REVIEW

Arrhythmia Risk and Stratification

Arrhythmogenesis of Sports: Myth or Reality?

Saad Fyyaz and Michael Papadakis

Cardiovascular Clinical Academic Group, St George’s, University of London, St George’s University Hospitals NHS Foundation Trust, London, UK

Abstract
Regular exercise confers health benefits with cardiovascular mortality risk reduction through a variety of mechanisms. At a population level,
evidence suggests that undertaking more exercise has greater benefits. In the modern era of sport, there has been an exponential rise in
professional and amateur athletes participating in endurance events, with a progressively better understanding of the associated cardiac
adaptations, collectively termed ‘athletes heart’. However, emerging data raise questions regarding the risk of potential harm from endurance
exercise, with an increased risk of arrhythmia from adverse cardiac remodelling. Cross-sectional studies have demonstrated that athletes may
exhibit a higher burden of AF, conduction tissue disease, ventricular arrhythmias, a cardiomyopathy-like phenotype and coronary artery disease.
In an attempt to separate myth from reality, this review reports on the evidence supporting the notion of ‘too much exercise’, the purported
mechanisms of exercise-induced cardiac arrhythmia and complex interplay with sporting discipline, demographics, genetics and acquired factors.

Keywords
Endurance athlete, masters athlete, AF, coronary artery disease, myocardial fibrosis, exercise dose

Disclosure: SF is funded by research grants from Cardiac Risk in the Young, which advocates for preparticipation cardiac screening of young athletes. MP has received
research grants from Cardiac Risk in the Young.
Received: 14 December 2021 Accepted: 17 March 2022 Citation: Arrhythmia & Electrophysiology Review 2022;11:e05. DOI: https://doi.org/10.15420/aer.2021.68
Correspondence: Michael Papadakis, Cardiovascular Clinical Academic Group, St George’s, University of London, Cranmer Terrace, London SW17 0RE, UK.
E: mipapada@sgul.ac.uk

Open Access: This work is open access under the CC-BY-NC 4.0 License which allows users to copy, redistribute and make derivative works for non-commercial
purposes, provided the original work is cited correctly.

The health benefits of exercise are well established and extend beyond discipline, ethnicity, age and sex, and can overlap with mild phenotypes of
the cardiovascular system.1 These benefits accrue from the modulation conditions associated with arrhythmias and sudden cardiac death (SCD).11
of traditional risk factors for atherosclerotic cardiovascular disease, as Extreme cavity dilatation, left ventricular (LV) hypertrophy, elevated
well as through an anti-inflammatory effect on the vascular endothelium coronary artery calcium (CAC) scores, acute cardiac biomarker release,
and changes in autonomic regulation.2 A meta-analysis in almost myocardial fibrosis and cardiac arrhythmias have all been reported,
900,000 individuals demonstrated that the physically active group had raising concern of a reverse U-shaped relationship between the volume
a 35% reduction in the risk of cardiovascular death and 33% reduction in of exercise and cardiovascular health, with diminishing cardiovascular
all‑cause mortality.3 benefit and potential harm.12–15 Therefore, there is ongoing debate as to
whether there is a threshold that constitutes ‘excess of exercise’, which
The WHO recommends a minimum of 150 minutes of moderate-intensity may induce harm. To separate myth from reality, this review reports on the
exercise or 75 minutes of vigorous-intensity exercise per week. 4 A cohort evidence supporting the notion of ‘too much exercise’ and the proposed
of nearly 650,000 individuals participating in physical activity at half these mechanisms of exercise-induced cardiac arrhythmias in ostensibly healthy
recommended levels, at the recommended levels and at three times the athletes.
recommended levels, gained 1.8, 3.4 and 4.3 years of life, respectively.5
Higher cardiorespiratory fitness levels correlate with greater benefit, with AF
a mortality risk reduction of 13% for each additional metabolic equivalent AF is the most common sustained arrhythmia in the general population; it
(MET) increase in exercise capacity.6,7 These data suggest that, at the is a major cause of ischaemic stroke, heart failure and impairment in
population level, a greater volume of exercise results in greater cognition and quality of life, and increases the risk of death.16–18 The
cardiovascular benefit. A more cautious approach is necessary in incidence of AF increases with age, given that age in itself is a determinant
individuals with established heart disease, where the volume and intensity of AF. Moreover, advanced age is associated with cardiovascular risk
of exercise may need to be moderated.8 factors, heart failure, structural heart disease, coronary artery disease and
chronic kidney disease, all of which are linked with an increased risk of
Endurance athletes routinely exercise far beyond the WHO AF.19 It is well established that exercise mitigates such risk factors and, as
recommendations.9,10 The sustained elevation of cardiac pressure and such, regular exercise can prevent AF onset, as well as also improve
volume loads associated with regular exercise promote a series of symptoms, morbidity and mortality in those with established AF.20–22 A
electrical, structural and functional adaptations, collectively termed study of 6,000 veterans with a mean age of 56.8 years undergoing a
‘athlete’s heart’. The nature and magnitude of changes vary by sporting symptom-limited exercise tolerance test found exercise capacity to be

