Rapid cooling-induced contractures in rat skinned skeletal muscle fibres originate from sarcoplasmic reticulum Ca2+ release through ryanodine and inositol trisphosphate receptors.

Previous reports have shown that cooling striated muscles induces contractile responses that are related to Ca2+ release from the sarcoplasmic reticulum. However, the effect of cooling has generally been studied in the presence of pharmacological agents that potentiate rapid cooling-induced contractures. The present study shows that in saponin-skinned rat skeletal muscle preparations, a drop in temperature from 22 degrees C to 2 degrees C per se induces a contracture which relaxes on return to 22 degrees C. In fast-twitch fibres, rapid cooling-induced contractures are fully blocked by ryanodine, an inhibitor of ryanodine receptors. By contrast, in slow-twitch fibres, ryanodine partially inhibits the rapid cooling-induced contractile response, leaving a residual tension that dissipates after application of inositol 1,4,5-trisphosphate (InsP3). At low concentrations, heparin, an inhibitor of InsP3 receptors, decreases rapid cooling-induced contractures in both types of muscle. The present results suggest that in skeletal muscle, rapid cooling-induced contractures are due to both ryanodine-sensitive and InsP3-sensitive Ca2+ release from the sarcoplasmic reticulum.