Research
Macro partitioning
Sustained hyperactivation of mTORC1 in skeletal muscle eventually causes atrophy and myopathy by inhibiting autophagy, whereas acute activation promotes hypertrophy.
While building muscle requires turning on growth signals, keeping them on constantly can damage muscle over time. Regular periods of rest and low signaling (like fasting or rest days) allow your muscles to recycle damaged parts, preventing long-term deterioration.
GoodQualifiesHIGH confidence
sustained mTORC1 hyperactivation eventually precipitates atrophy in most muscles and premature death... The features of this myopathy are very similar to the ones developed by mice with a specific deletion of Atg7 in the skeletal muscle
Why this rating
Based on genetic mouse models (Tsc1 KO, Raptor KO) showing clear phenotypic differences between acute and chronic mTORC1 states.
Source
The mTOR–Autophagy Axis and the Control of Metabolism
Nerea Deleyto-Seldas et al. · Frontiers in Cell and Developmental Biology · 2021
DOI 10.3389/fcell.2021.655731
narrative_reviewCited 325×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Inhibition of mTORC1 activity is a necessary physiological trigger for initiating autophagy during nutrient deprivation, which recycles cellular components to sustain blood glucose and amino acid levels.Good
- Enhancing autophagy through genetic or pharmacological means improves glucose tolerance, insulin sensitivity, and resistance to obesity in high-fat diet models.Good
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