Barbell Medicine Podcast

Three weeks of stalled squats. The conventional answer is to switch programs because you've crossed into intermediate territory. The data says something else. In Part 3 of the Progressive Loading series, Dr. Jordan Feigenbaum and Dr. Austin Baraki walk through why the standard novice / intermediate / advanced framework runs into trouble in real training, what the four adaptive systems are actually doing across a training career, and why most of what gets called a stall is impatience with the noise floor at your current strength level.
This is Part 3 of the Progressive Loading series. Part 1 covered why loading should react to demonstrated adaptation. Part 2 covered RPE-based autoregulation and the artificial-momentum approach. Today is the mechanism layer.

Timestamps
0:00 - Why your lifts aren't moving
1:52 - The novice / intermediate / advanced framework, three claims to test
13:23 - What 17 years of powerlifting data show about how long you keep getting stronger
32:28 - How getting stronger actually works (four systems on four clocks)
38:00 - What early growth is actually made of (the Damas 2016 deuterium study)
50:33 - The connective tissue lag and why early-training injuries happen
58:32 - Why heavy lifting works for bone density (and why "walk on a treadmill" advice misses)
1:05:10 - Why new lifters get hurt 3 to 10 times more than experienced lifters
1:12:56 - Fatigue is at least four different things (and most coaches treat it as one)
1:26:19 - The CNS fatigue myth (and what the data actually says)
1:33:52 - When the bar isn't moving: how to actually diagnose a stall
1:45:51 - Takeaways and next week's tease: leptin and low testosterone

What we cover 
- The novice / intermediate / advanced framework: three claims and why each one fails the data test
- The 17-year IPF strength curve and what the no-kink finding does and does not establish (Latella 2024)
- The four adaptive systems and their separate timescales (neural, muscle, connective tissue, bone)
- What early growth actually is, including the deuterium-oxide finding that most week-3 size is fluid (Damas 2016)
- Why connective tissue lags muscle by six to eight weeks, and why that produces patellar tendinopathy four months in
- The 9.5 vs 0.74 to 3.3 injury rate gap between novice and experienced CrossFit participants
- The CNS fatigue myth and the Skarabot 2018 finding that locates the fatigue in the muscle, not the brain
- Why the LIFTMOR trial result (heavy lifting for bone density in women in their 60s and 70s) is being missed by primary care
- A practical decision tree for stalls: environment first, then load, then program
- Tease for next week: leptin, the HPG axis, and the metabolic driver of low testosterone almost nobody connects

Resources 
Training Plateau Action Plan (free): https://www.barbellmedicine.com/training-plateau-action-plan/
Progressive Loading article series: https://www.barbellmedicine.com/blog/progressive-loading/
Beyond Progressive Overload (Part 2 article): https://www.barbellmedicine.com/blog/beyond-progressive-overload/
BBM Programs and Coaching: https://www.barbellmedicine.com/
Support our work on barbellmedicine.supercast.com
Latella C et al. Using powerlifting athletes to determine strength adaptations across ages in males and females. Sports Med. 2024. https://pubmed.ncbi.nlm.nih.gov/

Del Vecchio A et al. The increase in muscle force after 4 weeks of strength training is mediated by adaptations in motor unit recruitment and rate coding. J Physiol. 2019. https://pubmed.ncbi.nlm.nih.gov/30644584/

Lecce E et al. Resistance training-induced adaptations in the neuromuscular system. J Physiol. 2025.

Balshaw TG et al. Neural adaptations after 4 years vs 12 weeks of resistance training. Scand J Med Sci Sports. 2019. https://pubmed.ncbi.nlm.nih.gov/30474171/

Skarabot J et al. Voluntary activation and agonist EMG amplitude in resistance-trained men. J Appl Physiol. 2021.

Roberts MD et al. Mechanisms of mechanical overload-induced skeletal muscle hypertrophy. Physiol Rev. 2023.

