- A 56-year-old cyclist (A) started to train extensively at 50. He trained at least 2 h almost every day in a group of cyclists from his club. In his words: every training was a small competition for him. He wanted to be faster than his peers. He also participated at competitions of all types with the only goal to win and he was very successful, receiving many gold medals in his age group. After 5 years of intensive training he started to feel symptoms of exhaustion and he was diagnosed with lone atrial fibrillation (AF). His AF is controlled by medications propafenone and clopidogrel. He has been advised to considerably reduce his level of exercise, and he no longer participates in races.
- A 56-year-old cyclist (B) does mountain cycling at least 2 h·d−1 and several hours on weekends. He started to train in his 40s. He cycles alone, in nature, without measuring speed. During a regular check-up his physical examination showed no abnormalities. However, he wanted to know whether it was safe to continue his current training schedule since he knows about the case of cyclist A and he had read about the risk of AF with endurance training in the scientific literature.
“Ne quid nimis” or “nothing in excess.” In recent studies and meta-analyses researchers wanted to validate this Latin proverb in relation to sports activities; however, there are many controversies and unproven statements in investigations regarding this topic. This seems to be one of the most controversial topics of modern sports medicine. With the massive growth of sports activities in recent decades on all continents and their proven benefits to health, information about the benefit spectrum for health is rapidly increasing with new scientific evidence. However, recent investigations demonstrated increased risk of heart rhythm abnormalities and coronary artery disease among middle-aged athletes who train for endurance sports disciplines such as running, cycling, cross-country skiing, and so on (1,2).
High-intensity endurance sport practice is listed as one of the risk factors of lone AF (3–6) and this is a topic of serious consideration for researchers since AF is known to substantially increase the risk of stroke, hospitalization, and mortality (7).
AF is the most common cardiac arrhythmia in athletes and it is usually paroxysmal with occasional crisis (8). According to some retrospective and observational studies, high-intensity endurance competitive athletes have from approximately a 2-fold to 10-fold increased risk of developing AF compared to the normal population (9,10). A definition of a new syndrome of lone AF associated with vigorous endurance exercise especially at a competitive level (based on the accumulated data in the literature) is proposed in Sanchis-Gomar et al. ( 11): paroxysmal AF in young and middle-aged athletes (PAFIYAMA).
There are several recent reviews that concluded that there is a U-shaped function, where the independent variable is the dose of sports activities and the dependant variable is the risk of AF and other heart problems (3). This means that there is a high risk with no exercise and a similar high risk with too much exercise. With moderate doses of exercise, the risk is minimized (3). Based on observations in individual studies and meta-analyses, a recent review suggests even worse effects, proposing a J-shaped function, meaning much smaller risk for sedentary individuals than for endurance athletes (12).
These findings caused a great deal of confusion and fear among middle-aged athletes who have been massively engaged in increased physical activity following previous studies which highlighted a need for physical activity for the prevention of diseases which can occur at that age. Therefore, it is essential to thoroughly investigate the hypothesis that vigorous exercises can cause AF, to discover the mechanisms, and to define precise activities and doses that may increase the risk for AF.
In this review, we will try to resolve seemingly contradictory research evidence: reliable evidence that demonstrated a great health benefit of regular exercise (including endurance exercise) and recent research evidence of increased AF risk in endurance (male competitive) athletes.
The studies up until now have concentrated mostly on the athletes who compete, but there is no evidence of AF prevalence among noncompetitive endurance athletes of the same age. Even if the risk exists for competitive athletes, middle-aged endurance athletes who do not compete might be at a lower risk of AF than their competitive peers. By competitive athletes we mean all who participate in marathons and other endurance races (even at the amateur level), not only the elite professional athletes.
The aim of this review is to theoretically elaborate on this hypothesis and to recommend it as a topic for future studies: Noncompetitive endurance athletes are at a lower risk of AF than competitive endurance athletes.
AF — Epidemiology, Pathophysiology, and Complications
According to some estimates, AF prevalence is 3% in adults ages 20 years or older, with greater prevalence in older people and with higher incidence and prevalence rates in developed countries (13). The prevalence of AF increases with age and in normal populations older than 65, it is around 9% (11). Approximately 25% of middle-aged adults in the EU and the United States will develop AF (13).
