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 O₂ delivery and regional tissue oxygenation. Changes in arterial O₂ saturation (SaO₂, oximeter), forearm muscle and cerebral tissue oxygenations (SmO₂ and ScO₂, near-infrared spectroscopy) were compared during five repeated hypoxia exposures (10±0.2% O₂ 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 O₂ (P_ETO ₂, mass spectrometer) and SaO₂ (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 CO₂, tidal volume and breathing frequency were similar. Arterial O₂ dissociation in terms of per unit decrease in P_ETO₂ during hypoxia, i.e. the slope of SaO₂/P_ETO₂, 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 O₂ extraction rate (SmO₂D, i.e. normalized difference between SaO₂ and SmO₂) progressively decreased (P< 0.01) during IH; however, fractional cerebral tissue O₂ extraction rate (ScO₂D, i.e. normalized difference between SaO₂ and ScO₂) did not decrease during hypoxia (P = 0.94). ScO₂D during normoxia tended to increase (P = 0.089) following repeated IH exposures. We conclude that enhanced arterial O₂ delivery with repeated IH exposures serves as a compensatory mechanism to potentiate O₂ availability during hypoxia.