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 Arrhythmogenesis of Sports: Myth or Reality?

Figure 1: Characteristics of AF in Masters Athletes (Age >40 years)

Athletes are at higher Adrenergic activation, vagal Younger male athletes Both mixed and endurance
risk of developing AF tone, inflammation, atrial (<55 years) at greater risk, sports are associated with
compared with dilatation and fibrosis are with a lifetime of 1,500–2,000 increased risk of AF
non-athletes potential mechanisms of AF training hours suggested
in atheletes as the risk threshold

inversely related to the incidence of AF during a median follow-up of endurance athletes, who would surpass the level of exercise undertaken
8 years. The fittest individuals were found to have the lowest risk of by the female participants of these studies.
developing AF, with a 21% decrease for each MET increase in exercise
capacity.20 The Cardiovascular Health Study of 5,446 adults aged The mechanism of AF in athletes is not well understood, with much of
>65 years identified greater leisure time activity and walking as being our knowledge based on animal models. Vagal tone, which is chronically
associated with a lower incidence of AF, with progressively lower risk with elevated in athletes, is thought to be one of the most important
greater activity levels, and a 44% risk reduction in those undertaking contributors to the development of AF.35 In addition, atrial remodelling, in
moderate physical activity.23 Importantly, however, risk reduction the form of atrial dilatation and fibrosis, is increasingly being recognised
diminished in those undertaking high-intensity exercise (>6 METs).23 as an important factor. Atrial remodelling in athletes is considered to
be a physiological response to exercise, because the overall reservoir
An emerging body of evidence has since supported a link between long- function appears to be preserved with atrial dilatation; however, given
term intense endurance exercise and AF in an ‘exercise paradox’ (Figure 1). that atrial dilatation in pathological conditions contributes to the
Larger epidemiological studies and several meta-analyses have development of AF, it remains to be seen how distinct atrial remodelling
demonstrated that the incidence of AF is two- to fivefold greater in in athletes is from that seen in pathological states.36,37 AF episodes are
endurance athletes than in non-athletes.24–29 The elevated risk in the most common during states of increased parasympathetic tone (rest,
athletic group dissipates with increasing age (>55 years) and the presence sleep), but sympathetic stimulation during exercise may also trigger AF,
of cardiovascular risk factors. There is evidence to support the notion that in association with atrial wall stretch and inflammatory cytokines.15 In
exercise intensity, duration and type of sport affect the onset of AF. In a a study of rat models of chronic endurance exercise, AF was induced
study of 52,755 cross-country skiers participating in a 90 km cross-country after 16 weeks of training with identifiable atrial dilatation, fibrosis in the
skiing race, the participants who completed more than five races were at atria and right ventricle (RV) and autonomic changes, which did not fully
highest risk of AF, and were more likely to develop AF than those who resolve with detraining.14
undertook one race (HR 1.29).24 Similar findings have been observed
among healthy, middle-aged male physicians, with those participating in Bradyarrhythmias
higher-intensity jogging having a 53% higher risk of AF compared with Sinus bradycardia and sinus pauses are common in endurance athletes.
men who did not exercise.30 This would suggest that the association In a study of 62 former professional male cyclists, compared with 62 well-
between exercise and AF is not restricted to elite athletes, and is also matched controls (male golfers), the former endurance athletes
observed in the general population. However, the exact dose of exercise demonstrated more frequent sinus bradycardia, sinus node dysfunction
that confers risk of AF remains unclear, with high-quality prospective and pacemaker implantation for bradyarrhythmias relative to the control
studies with well-defined study populations still lacking. A figure of around group.38 This is widely believed to be a consequence of high vagal tone,
1,500–2,000 lifetime exercise hours has been suggested as the threshold although, because these findings can persist despite detraining, adverse
at which AF risk increases, with a peak age of onset at >40 years.31 AF in remodelling and fibrosis of the conduction system are also thought to be
younger athletes is unusual and should prompt evaluation for underlying contributing factors.38 More recently, evidence suggests significant
heart disease.32,33 electrical remodelling within the sinus node, with downregulation of
potassium/sodium hyperpolarisation activated cyclic nucleotide-gated
Most studies investigating the relationship between AF and exercise channel 4 (HCN-4).39,40 A possible dose–response relationship has also
have focused on male elite athletes, who historically dominated the been suggested, with a study of cross-country skiers demonstrating that
landscape of elite sports. The link between exercise and AF in female those who participated in more races had a higher risk of sinus node
athletes is less clear. In a large cohort of more than 140,000 male and disease or third-degree atrioventricular block.24
160,000 female athletes, increasing levels of physical activity were
associated with AF in male, but not female, participants.34 A meta- Ventricular Arrythmias
analysis of 22 studies identified an increased risk of AF in men Premature Ventricular Beats
undertaking intense exercise but, conversely, intense exercise was Premature ventricular beats (PVB) are fairly common in athletes and are
protective in women.25 Similarly, a more recent meta-analysis also usually benign. However, they may be the only sign of heart disease,
concluded that the general risk of AF is lower in female than male often leading to comprehensive evaluation. It is well established that
athletes.27 However, there remains a lack of data on high-level female PVBs may reflect the broader phenotype of cardiomyopathies and help

