LONGITUDINAL EVALUATION OF EXERCISE PERFORMANCE DURING THE FIRST 2 YEARS AFTER HEART TRANSPLANTATION

Abstract

In heart transplant recipients (HTR) exercise performance remains impaired after surgery, due to a low maximal aerobic power and to a larger O2 deficit during increases in workrate. Previous longitudinal measurements of both these variables during the critical first 2 years after HT are missing. Fifteen male HTR (52.0 ± 9.9 yr, × ± SD), not engaged in programmed rehabilitation, were evaluated every 3 months throughout the first 2 years post-HT, and were compared to healthy sedentary controls (C, n = 11, 51.0 ± 1.0 yr). Peak values of pulmonary O2 uptake (VO2) and heart rate (HR) were determined during an incremental cycling exercise to voluntary exhaustion. HR (t of the on-response) and VO2 kinetics were determined during 5-min constant-load exercise at 60% of the ventilatory threshold. For the VO2 on-response, the mean response time (MRT) of the overall transient (no distinction between phase I and phase II), the duration of the ôcardiodynamicö phase I (TD2) and the time constant (τ) of phase II (τ2) were determined. For the VO2 off-transient, τ (τoff) was determined. VO2peak increased as a function of time post-HT, going from 15.2 ± 3.4 ml/kg/min at 3 months to 20.0 ± 3.6 at 24 months (both values significantly lower than C, 24.7 ± 4.0). All other variables were unchanged throughout the study. HRpeak was significantly lower in HTR (135 ± 16 b/min) vs C (162 ± 15). t HR on- was longer in HTR (95 ± 12 s) vs C (37 ± 5 s); this was associated with a longer TD2 (34 ± 12 in HTR vs 25 ± 7 s in C). τ2 was not significantly different in HTR (39 ± 11 s) vs C (36 ± 10 s). Thus, the longer MRT in HTR (58 ± 14 s) vs C (44 ± 12 s) was mainly attributable to a longer cardiodynamic phase. τoff was slower in HTR (57 ± 13 s) vs C (49 ± 10 s). In the absence of structured rehabilitation programs, and despite a reduced HRpeak, HTR show a significant improvement of VO2 peak during the first 2 years after HT. On the other hand, VO2 on-kinetics remains slower, mainly as a consequence of a sluggish cardiac response. Despite the normal τ2 of the VO2 on-, the slower VO2 off- kinetics would indicate an impairment of skeletal muscle oxidative metabolism. (Telethon Italy Grant n. 1161C)