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ENVIRONMENTAL, EXERCISE AND RESPIRATORY PHYSIOLOGY
1Centre for Sports Medicine and Human Performance, Brunel University, Uxbridge, United Kingdom; and 2John Rankin Laboratory of Pulmonary Medicine, Department of Population Health Sciences, Medical Sciences Center, University of Wisconsin, Madison, Wisconsin
Submitted 10 May 2005 ; accepted in final form 7 September 2005
The effect of exercise-induced arterial hypoxemia (EIAH) on quadriceps muscle fatigue was assessed in 11 male endurance-trained subjects [peak O2 uptake (
O2 peak) = 56.4 ± 2.8 ml·kg1·min1; mean ± SE]. Subjects exercised on a cycle ergometer at
90%
O2 peak 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 8494%) 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 O2 fraction (FIO2) = 0.250.31] that prevented EIAH (SaO2 = 9799%). Quadriceps muscle fatigue was assessed via supramaximal paired magnetic stimuli of the femoral nerve (1100 Hz). Immediately after exercise at FIO2 0.21, the mean force response across 1100 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 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 toward quadriceps muscle fatigue via a peripheral mechanism.
magnetic stimulation; low- and high-frequency fatigue; quadriceps twitch force; voluntary activation; peripheral fatigue; central fatigue
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