I Trained Hard for 25 Years. I Was Measuring the Wrong Fitness.

For twenty-five years, my fitness test was a mirror.

Every morning before the gym, I turned sideways, looked for what had changed, and let the reflection tell me the work was paying off. The mirror was the scoreboard, the coach, and the whole training plan. And it lied to me by omission, because it can only grade the one system you can see.

Ninety percent of my training was resistance work. Four, sometimes five hard sessions a week, an hour at a time, most sets pushed to failure. Cardio was a warm-up I skipped. Mobility was for other people. Recovery wasn't in my vocabulary. Every session was max effort toward one target: how I looked with my shirt off.

Here's the part that still stings. I've held a personal training certification for years, and my first job out of high school was as a fitness trainer. I knew the textbook answer to "what should a middle-aged man train for," and I coached the balanced version to every friend who asked. Then I went home and ran the vanity program on myself. For twenty-five years I never once turned that lens on my own training, right up until they threaded a stent into my right coronary artery at 44 and I finally read the literature I should have read at 20.

So let me be precise about what this is and isn't. I am not going to tell you my cardio fitness was garbage before the stent, because I never measured it. That's not a hedge. That's the whole indictment: a certified trainer with a stent in his heart who had never once measured one of the most powerful survival numbers in medicine, because he let a mirror tell him it didn't matter. I wasn't lazy and I wasn't unfit. I was highly trained in one dimension and completely untrained in another, and I couldn't see the gap because the half I trained was the half that shows.

That's the trap this whole post is about. A hard program is not the same as a complete one. The system you train best is the one that hides the systems you never test.

The Bottom Line I trained hard and narrow for twenty-five years: heavy lifting, almost no structured cardio, and I never measured my cardiorespiratory fitness once. I looked fit. That was the problem.

Cardiorespiratory fitness, the thing the mirror can't show you, carries one of the strongest survival signals we can measure. In treadmill-tested cohorts, fitter people keep dying less at every level, with no ceiling anyone has found. Strength training protects you too, but in the cohort data most of that survival benefit shows up fast, in the first 30 to 60 minutes a week, then flattens. I was doing five hours.

This isn't cardio versus weights, and it isn't "lifting gave me a stent." It's simpler and more uncomfortable: you can't judge a training program by the one system it builds best. I trained the mirror. I never trained the parts that decide how long you live.

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Vocabulary that matters

• VO₂max: the most oxygen your body can use at full effort. The single best lab number for cardio fitness.
• Cardiorespiratory fitness (CRF): how well your heart, lungs, and muscles move and use oxygen when you push hard.
• MET: a simple unit of effort. Sitting still is 1; the higher the number you can hold, the bigger your engine.
• Zone 2: easy aerobic work, right around the pace where you can still talk in full sentences but not sing. The intensity that builds your aerobic base.
• Epigenetic clocks: blood tests that estimate your biological age from chemical tags on your DNA that shift with age, lifestyle, and disease.

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Exercise doesn't play by the rules the last two did

My last two posts were about exposures that behave like a running tab. Carry a borderline-high LDL for twenty years and the damage stacks up. Same with blood pressure: every year above the line adds to the total your arteries have to eat. More exposure, more harm.

Exercise refuses to behave that cleanly. It isn't a "more is always better" story or a "less is always safer" one. It's a question of which kind, in what balance, and the honest answer moves as you age. The program that builds the body you want at twenty-five is not automatically the program that keeps your heart beating at fifty-five. Sometimes they're the same workout. Usually they're not.

The number I never measured

Start with the one I ignored completely: cardiorespiratory fitness. How well your heart, lungs, and muscles move and use oxygen when you push hard. The gold-standard version is VO₂max, the most oxygen your body can burn at full effort, estimated on a treadmill test in METs. Bigger number, bigger engine.

In 2018, Cleveland Clinic researchers ran the largest study of its kind: 122,007 adults who took a treadmill stress test, followed for a median of about eight years, more than 13,000 deaths across 1.1 million person-years.¹ Fitter people died less, and it didn't stop. At every level they measured, more fitness meant less death, with no ceiling where the benefit finally ran out.

Sit with the scale of that. In the same data, being unfit carried a mortality risk comparable to or greater than coronary artery disease, smoking, or diabetes. Low fitness tracked with as much excess death as the named diseases we spend billions screening for. And it's the one that doesn't get its own screening test.

