Introduction. We investigated possible physiological determinants of variability in hypoxia tolerance in subjects given a 5-minute normobaric exposure to 25,000 ft equivalent. Physiological tolerance to hypoxia was defined as the magnitude of decline in hemoglobin saturation (SpO2 - dependent variable).Methods. Pulmonary function, heart rate variability (HRV), total hemoglobin, a VO2 max estimation and resting oxygen consumption (VO2) were measured prior to the normobaric hypoxia exposure. Cerebral oximetry, ECG, middle cerebral artery blood flow velocity, noninvasive beat-to-beat arterial pressure and its first derivative, cardiac output, and left ventricular stroke volume, cerebral pulse oximetry, and hemoglobin oxygen saturation were recorded. Additionally, tidal volume and respiratory rate, breath-by-breath inhalation and end-tidal O2, CO2, and N2 tensions were measured and VO2 computed. Mixed venous PO2 and alveolar-capillary O2 gradient was calculated. Serum S100b, a putative marker for cerebral hypoxic insult, was also measured in 26 subjects.Results. Multivariate linear regression analysis was used to evaluate the ability of combinations of physiological measures to predict declines in SpO2 in 34 subjects. Seven variables were identified that gave a statistically significant prediction model that accounted for 71% of the variance (R2 = .706; adjusted R2=.627).Discussion. The model predicted that subjects with large total lung diffusion capacities for O2, those with the highest end- alveolar PO2 and the lowest mixed venous PO2 at the end of the 5-min exposure, and those who maintained an O2 consumption rate that exceeded their resting levels had the smallest declines in SpO2. Additionally, cerebral oximetry declines were negatively correlated with SpO2 declines and suggest that greater O2 extraction at the tissue level may be a strategy for lowering oxygen tension in blood returning to the lungs, thus providing a larger gradient for diffusion.
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