Hormonal
Chronic activation of mTORC1 signaling in aging skeletal muscle leads to mitochondrial dysfunction, oxidative stress, and muscle senescence, resulting in sarcopenia rather than hypertrophy.
While stimulating muscle growth pathways like mTOR is essential for building muscle, doing so chronically without adequate recovery or in older age can backfire, leading to muscle loss and cellular aging. Focus on balanced training and nutrition that supports both synthesis and cellular cleanup (autophagy) rather than constant, maximal stimulation.
A mounting body of evidence implicates the chronic activation of mTOR in aging skeletal muscle, where mTORC1 signaling is hyperactivated in muscle of sarcopenic mice and humans [24,25]. Chronic activation of mTOR in TSC1 knockout muscle results in mitochondrial dysfunction and increased oxidative stress, which over time ultimately leads to fiber decay.
Why this rating
The paper is a review summarizing multiple studies (including mouse models and human observations), but lacks a single definitive clinical trial establishing causality in humans.
Source
Signaling Pathways That Control Muscle Mass
Anna Vainshtein et al. · International Journal of Molecular Sciences · 2020
DOI 10.3390/ijms21134759
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