A look at Master@Heart, coronary plaque and ACC guidance on individualized cardiovascular assessment for endurance athletes over 35.
Brady Holmer’s Physiology Friday #341: The Athlete’s Heart Paradox, published October 23, 2026, revisits a finding that deserves attention without alarm: highly trained endurance athletes can have coronary plaque. His analysis centers on Master@Heart, a study published in 2023 that compared lifelong athletes with later-starting athletes and healthy non-athletes.
The practical question is not whether endurance exercise remains worthwhile. Holmer emphasizes its overall benefits. The question is how ambitious athletes should understand cardiovascular risk when strong fitness and plaque appear in the same person.
In Holmer’s account of Master@Heart, average coronary artery calcium scores were low or near zero across the groups. The number of plaques per person was also similar. Yet lifelong athletes had higher scores for the severity of arterial narrowing and the extent of artery involvement than non-athlete controls.
Those findings matter because a calcium score was not the whole picture. The study also assessed plaque characteristics and narrowing. Similar average calcium scores therefore did not mean the groups had identical coronary imaging findings.
Compared with controls, lifelong athletes had higher odds of several plaque findings. These included calcified and non-calcified plaques as well as mixed plaques. They also had higher odds of multiple plaques and plaques in proximal coronary segments.
The comparison between athlete groups added another distinction. Lifelong athletes were more likely than later-starting athletes to have a coronary segment narrowed by at least 50%. However, vulnerable plaques were uncommon across all groups and less frequent among lifelong athletes.
Holmer’s interpretation is that the familiar “stable plaque” explanation is too simple. The results did not show a uniquely benign plaque mix in lifelong athletes. They showed a more complicated pattern across several imaging measures.
For the reader, the central finding is straightforward: high fitness and coronary atherosclerosis can coexist. Neither a strong training history nor a low average calcium score captured every aspect of the arteries examined.
According to Holmer’s summary, Master@Heart compared groups averaging about 56 years old:
The athletes were fitter on the reported VO₂ peak measure and trained substantially more than the controls. The comparison therefore put the central tension into focus: better measured fitness did not correspond to uniformly more favorable coronary imaging.
The distinction between lifelong and later-starting athletes also matters. This was not simply a comparison between people who exercised and people who did not. It examined different training histories alongside the coronary findings.
Holmer also discusses a related MARC-2 analysis of 289 male athletes averaging 60 years old. In that cohort, family history of coronary artery disease was the strongest predictor of severe coronary artery calcium, or CAC.
The article reports associations involving age and systolic blood pressure. Smoking history and training load were also associated with CAC, alongside energy intake and dietary fat. That broader picture puts training into context rather than treating it as the only relevant exposure.
MARC-2 follow-up results summarized by Holmer showed changes over about seven years:
Total exercise volume did not predict plaque progression in that cohort. Very-vigorous exercise was associated with faster progression, mostly through calcified plaque. The distinction between total volume and intensity is important when interpreting a headline about “too much exercise.” Those are different exposures and should not be treated as interchangeable.
The central limitation belongs here: Master@Heart assessed coronary imaging rather than subsequent heart-attack rates. Holmer reports that clinical follow-up was planned but does not provide those outcomes. Its findings therefore do not demonstrate that lifelong endurance exercise causes more heart attacks.
The MARC-2 relationships are associations rather than proof of cause. That includes the relationship involving very-vigorous exercise. Holmer also characterizes the dietary interpretation as speculative, so these observations do not establish a diet prescription.
The MARC-2 analysis concerned male athletes. The American College of Cardiology’s related prevalence comparison also concerns male endurance masters athletes. These findings should not be treated as a universal coronary profile for everyone who trains.
The American College of Cardiology’s 2026 Sports Cardiology Research and Guideline Highlights provides the clinical context. It defines masters athletes as people aged 35 and older who regularly participate in competitive or high-intensity recreational exercise.
The overview says male endurance masters athletes have a higher prevalence of coronary calcium and atherosclerosis than sedentary peers. It also states that fitness reduces the cardiovascular risk associated with higher CAC but does not eliminate that risk.
For an athlete aged 35 to 65, that supports a balanced approach. Fitness remains valuable. It simply should not be used as a substitute for considering family history or blood pressure, nor as a reason to dismiss lipid results or an existing CAC finding.
Reendure’s focus is on performance today and the ability to keep racing for decades. In that frame, cardiovascular assessment belongs alongside athletic ambition rather than in opposition to it. A risk discussion does not need to begin with the assumption that training has become a problem.
The useful conversation with a qualified clinician includes more than weekly hours or race performance. Holmer’s analysis points toward family history and blood pressure as relevant considerations. He also urges athletes to take lipids and elevated CAC seriously.
That does not require turning every training decision into a medical calculation. It means giving health information its own place rather than judging it through the training log alone. An athlete can value a strong season while also asking whether their cardiovascular risk assessment is appropriate.
For a personal appointment, questions consistent with this evidence include:
These are conversation starters rather than a screening protocol. Our discussion of approaching cardiovascular assessment as an athlete offers a related perspective on separating athletic performance from assumptions about heart health.
The ACC overview says an elevated CAC score alone does not require exercise restrictions when concerning symptoms are absent. That is a specific point about interpreting the score, not a blanket clearance for every athlete or every training situation.
Screening and training decisions should therefore remain individualized with a qualified clinician. The sources do not establish a universal program of scans or stress tests for asymptomatic endurance athletes. They also do not supply a weekly training ceiling that follows from these plaque findings.
For everyday planning, the practical task is to keep cardiovascular care within the broader picture of an athletic life. That fits with making room for training alongside other responsibilities. A sustainable approach leaves space for both sporting goals and informed health decisions without assuming that one must displace the other.
The athlete’s heart paradox does not demand a choice between endurance training and cardiovascular awareness. It challenges the assumption that being highly fit means being free of coronary plaque.
The evidence supports taking conventional risk factors seriously while retaining the overall value of exercise. For masters athletes, the modest takeaway is to discuss personal cardiovascular assessment with a qualified clinician rather than assume fitness settles the question. Keep athletic ambition, but give health information a place beside it.
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