This study utilized a hypobaric chamber to compare the effects of mild hypobaria (MH; 50 mmHg, approximately 580 m altitude) on blood O2 status and maximal O2 consumption (VO2max) in 9 untrained and 11 trained (T) cyclists with VO2max values of 51 +/- 3 and 77 +/- 1 ml.kg-1.min-1, respectively. In both groups, arterial O2 saturation (SaO2) decreased significantly during maximal exercise, and this effect was enhanced with MH. Both these responses were significantly greater in the T cyclists in whom the final SaO2 during MH was 86.5 +/- 0.9%. When the group data were combined, approximately 65% of the variance in SaO2 could be attributed to a widened alveolar-arterial Po2 difference. The arterial PO2 during maximal exercise at sea level in the T group was on the steeper portion of the hemoglobin-O2-loading curve (T, 68.3 +/- 1.3 Torr; untrained, 89.0 +/- 2.9 Torr) such that a similar decrease in arterial PO2 in the two groups in response to MH resulted in a significantly greater fall in both SaO2 and calculated O2 content in the Tgroup. As a consequence, the VO2max fell significantly only in the T group (mean change, -6.8 +/- 1.5%; range, + 1.2 to - 12.3%), with approximately 70% of this decrease being due to a fall in O2 content. This is the lowest altitude reported to decrease VO2max, suggesting that T athletes are more susceptible to a fall in inspired PO2.
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