Article Text

Download PDFPDF

Atrial fibrillation in endurance-trained athletes
  1. A V Sorokin1,
  2. C G S Araujo2,
  3. S Zweibel1,
  4. P D Thompson1
  1. 1Division of Cardiology, Hartford Hospital, University of Connecticut School of Medicine, Hartford, CT, USA
  2. 2Clinica de Medicina do Exercico, Rio de Janeiro, Brazil
  1. Correspondence to Dr P D Thompson, Cardiology, Hartford Hospital, 81 Seymour Street, Hartford, CT 06102, USA; pthomps{at}


Background Endurance exercise training produces multiple cardiac adaptations including changes in electrophysiological function that may make endurance-trained athletes more vulnerable to atrial fibrillation (AF). This possible association is not recognised by many practising cardiologists and sports physicians. Consequently, we performed a literature review to examine the relationship between atrial fibrillation and endurance exercise training among athletes. PubMed was searched from January 1960 through December 2008 to identify articles examining the relationship between endurance exercise training and AF.

Results Evidence suggests that athletes are at increased risk for development of AF. Possible factors increasing AF in this population include increased parasympathetic tone, reduced sympathetic tone, increased atrial size and increased inflammation.

Discussion Suggested management of AF in athletes should follow similar principles to those used to manage AF in the general population.

View Full Text

Statistics from

Endurance exercise training produces multiple cardiac adaptations including changes in sinus node function, atrial electrophysiological properties and atrioventricular node (AV) conduction.1 These changes are related to enhanced resting parasympathetic tone and may make endurance trained athletes more vulnerable to atrial fibrillation (AF).1 This possible association is not recognised by many practising cardiologists and sports physicians. Consequently, we performed a literature review to examine the relationship between atrial fibrillation and endurance exercise training among athletes.


English-, German- and Spanish-language articles addressing the relationship between athletic physical training and atrial fibrillation (AF) were identified by searching PubMed from January 1960 through December 2008 using the key words “atrial fibrillation,” “athlete,” “physical training” and “autonomic nervous system” alone and in various combinations. Abstracts were reviewed, and those articles pertinent to AF and endurance exercise training were reviewed in full. Endurance exercise training was defined as physical activity requiring prolonged exercise at a sustained increased heart rate. No articles were identified discussing AF in non-endurance athletes, except one cross-sectional study2 that included two weight lifters.

Frequency of atrial fibrillation in athletes

Few studies and reviews have examined the frequency of atrial fibrillation among athletes (table 1). A cross-sectional study2 compared the frequency of lone atrial fibrillation between athletes and the general Catalonian population with similar demographic characteristics. Seventy patients <65 years of age with lone atrial fibrillation (LAF) were identified from an arrhythmia outpatient clinic.2 Of the 70 LAF patients, 32 were either habitually endurance trained (n = 30) or weight lifters (n = 2). LAF was considered vagally mediated if it occurred nocturnally or postprandially,3 since vagal tone is increased both during sleep and after meals. Athletes were more likely to have vagally mediated AF than sedentary subjects (57% vs 18% p<0.01). The proportion of athletes with lone AF was significantly higher than that reported in the comparison group (63% vs 15%; p<0.05).2

Table 1

Incidence and prevalence of atrial fibrillation (AF) in endurance athletes

Some of these same authors2 also compared 51 consecutive outpatient men with LAF and 109 patients from the general population.3 It is not clear how many from this larger LAF sample were included in the authors’ prior study.2 Patients with LAF were more than three times more likely to be athletes than were the comparison subjects (odds ratio (OR) = 3.13, 95% CI 1.39 to 7.05 p = 0.006). Vagally mediated LAF was present in 20 of the athletes and was more frequent in the athletes than in the control group (OR = 3.13, 95% CI 1.4 to 19.0, p = 0.046).

A retrospective cohort study4 compared the incidence of AF in a group of marathon runners (n = 252) and a population-based sample of sedentary men (n = 305) recruited in 1990–2 and followed up in 2002–3. The annual incidence rate of LAF among marathon runners and sedentary men was 0.43/100 and 0.11/100, respectively. Endurance sport practice was associated with a higher risk of incident LAF in the multivariate age- and blood pressure-adjusted Cox regression models (heart rate = 8.80; 95% CI 1.26 to 61.29). In the group of marathon runners, left atrial diameter and left atrial volume were both associated with a higher risk of incident LAF.

An additional case control study5 compared questionnaires obtained in 1985 and 1995 from 300 top-ranked orienteers (mean age at baseline 47.5 years) and 495 healthy men (mean age at baseline 49.6 years). The questionnaire queried physical activity history and the occurrence of AF. The orienteers without known AF risk factors experienced more episodes of AF than controls (5.3% vs 0.9%; p = 0.012) although mortality was significantly lower over the 10-year follow-up in the orienteers. (1.7% vs 8.5%; p = 0.05).

These studies suggest that AF is more common in athletes, but larger cross-sectional and prospective studies using additional cohorts are required to further confirm this hypothesis.

