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Inhibition of stretch-activated channels during eccentric muscle contraction attenuates p70^S6K activation

¹Exercise Biology Program, Division of Biological Sciences, and ²Department of Physiology and Membrane Biology, School of Medicine, University of California-Davis, Davis; and ³Department of Biology, California State University, Bakersfield, California

Submitted 24 May 2005 ; accepted in final form 15 September 2005

Eccentric contractions (EC) are known to result in muscle hypertrophy, potentially through activation of the Akt-mammalian target of rapamycin-p70 S6 kinase (p70^S6K) signaling pathway. Previous work has also demonstrated that EC result in the opening of stretch-activated channels (SAC), and inhibition of these channels resulted in an attenuation of EC-induced muscle hypertrophy. The purpose of this study was to test the hypothesis that a known intracellular pathway directly associated with muscle hypertrophy is coupled to the opening of SAC. Specifically, we measured the activation of the Akt, GSK-3, p70^S6K, and ribosomal protein S6 following a single bout of EC in the rat tibialis anterior (TA) muscle. The TA muscles performed four sets of six repetitions of EC. In vivo blockade of SAC was performed by a continuous oral treatment with streptomycin in the drinking water (4 g/l) or by intravenous infusion of 80 µmol/kg gadolinium (Gd³⁺). EC increased the degree of Akt and p70^S6K phosphorylation in the TA muscle, whereas in animals in which SAC had been inhibited, there was a reduced capacity for EC to induce Akt or p70^S6K phosphorylation. Accompanying this reduced activation of Akt and p70^S6K was a failure to phosphorylate GSK-3 or S6 when SAC were inhibited. The results from these data indicate the necessity of functional SAC for the complete activation of Akt and p70^S6K pathway in response to EC.

skeletal muscle; hypertrophy; Akt; membrane; ions

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