Why fit endurance athletes still die of heart attacks

Everyone who follows endurance sport knows a version of the story. A cyclist in his late forties, lean, training fifteen hours a week, resting pulse in the low forties. A rower, a marathon runner, a triathlete. Then a cardiac arrest — sometimes mid-ride, sometimes on an ordinary Tuesday morning.

It does not fit what we are told about exercise. Endurance training is supposed to be the thing that protects the heart. Every article on this site, including the one arguing that VO₂max is the strongest predictor of mortality we have, points in that direction.

So how do the people with the best hearts keep dying of heart disease?

The answer turns out to involve three separate things that are usually confused with one another. Getting them apart is what makes the picture make sense.

First: it is almost always ordinary coronary disease

This is the part that surprises people most, because they expect something exotic — a hidden congenital defect, a freak arrhythmia.

In athletes under 35, that expectation is correct. Sudden cardiac death in that group is dominated by inherited and structural conditions: hypertrophic cardiomyopathy, arrhythmogenic cardiomyopathy, congenital coronary artery anomalies, channelopathies.

Above 35, the picture flips almost entirely. In masters athletes, sudden cardiac death during exercise is most commonly caused by atherosclerotic coronary artery disease — the same furred-up arteries that kill sedentary people. One review puts coronary disease at around 80% of exercise-related sudden deaths in older athletes.

The mechanism is usually one of two. A plaque ruptures, a clot forms, and an artery closes — a conventional heart attack. Or a stable narrowing that causes no trouble at rest cannot supply enough blood at 90% of maximum effort, and the resulting ischaemia triggers a fatal arrhythmia.

Nothing about being fit prevents plaque from existing. It just means the plaque has to compete for attention with a resting heart rate of 42, which does not look like a person with heart disease.

Second: fitness hides the warning signs

This is the cruellest part of the pattern, and it explains why so many of these deaths appear to come from nowhere.

The usual early symptom of coronary disease is reduced exercise tolerance — getting breathless on a hill you used to manage. In a trained cyclist, the margin is so large that a meaningful narrowing can develop without ever producing a symptom in normal training. You have enough surplus capacity to absorb the loss.

The same applies to the standard clinical picture. High blood pressure at rest is often masked by training adaptation, showing up only on exertion or ambulatory monitoring. Lipid results can look reasonable. The athlete has none of the visible risk markers, so nobody investigates, and the athlete themselves reasons — sensibly — that a person who rides 300 km a week does not have heart disease.

When symptoms do appear, they are often dismissed by the person best placed to notice them. A drop in power output gets attributed to overtraining. Chest tightness on a climb gets attributed to effort. The interpretation that fits the identity is always available.

Third: the plaque finding nobody expected

Here the evidence gets genuinely uncomfortable, and it deserves to be reported straight rather than smoothed over.

The Master@Heart study, published in the European Heart Journal in 2023, used CT coronary angiography to compare three groups of men with a median age of 55 and low cardiovascular risk profiles: 191 lifelong endurance athletes, 191 late-onset athletes who started after 30, and 176 healthy non-athletes. The athletes were training 10 to 11 hours a week, mostly cycling and running, against about 1 hour for the controls.

The expectation was that the athletes would have less plaque, or at least more stable plaque.

They had more. Compared with the healthy non-athletic group, lifelong endurance athletes had higher odds of having at least one coronary plaque (odds ratio 1.86), at least one plaque in a proximal segment — the most dangerous location (1.96), and, contrary to the hopeful hypothesis, at least one non-calcified plaque (1.95), the softer, more rupture-prone kind. In proximal segments specifically, the odds ratio for non-calcified plaque was 2.80.

This was not the first hint. A 2008 study found higher coronary calcium scores in male marathon runners than in controls, and several cohorts since have pointed the same way.

What it does not mean. Master@Heart is observational, all-male, cycling-heavy, and — critically — it measured plaque, not events. Nobody has yet shown that these athletes go on to have more heart attacks, and the authors themselves say longitudinal research is needed to reconcile the imaging with outcomes. Other work, including the MARC study, has found that the most active men had fewer plaques with high-risk imaging features, suggesting the plaque they carry may behave differently.

The honest summary is that the imaging paradox is real and unexplained, and that translating it into personal risk is currently not something anyone can do responsibly.

The fourth thing, which is not fatal but is very common

If you follow masters cycling or skiing, you will know more people with atrial fibrillation than the general population would predict. That is not a coincidence.