Damas F et al. Resistance training-induced changes in integrated myofibrillar protein synthesis are related to hypertrophy only after attenuation of muscle damage. J Physiol. 2016. https://pubmed.ncbi.nlm.nih.gov/27219125/

Damas F et al. Early resistance training-induced increases in muscle cross-sectional area are concomitant with edema-induced muscle swelling. Eur J Appl Physiol. 2016. https://pubmed.ncbi.nlm.nih.gov/26280652/

Lazarczuk SL et al. Mechanical, material and morphological adaptations of healthy lower limb tendons. Sports Med. 2022. https://pubmed.ncbi.nlm.nih.gov/35657492/

Kubo K et al. Time course of changes in the human Achilles tendon properties. Eur J Appl Physiol. 2012. https://pubmed.ncbi.nlm.nih.gov/22105708/

Watson SL et al. High-intensity resistance and impact training improves bone mineral density in postmenopausal women: the LIFTMOR randomized controlled trial. J Bone Miner Res. 2018. https://pubmed.ncbi.nlm.nih.gov/28975661/

Aasa U et al. Injuries among weightlifters and powerlifters: a systematic review. Br J Sports Med. 2017. https://pubmed.ncbi.nlm.nih.gov/27445362/

Prieto-Gonzalez P et al. Injuries in novice participants during an eight-week start-up CrossFit program. Int J Environ Res Public Health. 2020. https://pubmed.ncbi.nlm.nih.gov/32155747/

Kanayama G et al. Tendon rupture in body builders. Sports Med. 2015.

Enoka RM, Duchateau J. Translating fatigue to human performance. Med Sci Sports Exerc. 2016. https://pubmed.ncbi.nlm.nih.gov/27015386/

Behrens M et al. Fatigue and human performance: an updated framework. Sports Med. 2023. https://pubmed.ncbi.nlm.nih.gov/

Halperin I et al. Accuracy in predicting repetitions to task failure: scoping review. Sports Med. 2022. https://pubmed.ncbi.nlm.nih.gov/

Skarabot J et al. Neuromuscular fatigue and recovery after heavy resistance, jump, and sprint training. Eur J Appl Physiol. 2018.

Garcia-Ramos A et al. Greater neuromuscular and perceptual fatigue after low-load to failure than heavy-load to failure. 2024.

Minor, Brian MS, CSCS1; Helms, Eric PhD, CSCS2; Schepis, Jacob3. RE: Mesocycle Progression in Hypertrophy: Volume Versus Intensity. Strength and Conditioning Journal 42(5):p 121-124, October 2020. | DOI: 10.1519/SSC.0000000000000581

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Out of 32 symptoms commonly attributed to low testosterone, only 3 actually correlate with it. All three are sexual. The other 29 — fatigue, brain fog, low mood, weight you can't lose, feeling not quite like yourself — are real, but they are produced by something else, and the wellness-clinic funnel runs on getting that wrong.
 
Episode 2 of our Signal book launch series. Dr. Jordan Feigenbaum and Dr. Austin Baraki cover how testosterone actually works, what the number on your lab report is really measuring, and what a real evaluation of low T looks like.

Timestamps:
00:00 Mark, revisited (cold open)
02:00 How testosterone actually works (HPG axis)
06:14 Why "in range" can still be abnormal
09:24 What your lab number actually measures
12:25 Case: total 230, low SHBG — does this guy need TRT?
17:04 The saturation model — why higher isn't better
21:11 A patient at 480 wants 900: how the conversation goes
28:57 What "in range" actually means (and why 264 is the cutoff)
34:41 The 3 symptoms that matter (out of 32)
37:16 Walking back a 10-symptom checklist
42:31 How a real testosterone workup gets done
46:42 Chasland trial — TRT vs. exercise at low-normal T
49:31 A warning for hard-training men
58:48 Takeaways, tease, and what's coming next 
What we cover:
The HPG axis explained — and why one low total testosterone reading tells you almost nothing about where the problem actually sits.
The difference between total, free, and bioavailable testosterone — and why SHBG, the binding protein the wellness-clinic workup almost always ignores, is what determines whether the number on your lab report is misleading you in either direction.
The saturation model: above roughly 250 ng/dL, the prostate androgen receptor is saturated. Libido follows the same plateau. Pushing a normal man from 500 to 900 isn't doing what the marketing implies.
The EMAS study finding: of 32 symptoms men commonly attribute to low testosterone, only 3 actually correlate. Every other symptom needs a different workup.
How a real testosterone workup gets done — morning sample, fasted, repeat draw, LH/FSH/SHBG to localize and contextualize.
The Chasland 2021 trial: when standard TRT is prescribed properly to middle-aged men with low-normal levels, does it beat exercise? The answer is what most of the wellness-clinic industry is built on getting wrong.
A note for hard-training men: the exercise-hypogonadal-male pattern, what "low-normal" means in someone whose levels are an adaptation to training load rather than a baseline deficit, and why a textbook TRT dose in that man may functionally act as a performance enhancer.
If you have a lab report on your kitchen counter right now, this is what we wrote for you. Signal, the book, drops in May. Pre-order available soon at barbellmedicine.com.

