JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 3, NO.

9, 2017

ª 2017 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION ISSN 2405-500X/$36.00

PUBLISHED BY ELSEVIER http://dx.doi.org/10.1016/j.jacep.2017.03.019

STATE-OF-THE-ART REVIEW

Atrial Fibrillation in Athletes

A Lesson in the Virtue of Moderation

N.A. Mark Estes III, MD, Christopher Madias, MD

ABSTRACT

Although the cardiovascular benefits of moderate exercise are well established, there is growing epidemiological support
for the notion that high-intensity endurance athletics increases the risk of atrial fibrillation (AF). There are many gaps in
evidence related to epidemiology and mechanisms of AF in endurance athletes. The proposed pathophysiological
mechanisms include alterations of autonomic tone, electrical remodeling, anatomical remodeling, fibrosis, and inflam-
mation. Clinical management of the athlete with AF often includes a period of decreased frequency, intensity, and
duration of exercise with assessment for improvement in AF recurrence. Based on symptoms, a strategy of rate or rhythm
control should be selected; however, due to side effects and intolerance of medications, ablation may be a preferred
approach. The risks and benefits of anticoagulation for stroke prevention must be carefully assessed in the athlete with
AF. All patients should be encouraged to be physically active with moderation; however, men should be advised of the
higher risk of AF with long-term, high-intensity endurance training. (J Am Coll Cardiol EP 2017;3:921–8)
© 2017 by the American College of Cardiology Foundation.

T
dén ágan) is
he phrase “ mhdέn ά gan ” (m e
carved into the Temple of Apollo at Delphi.
This ancient Greek proverb—“nothing in
excess”—characterizes the belief that a healthy life is
achieved by following the principle of moderation.
Atrial fibrillation (AF) in the high-intensity endurance
athlete brings to the forefront the concept that even
healthy behaviors may have detrimental effects
when they are performed in excess. Although athletes
with AF represent a small subset of all patients with
this common arrhythmia, this niche athletic popula-
tion intrigues the medical community and public. His-
torically, and in contemporary culture, athletes are
symbols of health. Exercise as a driver in the patho-
physiology of arrhythmia stands out as an apparent
contradiction of the known cardiovascular benefits
of physical activity (1–6). Exercise decreases the risk
of cardiovascular disease by reducing hypertension,
diabetes mellitus, and obesity (1–6). The benefits of
exercise also include improvements in the lipid pro-
file, insulin sensitivity, and all-cause mortality (1–6).
Advanced levels of endurance training are widely
believed to further improve these health outcomes;
however, it remains controversial whether there is in-
cremental benefit over moderate exercise (1–6).
Because of the robust objective evidence that supports
the health benefits of exercise, the paradox that phys-
ical activity may also promote adverse cardiovascular
effects merits careful consideration. Although many
gaps in current knowledge persist regarding the epide-
miology, mechanisms, and management of AF in ath-
letes, clinicians must use the best available evidence
to care for this unique patient population (7–31).
EPIDEMIOLOGY
A considerable body of evidence has emerged
that supports an increased incidence of AF in

From the New England Cardiac Arrhythmia Center, The Cardiovascular Center, Tufts Medical Center, Tufts University School of
Medicine, Boston, Massachusetts. The authors have reported that they have no relationships relevant to the contents of this paper
to disclose.
All authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’
institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information,
visit the JACC: Clinical Electrophysiology author instructions page.

