Pathway link LOAD-MTORC1
Resistance exercise / mechanical load mTORC1
Resistance exercise / mechanical load activates mTORC1.
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.
The conditions it 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.
- Time it takes
- hours
- Step
- indirect (through steps not drawn here)
- Measured in
- human, mouse
- Where in the cell
- lysosome
- Reaches people?
- shown in people
- How settled
- settled in the literature
Studies behind it
| Year | Evidence | Study |
|---|---|---|
| 2009 | H | Rapamycin administration in humans blocks the contraction-induced increase in skeletal muscle protein synthesisDRU2009 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 vivoBOD2001 Akt/mTOR signalling is necessary and sufficient to drive skeletal-muscle hypertrophy and counteract atrophy in vivo. |
Points the other way
No study in the Atlas contradicts this link. That means none in this curated set, not none in the literature.
Who has checked this
- Checked by
- No researcher outside the project has checked this link yet.
- Curator sign-off
- Not signed off yet. This link was drafted with AI help and has not been reviewed link by link; treat it as a proposal until it is.
- Curated by
- Oliver Barton, with AI help for drafting; see how links are checked.
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