Here's the honesty this brand runs on, and it cuts both ways. This was an observational study. It shows a brutal association, not proof of cause. Fit people differ from unfit people in a hundred ways a model can't fully catch, and some of those differences move the survival needle on their own. So I won't tell you fitness causes the lower death rate. I'll tell you it's one of the strongest, most consistent associations in all of preventive cardiology, and it holds whether you cut the data by age, sex, or existing disease. That's not a number you get to wave off because it's "only" observational.

It's strong enough that in 2016 the American Heart Association argued fitness should be treated like a vital sign, measured as part of routine care.² A vital sign. And I was a certified trainer who ended up with a stent in his heart having never once taken the test.

The Read Aerobic fitness is one of the strongest survival signals we can measure, with no ceiling anyone has found. It's also the exact thing I spent decades treating as optional and never bothered to measure.

The gauge I was maxing out

Now the one I obsessed over: lifting. This reckoning is subtler, because the answer isn't "lifting was a mistake." Lifting is genuinely protective. The question is how much of that protection you can actually bank, and how fast you hit the wall.

A 2022 meta-analysis in the British Journal of Sports Medicine pooled sixteen long-term studies on muscle-strengthening activity.³ Independent of any cardio, strength work was associated with roughly a 10 to 17 percent lower risk of dying from any cause, and of getting or dying from heart disease, cancer, and diabetes.³ Real, meaningful, worth doing.

But the dose-response is what stopped me cold. It looked nothing like the fitness curve. It was front-loaded. The biggest risk reductions clustered around 30 to 60 minutes of strength work per week, then flattened. A separate 2022 meta-analysis found the same shape, with the largest mortality reduction near 60 minutes a week and shrinking returns past that.¹³

I was doing four to five hours.

Now here's the trap I almost walked into, and where a lot of "cardio beats weights" content face-plants. These two findings are not a head-to-head. They don't even measure the same kind of thing. The fitness study measured an objective physical capacity: your actual output on a treadmill. The strength studies measured reported behavior: how many minutes a week people said they lifted. One is a number a machine reads off your body. The other is a number you write on a questionnaire. Stacking them side by side and crowning a winner is comparing a blood test to a food diary.

So read the curves separately, for what each honestly says. Measured aerobic fitness keeps tracking with survival all the way up. Reported strength minutes buy most of their survival benefit early, then flatten. And here's what made me put down the barbell and pick up a heart-rate strap: I was four or five times past the point where the lifting signal peaked, while scoring a zero on the system with the bigger, steeper survival curve. Not because I was lazy. Because I only ever trained the gauge I could see in the mirror.

To be crystal clear about what that flat curve is not: it is not proof that lifting past an hour a week is bad for you. If your goal is muscle, strength, bone, or still being able to deadlift your grandkid at 80, more volume keeps paying off. It's a mortality curve, not a strength curve. What the data won't yet promise is that hour six of lifting buys you more years the way hour one of cardio does. The strength numbers are also pooled, often self-reported, and some outcomes were rated low-certainty. Directionally real, not carved in stone.

The Read Strength training lowers your risk, but in the cohort data the benefit is front-loaded, strongest in the first 30 to 60 minutes a week. More volume builds more muscle, strength, and bone. It just hasn't been shown to keep buying more years. And it was never measured the way treadmill fitness was, so don't read the two curves as a fair fight.

So the answer is endless cardio? Not so fast.

Before anyone reads this as "ditch the weights and run forever," the aerobic side has its own catch, and an honest post has to show it.

Scan the arteries of lifelong, high-volume endurance athletes and the most active ones often have more coronary calcium, not less. In the MARC study of 284 middle-aged male athletes, the highest-volume group had roughly three times the odds of detectable coronary calcium versus the least active.⁴ That scared a lot of runners for a while. But a parallel study of 152 masters endurance athletes, three decades of training behind them, looked at what kind of plaque was forming: in the male athletes, 73 percent of the plaques were the calcified, denser, more stable kind, while sedentary men skewed the other way, toward the mixed, more rupture-prone kind (62 percent).⁵ The training seemed to build a different type of plaque, not just more of it.

Then it gets more complicated, which is the honest part. A cohort of nearly 22,000 men found the very active were slightly more likely to have high calcium, but high activity was not tied to a higher death rate, even among those with elevated scores.⁶ Reassuring, but not a green light. In 2023 the MARC team followed up and traced the calcium signal to intensity, not volume: very vigorous exercise tracked with faster progression of coronary calcium, while total training volume on its own did not.⁷ And the newest cohort, MASTER@HEART, knocked down the tidy "athlete plaque is the safe kind" story: lifelong endurance athletes had more plaque of every type than healthy non-athletes, calcified, non-calcified, and mixed.¹⁶ Nobody has shown those plaques turn into more heart attacks. Nobody has shown they don't.

