Aerobic exercise conditioning: a nonpharmacological antiarrhythmic intervention.
Sudden, unexpected cardiac death due to ventricular fibrillation is the leading cause of death in most industrially developed countries. Yet, despite the enormity of this problem, the development of safe and effective antiarrhythmic therapies has proven to be an elusive goal. In fact, many initially promising antiarrhythmic medications were subsequently found to increase rather than to decrease cardiac mortality. It is now known that cardiac disease alters cardiac autonomic balance and that the patients with the greatest changes in this cardiac neural regulation (i.e., decreased parasympathetic coupled with increased sympathetic activity) are also the patients at the greatest risk for sudden death. A growing body of experimental and epidemiological data demonstrates that aerobic exercise conditioning can dramatically reduce cardiac mortality, even in patients with preexisting cardiac disease. Conversely, the lack of exercise is strongly associated with an increased incidence of many chronic debilitating diseases, including coronary heart disease. Because it is well established that aerobic exercise conditioning can alter autonomic balance (increasing parasympathetic tone and decreasing sympathetic activity), a prudently designed exercise program could prove to be an effective and nonpharmacological way to enhance cardiac electrical stability, thereby protecting against sudden cardiac death.
Billman
George E
GE
Department of Physiology and Cell Biology, The Ohio State University, Columbus, Ohio 43210, USA. billman.1@osu.edu
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000150:complications / Q000503:physiopathology / Q000628:therapy*; D001341:Autonomic Nervous System / Q000503:physiopathology; D003213:Conditioning, Psychological / Q000502:physiology*; D016757:Death, Sudden, Cardiac / Q000209:etiology / Q000517:prevention & control; D004198:Disease Susceptibility; D015444:Exercise / Q000502:physiology*; D006329:Heart Conduction System / Q000503:physiopathology; D006801:Humans