CO2-H+ stimuli and neural muscular drive to ventilation during dynamic exercise: comparison of stimuli at constant levels of ventilation.
In exercising man, the ventilatory responses to CO2-H+ stimuli and neural muscular drives were compared at constant ventilation (VE). For that purpose, a small increase of the CO2-H+ stimulus in exercise was to be counterbalanced by work load reductions in such a way that the magnitude of ventilation remained unchanged. Control of end-tidal PO2 and PCO2 (PETO2, PETCO2) was established to minimize the influence of changed mixed venous gas tensions on the arterial levels. Only in metabolic acidosis could the additional CO2 stimulus be compensated by work load reduction. This compensation was due to the concomitant decrease of acidosis. Below the 2 mmol X l-1 [La]a threshold, decrements of work load, VO2, and VCO2 showed no effect on VE, when PETCO2 and PETO2 were regulated at constant levels. After the termination of end-tidal clamps, the proportional relation of VE to VO2, VCO2, and work load was largely reestablished. The results show that neural muscular drives cannot decrease ventilation against a background of constant arterial feedback stimuli. Transient decreases of the CO2-H+ stimulus seem to be necessary to readjust the ventilation to a decreased CO2 flow to the lungs. It is suggested that the overall effect of decreasing CO2 is to inhibit the respiratory centers and that positive ventilatory effects of CO2 are the result of a disinhibitory influence.
D000138:Acidosis / Q000503:physiopathology; D000328:Adult; D002245:Carbon Dioxide / Q000502:physiology*; D006339:Heart Rate; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008297:Male; D009469:Neuromuscular Junction / Q000502:physiology*; D010101:Oxygen Consumption; D010313:Partial Pressure; D005082:Physical Exertion; D011659:Pulmonary Gas Exchange; D012119:Respiration; D012125:Respiratory Center / Q000502:physiology; D013990:Tidal Volume
D002245:Carbon Dioxide