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1 Department of Population Health Sciences, John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin, Madison, WI 53706, USA; School of Sport and Education, Brunel University, Middleses, UB8 3PH, United Kingdom
2 Department of Population Health Sciences, John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin, Madison, WI 53706, USA
* To whom correspondence should be addressed. E-mail: lee.romer{at}brunel.ac.uk.
The effect of exercise-induced arterial hypoxemia (EIAH) on quadriceps muscle fatigue was assessed in eleven male, endurance-trained subjects (mean ± S.E.M. peak O2 uptake [VO2peak] = 56.4 ± 2.8 ml kg-1 min-1). Subjects exercised on a cycle ergometer at
90% VO2peak to exhaustion (13.2 ± 0.8 min), during which time arterial O2 saturation (SaO2) fell from 97.7 ± 0.1% at rest to 91.9 ± 0.9% (range 84-94%) at end-exercise, due primarily to 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 (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 following exercise at FIO2 0.21, 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 sub-group of 4 less fit subjects, who showed minimal EIAH at FIO2 0.21 (SaO2 = 95.3 ± 0.7%), the decrease in evoked force was exacerbated by 35% (p < 0.05) in response to further desaturation induced via FIO2 0.17 (SaO2 = 87.8 ± 0.5%) for the same duration and intensity of exercise. We conclude that the arterial O2 desaturation that occurs in fit subjects during high-intensity exercise in normoxia (-6 ± 1%
SaO2 from rest) contributes significantly towards quadriceps muscle fatigue by a peripheral mechanism.
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