So hold the reassurance loosely, and here's the honest landing: the athlete-plaque literature is a reason not to treat extreme endurance volume as automatically protective. It is not a reason to skip ordinary aerobic exercise. Those are not the same thing.

Because the two cardio findings only sound contradictory. They measure different things. Measured fitness, the treadmill number, tracks with survival all the way up, though the biggest drop is getting off the bottom, from unfit to fit; the gap from "very fit" to "elite" is real but small. The scary plaque signal lives at the far extreme: ten-plus hours a week of hard racing for decades. For anyone aiming at aging instead of a podium, the math closes cleanly. Most of the survival protection is in getting off the floor of that fitness curve, and that takes maybe three to five hours a week of structured aerobic work: a Zone 2 base plus one harder session that actually pushes your VO₂max. The minimum effective dose for cardio isn't zero. It's moderate, structured, and consistent. You don't need the elite end. You need off the bottom.

Train both, and get honest about "reversing aging"

The same strength-training meta-analysis pointed straight at what I'd been ignoring: people who did both strength and aerobic work had roughly a 40 percent lower risk of dying from any cause, a bigger benefit than either kind of training managed on its own.³ Not one or the other. Both.

There's real biology under that. Aerobic training does its quiet work in your mitochondria, the tiny engines inside cells that fade with age, and on the endothelium, the living inner lining of your blood vessels where nitric oxide keeps the pipes flexible.⁸ Lifting protects a different set: muscle, bone, the machinery that clears glucose. The systems overlap, but neither one fully covers for the other. Train half the map and you leave the other half unguarded.

Now the part where the longevity influencers lose the plot.

You've heard it: this cardio zone "reverses your biological age," that protocol "turns back your epigenetic clock." Epigenetic clocks are blood tests that read chemical tags on your DNA to estimate how fast you're aging, and the newer ones (PhenoAge, GrimAge, DunedinPACE) are the closest thing we have to a real-time aging readout.⁹ They're early-stage and openly noisy: run the same person twice and the readings don't always agree, and plenty of serious aging researchers still think the tools need years more validation. But noisy isn't useless. Right now they're the best window we have into aging biology, and they're improving fast. I read them as the strongest imperfect tool on the table, not a verdict. Here's what the exercise data on them actually say.

The biggest look yet landed in 2026: a Lancet Healthy Longevity meta-analysis pooling 44 studies and 145,465 people.¹⁷ More activity did track with a younger biological age, echoing earlier cohorts where active adults read a year or two younger on the clocks.¹⁰ But read the fine print. Only seven cross-sectional studies made it into the pooled math. The effect showed up on two clocks, Horvath and GrimAge, and vanished on two others, Hannum and PhenoAge. And the size of it was tiny, fractions of a standard deviation. The authors say it outright: the evidence is mostly cross-sectional, which means it can't tell you exercise caused the younger reading, only that people who move more tend to show one.

The randomized data are thinner and less flattering. In DO-HEALTH, 777 older adults followed for three years, the exercise arm was a simple home strength program, and on its own it didn't meaningfully move the major clocks. The clearest signal came from omega-3, and the omega-3 plus vitamin D plus exercise combo nudged PhenoAge by the equivalent of looking a few months younger over three years.¹⁴ A small Finnish twin study lands the same punch: among older twins split by decades of leisure-time activity, the active twin's DNA-methylation age didn't clearly differ from the inactive one's.¹⁵

So here's the calibrated read, and I won't soften it: the mechanism is plausible, the observational signal is consistent, and the randomized evidence is nowhere near strong enough to say exercise reverses your systemic biological age. Anyone selling you a specific zone or protocol that "rewinds your clock" is running miles ahead of the data.

Where the modality-specific evidence does bite harder is one level down, at the hallmarks of aging, the actual machinery that drives aging in the first place. HIIT, short bursts of hard work with recovery between, threw one of the strongest mitochondrial signals in the Mayo Clinic training trial, especially in older adults, reversing age-related differences in mitochondrial proteins.¹¹ Resistance training, in a small muscle-biopsy study, rejuvenated the mitochondrial methylation pattern inside aged muscle.¹² Real levers, both. Different levers. Do only one and part of the machine goes untouched. That's the case for training both, not for crowning a winner.

