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Right and Left Ventricular Function and Mass in Male Elite Master Athletes: A Controlled Contrast-Enhanced Cardiovascular Magnetic Resonance Study.Bohm P, Schneider G, Linneweber L et al.Circulation. 2016 Apr 12. pii: CIRCULATIONAHA.115.020975. [Epub ahead of print]
Regular exercise of moderate intensity is widely accepted as the safest, cheapest and most effective way of preventing and treating cardiovascular diseases. It has anyway been suggested that there is a U-shaped relationship between exercise intensity and cardiovascular events, and that too much and too intense exercise could be as harmful as no exercise at all, at least in certain subjects.
Several studies published in the last two decades have speculated that long-term intense endurance exercise may be associated with arrhythmias, myocardial fibrosis and even coronary artery disease. According to the hypothesis developed by Heidbuchel and La Gerche (1), the disproportionate haemodynamic load that the right ventricle (RV) has to withstand during intense endurance exercise, would result in long-term RV chronic remodelling and arrhythmias.
The authors of the present study looked at evidence of RV function impairment and/or myocardial damage in thirty three asymptomatic white elite male master endurance athletes (30-60 yrs age, 16 former elite professional), still in regular competition and with a recent continuous training history of ≥10 hours/week during 29±8 years.
As expected, echocardiography (with tissue Doppler imaging and speckle tracking) and contrast-enhanced cardiovascular magnetic resonance (CMR) showed that indexed (per body surface area) left ventricular (LV) and RV mass and end diastolic volumes were significantly increased in athletes compared to control subjects. There was no significant difference in left and right ventricles ejection fraction between athletes and control subjects. CMR showed nonischemic pathological late enhancement only in one athlete. High sensitive troponin T was normal in all athletes and N-Terminal pro-brain natriuretic peptide did not differ significantly between athletes and control subjects. None of the athletes showed any arrhythmias during the maximal cardiopulmonary exercise test. As assumed by the authors, one of the main limitations of the study is its cross sectional design that might have led to recruitment bias. Although all athletes were asymptomatic and no arrhythmias were documented, exercise imaging would probably be of interest in future studies, for risk stratification of athletes in whom ventricular arrhythmias are suspected (La Gerche et al.) (2).
On the other side, and as the authors of the exercise induced arrhythmogenic right ventricular cardiomyopathy (ARVC) hypothesis recognize, the mechanistic insights of certain athletes proarrhythmic state remain speculative, and to date, proarrhythmic substrates (fibrosis) associated with intense endurance training have only been documented in an animal model (Benito el al.) (3). In addition, although maybe not only attributable to exercise training, former elite endurance athletes have been shown to live longer than referents (Sarna et al.) (4).
Based on the findings of the present and other previous studies performed in former elite endurance athletes, the hypothesis of a cause-effect and dose-response relationship between intense endurance exercise and an exercise induced RV arrhythmogenic cardiomyopathy should at least, still be questioned. More studies with larger samples of former elite athletes are needed, but definitely longitudinal prospective studies with follow-up of elite athletes, with and without pathological or borderline findings, are required to better understand the long-term consequences of years of intense endurance training and competition, and in the end, the dose-response relationship.
Seems to me that nowadays we should probably be more concerned about risk assesment in those “recreational” endurance and ultra-endurance athletes with a long history of physical inactivity, frequently associated with other cardiovascular risk factors.
The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.
1. Heidbüchel H, La Gerche A. The right heart in athletes. Evidence for exercise-induced arrhythmogenic right ventricular cardiomyopathy. Herzschrittmacherther Elektrophysiol. 2012;23:82-86.2. La Gerche A, Claessen G, Dymarkowski S et al. Exercise-induced right ventricular dysfunction is associated with ventricular arrhythmias in endurance athletes. Eur Heart J. 2015;36(30):1998-2010.3. Benito B, Gay-Jordi G, Serrano-Mollar A et al. Cardiac arrhythmogenic remodeling in a rat model of long-term intensive exercise training. Circulation 2011;123:13-22.4. Sarna S, Sahi T, Koskenvuo M, Kaprio J. Increased life expectancy of world class male athletes. Med Sci Sports Exerc. 1993;25:237–244.