The main nonmodifiable risk factors for AF are advanced age, male sex, and European ancestry. The modifiable risk factors include sedentary lifestyle, smoking, obesity, diabetes mellitus, obstructive sleep apnea, elevated blood pressure, hypertension, structural heart disease, chronic kidney disease, and thyroid disease (3,13). AF developed in patients without these traditional risk factors is defined as lone AF.
AF is associated with a 2-fold increased risk of mortality in women and a 1.5-fold increase in men (13). Heart failure, stroke, and thromboembolism are among complications of AF and around a quarter of the cases of ischemic stroke are connected to AF (13).
The exact mechanisms causing and sustaining AF are multifactorial and very complex. They are not understood fully and are under permanent investigation. AF is characterized by high frequency excitation of the atrium with the consequence in dyssynchronous atrial contraction and irregularity of ventricular excitation (14). A main factor in the genesis of AF is vulnerable atrial substrate, and AF is a result of numerous different pathophysiological processes in the atria (14). These pathophysiological changes, including electrophysiological remodeling and fibrosis, occur as AF progressively advances from an acute to a chronic phase. Structural abnormalities of the heart, including valvular heart disease, hypertension, and congestive heart failure, cause dilatation of the atria and consequently lead to AF. Electrical remodeling is connected to fundamental arrhythmia mechanism. Focal ectopic activity and re-entry within the pulmonary veins can trigger AF (13).
Several recent genetic studies demonstrated that AF and in particular lone AF have a genetic basis. Genetic variants associated with common forms of AF are identified: 17 independent signals for AF at 14 genomic regions are discovered and each factor has been shown to induce structural and electrical remodeling of the atria (14).
Mechanisms by Which Vigorous Exercise Predisposes to AF
It is well known that elite endurance athletes have a greater left atrium size than the normal population. However, a study (15) concluded that left atrium remodeling of the athlete’s heart is not associated with increased left atrium stiffness, which supports the benign nature of this phenomenon as physiological adaptation to exercise conditioning.
Several mechanisms were proposed to underlie the association between exercise and AF, but the exact pathophysiology remains unclear.
The atrial remodeling accompanied by autonomic alterations and inflammation might play a central role (16).
Some of the risk factors mentioned in the previous paragraph that are known to cause AF in nonathletes, and also might have correlates in athletes. Besides structural remodeling of the left atrium, the contributing factors might be elevated left atrial pressure, inflammation, myocardial fibrosis, increased vagal tone, sinus bradycardia, and genetic predispositions (9,12). According to Estes and Madias (9), besides the proven factors that can cause AF in endurance athletes, other possible factors might be intermittent and intense sympathetic activation, pulmonary vein triggers, and performance-enhancing agents.
There are factors closely linked to endurance sports that might increase the risk of AF (and not the sports activities themselves), like performance-enhancing agents, sports supplements, energy drinks, and electrolyte imbalance. The World Anti-Doping Agency was founded less than 20 years ago, and performance-enhancing agents were used more often than they are today during competitions since some of the substances were not banned during that timeframe. That might cause AF in a higher percentage of athletes that participated in competitions 20 to 30 years ago. Regarding younger generations, the taurine-containing “energy” drinks and sports supplements are often consumed before or during endurance sports activities, and such drinks and supplements also are listed as possible triggers of AF (11). Electrolyte imbalance in sweating also is listed as a possible modulator of AF (11).
As mentioned, one of the proposed risk factors of AF is increase in sympathetic tone that might cause the atrial inflammation leading to the autonomic imbalance and atrial fibrosis and finally to AF. Inflammation also may modulate the intrinsic cardiac nervous system of the heart, promoting nerve growth and autonomic variations. During endurance sport activities, the sympathetic tone is increased due to the stress generated by competitive sports, which, in turn, increases the risk of AF.
Research Evidence on Health and Exercise: More Is Better, No Risk Even for Vigorous Athletes
There is impressive research evidence proving the tremendous health benefit of regular exercise, also including top-level athletes.
Conclusions from scientifically rigorous systematic reviews and meta-analyses (17,18) with very large numbers of participants were that the data do not support a statistically significant association between regular physical activity and increased incidence of AF. In connection to part of the evidence regarding risk of AF for endurance athletes, it is noted that among studies considered, there were studies of poor quality with smaller numbers of participants that showed a borderline significant association of higher level of physical activity with AF (18). Besides, a meta-analysis of cohort studies (19) concluded that available evidence shows that top-level athletes live longer than the general population and have a lower risk of cardiovascular disease. It is suggested that regular vigorous physical activity should be further endorsed in clinical and public health activity guidelines to maximize the population benefits of physical activity (20).
