Published online Jun 26, 2017. doi: 10.4330/wjc.v9.i6.470
Peer-review started: January 11, 2017
First decision: February 17, 2017
Revised: March 14, 2017
Accepted: April 6, 2017
Article in press: April 10, 2017
Published online: June 26, 2017
Intense exercise may cause heart remodeling to compensate increases in blood pressure or volume by increasing muscle mass. Cardiac changes do not involve only the left ventricle, but all heart chambers. Physiological cardiac modeling in athletes is associated with normal or enhanced cardiac function, but recent studies have documented decrements in left ventricular function during intense exercise and the release of cardiac markers of necrosis in athlete’s blood of uncertain significance. Furthermore, cardiac remodeling may predispose athletes to heart disease and result in electrical remodeling, responsible for arrhythmias. Athlete’s heart is a physiological condition and does not require a specific treatment. In some conditions, it is important to differentiate the physiological adaptations from pathological conditions, such as hypertrophic cardiomyopathy, arrhythmogenic dysplasia of the right ventricle, and non-compaction myocardium, for the greater risk of sudden cardiac death of these conditions. Moreover, some drugs and performance-enhancing drugs can cause structural alterations and arrhythmias, therefore, their use should be excluded.
Core tip: Athlete’s heart is a physiological condition that in some cases can simulate pathological disease, sometimes due to the use of doping drugs. Furthermore, exercise can induce atrial dilation and arrhythmias. Our objective is to analyze the current literature and to review the most important changes in the heart of athletes, from the different molecular pathways to the structural anomalies.