Mechanisms of atrial fibrillation in athletes: what we know and what we do not know

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.

Keywords: Atrial fibrillation; Atrial fibrosis; Endurance; Exercise; Vagal tone.

Fig. a

Schematic representation of the potential mechanisms underlying exercise-induced atrial fibrillation represented in a Coumel’s triangle of arrhythmogenesis, and their functional consequences

Fig. 1

Schematic representation of the potential mechanisms underlying exercise-induced atrial fibrillation represented in a Coumel’s triangle of arrhythmogenesis, and their functional consequences

Fig. 2

Potential factors leading to a pathological atrial remodelling in athletes (atrial fibrosis). Systemic blood pressure and, particularly, pulmonary pressure promote an increase in atrial intracavitary pressure during exercise. In the presence of chronically dilated atria and limited ability to increase wall thickness, atrial wall stretch has remarkably increased, which may promote the activation of profibrotic mechanisms. A pro-inflammatory status during each exercise bout and intake of an illicit performance enhancer may also contribute. RA right atrium, LA left atrium

Fig. 3

Representation of the factors contributing to the balance between the antiarrhythmic and the pro-arrhythmic effect of exercise