Muscle growth
mTORC1-dependent process of skeletal muscle fiber enlargement (hypertrophy); driven by growth factors and exercise, blocked by rapamycin.
Muscles getting bigger.
Raptor-null muscle is dystrophic and rapamycin blocks overload hypertrophy; but constitutive mTORC1 activation alone is not sufficient for healthy hypertrophy.
Evidence at a glance
| Evidence | What it means | Studies |
|---|---|---|
| H | Human study | 2 |
| M | Molecular — cells, biochemistry, structure | 1 |
Studies
| Year | Evidence | Study |
|---|---|---|
| 2025 | H | Influence of rapamycin on safety and healthspan metrics after one year: PEARL trial results MOE2025 First completed long-term RCT of rapamycin for healthy human aging (NCT04488601, 48 weeks, n=114). Primary endpoint (visceral fat by DXA) showed NO significant change (p=0.942) - a null result exactly as pre-registered. Secondary endpoints were more promising: women on the 10mg/week dose had significant improvements in lean muscle mass and self-reported pain. A textbook example of why the pre-registered primary endpoint, not the most exciting secondary finding, is what should drive the headline conclusion. |
| 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 | M | Mediation of IGF-1-induced skeletal myotube hypertrophy by PI(3)K/Akt/mTOR and PI(3)K/Akt/GSK3 pathways ROM2001 Shows IGF-1 drives muscle fiber hypertrophy specifically through the Akt-mTOR pathway, establishing mTORC1 as a central node for muscle growth signaling. |