Why the study?
Whether an upper limit exists for the cardiovascular benefits of exercise is unclear, prompting the need for a deeper mechanistic understanding of why lifetime high-volume endurance exercise is associated with increased coronary artery calcification.
What are the underlying molecular and cellular mechanisms explaining the paradox of increased coronary artery calcification in older men exposed to high volumes of endurance exercise?
What are the underlying molecular and cellular mechanisms explaining the paradox of increased coronary artery calcification in older men exposed to high volumes of endurance exercise?
This review explores the molecular and cellular mechanisms that may explain the paradoxical increase in coronary artery calcification observed in older male endurance athletes.
Hypothesis-generating for mechanisms of athlete coronary calcification; prospective studies required before clinical translation.
Regular exercise is widely known to exert beneficial effects on the cardiovascular system. Despite the widely accepted and numerous benefits of exercise, whether there is an upper limit to these benefits is unclear, particularly with regard to atherosclerotic disease. Observational cohort studies over the past 2 decades have identified a consistent signal of increased coronary artery calcification in older men, who have been exposed to high volumes of endurance exercise over their lifetime. The clinical ramifications of these findings are not fully known, as outcomes studies in these athletic populations are needed, but given the strong associations of coronary artery calcification with adverse cardiovascular events, a deeper mechanistic understanding of the link between endurance exercise and coronary artery calcification is needed. In this review, we describe the possible underlying mechanisms that may explain this conundrum of the athlete calcification paradox at the molecular and cellular levels.
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Hsu et al. (2025) studied this question.
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