There is a pandemic of physical inactivity that appears to parallel the widespread prevalence of cardiovascular disease (CVD). Yet, regular physical activity (PA) and exercise can play an important role not only in primary cardiovascular prevention but also in secondary prevention. This review discusses some of the main cardiovascular effects of PA/exercise and the mechanisms involved, including a healthier metabolic milieu with attenuation of systemic chronic inflammation, as well as adaptations at the vascular (antiatherogenic effects) and heart tissue (myocardial regeneration and cardioprotection) levels. The current evidence for safe implementation of PA and exercise in patients with CVD is also summarized.

There is a growing population of veteran endurance athletes, regularly participating in training and competition. Although the graded benefit of exercise on cardiovascular health and mortality is well established, recent studies have raised concern that prolonged and strenuous endurance exercise may predispose to atrial and ventricular arrhythmias. Atrial fibrillation (AF) and atrial flutter are facilitated by atrial remodelling, atrial ectopy, and an imbalance of the autonomic nervous system. Endurance sports practice has an impact on all of these factors and may therefore act as a promoter of these arrhythmias. In an animal model, long-term intensive exercise training induced fibrosis in both atria and increased susceptibility to AF. While the prevalence of AF is low in young competitive athletes, it increases substantially in the aging athlete, which is possibly associated with an accumulation of lifetime training hours and participation in competitions. A recent meta-analysis revealed a 5-fold increased risk of AF in middle-aged endurance athletes with a striking male predominance. Beside physical activity, height and absolute left atrial size are independent risk factors for lone AF and the stature of men per se may explain part of their higher risk of AF. Furthermore, for a comparable amount of training volume and performance, male non-elite athletes exhibit a higher blood pressure at rest and peak exercise, a more concentric type of left ventricular remodelling, and an altered diastolic function, possibly contributing to a more pronounced atrial remodelling. The sports cardiologist should be aware of the distinctive features of AF in athletes. Therapeutic recommendations should be given in close cooperation with an electrophysiologist. Reduction of training volume is often not desired and drug therapy not well tolerated. An early ablation strategy may be appropriate for some athletes with an impaired physical performance, especially when continuation of competitive activity is intended. This review focuses on the prevalence, risk factors, and mechanisms of AF in endurance athletes, and possible therapeutic options.

To assess cardiac morphologic and functional adaptations in elite triathletes with magnetic resonance (MR) imaging and to compare findings to those in recreationally active control subjects. The institutional review board approved the study, and written informed consent was obtained from all subjects. Twenty-six male triathletes (mean age ± standard deviation, 27.9 years ± 3.5; age range, 18-35 years) and 27 nonathletic male control subjects (mean age, 27.3 years ± 3.7; age range, 20-34 years) underwent cardiac MR imaging. Electrocardiographically gated steady-state free-precession cine MR imaging was used to measure indexed left ventricular (LV) and right ventricular (RV) myocardial mass, end-diastolic and end-systolic volumes, stroke volume, ejection fraction (EF), and cardiac index at rest. The ventricular remodeling index, which is indicative of the pattern of cardiac hypertrophy, was calculated. The maximum left atrial (LA) volume was calculated according to the biplane area-length method. Differences between means of athletes and control subjects were assessed by using the Student t test for independent samples. The atrial and ventricular volume and mass indexes in triathletes were significantly greater than those in control subjects (P < .001). In 25 of the 26 athletes, the LV and RV end-diastolic volumes were greater than the normal ranges reported in the literature for healthy, male, nonathletic control subjects (47-92 mL/m(2) and 55-105 mL/m(2), respectively). There was a strong positive correlation between end-diastolic volume and myocardial mass (P < .01). The mean LV and RV remodeling indexes of the athletes (0.73 g/mL ± 0.1 and 0.22 g/mL ± 0.01, respectively) were similar to those of the control subjects (0.71 g/mL ± 0.1 [P = .290] and 0.22 g/mL ± 0.01 [P = .614], respectively). There was a negative correlation between LA end-systolic volume and heart rate (P < .01). Changes in cardiac morphologic characteristics and function in elite triathletes, as measured with cardiac MR imaging, reflect a combination of eccentric and concentric remodeling with regulative enlargement of atrial and ventricular chambers. These findings are different from what has been observed in previous studies in other types of elite athletes.