Abstract
Heart transplantation is now currently performed in adult (A-HTR) as well as in pediatric cardiac patients (P-HTR). In A-HTR, heart denervation results in a delayed, blunted heart rate (HR) response to exercise onset, mainly sustained by the level of circulating catecholamines. At the offset of exercise HR resumes the pre-exercise level in 5 - 25 min, depending on the absolute work intensity. Peak HR is ∼ 140 beats/min. Maximal aerobic power is 19 O2/kg × min, i.e., ∼ 60 % than that of healthy age-matched sedentary subjects and exercise tolerance is therefore reduced. A functional impairment at the muscle level may also be present, as suggested by the slow kinetics of the V˙O2 readjustment (phase II) at the onset of submaximal aerobic exercise. P-HTR generally behave as A-HTR. However, recently, in a few P-HTR a fast HR response to exercise and greater peak HR values (172 ± 22 beats/min) were demonstrated. Maximal aerobic power of P-HTR was 32 ± 7 ml O2/kg × min, greater than that of A-HTR, but yet ∼ 60 % of that of healthy age-matched controls. It may be concluded that occasionally P-HTR may resume an almost normal cardiovascular response to exercise; nevertheless, their exercise tolerance is limited, likely by functional impairment at the muscle level, whose origin is still unknown.

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