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Regular physical activity over a long period of time increases the output of the cardiovascular system. That leads to development of a normal (physiological) athlete's heart. Bradycardia, cardiac hypertrophy, and arterial hypotension are three major characteristics of a normal athlete's heart. Changes in parameters of cardiovascular system and features of heart remodeling are determined by type, frequency, and duration of a physical activity. Excessive levels of physical activity could result in development of a pathologic athlete's heart, negatively affect hearts metabolism, and increase the risk of both atherosclerosis and myocardial infarction. Autopsy studies have shown that atherosclerosis, which leads to development of an ischemic heart disease, is often found in both young and elderly athletes. 56% of sudden deaths in all athletes were due to cardiovascular problems. Reports of ischemic heart disease in athletes of all ages have increased over the past few years. Echocardiographic features and clinical outcomes of stable angina and myocardial infarction in retired professional athletes are not well studied. Further studies are needed to improve diagnosis, prevention, treatment, and rehabilitation in elite athletes with ischemic heart disease.

The aim of this review was to study the role of the autonomic nervous system in the pathogenesis of atrial fibrillation (AF), as well as to establish the relationship of autonomic regulation with other mechanisms underlying the AF At present, the molecular and cellular mechanisms underlying the AF have not been precisely established. There is interest in evidence showing that both sympathetic outflow and an increased vagal tone can initiate and support AF. As modern studies have shown, autonomic cardiac regulation can be an important factor in the pathogenesis of AF.

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