I'll come back to clocks and hallmarks again and again, because they're the lens I now run every health claim through. For this post the takeaway is smaller and more honest than the influencer version: the evidence says balance aerobic and resistance work. It does not say any single kind of exercise turns back your biological clock.

The Read Exercise is one of the most defensible healthspan bets we have. But calling it proven biological-age reversal runs past the clock data, which is mostly cross-sectional, clock-dependent, and small. Train for the hallmarks it clearly moves, not for a clock number nobody has reversed on demand.

What I Changed

This is what I do now, offered as my own interpretation of the evidence and my own situation, not as a prescription for yours.

Change	Why
Lift 2–3x/week for approximately 30 mins instead of 4–5x/week at an hour per session	Strength is protective, but the survival benefit is front-loaded. I stopped assuming every extra hour of lifting buys another year of life.
Stop taking every session to failure	Recovery is now part of the intervention, not an afterthought.
Add real Zone 2 cardio	I needed the aerobic base I had treated as optional.
Add one weekly VO₂max-focused session	Cardiorespiratory fitness was the number I had never measured.
Treat mobility and recovery as training	The program was all output and almost no restoration.
Measure VO₂max	You cannot improve the number you refuse to look at.

What this still can't explain

I don't think the training style I've run since high school football is what put a stent in my heart at 44. Plenty of untrained men with worse habits than mine never get an 80 percent blockage that young. A lopsided program is a missing layer of protection, not a smoking gun. And here's the gap nobody names: almost all the "high training volume tracks with more coronary calcium" data is on endurance athletes, runners, cyclists, masters racers. I lifted heavy and skipped cardio. There is essentially no published cohort asking whether that pattern accelerates coronary disease. We don't know. That's a hole in the map, not a reassurance.

And that's the problem I keep hitting. Borderline LDL, borderline blood pressure, a diet I trusted that may not have suited me, a program tilted hard toward the mirror. Every one is a plausible contributor. Stack them all together and they still don't explain how an artery goes from clean to 80 percent blocked in the window I'm looking at. The math doesn't close.

Which raises the question I'd been dodging: what if the slow-buildup story is the wrong story for what happened to me? What if it wasn't slow?

The Calibrated Claim Audit

Claim	Mechanism strength	Evidence quality	What epi clocks say	My read	What would change my mind
Cardiorespiratory fitness is one of the strongest modifiable survival signals.	Strong	Strong observational data, especially objective treadmill cohorts	Suggestive observational signals, not decisive	Measure it and train it	Trials showing that raising CRF doesn't lower mortality
Resistance training lowers risk, but the mortality benefit looks front-loaded.	Strong	Moderate; mostly observational and often self-reported	Sparse systemically; some tissue-specific muscle data	Keep lifting, but stop making it the whole program	Objective cohorts showing high-volume lifting buys added years
High-volume endurance training can raise coronary calcium.	Plausible	Moderate; mostly male master-athlete cohorts	Not useful yet	Not a reason to avoid cardio; intensity, plaque type, and outcomes matter	Long-term CCTA studies linking athlete plaque patterns to actual events
Exercise reverses biological age.	Plausible, but often overstated	Observationally suggestive; randomized clock data weak for exercise alone	Mixed and early	Do not sell clock reversal yet	Larger exercise-specific RCTs with validated clocks and clinical outcomes

Commercial distortion risk: Moderate The main incentive ecosystem here is wearables, VO₂max testing, Zone 2 coaching apps, recovery devices, and influencers selling one modality as the answer. That doesn't make the claims wrong; it changes how carefully I read the evidence.

The Final Signal

• What this gets right. Strength training is genuinely protective. Cardiorespiratory fitness is one of the strongest survival signals we can measure. Both belong in an aging program. And if your goal is longevity, not winning a powerlifting meet or an ultra, the dose that gets you there is smaller than the one the mirror demanded.
• What gets oversold. The mortality benefit of lifting appears front-loaded in cohort data. Extra volume past roughly an hour a week may keep buying muscle, strength, and bone, but the longevity dividend is not yet established. And exercise as a standalone lever on reversing aging via systemic epigenetic clocks is mostly null in the randomized data we have.
• What I changed. Rebalanced to 2–3 strength sessions a week, stopped chasing failure on every set, added real Zone 2 cardio, added one weekly VO₂max-targeting session, started treating recovery as training, and measured my VO₂max.
• What would change my mind. Long-term cohorts or trials showing high-volume lifting buys clinically meaningful added longevity, or exercise-specific randomized clock data showing systemic biological-age reversal that maps to actual outcomes.
• What this opens next. I don't think lifting gave me a stent. I think a lopsided program left a layer of protection on the table. But none of my cracks, LDL, BP, diet, or training, alone or stacked together, fully explains how an artery goes from clean to 80 percent blocked in eight years. What if the standard slow-buildup story is the wrong story for what happened to me?