Endurance athletes have roughly a two- to five-fold higher prevalence of atrial fibrillation than matched controls, and the relationship is dose-dependent. In a Swedish cohort of more than 52,000 long-distance cross-country skiers, those who completed the most races and those with the fastest finishing times had the highest risk. Among former professional cyclists in their sixties, prevalence around 10% has been reported against essentially none in a comparison group.

AF is not usually what kills people. But it raises stroke risk, it is often what finally sends a lifelong athlete to a cardiologist, and it is the clearest example of the shape underlying all of this: the relationship between exercise and heart health is not a straight line.

Keeping the risk in proportion

None of this argues for training less, and the absolute numbers matter here.

Sudden cardiac death among trained participants in endurance events is estimated at roughly 0.39 per 100,000 marathon finishers, 0.54 per 100,000 in half-marathons, and 1.74 per 100,000 in triathlons. An older analysis of over 215,000 marathon finishers found four sudden deaths — a risk the authors described as around one in 50,000, and a fraction of the annual risk of simply being alive.

There is also a genuine paradox in the timing. Vigorous exertion transiently raises the risk of an acute cardiac event in someone with underlying disease — while habitual vigorous exercise lowers the risk of having that disease in the first place. The transient risk is highest in people who are unaccustomed to hard effort, and lowest in the well-trained. Reviewers consistently conclude that the overall mortality benefit of regular exercise outweighs the acute risk.

The athlete who dies on the bike was not killed by cycling. He had coronary disease that cycling did not prevent, that his fitness concealed, and that the ride exposed.

What this is actually useful for

The practical conclusion is narrow and worth stating precisely: being very fit is not evidence that you do not have coronary disease, and it should not be used as a reason to skip investigation.

That means taking seriously the things that are easy to explain away. Chest tightness, pressure or unusual breathlessness on exertion — particularly if it reliably appears at the same intensity and eases when you stop. Fainting or near-fainting during or just after exercise, which is never normal. Palpitations, especially if they arrive during recovery rather than effort. An unexplained decline in performance that does not respond to rest. A family history of sudden death or heart disease before 55 in men, 65 in women.

It also means having the standard risk factors checked at ordinary intervals rather than assuming your training exempts you. Lipids — ideally including ApoB — blood pressure measured properly, and blood glucose. If you have a family history or an abnormal result, a coronary calcium score is a conversation to have with a doctor.

There is no argument here for screening every masters athlete; the evidence does not support that, and the false-positive costs are real. The argument is for not dismissing symptoms because of a training log.

Endurance training remains one of the most powerful things you can do for how long and how well you live. It is simply not armour, and treating it as armour is what turns a treatable disease into a sudden one.

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This article is for general information and is not medical advice. If you have chest pain, breathlessness that is new or unexplained, fainting, or palpitations during or after exercise, stop and speak to a doctor. Chest pain with sweating, nausea, or pain spreading to the arm or jaw is a medical emergency — call 999 or 112.

Sources

1. De Bosscher R, Dausin C, Claus P, et al. Lifelong endurance exercise and its relation with coronary atherosclerosis. European Heart Journal, 2023;44(26):2388–2399. https://pubmed.ncbi.nlm.nih.gov/36881712/
2. American College of Cardiology. Sudden cardiac arrest and death in athletes: key points, 2024. https://www.acc.org/latest-in-cardiology/ten-points-to-remember/2024/12/10/16/37/a-contemporary-review-of
3. American College of Cardiology. Is the older athlete at risk for sudden cardiac death? 2015. https://www.acc.org/Latest-in-Cardiology/Articles/2015/07/28/07/19/Is-the-Older-Athlete-at-Risk-for-Sudden-Cardiac-Death
4. Maron BJ, Poliac LC, Roberts WO. Risk for sudden cardiac death associated with marathon running. Journal of the American College of Cardiology, 1996. https://pubmed.ncbi.nlm.nih.gov/8800121/
5. Andersen K, Farahmand B, Ahlbom A, et al. Risk of arrhythmias in 52,755 long-distance cross-country skiers: a cohort study. European Heart Journal, 2013;34:3624.
6. Coronary atherosclerosis in athletes: emerging concepts and preventive strategies. European Heart Journal, 2025;46(10):890. https://academic.oup.com/eurheartj/article/46/10/890/7951179
7. Atrial fibrillation in endurance athletes: epidemiology, proposed mechanisms and management. https://pmc.ncbi.nlm.nih.gov/articles/PMC4711509/