Abstract

We tested the hypothesis that endurance training results in changes in inositol triphosphate (InsP3) production from membrane phosphoinositides in trained muscles during contractile activity, which might have implications for fatigue involving calcium-release mechanisms. The extensor digitorum longus (EDL) muscles of endurance-trained rats were measured for membrane phosphoinositides, fatigability, and the production of inositol phosphates resulting from a 10-s tetanic contraction in vitro. In the latter, training resulted in a 22% increase in the production of inositol phosphates, in spite of lower phosphoinositides per muscle. In a separate group of animals, pretreatment of EDL in vitro for 15 min with 20 mM lithium resulted in a gradual decrease in tetanic forces at 100 Hz and increased fatigability. These results show for the first time that this metabolic system adapts to increased use and may contribute to the associated increased fatigue resistance, through its modulation of calcium release by sarcoplasmic reticulum.

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