Resources & links
Signal — Feigenbaum & Baraki (Barbell Medicine, 2026): coming soon
Episode 1 (Is the Testosterone Crisis Real?): https://stream.redcircle.com/episodes/b25a8006-57e5-4dc3-b74c-203f6fbcebc1/stream.mp3
Training Plateau Action Plan (free): barbellmedicine.com/training-plateau-action-plan
Barbell Medicine programs and consultations: barbellmedicine.com
To support us and get ad free listening, plus special product discounts, and exclusive content, go to supercast.barbellmedicine.com

Referenced studies
Wu FCW et al. 2010 - Identification of late-onset hypogonadism in middle-aged and elderly men. NEJM 363(2):123-135. [The EMAS 3-of-32 finding]
https://pubmed.ncbi.nlm.nih.gov/20554979/

Bhasin S et al. 2018 - Testosterone Therapy in Men With Hypogonadism: An Endocrine Society Clinical Practice Guideline. JCEM 103(5):1715-1744. [264 ng/dL threshold; first-draw protocol]
https://pubmed.ncbi.nlm.nih.gov/29562364/

Travison TG et al. 2008 - The natural history of symptomatic androgen deficiency in men. JAGS 56(5):831-839. [MMAS: ~50% of initially low values normalize on repeat]
https://pubmed.ncbi.nlm.nih.gov/18308002/

Travison TG et al. 2006 - The relationship between libido and testosterone levels in aging men. JCEM 91(7):2509-2513. [Libido plateau data, Framingham + HIM]
https://pubmed.ncbi.nlm.nih.gov/16670164/

Brambilla DJ et al. 2009 - The effect of diurnal variation on clinical measurement of serum testosterone. JCEM 94(3):907-913. [Why morning, fasted matters]
https://pubmed.ncbi.nlm.nih.gov/19112025/

Morgentaler A & Traish AM. 2009 - Shifting the paradigm of testosterone and prostate cancer: the saturation model and the limits of androgen-dependent growth. Eur Urol 55(2):310-320. [The saturation model]
https://pubmed.ncbi.nlm.nih.gov/18838208/

Trost LW & Mulhall JP. 2016 - Challenges in Testosterone Measurement, Data Interpretation, and Methodological Appraisal of Interventional Trials. J Sex Med 13(7):1029-1046. [Free T unreliability at the low end; equilibrium dialysis as the reference method]
https://pubmed.ncbi.nlm.nih.gov/27210182/

Vermeulen A et al. 1999 - A critical evaluation of simple methods for the estimation of free testosterone in serum. JCEM 84(10):3666-3672. [Calculated free T methodology]
https://pubmed.ncbi.nlm.nih.gov/10523012/

Chasland LC et al. 2021 - Testosterone and exercise: effects on fitness, body composition, and strength in middle-to-older aged men with low-normal serum testosterone levels. Am J Physiol Heart Circ Physiol 320(5):H1985-H1998. [The 12-week trial]
https://pubmed.ncbi.nlm.nih.gov/33739153/

Arun AS et al. 2025 - Reevaluating the Threshold for Low Total Testosterone. Clin Chem 71(5):609-611. [2025 NHANES strength-dissociation reference]
https://pubmed.ncbi.nlm.nih.gov/40066943/

Baillargeon J et al. 2015 - Trends in Androgen Prescribing in the United States, 2001-2011. JAMA Intern Med 175(8):1413-1415. [25% no preceding lab; the 50% no follow-up monitoring gap - referenced from Episode 1]
https://pubmed.ncbi.nlm.nih.gov/26075486/

