Reactive oxygen radicals are produced by skeletal muscle during exercise (Powers et al. 1999). Failure to remove these oxidants may result in cellular damage and/or an altered capability to develop tension. Recent evidence in vitro suggests maximal force is modulated by altered redox states (Plant et al. 2001). However, the mechanism by which this occurs is not fully understood. Likely targets for oxygen radicals include membrane systems and contractile elements, with all receiving little research attention during oxidising conditions. Therefore, the aim of this study was to investigate the effects of altered redox balance on skeletal muscle SR function.

Thirty male Wistar rats were used in this study. Anaesthetised animals (100 mg kg^-1 sodium pentobarbitone; I.P.) were killed by cervical dislocation, following which the hindlimb muscles extensor digitorum longus (EDL) and soleus were removed. Muscles were incubated in Krebs with (Treated, TR) or without (Control, CON) 5 mM H₂O₂ for 0, 10, 20, 30 or 40 min. Six (n = 6) EDL and soleus muscles were used at each time point for both groups. Following incubation, assays for SR Ca²⁺ uptake and release were performed using previously published methods (Warmington et al. 1996).

Results show no difference in SR Ca²⁺ release at all time points (in nM min^-1 mg^-1) between Control and Treated groups in both the EDL (127 ± 8 CON versus 117 ± 12 TR at t = 10) and soleus (65 ± 9 CON versus 85 ± 11 TR at t = 10). SR Ca²⁺ uptake was unchanged by H₂O₂ incubation at all time points in soleus (21.5 ± 3 CON versus 20 ± 4.2 TR at t = 10), although at 20, 30 and 40 min Treated groups showed a significantly reduced rate of SR Ca²⁺ uptake (74.5 ± 6.4 TR at t = 40) compared with Control groups in the EDL (99.9 ± 11.2 CON at t = 40) (P < 0.05, ANOVA).

These data suggest SR function is little affected by oxidative stress. Thus changes in muscle tension induced by oxygen radicals are more likely to arise via actions on other cell components such as the contractile apparatus, rather than alterations in calcium cycling during contraction. However, it seems likely, particularly in fast-twitch muscle (EDL), that a reduction in SR Ca²⁺ uptake following exposure to an oxidative stress may contribute to increased cellular damage or altered force generation during exercise.

This work was supported by The University of Dublin, Provost Academic Development Fund. The Committee for Protection of Animals used for Scientific/Medical Experiments, Department of Health and Children, Ireland, approved.