“…223,224 Among other factors, this can be explained by: 1) in the immediate post-transplant period, the allograft is devoid of sympathetic and parasympathetic innervation (autonomic denervation), causing an increase in resting HR, attenuating its natural elevation in response to exercise, and impairing recovery after exertion 224,225 ; 2 ) patients often exhibit skeletal muscle dysfunction (sometimes to the point of cachexia), in which immunosuppressive therapy and pre-transplant HF play prominent roles 226 ; and 3) impairment of vascular and diastolic function. 227 During the acute phase of exercise, the increase in cardiac output of HTx recipients depends fundamentally on the Frank-Starling mechanism, i.e., on increase in venous return, inotropy, chronotropy, and reduction in afterload. 228,229 In addition, there is an increase in the concentrations of circulating catecholamines, 227 which decrease slowly after the end of exercise, explaining the slow recovery of HR in these patients.…”