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Stop a GLP-1 and about two thirds of the weight loss comes back within a year. Three randomized withdrawal trials (SURMOUNT-4, STEP 1 extension, STEP 4) and a new BMJ 2026 systematic review of 37 RCTs and nearly 10,000 adults all land on the same signal. The cardiometabolic benefits, blood pressure, fasting glucose, lipids, drift back in parallel with the weight. The framing that actually fits the data: GLP-1s behave like a statin. There is a cumulative benefit during exposure, but this does not extend indefinitely,
This month's Direct Line covers two subscriber questions. The first asks what the new BMJ paper on GLP-1 cardiovascular protection after cessation actually shows, and how GLP-1 durability compares to lifestyle-only interventions. The second asks how a postmenopausal woman newly diagnosed with osteopenia should structure her lifting.
Studies referenced: SURMOUNT-4 (Jastreboff, JAMA 2024), STEP 1 extension (Wilding, Diabetes Obes Metab 2022), STEP 4 (Rubino, JAMA 2021), West et al. BMJ 2026 systematic review, Budini 2026 eClinicalMedicine regain meta-analysis, SELECT cardiovascular outcomes, FLOW renal outcomes, the Diabetes Prevention Program, Look AHEAD, POUNDS Lost, and LIFTMOR (Watson, JBMR 2018).
Full episode on BBM+ covers 8 additional subscriber questions. Join at https://barbellmedicine.supercast.com/
Timestamps
0:00 Intro
1:52 Q1: What happens when you stop a GLP-1
5:33 Lifestyle-only comparators: DPP, Look AHEAD, POUNDS Lost
8:15 Austin on the cessation conversation 1
2:41 BMJ 2026: weight and cardiometabolic regression
17:59 The statin framing
23:41 Austin: first 6 months off GLP-1
28:07 Q2: Osteopenia and heavy lifting
35:28 LIFTMOR protocol
38:00 Outro

Next Steps
For evidence-based resistance training programs: barbellmedicine.com/training-programs
For individualized training consultation: barbellmedicine.com/coaching
Explore our full library of articles on health and performance: barbellmedicine.com/resources
To consult with Drs. Baraki or Feigenbaum email us at [email protected]

Resources
Aronne, Louis J., et al. "Continued Treatment With Tirzepatide for Maintenance of Weight Reduction in Adults With Obesity: The SURMOUNT-4 Randomized Clinical Trial." JAMA, vol. 331, no. 1, 2024, pp. 38–48. https://jamanetwork.com/journals/jama/fullarticle/2812936
Wilding, John P. H., et al. "Weight Regain and Cardiometabolic Effects After Withdrawal of Semaglutide: The STEP 1 Trial Extension." Diabetes, Obesity and Metabolism, vol. 24, no. 8, Aug. 2022, pp. 1553–1564. https://dom-pubs.onlinelibrary.wiley.com/doi/10.1111/dom.14725
Rubino, Domenica, et al. "Effect of Continued Weekly Subcutaneous Semaglutide vs Placebo on Weight Loss Maintenance in Adults With Overweight or Obesity: The STEP 4 Randomized Clinical Trial." JAMA, vol. 325, no. 14, 2021, pp. 1414–1425. https://jamanetwork.com/journals/jama/fullarticle/2777886
West, Sam, et al. "Weight Regain After Cessation of Medication for Weight Management: Systematic Review and Meta-Analysis." BMJ, vol. 392, 7 Jan. 2026, article e085304. https://www.bmj.com/content/392/bmj-2025-085304
Budini, Brajan, et al. "Trajectory of Weight Regain After Cessation of GLP-1 Receptor Agonists: A Systematic Review and Nonlinear Meta-Regression." eClinicalMedicine, vol. 93, 4 Mar. 2026, article 103796. https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(26)00043-X/fulltext
Lincoff, A. Michael, et al. "Semaglutide and Cardiovascular Outcomes in Obesity Without Diabetes." New England Journal of Medicine, vol. 389, no. 24, 11 Nov. 2023, pp. 2221–2232. https://www.nejm.org/doi/full/10.1056/NEJMoa2307563
Perkovic, Vlado, et al. "Effects of Semaglutide on Chronic Kidney Disease in Patients with Type 2 Diabetes." New England Journal of Medicine, vol. 391, no. 2, 24 May 2024, pp. 109–121. https://www.nejm.org/doi/full/10.1056/NEJMoa2403347
Knowler, William C., et al. "Reduction in the Incidence of Type 2 Diabetes with Lifestyle Intervention or Metformin." New England Journal of Medicine, vol. 346, no. 6, 7 Feb. 2002, pp. 393–403. https://www.nejm.org/doi/full/10.1056/NEJMoa012512
Look AHEAD Research Group. "Cardiovascular Effects of Intensive Lifestyle Intervention in Type 2 Diabetes." New England Journal of Medicine, vol. 369, no. 2, 11 July 2013, pp. 145–154. https://www.nejm.org/doi/full/10.1056/NEJMoa1212914
Sacks, Frank M., et al. "Comparison of Weight-Loss Diets with Different Compositions of Fat, Protein, and Carbohydrates." New England Journal of Medicine, vol. 360, no. 9, 26 Feb. 2009, pp. 859–873. https://www.nejm.org/doi/full/10.1056/NEJMoa0804748
Watson, Shelley L., et al. "High-Intensity Resistance and Impact Training Improves Bone Mineral Density and Physical Function in Postmenopausal Women With Osteopenia and Osteoporosis: The LIFTMOR Randomized Controlled Trial." Journal of Bone and Mineral Research, vol. 33, no. 2, 2018, pp. 211–220. https://onlinelibrary.wiley.com/doi/10.1002/jbmr.3284

