Effects of exercise-induced arterial hypoxemia on limb muscle fatigue and performance

Abstract

1. Reductions in arterial O2 saturation (−5% to −10% SaO2 below rest) occur over time during sustained heavy-intensity exercise in a normoxic environment, caused primarily by the effects of acid pH and increased temperature on the position of the HbO2 dissociation curve. 2. We prevented the desaturation incurred during exercise at ∼90% √O2 MAX via increased fraction of inspired O2 (FiO2) (0.23 to 0.29) and showed that exercise time to exhaustion was increased. 3. We used supramaximal magnetic stimulation (1–100 Hz) of the femoral nerve to test for quadriceps fatigue. We used mildly hyperoxic inspirates (FiO2 0.23 to 0.29) to prevent O2 desaturation. We then compared the amount of quadriceps fatigue incurred following cycling exercise at SaO2 91% vs 98% with each trial carried out at identical work rates and for equal durations. 4. Preventing the normal exercise-induced O2 desaturation prevented about one-half the amount of exercise-induced quadriceps fatigue; plasma lactate and effort perception were also reduced. In a subset of less fit subjects who showed only minimal arterial hypoxaemia during sustained exercise (SaO2 ∼95%), breathing a mildly hypoxic inspirate (FiO2 0.17; SaO2 ∼88%) exacerbated the quadriceps fatigue. 5. We conclude that the normal exercise-induced O2 desaturation during heavy-intensity endurance exercise contributes significantly to exercise performance limitation in part because of its effect on locomotor muscle fatigue.