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1 The John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin-Madison Medical School, Madison, Wisconsin, United States
* To whom correspondence should be addressed. E-mail: amann{at}wisc.edu.
Our aim was to isolate the independent effects of a) the inspiratory muscle work (Wb) and b) arterial-hypoxemia, during heavy-intensity exercise in acute hypoxia on locomotor muscle fatigue. Eight cyclists exercised to exhaustion in hypoxia (FIO2=0.15, SaO2=81±1%; 8.6±0.5 min, 273±6 W; Hypoxia-CTRL) and at the same work-rate and duration in normoxia (SaO2=95±1%; Normoxia-CTRL). These trials were repeated, but with a 35 to 80% reduction in Wb achieved via proportional assist ventilation (PAV). Quadriceps fatigue was assessed via magnetic femoral nerve stimulation pre- and 2-min post-exercise. The isolated effects of Wb in hypoxia on quadriceps fatigue, independent of reductions in SaO2, were revealed by comparing Hypoxia-CTRL and Hypoxia-PAV at equal levels of SaO2 (P=0.10). Immediately after hypoxic exercise, potentiated-twitch force of the quadriceps (Qtw,pot) decreased by 30±3% below pre-exercise baseline and this reduction was attenuated by about one-third following PAV exercise (21±4%; P<0.05). This effect of Wb on quadriceps fatigue occurred at exercise work-rates during which, in normoxia, reducing Wb had no significant effect on fatigue. The isolated effects of SaO2 on quadriceps fatigue, independent of changes in Wb, were revealed by comparing Hypoxia-PAV and Normoxia-PAV at equal levels of Wb. Qtw,pot decreased by 16±2% below pre-exercise baseline following Normoxia-PAV and this reduction was exacerbated by about one-third following Hypoxia-PAV (-21±4%; P<0.05). We conclude that both arterial-hypoxemia and Wb contribute significantly to the rate of development of locomotor muscle fatigue during exercise in acute hypoxia; this occurs at work-rates during which, in normoxia, the Wb has no effect on peripheral fatigue.
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