Regarding the dose-response relationship, a detailed pooled analysis based on a large number of participants showed that there is no evidence of harm (in regard to mortality) even with 10 times more than a suggested minimum of 75 min of vigorous-intensity or 150 min of moderate-intensity exercise per week (21). That means no harm with 750 min or 12.5 vigorous sports activity hours per week. It is suggested that there is no need to discourage adults who participate at higher levels of physical activity (21,22).
Considering the evidence, the conclusion from Bosomworth (23) is that AF is less common as physical activity increases, with a dose-response relationship, it is only in men exercising at very intensive levels that the risk might exceed that of the sedentary population.
Research Evidence on Health and Exercise: Better Not Do Too Much (Risk of AF in Endurance Competitive Athletes Is Increased)
In the review by Lavie et al. (1) both types of evidence are discussed; the one proving the great benefit of regular exercise training and the other demonstrating that high levels of endurance training may be associated with increased risk of AF, coronary artery disease, and malignant ventricular arrhythmias. It is stated that the latter are studies whose participants have been exercising for many days and many hours to compete in long races. Participants in the studies leading to conclusions that the probability of AF is increased with vigorous exercise were mostly competitive endurance athletes.
There are specific reviews and meta-analysis that have considered data gathered in relatively small populations, comparing elite competitive athletes with the rest of the population, establishing a connection between AF and intensive endurance exercise.
One of the typical studies showing that lone AF is associated with endurance sports practice is a retrospective cohort study (5) comparing two groups: marathon runners and sedentary men. Results of another study of this type, a 28 to 30 year follow up study based on cross-country skiers, demonstrated a prevalence of 12.8% of lone AF in this population (that is higher than in the normal population in this age group) (4).
A systematic review and meta-analysis (24) concluded that the risk of AF is significantly higher in athletes compared with nonathletes; the studies reviewed included mostly competitive endurance athletes.
In the Norwegian longitudinal cohort study (25), a population was observed in connection to drugs that were prescribed mostly for AF. All participants were divided into 4 groups according to the level of sports activity, and it was concluded only in the group of male competitive athletes (defined by regular participation in hard trainings or sports competitions), that the percentage of drug treated AF is considerably higher than average.
Another cohort study included competitive cross-country skiers out of which 1.7% were diagnosed with arrhythmias. It is indicated that the faster finishing time in races and the number of completed races were associated with higher incidence of AF and bradyarrhythmias (26).
Two more studies, the Physicians’ Health Study, a large-scale observational study (27) and a Swedish study (28), concluded that vigorous exercise at a young age is associated with an increased risk of AF, but that this risk is diminished in the older population. In the latter study, it is indicated that exercising for more than 5 h·wk−1 at the age of 30 years carries a risk of developing AF later in life.
There are studies trying to deduce the threshold of a number of lifetime training hours before the risk of AF rises. The conclusion of a study by Brugger et al. (29) is that a measurable “dose–response” effect of lifetime endurance training on left atrium mechanical function does not exist. Another study with ski racers demonstrated different results: there is a graded dose-response relationship between cumulative years of regular endurance exercise and a risk for AF and atrial flutter (30).
In Calvo et al. (3), it is claimed that the risk started to increase after 2000 h of accumulated lifetime endurance sports activity. If we accept that there is a risk with 2000 lifetime training hours, a small calculation shows that any athlete who trains intensively for 5 h·wk−1 would be at a higher risk of AF after 8 years of training. Nevertheless, it is mentioned in Calvo et al. (3) that it is necessary to undertake further epidemiological studies to confirm the threshold and that clinical decisions should be individualized.
As pointed out in Flannery et al. (12) most studies that associate endurance sports with increased risk of AF up until now were retrospective cohort or case control studies of modest size, and further adequately powered prospective cohort studies with careful quantification of exercise exposure should be performed.
Long-term Endurance Training Protects Women Against AF?
No study demonstrated that long-term endurance exercise increases the risk of AF in women. However, the majority of participants (93%) in all cohort and case control studies combined in a recent meta-analysis were men (12). Nevertheless, the available studies show that the intense exercise as well as moderate exercise lowers the risk of AF in women (9). A meta-analysis based on seven studies (31) that included both sexes concluded that moderate physical activity reduces the risk of AF for both sexes while vigorous exercise lowers the risk only for women. The Swedish study (32) that included 36,513 healthy women also demonstrated that physical activity in general is associated with a lower risk of AF in females.
