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Degree of arterial desaturation in normoxia influences O2max decline in mild hypoxia. Med. Sci. Sports Exerc., Vol. 31, No. 5, pp. 658-663, 1999.Elite endurance athletes display varying degrees of pulmonary gas exchange limitations during maximal normoxic exercise and many demonstrate reduced arterial O2 saturations (SaO2) at O2max-a condition referred to as exercise induced arterial hypoxemia (EIH). We asked whether mild hypoxia would cause significant declines in SaO2 and O2max in EIH athletes while non-EIH athletes would be unaffected.Nineteen highly trained males were divided into EIH (N = 8) or Non-EIH (N = 6) groups based on SaO2 at O2max (EIH < 90%, Non-EIH > 92%). Athletes with intermediate SaO2 values (N = 5) were only included in correlational analyses. Two randomized incremental treadmill tests to exhaustion were completed-one in normoxia, one in mild hypoxia (FIO2 = 0.187; ∼1,000m).EIH subjects demonstrated a significant decline in O2max from normoxia to mild hypoxia (71.1 ± 5.3 vs 68.1 ± 5.0 mL·kg−1·min−1, P < 0.01), whereas the non-EIH group did not show a significant ΔO2max (67.2 ± 7.6 vs 66.2 ± 8.4 mL·kg−1·min−1). For all 19 athletes, SaO2 during maximal exercise in normoxia correlated with the change in O2max from normoxia to mild hypoxia (r = −0.54, P < 0.05). However, the change in SaO2 and arterial O2 content from normoxia to mild hypoxia was equal for both EIH and Non-EIH (ΔSaO2 = 5.2% for both groups), bringing into question the mechanism by which changes in SaO2 affect O2max in mild hypoxia.We conclude that athletes who display reduced measures of SaO2 during maximal exercise in normoxia are more susceptible to declines in O2max in mild hypoxia compared with normoxemic athletes.