Acute intermittent hypoxia exposures enhance arterial oxygen delivery

Physiological adaptations to intermittent hypoxia (IH) conditioning are based on the cumulative effect of repeated IH exposures. The present study sought to test the hypothesis that acute IH exposures would promote arterial O(2) delivery and regional tissue oxygenation. Changes in arterial O(2) saturation (SaO(2), oximeter), forearm muscle and cerebral tissue oxygenations (SmO(2) and ScO(2), near-infrared spectroscopy) were compared during five repeated hypoxia exposures (10 +/- 0.2% O(2) for 5-min each) interposed with four-minute inhalation of room air in 11 healthy subjects (24 +/- 0.9 y). Baseline, prehypoxia partial pressure of end-tidal O(2) (P(ET)O(2), mass spectrometer) and SaO(2) (107 +/- 2 mmHg and 97.3 +/- 0.3%) were decreased (P < 0.05) after the first bout as compared with those during normoxia prior to the second (94 +/- 2 mmHg and 96.2 +/- 0.4%) and the fifth (92 +/- 3 mmHg and 95.7 +/- 0.7%) episodes of IH exposures, whereas partial pressure of end-tidal CO(2), tidal volume and breathing frequency were similar. Arterial O(2) dissociation in terms of per unit decrease in P(ET)O(2) during hypoxia, i.e. the slope of SaO(2)/P(ET)O(2), was augmented (P = 0.0025) from 0.71 +/- 0.09%/mmHg during the first hypoxia bout to 1.39 +/- 0.15%/mmHg and 1.47 +/- 0.16%/mmHg during the second and the fifth bouts, respectively. Fractional muscle tissue O(2) extraction rate (SmO(2)D, i.e. normalized difference between SaO(2) and SmO(2)) progressively decreased (P < 0.01) during IH; however, fractional cerebral tissue O(2) extraction rate (ScO(2)D, i.e. normalized difference between SaO(2) and ScO(2)) did not decrease during hypoxia (P = 0.94). ScO(2)D during normoxia tended to increase (P = 0.089) following repeated IH exposures. We conclude that enhanced arterial O(2) delivery with repeated IH exposures serves as a compensatory mechanism to potentiate O(2) availability during hypoxia.