VENTILATORY RESPONSE TO EXERCISE AFTER HEART AND LUNG DENERVATION IN HUMANS

This study, aimed at investigating some aspects of breathing control a t work, was conducted on 8 heart and lung transplant recipients (HLTR) (age 33 +/- 13 years, mean +/- SD; 10 +/- 6 months post-transplantati on) and on two control groups, i.e. 11 heart transplant recipients (HT R) and 11 healthy untrained subjects (C). The patients performed a ser ies of 2 to 6 1-min exercise bouts (at 25 or 50 W, corresponding to ab out 50% of their V(O2)max) on a bicycle ergometer, followed by a 5 min 25 or 50 W constant load. C exercised both at 50 W (C1) and at 50% of their V(O2)max (C2). Inspiratory (VI) and expiratory (VE) ventilation , tidal volume (VT), respiratory frequency (fR), end-tidal O2 and CO2 Partial pressures (PET(O2) and PET(CO2) and gas exchange (V(O2) and V( CO)) were measured breath-by-breath. ''Phase I'' ventilatory response (ph I) was determined as the mean changes of VI, VE, VT, fR, PET(O2) a nd PET(CO2), compared to rest, during the first two respiratory cycles following exercise onset. In HLTR ph I did not significantly differ f rom that of C1 and C2, whereas the response was lower in HTR. VE, V(O2 ) and V(CO2) responses during ''phase II'' (t 1/2 on-) and ''phase III '' (steady state exercise) were similar in HLTR and in HTR. t 1/2 on- were longer in HLTR and in HTR compared to C1. In 3 HLTR the ventilato ry pattern during the 5 min constant loads was similar to that of HTR and C, whereas 4 HLTR presented higher VT and lower fR values. It is c oncluded that: 1) The ventilatory response to exercise, in all its pha ses, is substantially preserved despite lung denervation. When slight alterations are found (.i.e. the slower phase II), they are presumably of peripheral origin. 2) The normal ph I in HLTR indicates that cardi ac and/or pulmonary inputs to the respiratory centers are not involved in its regulation, or that their role can be subserved by other venti latory control mechanisms.