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 Arrhythmogenesis of Sports: Myth or Reality?

Figure 2: Predictors of Malignant Ventricular Premature Beats in Athletes

Symptoms Family history of sudden Increased frequency of Structural LBBB with

cardiac death (<50 years) PVBs on exercise heart disease intermediate/superior axis
or inherited cardiac Atypical RBBB with
conditions QRS >130 ms
Complex PVBs
Short coupled PVBs

LBBB = left bundle branch block; PVBs = premature ventricular beats; RBBB = right bundle branch block.

differentiate pathology from physiological adaptation to exercise, considerable challenges in differentiating physiological adaptation from
particularly in athletes with mild phenotypic expression, often referred to congenital LQTS, and potentially offering false reassurance to athletes at
as the ‘grey zone’. risk. A recent study demonstrated an exercise-induced QT prolongation
phenotype, mimicking congenital LQTS, which reverts back to normal after
Data supporting the notion that PVBs are more frequent in athletes a period of detraining.54 Although no arrhythmic events were recorded,
and may represent a feature of athletic adaptation are contrasted by more data are needed to fully understand the arrhythmic risk in individuals
studies that show similar burden of ectopy in athletic and non-athletic with acquired QT prolongation.54
individuals.41–43 Comparisons between studies are challenging due to
differences in methodologies to record and report PVBs, as well as the Similarly, repolarisation patterns on the athlete’s ECG may overlap with
absence of a standardised protocol guiding further investigation. PVBs the Brugada phenotype, causing a diagnostic conundrum.55 Although
have been reported in up to 14% of young athletes and 26% of veteran there are no clear data supporting a relationship between exercise and
athletes, with no convincing association between sporting discipline, SCD in patients with Brugada syndrome, enhanced vagal tone at rest and
volume or intensity of exercise, years of sports participation and burden or in early recovery following exercise has been postulated as a precipitant
complexity of PVBs.42–44 Furthermore, the overall burden of PVBs increases of arrhythmia in athletes with Brugada syndrome.56
with age. These findings do not support the hypothesis that endurance
sports activity increases the burden of ventricular arrhythmias.42–44 The Left Ventricle
Elevations in cardiac preload and afterload with chronic exercise are
The PVB characteristics that imply association with disease are evolving associated with cardiac chamber enlargement, with a 10–20% increase in
(Figure 2). Traditionally, a frequency in excess of 2,000 PVBs/24 hours has wall thickness and 10–15% increase in ventricular cavity dimensions.
been considered a red flag.41 Recently, however, evaluation of the Consequently, differentiation between athletic adaptation to exercise and
morphology of PVBs, as a surrogate of ventricular origin, has emerged as a mild phenotype of primary cardiomyopathies may be challenging even
the key factor in differentiating benign from potentially sinister PVBs.44–46 for the most experienced of sports cardiologists. Male endurance athletes
Frequent PVBs as a result of focal automaticity, emerging from the outflow are typically observed with the largest cavity dimensions, with up to 14%
tracts or from the fascicles of the left bundle branches, are relatively exceeding 60 mm, a threshold that typically raises suspicion of a primary
common and, in the absence of structural heart disease, should be dilated cardiomyopathy.57 Ethnicity is important to consider in the
considered benign.42,43 Other morphologies, such as PVBs with left or evaluation of LV wall thickness. For example, an LV wall thickness of
wide right bundle branch block or with intermediate or superior axis, are >13 mm is rare among white athletes, whereas it is more prevalent in
relatively uncommon and should be investigated further.46–48 Similarly, black athletes (2% versus 12%, respectively).55,58 Crucially, regardless of
short coupling intervals, increasing PVB frequency during exercise and ethnicity, a maximum wall thickness exceeding 16 mm is uncommon and
multifocal ectopy should prompt further evaluation. In particular, exercise- should prompt consideration and further evaluation for hypertrophic
induced PVBs with multiple and/or alternating morphologies (bidirectional) cardiomyopathy. In addition, LV cavity dilatation and hypertrophy may
may raise suspicion of underlying catecholaminergic polymorphic persist in up to 20% of athletes, despite detraining, suggesting that
ventricular tachycardia.49 extremes of cardiovascular adaptation to exercise may be irreversible.59
In a study by Finocchiaro et al., none of the first-degree relatives of
Effects on Ion Channels decedents with unexplained LV hypertrophy (30% competitive athletes)
Regular exercise exerts a significant effect on the expression and function of were diagnosed with hypertrophic cardiomyopathy, suggesting that
cardiac ion channels. Athletes exhibit longer QT intervals than sedentary extreme LV hypertrophy may be a source of arrhythmias.60
individuals, with corrected QT intervals of 470 ms in male athletes and
480 ms in female athletes accepted as the upper limits of normal.8 Exercise- The Right Ventricle
induced QT prolongation may confer an increased risk in individuals with At rest, the RV functions against a very low resistance and high compliance
underlying long QT syndrome (LQTS) because adrenergic surges and pulmonary circulation. However, during exercise, RV wall stress increases
emotional stress may trigger arrhythmias in LQT1 and LQT2, respectively.50–53 30-fold, reflecting a minimal reduction in pulmonary vascular resistance
Moreover, exercise-induced prolongation of the QT interval may pose and a significant rise in pulmonary artery systolic pressures. This raises the

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 Arrhythmogenesis of Sports: Myth or Reality?

Figure 3: Proposed Mechanisms of Adverse Cardiac Remodelling that

May Predispose to Arrhythmias in Endurance Athletes

↑ RV pressures

Myocyte necrosis
(troponin release)
Sport, sex,
ethnicity, age, Autonomic dysfunction
genetics, acquired
ARVC-like phenotype factors

Ion channel remodelling

Adverse
Fibrosis cardiac
remodelling

Atrial dilatation

Excessive LV remodelling

Arrhythmias Atherosclerosis

DCM-like phenotype
HCM-like phenotype

Sinus node disease

AF
AV block

Ventricular arrhythmias

Strength of evidence

The figure underscores the complex interaction of demographics, sporting discipline, genetics and acquired factors. ARVC = arrhythmogenic right ventricular cardiomyopathy; AV = atrioventricular block;
DCM = dilated cardiomyopathy; HCM = hypertrophic cardiomyopathy; LV = left ventricle; RV = right ventricle.

