Neurohormonal abnormalities in heart failure: impact of exercise training

Endurance exercise training appears to beneficially alter the clinical course of chronic heart failure. The specific mechanisms responsible for exercise-induced benefits, however, are not completely understood. This review examines the impact of endurance exercise training on neurohormonal mechanisms, which play a central role in the progression of chronic heart failure. Few studies, however, have been specifically designed to elucidate exercise-induced mechanisms responsible for the suppression of neurohormonal activation in patients with chronic heart failure and the literature on this topic is derived from a limited number of small, single-center studies. The available data suggests that endurance exercise training programs of moderate duration (approximately 16 weeks) are efficacious in suppressing circulating levels of catecholamines, angiotensin II, arginine vasopressin, and aldosterone. Additionally, endurance exercise training improves baroreceptor sensitivity and heart rate variability, suggesting that exercise ameliorates the autonomic derangement in chronic heart failure by increasing the parasympathetically mediated component of heart rate variability. Pharmacologic suppression of sympathetic activity has proved, by and large, to be successful at reducing mortality in patients with chronic heart failure. Exercise-induced modulation of sympathetic activity may also be instrumental at reducing morbidity and mortality but this has not been carefully investigated and is a fertile area for further research.