Comparison between ventilatory and mouth occlusion pressure responses to hypoxia and hypercapnia in healthy sleeping man

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Abstract
Ventilatory and mouth occlusion pressure (Po.1) responses to progressive isocapnic-hypoxia and hyperoxic-hypercapnia were compared in eleven healthy sleeping men during the same night. Hypoxic and hypercapnic responses were determined during wakefulness, non-rapid and rapid-eye-movement sleep. The following parameters were measured: minute ventilation (.ovrhdot.VE) tidal volume (VT), ''duty cycle'' (TI/TT), mean inspiratory flow rate (VT/TI) and P0.1, an index of the neuromuscular inspiratory drive. To allow a direct comparison between the two types of chemostimuli, responses were characterized by the value of the different parameters at ''equivalent'' levels of hypoxia and hypercapnia, i.e., at levels which produced the same P0.1 during wakefulness: an oxyhaemoglobin saturation (SaO2) of 94% during the isocapnic-hypoxic tests (PETCO2 = 42.5 .+-. 1.2 mmHg) was found to be equivalent to a PETCO2 of 47.4 .+-. 3.7 mmHg during hypoxic-hypercapnic tests. For both tests, the arousal levels of the stimulus and of P0.1 were similar in all sleep stages. Sleep did not significantly modify P0.1 or breathing pattern responses to hypoxia (SaO2 = 94%). In contrast, at the ''equivalent'' level of hypercapnic stimulation, P0.1 (P < 0.05) and .ovrhdot.VE (P < 0.01) responses were significantly impaired, particularly in REM sleep, with a decrease in VT (P < 0.01) and VT/TI (P < 0.05) responses. The results suggest that CO2 intracranial receptor mechanisms are more affected by sleep than the O2 peripheral receptor activity.