Hydrogen peroxide disrupts ca2+ release from the sarcoplasmic reticulum of rat skeletal muscle fibers. Brotto, M. A. P., and T. M. Nosek. Muscle Cell Biology Research Group, Department of Physiology and Endocrinology, Medical College of Georgia, Augusta, Georgia 30912 -3000
APStracts 3:0152A, 1996.
Reactive oxygen species such as superoxide (O2- ) and hydrogen peroxide (H2O2) are produced at low levels in resting muscles and at substantially higher levels in exercising muscles. Increased respiratory activity with exercise leads to O2- production by the NADPH oxidase reaction and the subsequent generation of H2O2 from O2 -, either by spontaneous dismutation or by the superoxide dismutase reaction. The long lasting (24 hour) depression of contractile function following exercise has been linked to damage of one or more proteins important in the excitation-contraction coupling (ECC) process. We studied mechanically and chemically skinned fibers from the extensor digitorum longus muscle of the rat to evaluate the effects of a 5 min. exposure to 1.0 mM H2O2 on muscle function. We found that H2O2 had no effect on the isometric force producing properties of the contractile apparatus nor on Ca2+ uptake by the sarcoplasmic reticulum (SR). It did, however, significantly affect Ca2+ release from the SR. Maximum depolarization-induced Ca2+ release was inhibited and the sensitivity to depolarization decreased. Ca2+ -induced release was completely blocked. We conclude that elevated levels of H2O2 with exercise are capable of damaging one or more proteins of the ECC process to produce a disruption in function that can account, at least in part, for the long-lasting effects of fatiguing stimulation. 

Received 13 November 1995; accepted in final form 11 March 1996.
APS Manuscript Number A1194-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 27 March 96