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Every week there's a new headline saying men are losing testosterone. A quarter of men now start testosterone replacement therapy without ever getting their blood tested. The supplement aisle is full of boosters that either do nothing or contain undisclosed steroids. And the lab test that gets everybody to the pharmacy? Half of low results normalize on their own.
In Episode 1 of the Signal launch series, Dr. Jordan Feigenbaum and Dr. Austin Baraki (both MDs and strength coaches) walk through the three-layer problem with how testosterone gets diagnosed and treated in 2026, then take apart the "testosterone is crashing" headline with the most current data available, including a 2025 meta-analysis of more than one million men.
Timestamps
0:00 Mark's story: treating the number, not the patient
1:18 Welcome to the Barbell Medicine Podcast
1:41 Problem 1: A quarter of men start TRT with no lab work
3:36 Problem 2: Why testosterone boosters do not work (and what is in them)
13:40 Problem 3: Why one low testosterone lab is not a diagnosis
19:19 Setup: Is the testosterone crisis headline real?
20:04 The MMAS data and the 1%-per-year number
20:52 The 2025 meta-analysis of over 1 million men
22:02 Why the headline is inflated: three causes
22:27 Cause 1: The testing method changed (immunoassay to mass spec)
25:58 Cause 2: BMI cannot see visceral fat
29:37 The Nyante study: when you fix both problems, the decline vanishes
33:58 What this actually means for you
37:05 The broken testosterone system, summarized
38:24 Five takeaways from this episode
39:14 Next week: How testosterone actually works
39:39 About Signal and credits

What you'll learn in this episode:
 Why 25% of new TRT prescriptions are written without any pre-treatment lab work (JAMA, 2015)
What actually happens when researchers test 50+ "testosterone booster" supplements (spoiler: 12% are contaminated with undisclosed steroids)
Why a single low testosterone reading is not a diagnosis, and the Massachusetts Male Aging Study data that proves it
The real size of the population-level testosterone decline (much smaller than 1% per year)
Why BMI cannot see the visceral fat that is driving most of the genuine decline
The Nyante study that shows the decline essentially vanishes when you use an accurate test and measure waist circumference
Five practical takeaways you can apply before your next lab draw

This is Episode 1 of a four-part series built around our upcoming book, Signal. Over the next four weeks we cover what testosterone actually is, how to tell when it is genuinely low, what is really driving population-level changes, and what the evidence says you can do about it.
Next Steps
Check out our new book, Signal (coming soon)
For evidence-based resistance training programs: barbellmedicine.com/training-programs
For individualized training consultation: barbellmedicine.com/coaching
Explore our full library of articles on health and performance: barbellmedicine.com/resources
To consult with Drs. Baraki or Feigenbaum email us at [email protected]
To support us and get ad free listening, plus special product discounts, and exclusive content, go to supercast.barbellmedicine.com
Resources

Baillargeon, J., et al. (2015). Trends in Androgen Prescribing in the United States, 2001–2011. JAMA Intern Med, 175(8), 1413–1415. — 25% no preceding lab; post-prescription monitoring gap.

Rao, P.K., et al. (2017). Trends in Testosterone Replacement Therapy Use from 2003 to 2013 among Reproductive-Age Men in the United States. J Urol, 197(4), 1121–1126. — Prescription volume growth.