possibility that repetitive intense exercise can induce structural changes Subsequent genetic analysis of genes associated with ARVC, identified
and arrhythmias overlapping with arrhythmogenic right ventricular pathogenic variants in only 12.8% of athletes, compared with 30–50%
cardiomyopathy (ARVC), referred to as ‘exercise-induced ARVC’.61 expected in ARVC.68 Although these studies support the notion of
exercise-induced ARVC, it is important to note that they included a
Data from an animal model of endurance training demonstrated highly selected cohort of athletes presenting with ventricular
training-dependent RV fibrosis and tendency to arrhythmia following a arrhythmias, and the genetic yield in ARVC may be far lower than 50%
16-week exercise regime, which reversed after 8 weeks of exercise in the context of sporadic rather than familial disease. Moreover, other
cessation.62 In a study of more than 300 athletes, RV enlargement studies in elite Olympic athletes competing over many years have failed
meeting criteria for ARVC was seen in up to 45% of black athletes and to demonstrate significant pathological RV remodelling, suggesting that
59% of white athletes, although none was diagnosed with ARVC.63 this may be applicable to the very extremes of endurance training in
Studies have also reported transient RV dysfunction following endurance individuals with some genetic predisposition, although it may not
exercise, with greater dysfunction associated with more prolonged represent the classic ARVC genotype.69
intense exercise, such as ultra-endurance events. In most studies there
was no associated LV dysfunction, but there was correlation between By the same token, repetitive exercise in those with an established
the degree of RV dysfunction and elevation of troponin levels.64–66 diagnosis of ARVC is well recognised to increase the risk of SCD through
Moreover, an evaluation of 46 endurance athletes presenting with the acceleration of RV dysfunction and induction of ventricular
arrhythmias by Heidbüchel et al. reported that 80% of arrhythmias were arrhythmias.70,71 A North American multidisciplinary study reported that
of RV origin and 89% of athletes fulfilled either definite (59%) or patients engaging in competitive sports were at a twofold increased risk
borderline/possible (30%) diagnostic criteria for ARVC.67 During a of ventricular tachyarrhythmias or death and earlier presentation of
median follow-up of 5 years, 40% of athletes experienced major symptoms than patients who participated in recreational sports and
arrhythmic events defined as SCD, ICD shock or ventricular tachycardia. sedentary individuals.72 Similar results have been confirmed in

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 Arrhythmogenesis of Sports: Myth or Reality?

