Effect of exercise-induced arterial hypoxemia on quadriceps muscle fatigue in healthy humans

The effect of exercise- induced arterial hypoxemia (EIAH) on quadriceps muscle fatigue was assessed in 11 male endurance-trained subjects [peak O-2 uptake (VO2 peak) = 56.4 +/- 2.8 ml (.) kg(-1) (.) min(-1); mean +/- SE]. Subjects exercised on a cycle ergometer at >= 90% VO2 peak to exhaustion (13.2 +/- 0.8 min), during which time arterial O-2 saturation (Sa(O2)) fell from 97.7 +/- 0.1% at rest to 91.9 +/- 0.9% (range 84-94%) at end exercise, primarily because of changes in blood pH (7.183 +/- 0.017) and body temperature (38.9 +/- 0.2 degrees C). On a separate occasion, subjects repeated the exercise, for the same duration and at the same power output as before, but breathed gas mixtures [inspired O-2 fraction (FIO2) = 0.25-0.31] that prevented EIAH (Sa(O2) = 97-99%). Quadriceps muscle fatigue was assessed via supramaximal paired magnetic stimuli of the femoral nerve (1-100 Hz). Immediately after exercise at FIO2 0.21, the mean force response across 1-100 Hz decreased 335% compared with only 15 +/- 5% when EIAH was prevented (P < 0.05). In a subgroup of four less fit subjects, who showed minimal EIAH at FIO2 0.21 (Sa(O2) = 95.3 +/- 0.7%), the decrease in evoked force was exacerbated by 35% ( P < 0.05) in response to further desaturation induced via FIO2 0.17 (Sa(O2) = 87.8 +/- 0.5%) for the same duration and intensity of exercise. We conclude that the arterial O-2 desaturation that occurs in fit subjects during high-intensity exercise in normoxia (-6 +/- 1% Delta Sa(O2) from rest) contributes significantly toward quadriceps muscle fatigue via a peripheral mechanism.