Key result
Heavy endurance training increases the risk of atrial fibrillation by 3 to 8-fold in athletes, potentially driven by vagal enhancement, atrial dilation, and atrial fibrosis.
Exercise-induced atrial fibrillation in endurance athletes is likely driven by a combination of vagal enhancement, atrial dilation, and cumulative microstructural damage leading to atrial fibrosis, though significant knowledge gaps remain.
May warrant AF monitoring in endurance athletes; leaves open causal mechanisms and prevention strategies.
Exercise is an emerging cause of atrial fibrillation (AF) in young individuals without coexisting cardiovascular risk factors. The causes of exercise-induced atrial fibrillation remain largely unknown, and conclusions are jeopardised by apparently conflicting data. Some components of the athlete's heart are known to be arrhythmogenic in other settings. Bradycardia, atrial dilatation and, possibly, atrial premature beats are therefore biologically plausible contributors to exercise-induced AF. Challenging findings in an animal model suggest that exercise might also prompt the development of atrial fibrosis, possibly due to cumulative minor structural damage after each exercise bout. However, there is very limited, indirect data supporting this hypothesis in athletes. Age, sex, the presence of comorbidities and cardiovascular risk factors, and genetic individual variability might serve to flag those athletes who are at the higher risk of exercise-induced AF. In this review, we will critically address current knowledge on the mechanisms of exercise-induced AF.
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Guasch et al. (2018) conducted a review in Exercise-induced atrial fibrillation. Endurance exercise was evaluated. Heavy endurance training increases the risk of atrial fibrillation by 3 to 8-fold in athletes, potentially driven by vagal enhancement, atrial dilation, and atrial fibrosis.
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