Selinger, S., & Thallapureddy, A. (2024). Cross-sectional analysis of national testosterone prescribing through prescription drug monitoring programs, 2018–2022. PLoS One, 19(8), e0309160. — Recent prescribing data, 3-4 million estimate.

Vesper, H.W., et al. (2015). Serum Total Testosterone Concentrations in the US Household Population from the NHANES 2011–2012 Study Population. Clin Chem, 61(12), 1495–1504. — Population testosterone levels, NHANES data.

Clemesha, C.G., et al. (2020). "Testosterone Boosting" Supplements Composition and Claims Are Not Supported by the Academic Literature. World J Men's Health, 38(1), 115–122. — 62% no published data, 10% decreased T.

Tucker, J., et al. (2018). Unapproved Pharmaceutical Ingredients Included in Dietary Supplements Associated With US FDA Warnings. JAMA Network Open, 1(6), e183337. — 12% adulterated with undisclosed steroids.

Trost, L.W., & Mulhall, J.P. (2016). Challenges in Testosterone Measurement, Data Interpretation, and Methodological Appraisal of Interventional Trials. J Sex Med, 13(7), 1029–1046. — Half of low results normalize on repeat.

Travison, T.G., et al. (2008). The Natural History of Symptomatic Androgen Deficiency in Men: Onset, Progression, and Spontaneous Remission. JCEM. MMAS data — 50%+ spontaneous normalization.

Travison, T.G., et al. (2007). A Population-Level Decline in Serum Testosterone Levels in American Men. JCEM, 92(1), 196–202. — Original MMAS secular decline, 15–20% lower across cohorts.
Santi, D., et al. (2025). Meta-analysis of secular trend in total testosterone levels, 1971–2024. 1,256 studies, N > 1,000,000. — 0.56%/year adjusted; LH parallel decline; mass spec subgroup no significant decline.
 Methods note on the ~0.56% per year figure cited in this episode: the Santi paper does not report a single percentage rate. The headline adjusted meta-regression coefficient (−0.6 nmol/L/year) is inflated by the random-effects weighting scheme and is not a biological rate. The 0.5–0.6% per year approximation comes from the pre-2000 stratified subgroup (Fig. 5, coefficient −0.1 nmol/L/year) divided by the dataset mean of 18.5 nmol/L. The post-2000 stratum runs larger (~1.1%), and the age-stratified coefficients in Table 5 cluster in the 0.4–0.9% range. The mass spectrometry subgroup (Table 3, Group 4) showed no significant trend (p = 0.845). The episode uses the conservative end of this range as the most defensible estimate of the real population-level rate after accounting for assay drift.

Nyante, S.J., Graubard, B.I., Li, Y., McQuillan, G.M., Platz, E.A., Rohrmann, S., Bradwin, G., & McGlynn, K.A. (2012). Trends in sex hormone concentrations in US males: 1988–1991 to 1999–2004. Int J Androl, 35(3), 456–466. doi: 10.1111/j.1365-2605.2011.01230.x. — Archived NHANES samples, same platform, waist circumference added; no significant decline in total or free testosterone.

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A 43-year-old man starts exercising and ends up in the ER with a CK over 100x the upper limit of normal. His doctor says it’s from training. We don’t think so. In this episode, Dr. Jordan Feigenbaum and Dr. Austin Baraki walk through the full case — history, labs, diagnosis, and what actually went wrong — then break down the mechanisms behind the answer, the nocebo research, and what the brand-new 2026 guidelines mean for the 40 million Americans on a drug class you’ve definitely heard of.

We also cover the STOMP trial (do statins actually impair strength gains?), the SAMSON trial (how much of statin intolerance is nocebo?), the difference between myalgia, myositis, and rhabdomyolysis, Austin’s clinical approach to a patient whose strength is declining on a statin, and the treatment escalation pathway for statin-intolerant patients including bempedoic acid, PCSK9 inhibitors, and inclisiran. Plus, where GLP-1 receptor agonists like tirzepatide fit into the cardiovascular risk picture.
Timestamps
0:00 — A 43-year-old man is getting weaker, not stronger
2:09 — Taking the history: Medications, lifestyle, and red flags
12:53 — The labs come back: CK at 18,979
16:05 — Metabolic syndrome and the modern treatment approach
23:15 — Rhabdomyolysis: What it is and why it’s dangerous
29:50 — Final diagnosis and what went wrong with the medications
37:15 — 2026 ACC lipid guidelines: What changed
40:32 — Three mechanisms: How statins affect muscle
47:02 — The nocebo effect and the SAMSON trial
54:17 — Do statins impair training? The STOMP trial
1:00:30 — Who’s at highest risk for statin muscle problems
1:07:36 — What happened to the patient and options if this is you
1:14:12 — Five takeaways

