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Rapamycin prevents muscle growth and the increase in MHCIIa induced by voluntary wheel running
Author(s) -
Patchen Bonnie,
Swoap Steven J
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1086.24
Subject(s) - pi3k/akt/mtor pathway , wheel running , muscle hypertrophy , soleus muscle , skeletal muscle , endocrinology , medicine , western blot , chemistry , microbiology and biotechnology , biology , signal transduction , biochemistry , gene
Mammalian target of rapamycin (mTOR) and its downstream signaling proteins are known to be involved in skeletal muscle adaptation in response to resistance training. As both muscle hypertrophy and endurance running induce a transition to a slower muscle fiber phenotype, we tested the hypothesis that inhibition of the mTOR pathway with oral rapamycin would prevent the fast‐to‐slow transition in response to voluntary wheel running. C57Bl/6J mice were randomly assigned to a control diet or a diet containing rapamycin and fed for 5 weeks. Mice were then given access to a running wheel or a locked wheel for 7 additional weeks. Rapamycin had no effect on body mass or daily running distance, suggesting that rapamycin treatment did not adversely affect running performance. Western blot analysis of mTOR targets demonstrated that rapamycin inhibited mTOR signaling. Wheel running elevated soleus to body mass ratios only in control fed mice. Wheel running increased the expression of the MHCIIa isoform in the triceps, which was prevented by rapamycin. These data support the hypothesis that the mTOR signaling pathway plays a role in the phenotypic changes that occur in muscle with wheel running.