Resistance exercise / mechanical load
Mechanical loading of skeletal muscle, the physiological stimulus for hypertrophy, acting through mTORC1.
Lifting something heavy. Lifting something heavy.
One of the very few places in this map where the causal chain has been interrupted in living humans: rapamycin blocks the contraction-induced rise in muscle protein synthesis (DRU2009). The upstream route is only partly IGF-1-dependent – mechanical load reaches mTORC1 through mechanisms that do not require circulating growth factor, which is why loading and hormone signalling are not interchangeable.
TL;DR. Resistance exercise / mechanical load appears in 2 curated studies in Oliver's mTOR Atlas: 1 in people (1 human study); 1 in animal models. It has 1 interaction in the curated pathway model.
In the pathway model
| Interaction | Mechanism | Evidence | Studies |
|---|---|---|---|
| Resistance exercise / mechanical load activates mTORC1 mechanism: signal-relay · this link in full · on the map table | Working a muscle raises mTORC1 activity in it. When volunteers took rapamycin, the rise in muscle protein building after exercise was blocked, so in people, and not only in cell dishes, mTORC1 sits between the effort and the response. The map draws one arrow, but load reaches mTORC1 by several routes, and this result does not show which one carries the signal. Mechanical loading raises mTORC1 signalling in skeletal muscle. Rapamycin given to human volunteers blocks the contraction-induced increase in muscle protein synthesis, placing mTORC1 causally between the load and the response. Mechanical loading raises mTORC1 signalling in skeletal muscle. Rapamycin given to human volunteers blocks the contraction-induced increase in muscle protein synthesis, placing mTORC1 causally between the load and the response. Holds under: Compressed: load reaches mTORC1 through several routes, only some of which need IGF-1, and the map draws one arrow. The human evidence establishes that mTORC1 is required, not which upstream route carries the signal. shown in people · settled in the literature | H | DRU2009, BOD2001 |
Evidence at a glance
| Evidence | What it means | Studies |
|---|---|---|
| H | Human study | 1 |
| A | Animal model | 1 |
Studies
| Year | Evidence | Study |
|---|---|---|
| 2009 | H | Rapamycin administration in humans blocks the contraction-induced increase in skeletal muscle protein synthesis DRU2009 Rapamycin given before resistance exercise completely blocked the normal post-exercise increase in human muscle protein synthesis. |
| 2001 | A | Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo BOD2001 Akt/mTOR signalling is necessary and sufficient to drive skeletal-muscle hypertrophy and counteract atrophy in vivo. |
Related entities
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