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Department of Kinesiology, University of Waterloo, Waterloo, Ontario, Canada N2L 3G1
Submitted 5 September 2003 ; accepted in final form 9 January 2004
This study examined the effects of progressive exercise to fatigue in normoxia (N) on muscle sarcoplasmic reticulum (SR) Ca2+ cycling and whether alterations in SR Ca2+ cycling are related to the blunted peak mechanical power output (POpeak) and peak oxygen consumption (
O2 peak) observed during progressive exercise in hypoxia (H). Nine untrained men (20.7 ± 0.42 yr) performed progressive cycle exercise to fatigue on two occasions, namely during N (inspired oxygen fraction = 0.21) and during H (inspired oxygen fraction = 0.14). Tissue extracted from the vastus lateralis before exercise and at power output corresponding to 50 and 70% of O2 peak (as determined during N) and at fatigue was used to investigate changes in homogenate SR Ca2+-cycling properties. Exercise in H compared with N resulted in a 19 and 21% lower (P < 0.05) POpeak and O2 peak, respectively. During progressive exercise in N, Ca2+-ATPase kinetics, as determined by maximal activity, the Hill coefficient, and the Ca2+ concentration at one-half maximal activity were not altered. However, reductions with exercise in N were noted in Ca2+ uptake (before exercise = 357 ± 29 µmol·min–1·g protein–1; at fatigue = 306 ± 26 µmol·min–1·g protein–1; P < 0.05) when measured at free Ca2+ concentration of 2 µM and in phase 2 Ca2+ release (before exercise = 716 ± 33 µmol·min–1·g protein–1; at fatigue = 500 ± 53 µmol·min–1·g protein–1; P < 0.05) when measured in vitro in whole muscle homogenates. No differences were noted between N and H conditions at comparable power output or at fatigue. It is concluded that, although structural changes in SR Ca2+-cycling proteins may explain fatigue during progressive exercise in N, they cannot explain the lower POpeak and O2 peak observed during H.
calcium cycling; muscle; normoxia; fatigue
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