THE ROLE OF PULMONARY CO2 FLOW IN THE CONTROL OF THE PHASE-I VENTILATORY RESPONSE TO EXERCISE IN HUMANS

To gain an insight into the origin of the phase I ventilatory response to exercise (ph I) in humans, pulmonary ventilation (V-E) and end-tid al partial pressures of oxygen and carbon dioxide (PETO2 and PETCO2, r espectively) were measured breath-by-breath in six male subjects durin g constant-intensity exercise on the cycle ergometer at 50, 100 and 15 0 W, with eupnoeic normocapnia (N) or hyperpnoeic hypocapnia (H) estab lished prior to the exercise test. Cardiac output (Q(c)) was also dete rmined beat-by-beat by impedance cardiography on eight subjects during moderate exercise (50 W), and the CO2 flow to the lungs (Q(c) . C-(v over bar)CO2 where C (v) over bar CO2 is concentration of CO2 in mixed veneous blood) was estimated with a time resolution of one breathing cycle. In N, the initial abrupt increase of V-E during ph I (Delta V-E approximately 18 l . min(-1) above rest) was followed by a transient fall. When PETCO2 started to increase (and PETO2 decreased) V-E increa sed again (phase II ventilatory response, ph II). In H, during ph I De lta V-E was similar to that of N. By contrast, during ph II Delta V-E kept gradually decreasing and started to increase only when PETCO2 had returned to approximately 40 mmHg (5.3 kPa). Thus, as a result of the prevailing initial conditions (N or H) a temporal shift of the time-c ourse of V-E during ph II became apparent. No correlation was found be tween CO2 flow to the lungs and V-E during ph I. These results are int erpreted as suggesting that an increased CO2 flow to the lungs does no t constitute an important factor for the initial hyperventilatory resp onse to exercise. They are rather compatible with a neural origin of p h I, and would support the ''neurohumoral'' theory of ventilatory cont rol during exercise.