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

1. Reductions in arterial O-2 saturation (-5% to -10%S-a 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 HbO(2) dissociation curve. 2. We prevented the desaturation incurred during exercise at similar to 90% VO2 MAX via increased fraction of inspired O-2 (F(1)o(2)) (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 (F(1)o(2) 0.23 to 0.29) to prevent O-2 desaturation. We then compared the amount of quadriceps fatigue incurred following cycling exercise at S(a)o(2) 91% vs 98% with each trial carried out at identical work rates and for equal durations. 4. Preventing the normal exercise-induced O-2 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 (S(a)o(2)similar to 95%), breathing a mildly hypoxic inspirate (F(i)o(2) 0.17; S(a)o(2)similar to 88%) exacerbated the quadriceps fatigue. 5. We conclude that the normal exercise-induced O-2 desaturation during heavy-intensity endurance exercise contributes significantly to exercise performance limitation in part because of its effect on locomotor muscle fatigue.