Factors possibly contributing to AF in athletes

Parasympathetic tone

Resting bradycardia mediated by increased parasympathetic and reduced sympathetic tone at rest is characteristic of aerobically trained athletes.6 Augmented vagal tone shortens the atrial refractory period7 by decreasing inward current through L-type calcium channels.8 A shortened refractory period or slowed conduction shortens the excitation wavelength and thus facilitates re-entry. This is thought to be the core mechanism of atrial fibrillation induction when vagal tone is predominant.7

Analysis of heart rate variability (HRV) from electrocardiographic monitoring has provided the most relevant information about activity of both branches of the autonomic nervous system immediately preceding the onset of AF.9 There are multiple studies and experimental models suggesting that vagal stimulation shortens the atrial effective refractory period (AERP) and increases AERP heterogeneity.10 11 However, these data may not be applicable to an endurance athlete population, since changes in AERP due to vagally mediated bradycardia among athletes have not been studied.

Sympathetic tone

As noted above1 3 vagally influenced AF appears more common in athletes. Adrenergic stimulation can also induce AF primarily in association with vigorous physical exertion. Increased sympathetic activity shortens the atrial action potential, which increases the risk of AF, but most authorities suspect that sympathetically induced micro-re-entry due to adrenergic stimulation during exercise is more likely to produce AF in this situation.12

Structural and metabolic factors contributing to AF

Atrial enlargement

Endurance exercise training is associated with increased left and right atrial size.13 The clinical significance and long-term arrhythmic consequences of left atrial (LA) enlargement in competitive athletes have been widely debated in the literature and remain unresolved.13 An association between the increased atrial size and AF has not been shown in recent cross-sectional analysis among professional athletes.13 LA dimensions and the prevalence of supraventricular tachyarrhythmias were evaluated in 1777 competitive athletes free of structural cardiovascular disease. The diagnosis of AF was considered when the athlete had experienced prolonged palpitations either during exercise or at rest confirmed by the occurrence of AF by 24 h ECG monitoring or exercise testing or induced by electrophysiological study. AF was documented in 0.28% of athletes with, and 0.27% of athletes without, LA enlargement (defined as an LA transverse dimension of 40 mm). Atrial fibrillation can be transient and asymptomatic, and thus very difficult to detect with standard ECG or even ambulatory ECG monitoring.14 Therefore, athletes with asymptomatic or nocturnal intermittent AF would not have been included in this analysis.

AF can also occur in patients who have regular rate tachycardia such at AV nodal reentrant tachycardia.15 A significant portion of such patients with AF and other regular tachycardia have accessory pathways that can be treated with radiofrequency ablation.

Inflammatory markers

Prolonged, intense endurance exercise acutely increases serum concentration of the inflammatory markers: IL-6 and C reactive protein (CRP).16 Despite this acute inflammatory reaction, regular moderate endurance exercise training generally reduces inflammatory markers.16 although high-intensity exercise such as a marathon race may transiently produce a sustained systemic inflammatory response17 and elevated CRP levels.18 Epidemiological studies have noted an association between elevated CRP levels and both the presence of AF and the future risk of developing AF.19 Such observations suggest that sustained intense over training could produce a chronic inflammatory response in athletes that increases their risk for AF.20 This concept is speculative because we know of no studies linking AF and inflammation in athletes.

Management of AF in endurance athletes

Although AF may be more common in normal, healthy athletes1,,5 the initial evaluation of athletes with AF should exclude metabolic, pharmacological and structural causes. Hyperthyroidism is a well-recognised cause of AF and must be excluded in all AF patients, especially those with newly diagnosed, persistent AF.21 Sympathomimetic agents including legal sympathomimetics in over-the-counter cold remedies, stimulants such as caffeine and illegal sympathomimetics such as cocaine should be considered and excluded as a possible cause of AF in athletes. The use of anabolic steroids alone or in combination with creatinine has been associated with AF.22

The ECG in athletes with intermittent AF should be examined for evidence of any cardiac disease that can provoke AF including pericarditis, hypertrophic cardiomyopathy, and an acute cardiac event. In addition, the ECG should be examined for a delta wave which reveals the presence of accessory pathway conduction such as that seen with the Wolff–Parkinson–White (WPW) ECG pattern. AF in such patients can lead to rapid conduction down the accessory pathway and ventricular fibrillation. Athletes with newly diagnosed WPW must have the conduction velocity of their accessory pathway evaluated by either non-invasive or invasive testing before the athlete is allowed to participate in training or competitive athletics.23 There is no need to exclude an athlete from an athletic activity if they cannot conduct rapidly along the accessory pathway. Consequently, athletes with both regular tachycardia and AF should be considered for electrophysiolgical study if their symptoms are difficult to manage medically.

An echocardiogram with Doppler interrogation should also be obtained in athletes with AF to exclude valvular pathology, hypertrophic cardiomyopathy24 and other structural abnormalities. Five of 19 athletes evaluated for palpitations had paroxysmal AF,25 and were evaluated by resting electrocardiography, echocardiography and electrophysiological studies. Mitral valve prolapse (MVP) was reported in four athletes and WPW syndrome in one. This article probably overestimated the frequency of MVP in such patients, since it was published when diagnostic criteria for MVP were less stringent.

