Abstract

Aim. The role of mitochondrial KATP (mitoKATP) channels on muscle fatigue was assessed in adult mouse skeletal muscle fibers.Methods. Muscle fatigue was produced by eliciting short repetitive tetani. Isometric tension and the rate of production of reactive oxygen species (ROS) were measured at room temperature (20-22°C) using a force transducer and the fluorescent indicator CM-H2DCFDA.Results. We found that opening mitoKATP channels with diazoxide (100 ∈μM) significantly reduced muscle fatigue. Fatigue tension was 34% higher in diazoxide-treated fibers relative to controls. This effect was blocked by the mitoKATP channel blocker 5-Hydroxydecanoate (5-HD), by the protein kinase C (PKC) inhibitor chelerythrine, and by the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine methyl ester hydrochloride (L-NAME). We found that the rate of ROS production in muscle fibers incubated with diazoxide under non-fatigue and fatigue conditions was similar to control experiments, but that the increase in the rate of ROS production during recovery from fatigue was greatly reduced.Conclusions. A physiological role of mitoKATP channels on muscle fatigue is proposed.Diazoxide, an opener of mitoKATP channels, reduces muscle fatigue possibly through a preservation of mitochondrial volume and function.This work was supported in part by CONACYT grants 82667 (JS) and 60880 (MCG).

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