That's where this goes next.

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This is not medical advice. It's one clinician's experience and a review of the published data. Talk to your doctor about what exercise programming and screening is appropriate for your individual risk profile.

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References

1. Mandsager K, Harb S, Cremer P, Phelan D, Nissen SE, Jaber W. Association of Cardiorespiratory Fitness With Long-term Mortality Among Adults Undergoing Exercise Treadmill Testing. JAMA Netw Open. 2018;1(6):e183605. PMID: 30646252 [Finding: In 122,007 adults given treadmill stress tests, higher cardiorespiratory fitness tracked with lower death at every level, with no upper limit of benefit found, and being unfit carried a mortality risk comparable to or greater than coronary disease, smoking, or diabetes. Observational, so it shows a strong association, not proof of cause.]
2. Ross R, Blair SN, Arena R, et al. Importance of Assessing Cardiorespiratory Fitness in Clinical Practice: A Case for Fitness as a Clinical Vital Sign: A Scientific Statement From the American Heart Association. Circulation. 2016;134(24):e653–e699. PMID: 27881567 [Finding: An American Heart Association scientific statement making the case that cardiorespiratory fitness predicts mortality as strongly as smoking, hypertension, or diabetes, and should be measured in routine care as a clinical vital sign.]
3. Momma H, Kawakami R, Honda T, Sawada SS. Muscle-strengthening activities are associated with lower risk and mortality in major non-communicable diseases: a systematic review and meta-analysis of cohort studies. Br J Sports Med. 2022;56(13):755–763. PMID: 35228201 [Finding: Pooling 16 cohort studies, muscle-strengthening activity was tied to a 10 to 17 percent lower risk of death and major disease independent of cardio, with the benefit peaking around 30 to 60 minutes a week. Doing both strength and aerobic work carried a larger benefit than either alone.]
4. Aengevaeren VL, Mosterd A, Braber TL, et al. Relationship Between Lifelong Exercise Volume and Coronary Atherosclerosis in Athletes. Circulation. 2017;136(2):138–148. PMID: 28450347 [Finding: In 284 middle-aged male athletes, the highest training volume (over 2,000 MET-minutes a week) carried roughly triple the odds of coronary calcium and plaque, though that plaque skewed toward the more stable calcified type. Observational and male-only.]
5. Merghani A, Maestrini V, Rosmini S, et al. Prevalence of Subclinical Coronary Artery Disease in Masters Endurance Athletes With a Low Atherosclerotic Risk Profile. Circulation. 2017;136(2):126–137. PMID: 28465287 [Finding: Among 152 lifelong masters endurance athletes with low risk profiles, most had normal calcium scores, but the male athletes who did have plaque skewed toward calcified, more stable plaque (about 73 percent) versus mixed, rupture-prone plaque in sedentary men. What that means for real-world risk is uncertain.]
6. DeFina LF, Radford NB, Barlow CE, et al. Association of All-Cause and Cardiovascular Mortality With High Levels of Physical Activity and Concurrent Coronary Artery Calcification. JAMA Cardiol. 2019;4(2):174–181. PMID: 30698608 [Finding: In about 21,800 healthy men, the most active (over 3,000 MET-minutes a week) were slightly more likely to have high coronary calcium, but that high activity was not linked to higher all-cause or cardiovascular death, even when calcium was elevated.]
7. Aengevaeren VL, Mosterd A, Bakker EA, et al. Exercise Volume Versus Intensity and the Progression of Coronary Atherosclerosis in Middle-Aged and Older Athletes: Findings From the MARC-2 Study. Circulation. 2023;147(13):993–1003. PMID: 36597865 [Finding: Following 289 athletes for six years, exercise intensity rather than volume tracked with coronary calcium progression: very vigorous exercise was tied to faster calcium buildup, while total training volume on its own was not.]
8. López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. Hallmarks of aging: An expanding universe. Cell. 2023;186(2):243–278. PMID: 36599349 [Finding: The landmark review defining the twelve hallmarks of aging, including mitochondrial dysfunction, epigenetic alterations, and altered intercellular communication, the interconnected biological processes that drive aging and that interventions aim to slow.]
