期刊
JOURNAL OF PHYSIOLOGY-LONDON
卷 575, 期 3, 页码 937-952出版社
BLACKWELL PUBLISHING
DOI: 10.1113/jphysiol.2006.113936
关键词
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资金
- NHLBI NIH HHS [T32 HL007654, R01 HL-15469, R01 HL015469, T32 HL-07654] Funding Source: Medline
Changing arterial oxygen content (C-aO2) has a highly sensitive influence on the rate of peripheral locomotor muscle fatigue development. we examined the effects of C-aO2 on exercise performance and its interaction with peripheral quadriceps fatigue. Eight trained males performed four 5 km cycling time trials (power output voluntarily adjustable) at four levels of C-aO2 (17.6-24.4 ml O-2 dl(-1)), induced by variations in inspired O-2 fraction (0.15-1.0). Peripheral quadriceps fatigue was assessed via changes in forced output pre- versus post-exercise in response to supra-maximal magnetic femoral nerve stimulation (Delta Q(tw); 1-100 Hz). Central neural drive during the time trials was estimated via quadriceps electromyogram. Increased C-aO2 from hypoxia to hyperoxia resulted in parallel increases in central neural output (43%) and power output (30%) during cycling and improved time trial performance (12%); however, the magnitude of Delta Q(tw) (-33 to -35%) induced by the exercise was not different among the four time trials (P > 0.2). These effects of C-aO2 also effected performance time to exhaustion at a fixed work rate, but similarly there was no effect of C-aO2 on locomotor muscle power output and exercise performance time is determined to a significant extent by the regulation of central motor output to the working muscle in order that peripheral muscle fatigue does not exceed a critical threshold.
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