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 contracti le responses that are related to Ca2+ release from the sarcoplasmic reticul um. However, the effect of cooling has generally been studied in the presen ce of pharmacological agents that potentiate rapid cooling-induced contract ures. The present study shows that in saponin-skinned rat skeletal muscle p reparations, a drop in temperature from 22 degreesC to 2 degreesC per se in duces a contracture which relaxes on return to 22 degreesC. In fast-twitch fibres, rapid cooling-induced contractures are fully blocked by ryanodine, an inhibitor of ryanodine receptors. By contrast, in slow-twitch fibres, ry anodine partially inhibits the rapid cooling-induced contractile response, leaving a residual tension that dissipates after application of inositol 1, 4,5-trisphosphate (InsP(3)). At low concentrations, heparin, an inhibitor o f InsP(3) receptors, decreases rapid cooling-induced contractures in both t ypes of muscle. The present results suggest that in skeletal muscle, rapid cooling-induced contractures are due to both ryanodine-sensitive and InsP(3 )-sensitive Ca2+ release from the sarcoplasmic reticulum.