THE ARISING · Longevity & Healthspan
Review Weighs Whether Years of Intense Endurance Training Harm Athletes' Arteries
Exercise is among the best-established ways to protect the heart. Yet a new review asks an uncomfortable question: do years of very hard endurance training leave some athletes with more calcium in their heart arteries than expected?

The paper is a narrative review, published in 2026 in the Journal of Clinical Medicine by Z. Kampka and M. T. Wybraniec. It pulls together existing research on coronary artery disease (CAD) in male athletes. It does not report a new trial or new participant data, and it does not give a single sample size. The authors searched PubMed, Scopus and Web of Science and gave priority to original studies, meta-analyses, systematic reviews and clinical guidelines.
The headline figure is a wide range. According to the review, studies find coronary plaques or CAD in 13.7% to 71% of middle-aged male endurance athletes. The authors say that spread reflects differences in study design, age, race, cardiovascular risk profiles, and the type, intensity and total amount of training. Studies of older veteran endurance athletes report more CAD than studies of younger athletes. The authors stress that athletes are a mixed group, and the CAD seen cannot be blamed on exercise alone.
The review says research on physical activity and coronary artery calcification (CAC) gives mixed results. Some studies find less calcium with more activity. Others find a Uor J-shaped pattern, a positive link, or no link. Still, the authors report that higher calcium scores are common in athletes who do high volumes of endurance training.
Why might that happen? The authors say the cause is probably multifactorial, and the relationship is not well established. Possible contributors include stress from blood flow on artery walls, extra reactive oxygen species (unstable oxygencontaining molecules), inflammatory mediators, and repeated short rises in parathyroid hormone, which helps control calcium. Testosterone is also discussed. The review says normal levels do not seem to harm the heart, but abuse of anabolic– androgenic steroids builds up plaque. It adds that calcification is mostly seen in male athletes. These are proposed mechanisms, not proven ones. The authors note some of the supporting studies are small.
The review also offers some reassurance. It says athletes have better coronary vasodilatory capacity (the arteries widen well) and more coronary collateralization (extra small vessels that can route blood around a narrowing). Because of this, athletes are rarely affected by blockages that significantly limit blood flow. Their plaques are mostly of a benign, calcified type. The authors also note that earlier risk factors such as smoking, high blood pressure and high cholesterol are not erased by taking up more sport.
Even so, CAD matters. The review says it is responsible for the majority of sudden cardiac death in athletes over 30, and for over 95% of such cases in athletes over 40. The authors note that standard risk estimates may underestimate risk in athletes. A CT scan that measures a coronary calcium score may help.
On screening, the basics are medical history, a cardiovascular risk assessment and a resting electrocardiogram (ECG). The review calls resting ECG imperfect but more sensitive than history and physical examination alone. There are no official guidelines for managing athletes with no symptoms but calcium on imaging. The 2020 European Society of Cardiology guidelines advise screening master athletes over 35 based on symptoms and maximal exercise test results. The authors warn that people with mild to moderate plaques may go unidentified.
Exercise stress ECG has limits in athletes, because their strong vasodilatory capacity can hide disease. In the SEEPRED study, as described by the review, it was useful in high-risk athletes over 35 with at least two risk factors. There it had a negative predictive value above 99%, sensitivity of 77% and specificity of 93%. The authors suggest it may be considered in athletes with a calcium score of 400 Agatston units or more, or narrowing above 50%. They add that tests may need to run to maximal capacity rather than stop at a preset heart rate.
This is a review focused on men, and it cannot show that training causes plaque. What it does show is that the question is open and that screening in serious older athletes lacks firm guidance. Researchers will need larger studies that track athletes over time to sort out how training amount, risk factors and calcium relate to real heart outcomes.
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