The ventilatory responses to step changes from rest to 100 W cycling exercise were studied in five healthy human subjects. Exercise was performed in hypoxia (end-tidal O2 pressure, PET,O2, 50-55 mmHg), a condition characterized by a marked enhancement of arterial chemoreceptor activity, and in hyperoxia (PET,O2 greater than 250 mmHg), a condition in which arterial chemoreceptor activity is largely suppressed. The subjects were studied at each O2 level after placebo and after an oral dose of 120 mg propranolol. 2. The magnitude of phase 1, the immediate, rapid ventilatory response at the onset of work, was unaffected by hypoxia and at both oxygen levels it was also unaffected by propranolol. 3. Phase 2, analysed from 20 to 120 s after the onset of exercise, was significantly affected by both O2 level and beta-blockade. The kinetics of the ventilatory changes in this phase were well described in all four conditions by a simple exponential function. The overall mean time constants after placebo were shorter in hypoxia (31.0 s) than in hyperoxia (40.2 s), and at each O2 level longer after propranolol, in hypoxia 61.3 s and in hyperoxia 106.0 s. 4. Continuous analysis of gas sampled at the mouth with a mass spectrometer showed constancy of end-tidal PCO2 throughout the step change in hypoxia both with and without beta-blockade. In contrast, in both hyperoxic conditions PET,CO2 rose, mainly in phase 2, to a value 5-6 mmHg higher than the starting value. 5. The steady-state ventilation was higher in hypoxia than in hyperoxia, and end-tidal CO2 pressure, PET,CO2, correspondingly lower. Neither ventilation nor PCO2 were, however, affected by propranolol in either condition. 6. It is concluded that the arterial chemoreceptors are important for both the rate of adaptation of ventilation to a new rate of metabolism during a step change of work rate, and for the matching of ventilation to CO2 flow which normally ensures isocapnia. The further slowing of the dynamics of the ventilatory response in hyperoxia as well as the preserved isocapnia in hypoxia after beta-blockade argue against any major role of beta-adrenergic mechanisms for these functions of the arterial chemoreceptors. The observed effects are considered to be secondary to the reduced cardiac output and an increased CO2 storage initially during exercise following beta-adrenergic blockade.
