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As physicians, we often face patients with cardiovascular risk factors or different kinds of heart disease. We prescribe statins, ACE inhibitors or β-blockers, but also (should) encourage our patients to engage in regular physical activity to reduce cardiovascular disease burden. Physical exercise, as a part of cardiac rehabilitation or a primary prevention programme, is seemingly one of a kind. ‘For most health outcomes, additional benefits occur as the amount of physical activity increases through higher intensity, greater frequency, and/or longer duration’.1 No other known therapy offers such advantageous characteristics. This even led some researchers to speculate, some 40 years ago, that marathon runners were immune to atherosclerosis.2 Running a marathon was quite unusual at that time, and cardiovascular adaptation to such a high load of exercise had been scarcely explored. Since then, the late 70s, the number of non-professional runners finishing a marathon has increased 20-fold, and current observational studies are jeopardising the notion of exercise as risk-free. Increased sudden death risk during exercise bouts is well established but extremely rare. An evolving core of evidence supports the hypothesis that regular exercise increases the risk of atrial fibrillation (AF), ventricular arrhythmias or even ischaemic heart disease.3 How do these findings fit with the well-known benefits of exercise? Two papers explore this subject4 ,5 and provide important insights.
By assessing outcomes such as AF incidence4 and cardiovascular or total mortality,5 both groups elegantly suggest in two large cohorts that exercise intensity and duration are key players in this association. They describe a similar U-shaped or reverse J-shaped pattern for the dose–response effect of exercise: maximum cardiovascular benefits are obtained if performed at moderate doses, while these benefits are lost with (very) high-intensity and prolonged efforts.
Both groups took previously collected data on exercise performance …
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