein hydrolysates, beetroot juice, and exogenous ketones.
Outside of academia, through his sporting career as an Gaelic footballer, Brendan has had a lifelong association with sport, training and performance at all levels of competition from grassroots to elite level, and also practices in the field as a performance nutritionist with emphasis on intermittent field-based team sports, and endurance athletes, most recently with the Dublin Hurlers and the Irish Paratriathlon team.
Find Brendan's work here: https://www.researchgate.net/profile/Brendan-Egan and contact info here: https://www.dcu.ie/researchsupport/research-profile?person_id=35443
https://sigmanutrition.com/episode591/
Discussion Points
Personal Peak & Glide Path— peak as high and as late as possible, then hang on baby.
“Use it or lose it”. It’s an old thing but now we lose faster and it’s harder to get back. Consistency is the name of the game now. Spikes in training load and intensity lead to injury which leads to inconsistent training. DO NOT GET INJURED!
“I’m not what I was” — so true. I can't train like I used to because I can’t recover as quickly. (And don’t have as much time?)... and my body doesn’t respond to stimulus as well as it used to either...ergo, I'm not what I was.
What to consider for improved recovery? Sleep, adequate protein, adequate carbohydrate fueling, hot/cold exposure, hydration, hypoxia exposure. Dr Egan likes a hot bath (me too).
Testosterone falling? What else isn’t what it was? How important to get back to more youthful function of the body?
Balancing calories surplus against calorie deficit. Keep fat and protein steady; ramp carbs to match activity (“fuel for the work required")
Protein load: active older athletes probably don’t have anabolic resistance. May not need extra protein for age but probably do need extra for extra exercise. (1.5-1.6g/kg per day). It’s not a silver bullet of course.
Collagen for tendons? It can t hurt. Get collagen into bloodstream right before (30 min?) workouts. Wallsits might help.
Periodization of training. (3-5 weeks cycles). Keep it fun. Cover your bases. Build in time for recovery day to day as well as deep recovery every few weeks.
Minimum effective dose? What is the least attention I can put into an area of fitness to keep it alive. Is there Inverted U shaped curve for fitness. More is better but too much is possible. Is that true? Too little time in other key elements of fitness?
Performance vs. health and athletic longevity: with time and recovery constraints, older athletes in particular have serious limitations. If you put too much into one area of athleticism, you necessarily have to neglect others. What don’t you care about losing?
What is happening beyond Use It or Lose It?
gradual loss of recovery / healing / muscle growth ability
declining growth hormone / sex hormones (anabolic resistance?)
declining melatonin (sleep quality?)
poorer blood flow (lower NO, damage to blood vessels)
gradual increase in metabolic dysfunction
less autophagy/ mitophagy (senescence, aging blood factors, ROS, lower cellular energy)
higher insulin resistance
higher chronic inflammation (over active immune function, visceral fat, viral load)
Related Episodes & Links:
Episode 154 Adaptive Range Expansion for Peak Performance | Mike T Nelson PhD
Episode 144 | Muscle for Athletic Performance | Mark Tarnopolsky MD PhD
Episode 116 | Grow Old -- Get Fast -- Don't Die | Phil Cavelle
Episode 115 | Winning Athletic Longevity | Rick Cohen MD & Daniel Tawfik, Healthspan
Episode 102 | Maximizing Performance Health | Jim Lavalle R.Ph.
Episode 71 | Framework for Durability | Dr Nick Dinubile
Episode 65 | Optimizing Aging Muscle | Brendan Egan PhD
Help the show:
3 ways to support our show:
Leave a review (or share this episode)
Check out our Fullscript site to save big on high quality supplements. Thank you!
Email us your questions at [email protected].
