The cardiovascular benefit of regular moderate exercise is well established. Those exercising for 30 minutes five days per week will reduce their risk of coronary artery disease by 50% and gain approximately seven years of life, says Sanjay Sharma, St George's University of London.
However, there are emerging reports from large athlete cohorts that chronic intensive endurance exercise can promote cardiac arrhythmias, which may be associated with morbidity or even sudden death. Such arrhythmias most frequently manifest in veteran athletes who have exercised intensively for several decades. Perhaps the most commonly reported example is the five-fold greater prevalence of atrial fibrillation (AF) in middle aged athletes than in sedentary individuals of similar age.
Increased vagal tone superimposed on adverse atrial remodelling, atrial inflammation and fibrosis have been postulated by two recent animal studies. Data from the REGICOR study demonstrated that more than 1500 lifetime hours of intensive exercise was associated with a three-fold increase in AF prevalence in individuals with an otherwise normal heart. Furthermore, cessation of exercise has been shown to reverse AF in human and animal studies indicating a cause-effect relationship.
Our personal experience of evaluating large groups of veteran athletes has shown that over 40% exhibit asymptomatic paroxysmal AF. Thus, when consideration is given to the number of individuals engaged in gruelling endurance events in Europe each year (at least 1 million), it seems fair to assume that the question of AF amongst veteran athletes will become a burgeoning problem for cardiologists in the future. Such athletes are also prone to atrial flutter and symptomatic sino-atrial disease; the latter often requires pacemaker implantation.
Two large studies in almost 16,000 young Italian athletes (mean age 24 years) revealed that 2.2% showed at least three ventricular extra-systoles on their resting ECG and 71 athletes exhibited >2000 ventricular extra-systoles or bursts of non-sustained ventricular tachycardia. Detraining for a period of three months led to an 80% decrease in ventricular extra-systoles and 90% reduction in non-sustained ventricular tachycardia - implying that exercise also promotes ventricular arrhythmias in young athletes with a structurally normal heart.
The sudden death of several endurance cyclists from ventricular arrhythmias of right ventricular origin is probably the most extreme example of exercise-induced arrhythmias in young athletes. Chronic stretching of thin myocardial regions is thought to result in myocyte detachment and fibrotic myocardial repair akin to familial arrhythmogenic right ventricular cardiomyopathy.
A SEDENTARY lifestyle and obesity, even-tually resulting in increased atherosclerotic disease, are a hallmark of many developed countries, says Lluis Mont, Thorax Insitute, Hospital Clinic, University of Barcelona.
Physical exercise is a cheap and efficient strategy to reduce the burden of cardiovascular disease and improve survival. With such huge therapeutic potential, it thus seems appropriate to think of exercise as a drug. Indeed, the degree of physical fitness correlates with improvement in survival in a dose-response relationship.
Certainly, in almost all therapeutic strategies, whether drug-based or non-pharmacological, a threshold has been identified beyond which benefits are blunted or overcome by side effects. This same observation might also apply to physical exercise. Several recent reports have suggested an increased incidence of AF and right ventricular arrhythmias in elite athletes.
However, studies carried out in the general population have shown no changes in AF risk dependent on physical activity. Remarkably, a recent meta-analysis failed to demonstrate any significant increase in AF incidence in the more active quartiles of the general population. Moderate to intense exercise might even reduce AF in some individuals, possibly through a decrease in risk factors such as hypertension and cardiomyopathies. Moreover, moderate endurance training might be beneficial in patients with permanent AF by reducing mean ventricular rate and improving exercise tolerance.
The evidence linking ventricular arrhythmias and endurance training is less well established. Athletes remain at a higher risk of sudden death during a marathon. Underlying cardiomyopathies might play the most important role, while exercise-induced ventricular arrhythmogenic substrate or factors such as ionic disturbances have not been clearly defined.
Exercise intensity and duration seem to be critical parameters, mediating a dual relationship between exercise and arrhythmias. Remarkably, up-to-date guidelines recommend moderate-to-intense exercise up to 180 minutes weekly; brisk walking is considered intense activity.
Notably, athletes suffering from exercise-induced arrhythmias have been characteristically engaged for ten or more years in very high-intensity endurance sports, several-fold more intense than recommended by scientific societies. These data suggest the existence of an intensity and/or duration threshold, beyond which exercise becomes excessive. Today, we lack solid evidences of a proarrhythmogenic effect below this threshold.
In summary, physical exercise at an intensity and duration recommended for cardiovascular health does not convey increased arrhythmic risk and should be strongly encouraged in both healthy individuals and patients with cardiovascular disease.
Nevertheless, elite athletes should be warned of potentially adverse events when exercise trespasses on ‘physiological’ limits. However, endurance sports AT PHYSIOLOGICAL LEVELS do not exert arrhythmogenic effects.