Abstract
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.
Highlights
Atrial fibrillation (AF) is the most frequent sustained arrhythmia in the developed world, bearing a poor quality of life and increasing the risk of stroke and mortality
Is AF only a marker of extreme physical adaptation or is it associated with a pathological substrate? If so, do we have any evidence in humans of a deleterious effect of physical activity on cardiac structures? Why does the healthy exercise become harmful? Do illicit performance-enhancing substances play a role? While clinical and epidemiological evidence for exercise-induced AF is compelling, there is little evidence for a deleterious effect in the left ventricle: why do these cardiac chambers behave so differently? And, why do only a few
Middle-aged males who have been engaged in strenuous endurance training for more than 10 years and who are otherwise healthy, are at the highest risk of developing AF caused by exercise
Summary
Atrial fibrillation (AF) is the most frequent sustained arrhythmia in the developed world, bearing a poor quality of life and increasing the risk of stroke and mortality. Prevalence of AF has been steadily increasing in recent years, and the number of individuals with AF is expected to double by 2060 [1]. The cause of AF in these young patients with no cardiovascular conditions has been the focus of extensive research in recent years, and obstructive sleep apnoea, obesity, tall stature and genetic predisposition have all been associated with increased risk of AF [2, 3]. Do we have any evidence in humans of a deleterious effect of physical activity on cardiac structures? While clinical and epidemiological evidence for exercise-induced AF is compelling, there is little evidence for a deleterious effect in the left ventricle: why do these cardiac chambers behave so differently? Is AF only a marker of extreme physical adaptation or is it associated with a pathological substrate? If so, do we have any evidence in humans of a deleterious effect of physical activity on cardiac structures? Why does the healthy exercise become harmful? Do illicit performance-enhancing substances play a role? While clinical and epidemiological evidence for exercise-induced AF is compelling, there is little evidence for a deleterious effect in the left ventricle: why do these cardiac chambers behave so differently? And, why do only a few
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