Modelling the relationships between arterial oxygen saturation, exercise intensity and the level of aerobic performance in acute hypoxia.

Purpose: The aim of this study was to establish a model to estimate the level of arterial oxygen saturation (SpO ₂ ) and help determine the appropriate hypoxic dose in humans exercising in acute hypoxia.
Methods: SpO ₂ values were collected in seven untrained (UTS) and seven endurance-trained male subjects (ETS) who performed six cycle incremental and maximal tests at sea level and at simulated altitudes of 1000, 1500, 2500, 3500 and 4500 m. Oxygen uptake was continuously measured and maximal oxygen uptake ([Formula: see text]) was determined in each subject and at each altitude. Intensity was expressed as percentage of [Formula: see text].
Results: There were strong non-linear relationships between altitude and SpO ₂ at low, moderate and high intensity both in ETS and UTS (r = 0.97, p < 0.001). SpO ₂ was significantly correlated to exercise intensity at sea level and at all simulated altitudes in ETS but only from 2500 m in UTS. There were inverse correlations between SpO ₂ and sea-level [Formula: see text] at all altitudes, which were stronger from 2500 m and with the increase in exercise intensity. The three-variable model we established predicts (p < 0.001) the SpO ₂ level of individuals exercising in acute hypoxia based on their sea-level [Formula: see text], the intensity of exercise and the altitude level.
Conclusion: The model demonstrates that the drop of SpO ₂ during exercise in acute hypoxia is larger with the increase in both sea-level [Formula: see text] and exercise intensity. The model also highlights that the pivotal altitude from which the fall in SpO ₂ is exacerbated is between 2000 and 2500 m, depending on both sea-level [Formula: see text] and exercise intensity.