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

Abstract

The effect of exercise-induced arterial hypoxemia (EIAH) on quadriceps muscle fatigue was assessed in 11 male endurance-trained subjects [peak O₂uptake (V̇o_{2 peak}) = 56.4 ± 2.8 ml·kg⁻¹·min⁻¹; mean ± SE]. Subjects exercised on a cycle ergometer at ≥90% V̇o_{2 peak}to exhaustion (13.2 ± 0.8 min), during which time arterial O₂saturation (SaO₂) 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°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 O₂fraction (FiO₂) = 0.25–0.31] that prevented EIAH (SaO₂= 97–99%). Quadriceps muscle fatigue was assessed via supramaximal paired magnetic stimuli of the femoral nerve (1–100 Hz). Immediately after exercise at FiO₂0.21, the mean force response across 1–100 Hz decreased 33 ± 5% 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 FiO₂0.21 (SaO₂= 95.3 ± 0.7%), the decrease in evoked force was exacerbated by 35% ( P < 0.05) in response to further desaturation induced via FiO₂0.17 (SaO₂= 87.8 ± 0.5%) for the same duration and intensity of exercise. We conclude that the arterial O₂desaturation that occurs in fit subjects during high-intensity exercise in normoxia (−6 ± 1% ΔSaO₂from rest) contributes significantly toward quadriceps muscle fatigue via a peripheral mechanism.