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Elevated O2• − production at 37°C reduces membrane excitability in isolated rat skeletal muscle

J.N. Edwards,1 W.A. Macdonald,2 C. Van Der Poel1 and D.G. Stephenson,1 1Department of Zoology, La Trobe University, Melbourne 3086, Australia and 2Institute of Physiology and Biophysics, University of Aarhus, Denmark.

When isolated mammalian skeletal muscle is exposed to 37°C, performance rapidly and irreversibly declines. Also, extracellularly measured superoxide (O2• −) is markedly greater at 37°C than at 23°C. This can reduce muscle performance at temperatures above 40°C, by reducing contractile apparatus function. We investigate which excitation-contraction coupling steps contribute to the decline in performance at 37°C. Rats were killed by cervical dislocation or by halothane overdose. Single mechanically-skinned fibres were prepared from EDL muscles kept in Krebs-Ringer Solution (KRS) at 22°C or 37°C (30min). Skinned fibres were then activated at 22°C in solutions of different pCa. The resting membrane potential (RMP) and intracellular action potential (AP) were measured at 22°C in single fibres before and after 40min incubation in KRS at 22°C or 37°C. Results show that exposure to 37°C (30min) caused no significant effect on either the maximum Ca2+-activated specific force or on the Ca2+-sensitivity of the contractile apparatus. However, the RMP became depolarized (∼10mV) and the AP amplitude was reduced by ∼35mV following 37°C treatment (40min). Additionally, the depolarisation and repolarisation rate was significantly slower compared to control fibres (22°C). Tempol (1mM) largely ameliorated the effects of 37°C on the RMP, AP amplitude and maximum rate of repolarisation. In summary, the increased rate of O2• − production at 37°C significantly reduces membrane excitability, explaining to a large extent the concomitant reduction in tetanic force observed in the isolated rat EDL muscle under the same conditions.