Manuscript received December 12, 2016; revised manuscript received March 20, 2017, accepted March 23, 2017.
922 Estes III and Madias
Atrial Fibrillation in Athletes
ABBREVIATIONS high-intensity endurance athletes (7–31).
AND ACRONYMS Several case–control studies and retrospec-
tive analyses first demonstrated a higher
AF = atrial fibrillation
prevalence of AF associated with long-term
CI = confidence interval
vigorous training (12,13). Since these re-
OR = odds ratio
ports, additional studies and subsequent
meta-analyses have supported these findings (7–31).
Based on the available data, the frequency of AF has
been estimated to be 2 to 10 times greater in high-
intensity endurance athletes versus sedentary in-
dividuals; however, the bulk of this evidence has the
limitations of being retrospective and observational
(7–31). In addition, much of these data have been
gathered in relatively small populations of athletes.
The latter limitation has been addressed in larger
studies. The Physicians’ Health Study prospectively
analyzed the amount and type of physical exercise
and the subsequent risk of AF in 16,921 apparently
healthy men. Vigorous exercise was associated with
an increased risk of developing AF in young men
(younger than 50 years of age) and joggers (26).
Compared with men who did not exercise vigorously,
men who jogged 5 to 7 times per week had a signifi-
cantly increased risk of developing AF (risk ratio [RR]:
1.53, 95% confidence interval [CI]: 1.12 to 2.09; p <
0.01). These observations were also supported by a
Norwegian longitudinal study of 162,078 women and
147,462 men (27). The investigators found that 575
(0.4%) men and 288 women (0.2%) were classified as
having AF. The risk of AF increased with levels of
self-reported physical activity (27). The frequency of
cardiac arrhythmias was also assessed in >52,000
competitive cross-country skiers in Sweden (17). AF
occurred in 681 skiers (hazard ratio [HR]: 13.2; 95% CI:
12.3 to 14.3/10,000 person-years at risk). The fre-
quency of AF in this cohort increased in proportion to
the number of completed 90-km races (HR: 1.29; 95%
CI: 1.04 to 1.61 for $5 completed races vs. 1 completed
race) (17). In another large cohort of cross-country
skiers, the investigators noted a 26% increase in the
risk of lone AF for every decade of training (odds ratio
[OR]: 1.26; 95% CI: 1.10 to 1.44). Other studies also
supported the concept of an apparent threshold ef-
fect, with >1,500 to 2,000 lifetime training hours
required to heighten the risk of AF (8,13,14,18).
Systematic reviews and meta-analyses provided
further useful insights into many aspects of the
epidemiology of AF in athletes (7,17,25,28,29).
Although inclusion and exclusion criteria varied, and
there was some overlap of studies among these meta-
analyses, there was a consistency of conclusions. One
meta-analysis directly assessed whether the risk of
AF was higher in athletes versus risk of AF in non-
athletes (7). This analysis of 6 case–control studies
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SEPTEMBER 2017:921–8
included 655 athletes and 895 control subjects (7).
The rate of AF was significantly higher in the athletes
compared with control subjects (OR: 5.29; 95% CI:
3.57 to 7.85; p ¼ 0.0001) (7).
In a more recent systematic review, meta-analysis
of 6 casecontrol studies showed that the risk of AF
increased >5-fold in athletes compared with nonath-
letic control subjects (OR: 5.3; 95% CI: 3.6 to 7.9;
p < 0.0001) (28). In a separate meta-analysis of 3 pro-
spective long-term studies that compared the effects
of intensity of exercise, moderate or high habitual
physical activity was associated with a significantly
reduced risk of AF compared with low intensity or no
physical activity (OR: 0.89; 95% CI: 0.83 to 0.96;
p < 0.0001) (28). The authors concluded that long-
term vigorous physical training or lack of physical
activity were both associated with an increased risk of
AF. In contrast, habitual moderate physical activity
was associated with reduced risk (28). Based on
observations in individual studies and meta-analyses,
the concept of a “J-shaped” pattern describing the
relationship between exercise and AF has been
advanced (21–29). Regular exercise of mild to moder-
ate intensity provides protection from cardiovascular
disease and AF, whereas more sustained endurance
exercise may increase the AF burden (7–29).
Much of the reported data on exercise and AF have
been largely focused on men. A recent meta-analysis
of the relationship of AF to exercise suggested there
may be a sex-specific effect (29). Although moderate
physical activity was protective in men (OR: 0.81; 95%
CI: 0.26 to 1.004; p ¼ 0.06), vigorous physical activity
was associated with a significantly increased AF risk
(OR: 3.30; 95% CI: 1.97 to 4.63; p ¼ 0.0002) (29). In
contrast, pooled analysis of data from 149,048
women showed those involved in moderate physical
activity had a 8.6% lower risk of developing AF (OR;
0.91; 95% CI: 0.77 to 0.97; p ¼ 0.002); intense exercise
was even more protective, imparting a 28% lower risk
of AF compared with sedentary control subjects (OR:
0.72; 95% CI: 0.57 to 0.88; p < 0.001) (29). These ob-
servations led the investigators to conclude that a
