title: Inspiratory muscle work in acute hypoxia influences locomotor muscle fatigue and exercise performance of healthy humans.
abstract: Our aim was to isolate the independent effects of 1) inspiratory muscle work (W(b)) and 2) arterial hypoxemia during heavy-intensity exercise in acute hypoxia on locomotor muscle fatigue. Eight cyclists exercised to exhaustion in hypoxia [inspired O(2) fraction (Fi(O(2))) = 0.15, arterial hemoglobin saturation (Sa(O(2))) = 81 +/- 1%; 8.6 +/- 0.5 min, 273 +/- 6 W; Hypoxia-control (Ctrl)] and at the same work rate and duration in normoxia (Sa(O(2)) = 95 +/- 1%; Normoxia-Ctrl). These trials were repeated, but with a 35-80% reduction in W(b) achieved via proportional assist ventilation (PAV). Quadriceps twitch force was assessed via magnetic femoral nerve stimulation before and 2 min after exercise. The isolated effects of W(b) in hypoxia on quadriceps fatigue, independent of reductions in Sa(O(2)), were revealed by comparing Hypoxia-Ctrl and Hypoxia-PAV at equal levels of Sa(O(2)) (P = 0.10). Immediately after hypoxic exercise potentiated twitch force of the quadriceps (Q(tw,pot)) decreased by 30 +/- 3% below preexercise baseline, and this reduction was attenuated by about one-third after PAV exercise (21 +/- 4%; P = 0.0007). This effect of W(b) on quadriceps fatigue occurred at exercise work rates during which, in normoxia, reducing W(b) had no significant effect on fatigue. The isolated effects of reduced Sa(O(2)) on quadriceps fatigue, independent of changes in W(b), were revealed by comparing Hypoxia-PAV and Normoxia-PAV at equal levels of W(b). Q(tw,pot) decreased by 15 +/- 2% below preexercise baseline after Normoxia-PAV, and this reduction was exacerbated by about one-third after Hypoxia-PAV (-22 +/- 3%; P = 0.034). We conclude that both arterial hypoxemia and W(b) 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, W(b) has no effect on peripheral fatigue.
authors: John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin-Madison Medical School, Madison, WI 53706, USA. amann@wisc.edu
authors: Markus
authors: M
authors: Amann
authors: David F
authors: DF
authors: Pegelow
authors: Anthony J
authors: AJ
authors: Jacques
authors: Jerome A
authors: JA
authors: Dempsey
mesh_terms: D000208:Acute Disease; D000328:Adult; D001642:Bicycling / Q000502:physiology; D004574:Electromagnetic Fields; D004576:Electromyography; D015444:Exercise / Q000502:physiology*; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology*; D008124:Locomotion / Q000502:physiology*; D008176:Lung Volume Measurements; D008297:Male; D009119:Muscle Contraction / Q000502:physiology; D018763:Muscle Fatigue / Q000502:physiology*; D018482:Muscle, Skeletal / Q000503:physiopathology*; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption / Q000502:physiology; D011659:Pulmonary Gas Exchange / Q000502:physiology; D015203:Reproducibility of Results; D012121:Respiration, Artificial; D012132:Respiratory Muscles / Q000503:physiopathology*
chemical_list: D010100:Oxygen