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Ventilatory acclimatization in response to very small changes in PO₂ in humans

University Laboratory of Physiology, University of Oxford, Oxford, United Kingdom

Submitted 10 September 2004 ; accepted in final form 8 December 2004

Ventilatory acclimatization to hypoxia (VAH) consists of a progressive increase in ventilation and decrease in end-tidal PCO₂ (PET_CO2). Underlying VAH, there are also increases in the acute ventilatory sensitivities to hypoxia and hypercapnia. To investigate whether these changes could be induced with very mild alterations in end-tidal PO₂ (PET_O2), two 5-day exposures were compared: 1) mild hypoxia, with PET_O2 held at 10 Torr below the subject's normal value; and 2) mild hyperoxia, with PET_O2 held at 10 Torr above the subject's normal value. During both exposures, PET_CO2 was uncontrolled. For each exposure, the entire protocol required measurements on 13 consecutive mornings: 3 mornings before the hypoxic or hyperoxic exposure, 5 mornings during the exposure, and 5 mornings postexposure. After the subjects breathed room air for at least 30 min, measurements were made of PET_CO2, PET_O2, and the acute ventilatory sensitivities to hypoxia and hypercapnia. Ten subjects completed both protocols. There was a significant increase in the acute ventilatory sensitivity to hypoxia (Gp) after exposure to mild hypoxia, and a significant decrease in Gp after exposure to mild hyperoxia (P < 0.05, repeated-measures ANOVA). No other variables were affected by mild hypoxia or hyperoxia. The results, when combined with those from other studies, suggest that Gp varies linearly with PET_O2, with a sensitivity of 3.5%/Torr (SE 1.0). This sensitivity is sufficient to suggest that Gp is continuously varying in response to normal physiological fluctuations in PET_O2. We conclude that at least some of the mechanisms underlying VAH may have a physiological role at sea level.

acclimatization to hypoxia; respiratory control; chemoreflexes; acute ventilatory response to hypoxia

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