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Received February 1, 2007
Revised February 13, 2007
Accepted after revision February 16, 2007
1 University of Wisconsin-Madison
2 Brunel University
3 University of Colorado at Colorado Springs
* To whom correspondence should be addressed. E-mail: amann{at}wisc.edu.
We examined the effects of hypoxia severity on peripheral vs. central determinants of exercise performance. Eight cyclists performed constant-load exercise to exhaustion at various levels of inspired O2 fraction (FIO2 0.21/0.15/0.10). At task-failure (pedal-frequency <70% target) arterial-hypoxemia was surreptitiously reversed via acute O2 supplementation (FIO2=0.30) and subjects were encouraged to continue exercising. Peripheral quadriceps fatigue was assessed via changes in potentiated quadriceps twitch force (Qtw,pot) as measured pre- vs. post-exercise in response to supra-maximal femoral nerve stimulation. At task-failure in normoxia [hemoglobin saturation (SpO2) ~94%, 656±82s] or moderate-hypoxia (SpO2 ~82%, 278±16s), hyperoxygenation had no significant effect on prolonging endurance-time. However, following task-failure in severe-hypoxia (SpO2 ~67%; 125±6s), hyperoxygenation elicited a significant prolongation of time-to-exhaustion (171±61%). The magnitude of Qtw,pot at exhaustion was not different among the three trials (-35 to -36%, P=0.8). Furthermore, quadriceps integrated EMG, blood-lactate, heart-rate, and effort-perceptions all rose significantly throughout exercise and to a similar extent at exhaustion following hyperoxygenation at all levels of arterial oxygenation. Since hyperoxygenation prolonged exercise time only in severe-hypoxia, we repeated this trial and assessed peripheral-fatigue following task-failure prior to hyperoxygenation (125±6s). Although the magnitude of Qtw,pot was reduced from pre-exercise baseline (-23%; P<0.01), peripheral-fatigue was substantially less (P<0.01) than that observed at task-failure in normoxia and moderate-hypoxia. We conclude that across the range of normoxia to severe-hypoxia the major determinants of central motor output and exercise performance switches from a predominantly peripheral origin of fatigue to a hypoxic-sensitive central component of fatigue, likely involving brain hypoxic effects on effort perception.
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