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University Laboratory of Physiology, University of Oxford, Oxford OX1 3PT, United Kingdom
In humans, 8 h of isocapnic hypoxia causes a progressive rise in ventilation associated with increases in the acute ventilatory responses to hypoxia (AHVR) and hypercapnia (AHCVR). To determine whether 8 h of hyperoxia causes the converse of these effects, three 8-h protocols were compared in 14 subjects: 1) poikilocapnic hyperoxia, with end-tidal PO2 (PETO2) = 300 Torr and end-tidal PCO2 (PETCO2) uncontrolled; 2) isocapnic hyperoxia, with PETO2 = 300 Torr and PETCO2 maintained at the subject's normal air-breathing level; and 3) control. Ventilation was measured hourly. AHVR and AHCVR were determined before and 0.5 h after each exposure. During isocapnic hyperoxia, after an initial increase, ventilation progressively declined (P < 0.01, ANOVA). After exposure to hyperoxia, 1) AHVR declined (P < 0.05); 2) ventilation at fixed PETCO2 decreased (P < 0.05); and 3) air-breathing PETCO2 increased (P < 0.05); but 4) no significant changes in AHCVR or intercept were demonstrated. In conclusion, 8 h of hyperoxia have some effects opposite to those found with 8 h of hypoxia, indicating that there may be some "acclimatization to hypoxia" at normal sea-level values of PO2.
ventilation; acute ventilatory response to hypoxia; acute ventilatory response to hypercapnia
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