sedentary lifestyle significantly increases AF risk in
both sexes, whereas moderate amounts of physical
activity reduces that risk. In contrast, it was sug-
gested that intensive exercise might have a sex-
specific association with AF risk (Figure 1) (29). It
was likely that these differences were previously
overlooked because this analysis included 4 studies
that included only women.
Much more work is required to shed light on the
influences of sex, genetics, ethnicity, type of exercise,
physical activity threshold, and other variables on the
risk of exercise-induced AF. Clinicians should be
JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 3, NO. 9, 2017
SEPTEMBER 2017:921–8
F I G U R E 1 Association Between Level of Physical Activity and
Risk of AF in Men and Women
A sedentary lifestyle is associated with an increased risk of atrial
fibrillation (AF) for both men and women, whereas moderate
exercise reduces this risk regardless of sex. High-intensity exer-
cise appears to increase risk of AF in men. Reprinted with
permission from Mohanty et al. (29).
mindful of the incomplete understanding of the
epidemiology of exercise-induced AF in counseling
patients about the intensity of physical activity.
PATHOPHYSIOLOGY
Clearly, there are multiple knowledge gaps regarding
the pathophysiological mechanisms that underlie the
development of AF in athletes. Proposed mechanisms
include alterations of autonomic tone, left atrial
enlargement and fibrosis, electrical remodeling, and
increased inflammation (30–47). Although these
mechanisms are complex and likely vary among in-
dividuals, there is a growing consensus that common
elements include autonomic, structural, and electro-
physiological remodeling that predispose to triggered
activity arising from the pulmonary veins or reentry
within the atrial tissue (30–47).
Clinical studies demonstrated that at rest and
during low-intensity physical activity, endurance
athletes have dominant vagal tone compared with
nonathletes (30–32). Recently, the association of
Estes III and Madias 923
Atrial Fibrillation in Athletes
increased vagal tone and low heart rates with the
incidence of AF was demonstrated to be particularly
strong in physically fit men (46). Enhanced vagal ac-
tivity is known to shorten the atrial refractory period
through activation of the iKach channel
(31,33,34,39,42). It was postulated that a vagal-
induced decrease in the refractory period and
slowed atrial conduction velocity could facilitate
reentry. Alterations of autonomic tone, including an
intermittent exercise-related increase in sympathetic
tone in endurance athletes, might also predispose to
AF (40–44). Increased basal vagal activity coupled
with adrenergic activation might precipitate AF
(42,45).
Mechanical and electrophysiological remodeling
was noted in endurance athletes (46–48). Bi atrial
enlargement commonly accompanies competitive
athletic training (46–48). Although echocardiographic
studies showed that left atrial dilatation occurs in up
to 20% of athletes, this finding was not associated
with an increase in AF prevalence in younger athletes
(46,47). In contrast, physical activity, height, and left
atrial size were noted to be independent risk factors
for lone AF in middle-aged healthy individuals (24).
Proposed pathophysiological mechanisms for a dif-
ferential sex response in AF are speculative (28).
These include smaller atria, shorter P-wave duration,
and lower left ventricular mass and wall thickness in
women, as well as differences in autonomic tone
compared with high-intensity male athletes (29).
In many athletes, AF occurs nocturnally when
vagal tone is more pronounced (41). In these in-
dividuals, sinus bradycardia and atrioventricular
block are commonly noted during sleep (41,42). These
observations have advanced the notion of a distinct
clinical syndrome of vagal-induced AF (41). Although
vagal AF has no universal definition, etiology, or
diagnostic criteria, it is believed to be a distinct clin-
ical syndrome (41).
Animal studies also support the notion that
exercise-induced AF results from adverse mechani-
cal, anatomical, and electrophysiological remodeling
(33,34). In a rat model of endurance athletics,
exercise-induced left atrial remodeling with an in-
crease in left atrial fibrosis was noted (34). Among the
signaling pathways potentially involved in this pro-
cess are those associated with transforming growth
factor beta 1, the renin-angiotensin-aldosterone
system, and oxidative stress (35). A role of tissue
necrosis factor in mediating fibrosis has also been
indicated (35). Animal studies have demonstrated
that inflammation plays a role in exercise-induced
atrial collagen deposition (38). High-intensity ath-
letic activity results in elevations of factors associated
924 Estes III and Madias
Atrial Fibrillation in Athletes
C E NT R AL IL L U STR AT IO N Proposed Pathophysiologic Mechanisms of AF in the Endurance Athlete
Estes III, N.A.M. et al. J Am Coll Cardiol EP. 2017;3(9):921–8.
Multiple factors contributing to atrial fibrillation (AF) with intense endurance exercise are shown with color coding according to the strength of the supporting evidence.
PV ¼ pulmonary vein.
with increased oxidative stress and inflammation,