Once metabolic, pharmacological and structural causes of AF are excluded, management depends primarily on symptoms and persistence of the arrhythmia.

Intermittent AF

The frequency of symptomatic AF episodes is best determined by an event recorder. If the AF is frequent and symptomatic or infrequent and highly symptomatic, we attempt to suppress the AF pharmacologically. Since AF is often vagally mediated in endurance athletes,6 we use flecainide 50 mg twice or three times daily, since flecainide is especially useful in preventing AF associated with high vagal tone. Encainide, a compound similar to flecainide, increased cardiac deaths in the CAST-I trial,26 a study of individuals after myocardial infarction. Consequently, flecainide should be avoided in athletes with structural heart disease. Also, flecainide can increase the velocity of A-V conduction, and therefore the ventricular rate if 1:1 A-V conduction of atrial flutter should occur so flecainide should be given with an agent to reduce A-V conduction such as a beta-blocker or calcium-channel blocker in patients with either AF or atrial flutter. Calcium blockers are often preferable in athletes, since beta blockers may not be well tolerated or permitted in athletes.

Persistent AF

In athletes with persistent AF, the approach is dependent on the duration of the atrial fibrillation. The key concern with cardioversion in persistent AF is the risk of systemic embolisation. If the athlete is known for certain to have been in atrial fibrillation for less than 48 h, the athlete can be cardioverted promptly without prolonged systemic anticoagulation. Left atrial thrombus and systemic embolism have been documented in patients with AF persisting for less than 48 h, but the need for anticoagulation is not clear in this instance.27 On the other hand, if the AF is of unknown duration or greater than 48 h, the athletes should be anticoagulated with warfarin for at least 3 weeks prior to and 4 weeks after cardioversion. A transesophageal echocardiogram can be performed before cardioversion to exclude the presence of atrial thrombus. This may permit more rapid cardioversion in a patient whose duration of AF is unknown. Nevertheless, since it may take several days to weeks for atrial contraction to return, the absence of thrombus before cardioversion does not exclude the development of thrombus during this ensuing period, and anticoagulation should still be considered.

According to the current guidelines,23 an athlete with a first episode of AF should have a period of detraining for 3 months to achieve and maintain sinus rhythm. Competitive sports can be resumed once sinus rhythm has been maintained for 3 months. This time period can be negotiated depending on the athlete and the clinical situation. We frequently restrict athletic training for only 1–2 weeks with the first episode.

Intermittent AF carries the same risk of embolisation among the general population as does sustained AF,28 so that the decision as to whether or not to anticoagulate a non-athletic patient depends on the presence of embolic risk factors such as structural cardiac disease, hypertension, age 75 years, congestive heart failure and diabetes mellitus.29 Accumulation of risk factors enhances the prothrombotic state in atrial fibrillation but not the persistence of the AF. We are unaware of any data on the incidence of stroke in otherwise healthy athletes without structural heart disease and with paroxysmal LAF. Consequently, the decision to administer long-term anticoagulation therapy in an active athlete must be based on guidelines applicable to the general population. Most athletes with AF are healthy, usually lack risk factors for systemic embolisation and therefore do not require sustained anticoagulation. Long-term anticoagulation therapy excludes an athlete from participation in sports with a risk of bodily collision.23 Aspirin, 81–325 mg daily, is recommended as an alternative to vitamin K antagonists in low-risk patients or in those with contraindications to oral anticoagulation.27

If AF is persistent, recommendations for competitive sports participation largely depend on the ventricular rate during exertion and the athlete's ability to participate in activity during the episodes.23 Beta-adrenergic and calcium-channel blocking agents are recommended for rate control, sometimes in combination.23 It must be noted, however, that the use of beta-blockers is banned from some competitive sports,30 and so the use of this medication requires a therapeutic use exemption from governing antidoping agencies in certain competitive sports.

Ablation therapy

Radiofrequency ablation is an additional attractive treatment approach in athletes with AF whose symptoms and episodes cannot be adequately controlled with medications.27 There are no current outcome data available on efficacy of left atrial ablation and pulmonary vein isolation in active endurance athletes with AF, although it is possible that athletes may have higher recurrence rates of AF compared with the general population. A study by Heidbüchel et al showed that athletic participation may be a risk factor for atrial flutter (AFL) recurrence after AF/AFL ablation therapy.31 Athletes who are candidates for oral anticoagulation prior to an ablation procedure will likely remain so after the procedure. Therefore, an ablation procedure should not be recommended in these patients with the goal being discontinuation of anticoagulation therapy.


Evidence suggests that athletes are at increased risk for development of AF, but this has been examined in only a few studies, and this conclusion has not been established with certainty. Increased AF in athletes is likely due to changes in autonomic tone including increased parasympathetic tone at rest and increased sympathetic tone during exercise. Management of AF in athletes should follow guidelines provided for the general population.


View Abstract


  • Competing interests None.

  • Provenance and Peer review Commissioned; not externally peer reviewed.

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.