desmosomal mutation carriers with no phenotypic expression, controls.13 Furthermore, male athletes demonstrated twice as many
underscoring the impact of exercise on the RV.73 Further studies and atherosclerotic plaques (44% versus 22%), and 7.5% of male athletes
longitudinal data are required to better understand the interplay between demonstrated a luminal stenosis >50%, compared with none of the
exercise and the RV in health and disease states. controls.13 Importantly, the significance of the elevated CAC scores may
be mitigated by the plaque composition among athletes, which
Myocardial Fibrosis demonstrate a greater proportion of calcified plaques, which are
In patient populations, the presence of late gadolinium enhancement considered more stable and less prone to rupture. In a study of 284
(LGE) is an established adverse risk factor for malignant arrhythmia, and in athletes, divided by lifelong exercise volume (<1,000, 1,000–2,000 and
athletes has been associated with a risk of complex VA.47,48,74,75 >2,000 MET-min/week), Aengevaeren et al. demonstrated that the most
active athletes had a higher CAC score and more atherosclerotic plaque,
A small number of studies have demonstrated myocardial fibrosis in but also a higher prevalence of calcified plaque.82 The longer-term
ostensibly fit male masters athletes engaging in endurance exercise. In a longitudinal outcomes of endurance athletes remain unknown and
study of 102 middle-aged marathon runners, 12% demonstrated further studies are warranted. In the Cooper Centre Longitudinal Study
myocardial fibrosis (compared with 4% of controls), of which 42% of more than 20,000 male participants, those performing >3,000 MET-
demonstrated a pattern consistent with MI predominantly in the territory min of exercise per week were more likely to have CAC, without
of the left anterior descending artery.15 Furthermore, there was suggestion increased all-cause or cardiovascular mortality after a decade of follow-
of a dose–response relationship because participation in a greater up.83 Another study reported on 8,425 men who underwent an
number of marathons was an independent predictor for the presence of assessment of cardiorespiratory fitness and CAC and, over a 8.4-year
LGE.76 Similarly, in a study of 106 male masters endurance athletes, 14% follow-up, identified that each additional MET of fitness corresponded
demonstrated myocardial fibrosis, with almost half demonstrating a to a 14% lower risk of cardiovascular death in an adjusted model and
pattern consistent with a previous MI.13 Of those with evidence of MI, only attenuated the risk associated with higher CAC levels.84
half demonstrated coronary stenosis in the relevant coronary artery,
raising the possibility of subclinical infarction, due to demand ischaemia, Conclusion
coronary spasm or plaque rupture.13 Exercise remains one of the most potent, cost-effective treatments
against cardiovascular disease and cardiovascular mortality. Currently,
In a study of 83 asymptomatic middle-aged triathletes, participation in evidence suggests that even high-intensity, high-volume exercise, and
longer swimming distances and cycling races was an independent the associated lifestyle of elite endurance athletes, confers significant
predictor for the presence of non-ischaemic LGE, affecting 17% of male benefits, with athletes gaining an average of 5–7 years of life compared
athletes but none of the female athletes.77 A recent meta-analysis with sedentary individuals.85 Life-threatening arrhythmias remain
concluded that the incidence of LGE was almost sevenfold higher in overwhelmingly low, and mostly reflect underlying hereditary or congenital