which can contribute to atrial fibrosis (37,46). The
potential mechanisms through which exercise might
induce AF are shown in the Central Illustration.
CLINICAL EVALUATION AND MANAGEMENT
OF AF IN THE ENDURANCE ATHLETE
One of the fundamental tenets of evidence-based
medicine is that clinical practice is based on robust
data derived from appropriately designed clinical
trials. Although these standards are met with pro-
spective randomized clinical trials that evaluate rate,
rhythm, and anticoagulation strategies for AF, no
clinical trials are available specifically for exercise-
related AF (49–51). Consequently, clinical manage-
ment is based on extrapolation from nonathletic
populations, observational data, and expert opinion
(49–51). With these limitations in mind, the initial
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SEPTEMBER 2017:921–8
approach is to assess the athlete with a detailed his-
tory, with particular emphasis on the relationship of
AF to exercise and to AF-related symptoms (49–51). A
detailed social history, including the use of illicit and
performance enhancing drugs, is essential. Physical
examination, electrocardiography, and thyroid func-
tion tests should be performed. Echocardiography
and selected use of magnetic resonance imaging can
be useful to assess for structural heart disease,
including dilated cardiomyopathy, ventricular
dysplasia, and hypertrophic cardiomyopathy. In
young patients with AF, inherited channelopathies
and the presence of bypass tracts must be considered.
Ambulatory monitoring to assess the AF burden,
ventricular rate control at rest and with exercise,
and arrhythmia-related symptoms is useful clinical
information (49–51). Stress testing can be selectively
done to assess for AF rates with exercise and func-
tional capacity, and for ischemia, as clinically
JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 3, NO. 9, 2017
SEPTEMBER 2017:921–8
F I G U R E 2 Evaluation and Management of AF in the Endurance Athlete
Clinical evaluation and management of the endurance athlete is shown related to rhythm versus rate control, anticoagulation, and athletic
participation. ECG ¼ electrocardiogram; ETT ¼ exercise treadmill test; TSH ¼ thyroid-stimulating hormone; other abbreviation as in Figure 1.
indicated. Figure 2 depicts the clinical evaluation and
management of the athlete with AF.
A common clinical recommendation is to have the
athlete with symptomatic AF reduce the duration and
intensity of exercise up to 3 months to assess the
relationship of exercise to AF. This approach is based
solely on anecdotal evidence and expert opinions
(30,45,52). One study of 1,772 athletes with a follow-up
of 5 years noted a marked decrease in AF with decon-
ditioning (45). Another investigator noted a marked
improvement in AF symptoms with abstinence from
athletics (48). Notably, these observational studies
lacked randomization, blinding, standard definitions
of deconditioning, objective assessment of athletic
restriction, or rigorous AF monitoring. Despite the lack
of robust evidence, a commonly used initial clinical
approach is to have the athlete restrict training. If this
results in a meaningful decrease in AF, it is reasonable
to allow resumption of less intense exercise and reas-
sess the symptoms related to AF. In the process of
shared decision making, some athletes may elect to
forego any reduction in the duration and intensity of
exercise. It is reasonable under these circumstances
for health care providers to respect the decision of the
Estes III and Madias 925
Atrial Fibrillation in Athletes
athlete and advance alternate therapeutic approaches
for the AF.
If decreasing the frequency and duration of exercise
is not successful or not chosen as the initial approach, 1
of 2 strategies should be considered (49–51). If the
patient has clinically important symptoms, attempts
should be made to maintain normal sinus rhythm
(49–51). In contrast, if the patient is minimally symp-
tomatic or asymptomatic, the strategy of rate control is
preferred. There are no standard definitions of target
resting and peak exercise heart rates in the athlete.
Commonly resting rates #90 beats/min and peak
exercise rates less than the maximum age-predicted
heart rate in sinus rhythm are used as clinical target
rates. A rate control strategy can prove challenging in
this population because baseline sinus rates are often
quite slow. In addition, agents such as beta-blockers
and calcium-channel blockers are poorly tolerated
due to side effects, including fatigue and decreased
athletic performance (49–51). Digoxin has no role
in rate control in the athlete with AF because the
negative dromotropic effects are indirect through
enhanced vagal tone on the atrioventricular node.
These effects on slowing the ventricular response are
926 Estes III and Madias
Atrial Fibrillation in Athletes
withdrawn with exercise. On the basis of these con-
siderations, it is evident that the options for rate
control are limited in the athlete (49–51).
If rhythm control is not successful with decondi-
tioning in the athlete with symptomatic AF, the next
approach is most commonly a trial of an antiar-
rhythmic agent (49–51). There are no prospective
randomized trials that have assessed the safety and
