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

• Published in: Journal of applied physiology (1985) 2004-07, Vol.97 (1), p.188-196
• Main Authors: Duhamel, T. A, Green, H. J, Sandiford, S. D, Perco, J. G, Ouyang, J
• Format: Article
• Language: English
• Subjects: Adult; Aerobiosis; Bicycling; Biological and medical sciences; Calcium; Calcium - metabolism; Calcium-Transporting ATPases - metabolism; Cross-Over Studies; Effects; Exercise; Exercise - physiology; Fatigue; Fundamental and applied biological sciences. Psychology; Humans; Hypoxia - physiopathology; Kinetics; Male; Muscular system; Oxygen Consumption - physiology; Physical Fitness - physiology; Pulmonary Gas Exchange; Sarcoplasmic Reticulum - metabolism
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/japplphysiol.00958.2003

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) Ca 2+ cycling and whether alterations in SR Ca 2+ cycling are related to the blunted peak mechanical power output (PO peak ) and peak oxygen consumption ( O 2 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 O 2 peak (as determined during N) and at fatigue was used to investigate changes in homogenate SR Ca 2+ -cycling properties. Exercise in H compared with N resulted in a 19 and 21% lower ( P < 0.05) PO peak and O 2 peak , respectively. During progressive exercise in N, Ca 2+ -ATPase kinetics, as determined by maximal activity, the Hill coefficient, and the Ca 2+ concentration at one-half maximal activity were not altered. However, reductions with exercise in N were noted in Ca 2+ 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 Ca 2+ concentration of 2 µM and in phase 2 Ca 2+ 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 Ca 2+ -cycling proteins may explain fatigue during progressive exercise in N, they cannot explain the lower PO peak and O 2 peak observed during H. calcium cycling; muscle; normoxia; fatigue Address for reprint requests and other correspondence: H. J. Green, Dept. of Kinesiology, Univ. of Waterloo, Waterloo, Ontario, Canada N2L 3G1 (E-mail: green{at}healthy.uwaterloo.ca ).