Decrease in peak heart rate with acute hypoxia in relation to sea level V(over dot)O2max

The aim of this study was to evaluate the influence of arterial oxygen saturation (SaO(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 ((V) over dot O-2max): high [GH, (V) over dot O-2max=64.2 (3.3) ml.min(-1).kg(-1)], medium [GM, 50.8 (3.9) ml.min(-1).kg(-1)] and low [GL, 41.0 (1.9) ml.min(-1).kg(-1)]. All subjects performed a maximal exercise test in two conditions of inspired oxygen tension (PIO2, (149 mmHg and 70 mmHg). Among the GM group, seven subjects performed five supplementary incremental exercise tests at PIO2 136, 118, 104, 92, and 80 mmHg. Measurements of (V) over dot O-2max and SaO(2) using an ear-oxymeter were carried out at all levels of PIO2. The decrease in SaO(2) and peak heart rate (HRpeak) with PIO2 became significant from 104 and 92 mmHg. SaO(2) correlated with the decrease in HRpeak. For PIO2=70 mmHg, the decrease in (V) over dot O-2max, SaO(2) and HRpeak 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(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 HRpeak 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(2), due either to lower PIO2 or to training status, is associated with lower HRpeak.