effectiveness of antiarrhythmic drugs in athletes with
AF (49–51). Recommendations related to selection of
antiarrhythmic agents should be guided by the best
available evidence extrapolated from other pop-
ulations of AF patients (49–51). The subgroup of
athletes with exercise-induced AF that may be char-
acterized as vagal-mediated might benefit from the
anticholineric effects of disopyramide (53). This class
I antiarrhythmic agent has been reported to be rela-
tively effective in this niche population of athletes
with AF, with success in 67% of patients at 6 months
and 54% at 1 year (53).
Although there are multiple, prospective, ran-
domized controlled trials of antiarrhythmic agents
compared with ablation, the data are limited with
regard to AF ablation in endurance athletes (54–57).
An initial study of 20 athletes reported freedom from
AF off antiarrhythmic therapy in all patients at 36 
12.7 months after pulmonary vein isolation (56). After
6 months, all of the athletes became eligible for ath-
letic participation, and experienced improvement in
exercise capacity and quality of life as measured by
self-assessment questionnaire (56). Another study of
182 subjects reported similar freedom from recurrent
AF in athletes versus nonathlete control subjects who
underwent pulmonary vein ablation (59% vs. 48%;
p ¼ 0.44). The complication rates (7.1% vs. 4.3%; p ¼
0.45) and repeat ablation (40.5% vs. 37.3%; p ¼ 0.50)
were similar in the 2 groups (57). In a series of 59
endurance athletes with paroxysmal AF, pulmonary
vein isolation was as effective in athletes as in non-
athletes after 3 years of follow-up (58). These studies
were all limited by nonrandomized design, absence of
blinding, and no standardized assessment of AF
recurrence. Nonetheless, when considered in the
context of the available literature regarding outcomes
in nonathletes with paroxysmal AF, ablation appears
to be a reasonable option in athletes with symptom-
atic AF that is not responsive to deconditioning or at
least 1 antiarrhythmic agent (53,56,57). An early
invasive approach with catheter ablation might be
reasonable in selected athletes who elect ablation as a
first-line strategy and in those who quickly prove
intolerant to medical therapy.
In addition to choosing a strategy of rate control or
rhythm control for the endurance athlete,
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SEPTEMBER 2017:921–8
anticoagulant therapy needs to be considered,
weighing the risk of stroke using the CHA2 DS2-VASc
(congestive heart failure, hypertension, age $75
years, diabetes mellitus, prior stroke or transient
ischemic attack or thromboembolism, vascular dis-
ease, age 65 to 74 years, sex category) score and the
risk of bleeding. Due to their overall cardiovascular
health, many endurance athletes will likely lack
traditional stroke risk factors and prove to have low
CHA 2DS2-VASc scores. Standardized methods of
assessing bleeding risks of anticoagulant therapy in AF
patients, such as the HAS-BLED (hypertension,
abnormal renal and liver function, stroke, bleeding,
labile international normalized ratio, elderly, drugs or
alcohol) or ATRIA (Anticoagulation and Risk Factors in
Atrial Fibrillation) study scores, do not incorporate
any metric of risk attributable to athletic participation
(49–51). In athletes with AF who require antith-
rombotic therapy, it is reasonable to consider the
bleeding risk in the context of the particular sport
before clearance for participation is recommended,
especially in any athletic activity with the potential for
bodily harm (58). Recommendations regarding
continued sports participation for the competitive
athlete have been recently updated and can guide
clinicians in advising athletes with AF (58). Of note,
athletes with AF that is well tolerated and self-
terminating may participate in competitive sports
without the need for any therapy (58). It should be
noted that these recommendations, like all guidance
for AF management in the athlete, are based on
observational studies and expert opinion.
CONCLUSIONS
Many gaps in evidence related to epidemiology,
mechanisms, and management of endurance athletes
with AF persist. Clinicians must use the limited, but
best available data to manage these patients. To the
extent that the cardiovascular benefits of exercise are
well established, all patients should be encouraged to
be physically active with moderation. The evidence is
conclusive that sedentary lifestyles contribute to AF
development independent of sex. Physical activity in
moderation decreases the risk of AF in men and
women; however, men should be advised of the
potentially increased risk of AF with long-term, high-
intensity endurance training.
ADDRESS FOR CORRESPONDENCE: Dr. N.A. Mark
Estes III, New England Cardiac Arrhythmia Center,
The Cardiovascular Center, Tufts Medical Center, 800
Washington Street, Boston, Massachusetts 02111.
E-mail: nestes@tuftsmedicalcenter.org.
JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 3, NO. 9, 2017
SEPTEMBER 2017:921–8
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Force on Catheter and Surgical Ablation of Atrial KEY WORDS arrhythmia, athlete, atrial
Fibrillation. Heart Rhythm 2012;9:632–96. fibrillation, exercise