{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T22:21:07Z","timestamp":1791066067507,"version":"4.1.0"},"reference-count":56,"publisher":"Wiley","issue":"22","license":[{"start":{"date-parts":[[2011,11,14]],"date-time":"2011-11-14T00:00:00Z","timestamp":1321228800000},"content-version":"vor","delay-in-days":13,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2011,11]]},"abstract":"<jats:p>\n                    <jats:bold>Non\u2010Technical Summary\u2002<\/jats:bold>\n                    Chronic mechanical loading (CML) of skeletal muscle induces growth and this effect can be blocked by the drug rapamycin. Rapamycin is considered to be a highly specific inhibitor of the mammalian target of rapamycin (mTOR), and thus, many have concluded that mTOR plays a key role in CML\u2010induced growth. However, direct evidence that mTOR confers the CML\u2010induced activation of growth promoting events such as hypertrophy, hyperplasia and ribosome biogenesis is lacking. This study addressed that gap in knowledge by using a specialized line of transgenic mice. Surprisingly, the results indicate that only a few of the growth promoting events induced by CML are fully dependent on mTOR signalling (e.g. hypertrophy). 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