Letter to the Editor

Does endurance exercise cause atrial fibrillation in women?

Higher levels of physical activity (PA) and cardiorespiratory fitness (CRF) are associated with lower risk of incident cardiovascular disease (CVD). However, the relationship of aerobic PA and CRF with risk of atherosclerotic CVD outcomes and heart failure (HF) seem to be distinct. Furthermore, recent studies have raised concerns of potential toxicity associated with extreme levels of aerobic exercise, with higher levels of coronary artery calcium and incident atrial fibrillation noted among individuals with very high PA levels. In contrast, the relationship between PA levels and measures of left ventricular structure and function and risk of HF is more linear. Thus, personalizing exercise levels to optimal doses may be key to achieving beneficial outcomes and preventing adverse CVD events among high risk individuals. In this report, we provide a comprehensive review of the literature on the associations of aerobic PA and CRF levels with risk of adverse CVD outcomes and the preceding subclinical cardiac phenotypes to better characterize the optimal exercise dose needed to favorably modify CVD risk.

It has been documented that physical activity may increase the risk of atrial fibrillation (AF) in active or former competitive athletes. Different mechanisms are involved and responsible for the development of the arrhythmia, such as structural changes of the left atrium, influences of autonomic nervous system with enhanced vagal tone, and the use of prohibited substances with arrhythmogenic effects. Difficulties in the management of AF in athletes may derive from the low compliance to antiarrhythmic therapy and the selection of the most appropriate strategy for thromboembolic risk prevention. In fact, the majority of athletes are young, healthy, without any particular risk factor, except for arterial hypertension which can be the only risk factor in the evaluation of antithrombotic therapy with the CHA₂DS₂-VASc score. The integration of actual score with serum biomarkers and other clinical factors may be useful to identify patients who will benefit the most from anticoagulation. Nowadays the non-vitamin K antagonist oral anticoagulants (NOACs) may represent a valid alternative to vitamin K antagonists (VKA) in the prevention of ischemic stroke due to AF with a better safety profile.

Atrial fibrillation (AF) is a recognised arrhythmic risk of endurance sports participation, predominantly affecting middle-aged men who are lifelong athletes. Affected athletes were historically included in the category of lone AF, although specific pathophysiological processes apply to this condition, referred to as exercise-related AF. Younger non-endurance athletes may also present with AF, particularly when associated with co-existing cardiomyopathy or arrhythmia syndrome.

Management of exercise-related AF is largely based on evidence from randomised trials in non-athletes. Cornerstones of treatment are, thus, thromboembolic risk reduction and risk factor modification. Rhythm control is generally preferred over rate control due to frequent presentation with symptomatic AF during the paroxysmal phase.

Many therapies specific to athletes are based on expert consensus alongside observational data in athletic populations. These include: recommendations to detrain; treatment of symptomatic oesophageal reflux; and preferential use of anticholinergic antidysrhythmic agents to address the predominance of “vagal” AF in athletes.

Ongoing research involving cardiac ion channel remodelling and systemic inflammation as mediators of AF genesis may provide future novel therapeutic targets for exercise-related AF. Ablative therapy shows promise in the athletic population with AF, although evidence remains limited. International consensus guidance for disqualification from competitive sports exists to guide medical management alongside athletes’ preferences to continue to participate.

This review focusses on isolated exercise-related AF and reviews the evidence supporting postulated management recommendations of this unique patient population.

Exercise has substantial health benefits with pleomorphic vascular, metabolic, psychological and anti-neoplastic actions resulting in improved quality of life and longevity. Despite these many benefits, numerous studies have shown that endurance athletes are more likely to develop atrial fibrillation (AF) than non-athletes.

The type, intensity and amount of sport appears to influence the risk of developing AF. Several endurance sport activities have been shown to increase the risk of developing AF but an excess in AF has not been shown in non-endurance sports. Furthermore, lifetime hours of participation appear to increase the risk of developing AF. Intriguingly, women appear relatively protected and an association between endurance sport and AF has not been clearly demonstrated amongst female endurance athletes.

The mechanisms by which endurance sport promotes the development of AF are unclear. There are, however, a number of pathophysiological mechanisms which are known to increase the risk of AF in non-athletes which have correlates in athletes. These include structural remodelling of the left atrium, elevated left atrial pressure, inflammation, myocardial fibrosis, vagal tone, sinus bradycardia and genetic predisposition. In this article, we explore how some of these mechanisms may contribute to the development of AF in endurance athletes.