1 hr 9 min
February 03#177 | Bodycomp FMD | Renee Fitton MS RD
Professional Supplements for Wise Athletes (click to see the "always on" discount)
Renee Fitton MS RD
Renee is a Longevity Dietitian (she holds a masters degree in longevity nutrition earned with Dr Longo at UCLA) and she is the Director of Education at L-Nutra, the ProLon FMD company
Using Fasting-Mimicking Diet (FMD) to manage body comp
I’m not alone in my struggle to build muscle while reducing body fat. I recently completed an 18 month effort to do just that starting and ending with a Dexa scan to avoid any self deception. The results were not bad (16 —> 15% body) but I did not achieve my goal (I had essentially zero muscle growth and lost no visceral fat). I have always struggled with balancing calorie surplus (for recovery and adaption to exercise), with calorie deficit for body composition and achieving my goal of zero visceral fat. I guess I need more help, eh?
In my talk with Renee we explore the topic of finding the minimum calorie and protein consumption (over time; not everyday) needed for the life I, you, anyone may want,
And the use of cycles of growth (calorie surplus, high protein, hard exercise overload) and then rejuvenation (calorie deficit, low protein, fat loss, autophagy, mitophagy) to find the path that preserves vitality and health and builds a platform for a good life.
The devil is in the details but in my mind the key is avoiding becoming addicted to the parts that makes us feel good about ourselves: the group we belong to, the way we look, the feeling of accomplishing something important. Such addiction leads to short term misallocation of invested time which leads to long term straying from the selected path. This is my own battle.
Episode Resources
fittennutrition.com
Related episodes & links:
Episode 142 | Balance Muscle & Longevity w/FMD | Joseph Antoun MD PhD
Episode 137 | #1 Secret to Healthy Fat Loss | Vyvyane Loh MD
Episode 135 | What's Your Healthy Fat%? | Vyvyane Loh MD
Episode 144 | Muscle for Athletic Performance | Mark Tarnopolsky MD PhD
Help the show:
3 ways to support our show:
Leave a review (or share this episode)
Check out our Fullscript site to save big on high quality supplements. Thank you!
Email us your questions at [email protected].
51 min
January 17#176 | Truth in Cycling | Jim Martin PhD
Professional Supplements for Wise Athletes (click to see the "always on" discount)
Jim Martin – The Cycling Scientist
Dr. Jim Martin is a life-long competitive cyclist and well-known professor and researcher in exercise science whose work has had a strong impact on understanding cycling biomechanics and pedaling mechanics. He’s especially recognized for applying scientific methods to questions that many cyclists and coaches debate — like crank length, cadence, pedal stroke, and how muscles produce power on a bike.
Topics Discussed?
Crank length (mechanical advantage? Same crank length on all bikes for neuromuscular optimization?
Cadence (higher cadence allows faster response to attacks vs. standing up to accelerate which reduces muscular endurance). Faster cadence reduces variation in power generated during pedal stroke which preserves muscle endurance
Quad vs. glute power dominance / pedaling technique: unweight hands.
Pedaling technique: perfect circles like a mountain bike rider, mashing (like when standing up), pulling up to “unweight” the pedal coming up, and “scraping mud off shoe” (LeMond)
Any training recommendations? Single leg training? Why? How? Eccentric or muscle lengthening training? How to train it?
Papers
Reprint Determinants of Metabolic Cost JAP
Reprint Determinants of Maximal Cycling Power
Crank Length and Submaximal Biomechanics
Related episodes & links:
Episode 106 | Pain Free Cycling | Kevin Schmidt PT MSPT-CMP
Episode 98 | Myvelofit Professional-Quality Bike Fit from Home | Jesse Jarjour
Episode 87 | The Bike: Fun & Fitness Part 2 | Hunter Allen
Episode 86 | The Bike: Fun & Fitness Part 1 | Hunter Allen
Episode 9 | How to Pedal | Glen Winkel PhD, Masters World Champion
Help the show:
3 ways to support our show:
Leave a review (or share this episode)
Check out our Fullscript site to save big on high quality supplements. Thank you!
Email us your questions at [email protected].
1 hr 7 min

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