The controversial relationship between exercise and atrial fibrillation

Abstract

Atrial fibrillation is the most common clinically significant arrhythmia observed both in the general population and in competitive athletes. The most important risk factors are all preventable by regular physical activity. However, although the benefits of moderate physical activity in controlling cardiovascular risk factors and decreasing the risk of atrial fibrillation have been extensively proved, concerns have arisen about the potential negative effects of vigorous exercise, particularly in endurance athletes. Furthermore, in a subset of patients with atrial fibrillation younger than 60 years, routine evaluation does not reveal any cardiovascular disease or any other known causal factor. This condition is called 'lone atrial fibrillation', and the potential mechanisms underlying this condition are speculative and remain to be clarified. Atrial ectopy, increased vagal tone, changes in electrolytes, left atrial dilatation, and fibrosis have been proposed among others as potential mechanisms. However, no convincing data still exist. Particularly, the increase in left atrial size represents in athletes a physiological adaptation to exercise conditioning and the presence of biatrial fibrosis has not been demonstrated in humans. Thus, contrary to patients with cardiovascular disorders, the atrial substrate seems to play a secondary role in healthy athletes. This review article analyzes the controversial relationship between atrial fibrillation and physical activity, with a particular attention on the pathophysiological mechanisms that could be responsible for atrial fibrillation in the athletic population.

Age modifies the risk of atrial fibrillation among athletes: A systematic literature review and meta-analysis

“…The mechanism by which competitive sports predisposes athletes to AF is still a matter of intense speculation. It has been proposed that AF initiation and perpetuation occur due to an interplay of triggers, modulators, and an appropriate substrate [ 23 , 24 ]. Excessive parasympathetic and sympathetic stimulation, such as occurs in athletes, can trigger atrial ectopy and shorten action potential duration, thereby initiating and sustaining AF [ 25 , 26 ].…”

“…Excessive parasympathetic and sympathetic stimulation, such as occurs in athletes, can trigger atrial ectopy and shorten action potential duration, thereby initiating and sustaining AF [ 25 , 26 ]. Chronic pressure and volume overload from increased cardiac output leads to adverse anatomic and electrophysiologic remodeling, characterized by biatrial dilation, inflammation and myonecrosis, fibrosis and non-homogenous conduction [ [23] , [24] , [25] , [26] , [27] , [28] , [29] ]. Conversely, moderate exercise has been shown to be protective against remodeling [ 30 ].…”

“…It appears that each of the triggers and substrates are necessary but not sufficient causes for AF. For example, it is unclear if increased atrial ectopy by itself leads to more AF in athletes [ 24 ]. Furthermore, Guasch et al [ 29 ] showed that exercise increased AF susceptibility, vagal tone, atrial enlargement and fibrosis in mice that exercised for 16 weeks.…”

Differential Association of Exercise Intensity With Risk of Atrial Fibrillation in Men and Women: Evidence from a Meta‐Analysis

“…For the majority of health outcomes, a dose‐response relationship is believed to exist; additional benefits occur as the amount of physical activity increases through higher intensity, greater frequency, and/or longer duration . However, earlier studies have revealed conflicting associations between exercise intensity and atrial fibrillation (AF), a common form of cardiac rhythm disorder . Some trials reported a J‐shaped or U‐shaped correlation between physical activity level and AF with increased risk in sedentary individuals and vigorously exercising men .…”

Pathophysiology of atrial fibrillation in endurance athletes: an overview of recent findings

“…5 Others have also suggested that some endurance athletes may experience extensive stiffening of the heart muscle, which might trigger atrial fribrillation at high-intensity exercise. 6 A recently emphasized concept is that of vagal atrial fibrillation, 7 which usually affects young patients with otherwise normal hearts.…”