Five Takeaway
 Statin myopathy is real but relatively uncommon. The excess symptom rate above placebo is roughly 1–5% in controlled trials. But in exercising patients, especially on combination therapy, the risk can be higher.
There are three proposed mechanisms: reduced energy production from CoQ10 depletion, compromised muscle cell membranes from isoprenoid loss, and accelerated protein breakdown from calcium leak via the ryanodine receptor. Exercise amplifies all three, but the vast majority of people compensate.
If you’re on a statin and your strength is going down, talk to your doctor before stopping the medication or changing your training. A CK test can help separate a drug problem from a programming problem
The 2026 ACC guidelines list vigorous exercise as a risk factor for statin-associated muscle symptoms for the first time. They also provide statin-intolerant patients a clear escalation pathway: bempedoic acid, ezetimibe, PCSK9 inhibitors, and more.
Lower is better for LDL. There’s a 33% relative reduction in cardiovascular events at <55 vs. 70 mg/dL. Lower for longer. Healthy lifestyle changes plus effective lipid-lowering therapy are among the best things you can do for cardiovascular risk.

Next Steps
For evidence-based resistance training programs: barbellmedicine.com/training-programs
For individualized training consultation: barbellmedicine.com/coaching
Explore our full library of articles on health and performance: barbellmedicine.com/resources
To consult with Drs. Baraki or Feigenbaum email us at [email protected]
To support us and get ad free listening, plus special product discounts, and exclusive content, go to supercast.barbellmedicine.com

 Resources
Training Plateau Action Plan (free):
https://www.barbellmedicine.com/training-plateau-action-plan/
Fish oil episode:
https://open.spotify.com/episode/4kRtXZBMZWKkZPDdIKpu1S
Lp(a): https://www.barbellmedicine.com/blog/lipoprotein-a-testing-and-treatment/

Guidelines
Blumenthal RS, Morris PB, et al. 2026 ACC/AHA Guideline on the Management of Dyslipidemia. Circulation. 2026. DOI: 10.1161/CIR.0000000000001423

Case
László A, et al. Exercise and Statin-Fibrate Combination Therapy-Caused Myopathy. BMC Research Notes. 2013;6:52. https://pubmed.ncbi.nlm.nih.gov/23388500/
 
LDL Targets
Lee YJ, et al. (Ez-PAVE) Intensive LDL Cholesterol Targeting in Atherosclerotic Cardiovascular Disease. NEJM. 2026. PMID: 41910315

Mechanisms of Statin Myopathy
Meador BM, Huey KA. Statin-Associated Myopathy and Its Exacerbation with Exercise. Muscle Nerve. 2010;42(4):469–479. https://pubmed.ncbi.nlm.nih.gov/20878737/

Safitri N, et al. Statin-Induced Rhabdomyolysis: Mechanisms, Risk Factors, Management. Drug Healthc Patient Saf. 2021. https://pmc.ncbi.nlm.nih.gov/articles/PMC8593596/

Molinarolo S, et al. Cryo-electron microscopy reveals sequential binding and activation of Ryanodine Receptors by statin triplets. Nat Commun. 2025;16(1):11508. doi:10.1038/s41467-025-66522-0

Thompson PD, et al. Lovastatin Increases Exercise-Induced Skeletal Muscle Injury. Metabolism. 1997;46(10):1206–1210

Nocebo Effect and Statin Intolerance
Wood FA, et al. N-of-1 Trial of a Statin, Placebo, or No Treatment to Assess Side Effects (SAMSON). NEJM. 2020;383(22):2182–2184. https://pmc.ncbi.nlm.nih.gov/articles/PMC8453640/

Khan S, et al. Does Googling Lead to Statin Intolerance? Int J Cardiol. 2018;262:25–27. https://pubmed.ncbi.nlm.nih.gov/29706390/

