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Abstract
The aim of this study was to evaluate the influence of arterial oxygen saturation (SaO^sub 2^) on maximal heart rate during maximal exercise under conditions of acute hypoxia compared with normoxia. Forty-six males were divided into three groups depending on their sea level maximal oxygen consumption (VO^sub 2max^): high [GH, VO^sub 2max^=64.2 (3.3) ml.min^sup -1^.kg^sup -1^], medium [GM, 50.8 (3.9) ml.min^sup -1^.kg^sup -1^] and low [GL, 41.0 (1.9) ml.min^sup -1^.kg^sup -1^]. All subjects performed a maximal exercise test in two conditions of inspired oxygen tension (PIO^sub 2^, (149 mmHg and 70 mmHg). Among the GM group, seven subjects performed five supplementary incremental exercise tests at PIO^sub 2^ 136, 118, 104, 92, and 80 mmHg. Measurements of VO^sub 2max^ and SaO^sub 2^ using an ear-oxymeter were carried out at all levels of PIO^sub 2^. The decrease in SaO^sub 2^and peak heart rate (HR^sub peak^) with PIO^sub 2^ became significant from 104 and 92 mmHg. SaO^sub 2^ correlated with the decrease in HR^sub peak^. For PIO^sub 2^=70 mmHg, the decrease in VO^sub 2max^, SaO^sub 2^ and HR^sub peak^ was, respectively, 44%, 62%, and 17.0 bpm for GH, 38%, 68%, and 14.7 bpm for GM, and 34%, 68%, and 11.8 bpm for GL. During maximal exercise in hypoxia, SaO^sub 2^ was lower for GH than GM and GL (p<0.01). Among subjects in GH, five presented exercise-induced hypoxemia (EIH) when exercising in normoxia. The EIH group exhibited a greater decrement in HR^sub peak^ than the non-EIH group at maximal hypoxic exercise (21.2 bpm vs. 15.0 bpm; p<0.05). When subjects are exposed to acute hypoxia, the lower SaO^sub 2^, due either to lower PIO^sub 2^ or to training status, is associated with lower HR^sub peak^.[PUBLICATION ABSTRACT]