There are several possible explanations why there are differences between males and females regarding risks for AF. One of the explanations is that there might be similar relationships in females, but that it is not yet clearly demonstrated because there were not enough studies investigating female athletes’ risk of AF (12). However, if we accept the findings from the various studies that female endurance athletes are relatively protected against AF, the reason might be physiological differences (33). In the study of Alexander (2), women participants were younger and had lower prevalence of heart diseases, hypertension, and diabetes mellitus compared to the men included in the study. Another explanation might be evidence about electrophysiological changes which occur in male athletes and to a smaller extent in female athletes (12).
Limitations of What We Know and Future Directions
There are impressive research results proving the tremendous health benefit of regular exercise (including vigorous exercise on top-level). On the other hand, there are studies with a fewer number of participants showing an association of higher level of physical activity with AF (14), but the studies were mostly done on competitive athletes.
Sports behavior is a remedy that has a very beneficial effect, but if we accept the demonstrated hypothesis that after years of intensive sports practice a harmful effect could appear, it is of utmost importance to discover and explain the mechanisms of such a phenomenon.
Due to the contradictory evidence: some demonstrating unconditional benefits of sports in middle age and others showing that AF is more common with vigorous athletes, a sports medicine specialist can explain to middle-aged athletes, for example, the risk factors for Achilles tendon injury, but cannot accurately estimate the risk of AF. How much sports activity is too little and how much is too much?
Can we advise a middle-aged person to continue to run 1 h·d−1? According to Turagam et al. (8) no, since he/she has already accumulated too much endurance activities in life (Fig.). But then, he/she would pass into the opposite part of the U-shape, again not good for health. As stated in the study by Redpath and Back (34) there is not enough data to enable evidence-based recommendations to athletes regarding AF.
There are several studies that associate AF and psychological factors (35). Mattioli et al. (36) demonstrated that a Type A behavior pattern of personality and acute life stress are risk factors for developing AF. Type A behavior includes competitiveness, and moreover, preparations for competitions and competitions themselves produce an acute stress, so both risks for AF are present in competition.
The competition and stress increase the sympathetic tone that is already increased in sports activities, which can cause atrial inflammation leading to the autonomic imbalance and atrial fibrosis and consequently, to AF.
Can we advise athletes to continue vigorous endurance activities, but without measuring time, without competing with peers and trying to be faster? In line with Arem et al. and Bapat et al. (21,22), the answer would be yes.
As underlined in Aizer et al. (27), data on the role of vigorous exercise in the development of AF among men participating in exercise at a less competitive level is limited, and it is possible that the known beneficial effects of exercise counterbalance the potential risk. Even at the highest intensity levels health benefits probably outweigh the negative effects of exercise (37).
Most studies differentiate between elite and nonelite athletes. However, nonelite athletes also might be competitive. Not only marathoners, but 10 km runners also compete with their peers, with themselves trying to qualify, or trying to get a medal in their age group. Each jogger might be competitive, having a GPS measuring his/her current speed and comparing with his/her speed from 5 years ago and trying not to be slower.
Our hypothesis is that men as well as women are not in danger of AF as long as they are running (biking, skiing) without participating in competitions. This is based on the data from the literature and also on our experience with cardiovascular screening in athletes of different kinds.
Further adequately powered studies are necessary to confirm the proposed mechanisms of association between exercise and AF. The difference in risk of AF between competitive athletes and those engaged in endurance sports without competing should be examined. A real control group for this study should consist of individuals who run, cycle, or cross-country ski, possibly in nature, just for pleasure, without competing with peers and without measuring speed.
The vast majority of previous studies about the AF risk up until now have been concentrated on the AF of middle-aged endurance athletes participating in sports competitions, but there is no data on endurance athletes of the same age who do not compete. So, if harmful effects exist, this is demonstrated only in competitive athletes. The real risk factors might be competitiveness and stress connected to competitions, and not the endurance training itself.
Our advice to athlete B from the beginning of this article would be to continue activities in the same level, without competing.
The authors are grateful to the reviewers whose valuable comments were very helpful in improving the manuscript.
The authors declare no conflict of interest and do not have any financial disclosures.
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