Gupta A, et al. Adverse Events Associated with Unblinded, but Not with Blinded, Statin Therapy in the ASCOT-LLA. Lancet. 2017;389(10088):2473–2481. https://pubmed.ncbi.nlm.nih.gov/28476288/

Moon JC, et al. Examining the Nocebo Effect of Statins through the FDA AERS. Circ Cardiovasc Qual Outcomes. 2021;14(1):e007480. https://pubmed.ncbi.nlm.nih.gov/33161769

Statins and Exercise Outcomes
Parker BA, et al. Effect of Statins on Skeletal Muscle Function (STOMP). Circulation. 2013;127(1):96–103. https://pubmed.ncbi.nlm.nih.gov/23183941/

Parker BA, Thompson PD. Effect of Statins on Skeletal Muscle: Exercise, Myopathy, and Muscle Outcomes. Exerc Sport Sci Rev. 2012;40(4):188–194. https://pmc.ncbi.nlm.nih.gov/articles/PMC3463373/

Mikus CR, et al. Simvastatin Impairs Exercise Training Adaptations. JACC. 2013;62(8):709–714. https://pubmed.ncbi.nlm.nih.gov/23583255/

Slade JM, et al. The Impact of Statin Therapy and Aerobic Exercise Training. Am Heart J Plus. 2021;10:100028. https://pmc.ncbi.nlm.nih.gov/articles/PMC8477381/

Gui Y, et al. Efficacy and Safety of Statins and Exercise Combination Therapy. Eur J Prev Cardiol. 2017;24(9):907–916. DOI: 10.1177/2047487317691874 

Genetic Susceptibility
SEARCH Collaborative Group. SLCO1B1 Variants and Statin-Induced Myopathy — A Genomewide Study. NEJM. 2008;359(8):789–799

Autoimmune Myopathy
Barkhordarian M, et al. Statin-Induced Autoimmune Myopathy. Am J Case Rep. 2024;25:e944261. https://pubmed.ncbi.nlm.nih.gov/39219126/

Statin-Fibrate Interactions
Jones PH, Davidson MH. Reporting Rate of Rhabdomyolysis with Fenofibrate + Statin vs Gemfibrozil + Any Statin. Am J Cardiol. 2005;95(1):120–122

Bruckert E, et al. Mild to Moderate Muscular Symptoms with High-Dosage Statin Therapy (PRIMO Study). Cardiovasc Drugs Ther. 2005;19(6):403–414

Sinzinger H, O’Grady J. Professional Athletes Suffering from Familial Hypercholesterolaemia Rarely Tolerate Statin Treatment. Br J Clin Pharmacol. 2004;57(4):525–528

Tirzepatide and GLP-1 Agonists
Al-kuraishy HM, et al. The mechanistic role of tirzepatide in atherosclerosis. Int J Biol Macromol. 2025;329(1). https://doi.org/10.1016/j.ijbiomac.2025.147734

Effects of Tirzepatide on Lipid Profile: A Systematic Review and Meta-Analysis. 2024. https://pmc.ncbi.nlm.nih.gov/articles/PMC11704219/

Hamidi H, et al. Effect of tirzepatide on coronary atherosclerosis progression (T-Plaque trial design). Am Heart J. 2024;278:24–32. doi:10.1016/j.ahj.2024.08.015

Fish Oil and Omega-3 Fatty Acids
Bhatt DL, et al. Cardiovascular Risk Reduction with Icosapent Ethyl (REDUCE-IT). NEJM. 2019;380:11–22. https://pubmed.ncbi.nlm.nih.gov/30415628/

Abdelhamid AS, et al. Omega-3 Fatty Acids for Prevention of Cardiovascular Disease. Cochrane Database Syst Rev. 2020. https://pubmed.ncbi.nlm.nih.gov/32114706/

Manson JE, et al. Marine n-3 Fatty Acids and Prevention of CVD and Cancer (VITAL). NEJM. 2019;380:23–32. https://pubmed.ncbi.nlm.nih.gov/30415637/
 

Myopathy Classification
Selva-O’Callaghan A, et al. Statin-Induced Myalgia and Myositis: Pathogenesis and Clinical Recommendations. Expert Rev Clin Immunol. 2018;14(3):215–224. https://pmc.ncbi.nlm.nih.gov/articles/PMC6019601/

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