Effects of progressive exercise and hypoxia on human muscle sarcoplasmic reticulum function

Abstract

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 (V̇o2 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 V̇o2 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) POpeakand V̇o2 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 POpeakand V̇o2 peakobserved during H.