9. Belsky DW, Caspi A, Corcoran DL, et al. DunedinPACE, a DNA methylation biomarker of the pace of aging. eLife. 2022;11:e73420. PMID: 35029144 [Finding: Introduced DunedinPACE, a DNA-methylation blood test that estimates how fast a person is aging, built from two decades of within-person decline and shown to track with later illness, disability, and death.]
10. Ammous F, Peterson MD, Mitchell C, Faul JD. Physical Activity Is Associated With Decreased Epigenetic Aging: Findings From the Health and Retirement Study. J Cachexia Sarcopenia Muscle. 2025;16(3):e13873. PMID: 40511567 [Finding: In the Health and Retirement Study, physically active adults read one to two years younger on several epigenetic clocks than inactive adults. The main analysis was cross-sectional, so it shows association, not that exercise caused the younger reading.]
11. Robinson MM, Dasari S, Konopka AR, et al. Enhanced Protein Translation Underlies Improved Metabolic and Physical Adaptations to Different Exercise Training Modes in Young and Old Humans. Cell Metab. 2017;25(3):581–592. PMID: 28273480 [Finding: A 12-week Mayo Clinic trial found high-intensity interval training drove the strongest mitochondrial gains, especially in older adults, reversing many age-related differences in mitochondrial proteins. A small mechanistic study, not a mortality outcome.]
12. Ruple BA, Godwin JS, Mesquita PHC, et al. Resistance training rejuvenates the mitochondrial methylome in aged human skeletal muscle. FASEB J. 2021;35(9):e21864. PMID: 34423880 [Finding: In ten older men, six weeks of resistance training shifted the mitochondrial DNA methylation pattern in aged muscle toward a more youthful signature. A very small, short biopsy study, mechanistic rather than clinical.]
13. Shailendra P, Baldock KL, Li LSK, Bennie JA, Boyle T. Resistance Training and Mortality Risk: A Systematic Review and Meta-Analysis. Am J Prev Med. 2022;63(2):277–285. PMID: 35599175 [Finding: A meta-analysis of ten cohorts found any resistance training was tied to about 15 percent lower all-cause mortality, with the largest reduction (around 27 percent) near 60 minutes a week and benefits shrinking at higher volumes. Exposure was mostly self-reported.]
14. Bischoff-Ferrari HA, Gängler S, Wieczorek M, et al. Individual and additive effects of vitamin D, omega-3 and exercise on DNA methylation clocks of biological aging in older adults from the DO-HEALTH trial. Nat Aging. 2025;5:376–385. PMID: 39900648 [Finding: In this 3-year randomized trial of 777 older adults, a home exercise program on its own did not meaningfully move the major epigenetic clocks; omega-3 gave the clearest signal, and omega-3 plus vitamin D plus exercise together nudged PhenoAge by the equivalent of a few months younger.]
15. Sillanpää E, Ollikainen M, Kaprio J, et al. Leisure-time physical activity and DNA methylation age: a twin study. Clin Epigenetics. 2019;11(1):12. PMID: 30660189 [Finding: A co-twin study of older twins discordant in leisure activity for 32 years found essentially no difference in DNA-methylation age between the active and inactive twin, suggesting long-term activity has at most a minor effect on epigenetic aging once genetics are held constant.]
16. De Bosscher R, Dausin C, Claus P, et al.; Master@Heart Consortium. Lifelong endurance exercise and its relation with coronary atherosclerosis. Eur Heart J. 2023;44(26):2388–2399. PMID: 36881712 [Finding: In this well-balanced cohort, lifelong endurance athletes had more coronary plaque of every type (calcified, non-calcified, and mixed) than equally healthy non-athletes, undercutting the tidy idea that athlete plaque is uniformly the safe kind. Outcome data still needed.]
17. Shan J, Tay JH, Wang W, et al. Physical activity and biological age measured by DNA methylation clocks: a systematic review and meta-analysis. Lancet Healthy Longev. 2026;7(4):100835. PMID: 42068988 [Finding: Pooling 44 studies and 145,465 people, higher physical activity was associated with a younger biological age on two clocks (Horvath and GrimAge) but not two others (Hannum and PhenoAge), with very small effects and mostly cross-sectional data that cannot establish cause.]