BLOOD-GAS DYNAMICS AT THE ONSET OF EXERCISE IN HEART-TRANSPLANT RECIPIENTS

One hypothesis to explain the rapid neural component of exercise hyper pnea contends that afferent stimuli originating in the ventricles of t he heart act reflexly on the respiratory center at the onset of exerci se, ie, ''cardiodynamic hyperpnea.'' Orthotopic cardiac transplantatio n (Tx) results in die loss of afferent information from the ventricles . Thus, Tx possibly results in transient hypercapnia and hypoxemia in deafferented heart transplant recipients (HTR) at the onset of exercis e due to hypoventilation. To examine the cardiodynamic hypothesis, we collected serial arterial blood gas (ABG) samples during both the tran sient and the steady-state responses to moderate cycle exercise in 5 H TRs (55 +/- 7 years) 14 +/- 7 months post-Tx and 5 control subjects ma tched with respect to gender, age, and body composition. Forced vital capacity, forced expiratory volume in 1 s, total lung capacity, and di ffusion capacity did not differ (p greater-than-or-equal-to 0.05) betw een groups. Resting arterial PO2, PCO2, and pH did not differ between groups (p greater-than-or-equal-to 0.05). The ABGs were drawn every 30 s during the first 5 min and at 6, 8, and 10 min of constant load squ are wave cycle exercise at 40 percent of the peak power output (watts) . Absolute and relative changes in arterial PO2, PCO2, and pH were sim ilar (p greater-than-or-equal-to 0.05) between HTR and the control gro up at all measurement periods during exercise. Heart rate (%HRmax rese rve), rating of perceived exertion, and reductions in plasma volume (% DELTA from baseline) did not differ between HTR and control during exe rcise at 40 percent of peak power output (p greater-than-or-equal-to 0 .05). Our results demonstrate that there is no discernible abnormality in ABG dynamics during the transient response to exercise at 40 perce nt of peak power output in patients with known cardiac denervation. Th ese data do not support the cardiodynamic hyperpnea hypothesis of vent ilatory control in humans. The absence of hypercapnia in HTRs is furth er evidence for the existence of redundant mechanisms capable of stimu lating exercise hyperpnea.