middle-aged endurance athletes compared with non-athletes, with cardiac disease. Nevertheless, extremes of exercise may pose detrimental
most of this due to mid-myocardial or subepicardial LGE, with the next effects in an ‘exercise paradox’, with several routes of enquiry that require
most common pattern being insertion point fibrosis.78 Further further study (Figure 3). Life-long endurance athletes seem to be at
longitudinal studies are required to better understand the temporal increased risk of AF in their 40s and a small number who participate in the
association of non-ischaemic fibrosis with acquired risk factors, such as most extreme of endurance sports may be predisposed to RV-related
an episode of myocarditis, and its clinical relevance in masters athletes. arrhythmias. More research is needed in better-defined cohorts with long-
This is relevant in the era of the COVID-19 pandemic, which has ignited term follow-up.
interest about the prevalence and potential implications of asymptomatic
(subclinical) myocardial inflammation in elite athletes. A recent registry
of 1,597 competitive collegiate athletes infected with COVID-19 reported Clinical Perspective
symptomatic (clinical) myocarditis in five athletes (0.3%).79 The routine • The incidence of life-threatening arrhythmias in endurance
use of cardiac MRI (CMR) in all athletes increased the diagnostic yield of athletes is low, and commonly reflects hereditary or congenital
myocarditis by 7.4-fold to 2.3%.79 Importantly, follow-up CMR in 27 of the cardiac disease.
37 athletes diagnosed with myocarditis (73.0%) demonstrated resolution • Extremes of exercise may pose a detrimental effect; the
of myocardial oedema (T2 elevation) in all, and LGE indicative of proposed mechanisms are complex, with several routes of
myocardial fibrosis in 11 (41%).79 Similarly, in a cohort of more than 3,000 further enquiry ongoing.
athletes with COVID-19 infection, myocarditis was identified in 0.5% of • Athletes are at a higher risk of developing AF than non-athletes,
those who underwent clinically indicated CMR following clinical particularly in their 40s, with both mixed and endurance sports
assessment, but in 3% of the cohort of 198 athletes who underwent conferring risk.
screening CMR.80 • Premature ventricular beats are common in athletes and are
usually benign. Although ventricular arrhythmias have been
Coronary Artery Disease associated with an exercise-induced arrhythmogenic phenotype,
Exercise is well established to reduce traditional risk factors for coronary this seems to be applicable to the very extremes of endurance
artery disease, although masters athletes have been demonstrated to training in individuals with genetic predisposition.
show elevated CAC scores, which is a powerful adjunctive predictor of • Further research is needed to ascertain the long-term
future cardiovascular events in non-athletes.13,76,81 In a study of 152 significance of autonomic regulation and ion channel expression
masters endurance athletes with low Framingham risk scores (mean in endurance athletes, including extreme structural adaptations,
age 54 years), 19% of male athletes had a CAC score ≥100 Agatston coronary calcification, myocardial fibrosis and acute biomarker
units, compared with 4% among the controls, and 11% of athletes had a release.
CAC score >300 Agatston units, compared with none among the

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 Arrhythmogenesis of Sports: Myth or Reality?

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