The decline in maximal oxygen uptake (VO2max) with acute exposure to moderate altitude is dependent on the ability to maintain arterial oxyhemoglobin saturation (SaO2). Purpose: This study examined if factors related to VO2max at altitude are also related to the decline in race performance of elite athletes at altitude. Methods: Twenty-seven elite distance runners (18 men and 9 women, VO2max = 71.8 ± 7.2 mL/kg·min) performed a treadmill exercise at a constant speed that simulated their 3000-m race pace, both in normoxia and in 16.3% O2 (~2100 m). Separate 3000-m time trials were completed at sea level (18 h before altitude exposure) and at 2100 m (48 h after arrival at altitude). Statistical significance was set at P = 0.05. Results: Group 3000-m performance was significantly slower at altitude versus sea level (48.5 ± 12.7 s), and the declines were significant in men (48.4 ± 14.6 s) and women (48.6 ± 8.9 s). Athletes grouped by low SaO2 during race pace in normoxia (SaO2 < 91%, n = 7) had a significantly larger VO2 in hypoxia (-9.2 ± 2.1 mL/kg·min) and 3000-m time at altitude (54.0 ± 13.7 s) compared with athletes with high SaO2 in normoxia (SaO2 > 93%, n = 7, VO2 = -3.5 ± 2.0 mL/kg·min, 3000-m time = 38.9 ± 9.7 s). For all athletes, SaO2 during normoxic race pace running was significantly correlated with both VO2 (r = -0.68) and ?3000-m time (r = -0.38). Conclusions: These results indicate that the degree of arterial oxyhemoglobin desaturation, already known to influence VO2max at altitude, also contributes to the magnitude of decline in race performance at altitude.
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