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Journal of Applied Physiology, Vol 53, Issue 2 307-312, Copyright © 1982 by American Physiological Society
ARTICLES |
L. L. Hedemark and R. S. Kronenberg
Ventilatory and heart rate responses to hypoxia and hypercapnia were measured in eight normal subjects (5 women, 3 men, ages 22-27 yr) during wakefulness (W), slow-wave sleep (SWS), and rapid-eye-movement sleep (REM). Ventilatory responses to progressive isocapnic hypoxia were measured as k, the slope of the line relating the logarithm of incremental ventilation to alveolar O2 partial pressure (PAO2) and as the incremental ventilation at PAO2 = 40 Torr delta V 40. Values for k (mean +/- SE) were 40.5 +/- 2.4 Torr during W, 42.1 +/- 2.5 during SWS, and 29.9 +/- 2.3 (5 subj) during REM (P less than 0.02 vs. W). Comparable values for delta V 40 were 5.4 +/- 0.3, 6.3 +/- 1.0, and 5.4 +/- 0.31/min. Hypoxia increased heart rate 19 +/- 1.3% during W, 18 +/- 1.8% during SWS, and 15 +/- 2.2% during REM. Ventilatory responses to rebreathing CO2 (6 subj) were 1.7 +/- 0.3 1 X min-1 X Torr-1 during W and 1.3 +/- 0.2 during SWS. Hypercapnia consistently produced arousal from sleep in all eight subjects at levels between 6 and 15 Torr (11.2 +/- 1.1) above resting alveolar CO2 partial pressure. No consistent arousal was noted during hypoxia. Arousal occurred in 87% of the CO2-rebreathing tests compared with only 28% of the progressive isocapnic hypoxia tests (P less than 0.001). We conclude that ventilatory and heart rate responses to hypoxia and ventilatory responses to hypercapnia are not significantly altered by SWS. Arousal from sleep during hypercapnia is reproducible and predictable, but there is no consistent arousal during hypoxia.
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