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1 Department of Kinesiology, University of Waterloo, Waterloo, Ontario, Canada
* To whom correspondence should be addressed. E-mail: green{at}healthy.uwaterloo.ca.
This study examined the effects of progressive exercise to fatigue in normoxia 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 (VO2peak) observed during progressive exercise in hypoxia (H). Nine untrained males (20.7±0.42 yr; x± SE) performed progressive cycle exercise to fatigue on two occasions, namely during N (FIO2=0.21) and during H (FIO2=0.14). Tissue extracted from the vastus lateralis prior to exercise and at PO corresponding to 50% VO2peak, 70% VO2peak (as determined during N) and at fatigue was used to investigate changes in homogenate SR Ca2+-cycling properties. Exercise in H compared to N resulted in a 19 and 21% lower (P<0.05) POpeak and VO2peak, respectively. During progressive exercise in N, Ca2+-ATPase kinetics as determined by maximal activity (Vmax), the Hill coefficient (nH) and the Ca2+-concentration at 1/2 Vmax (Ca50) were not altered. However, reductions (µmol.min-1.g protein-1) with exercise in N were noted in Ca2+-uptake (Pre=357±29; Fatigue=306±26; P<0.05) when measured at 2 µM Ca2+f and in Phase Two Ca2+-release (Pre=716±33; Fatigue 500±53; P<0.05) when measured "in vitro" in whole muscle homogenates. No differences were noted between N and H conditions at comparable PO 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 VO2peak observed during H.
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