Mixed
Disuse atrophy involves complex, fiber-type-specific interactions between myonuclear domain maintenance, satellite cell (SC) dynamics, and molecular signaling pathways (MAFbx/MuRF1, IGF1-AKT-mTOR, Myostatin), where previous hypertrophy may protect against myonuclear loss.
Disuse atrophy is not a simple loss of muscle mass but a complex cellular response involving myonuclei, satellite cells, and signaling pathways. Previous muscle growth (hypertrophy) may protect against some aspects of atrophy, such as myonuclear loss. Recovery requires re-applying mechanical load, and nutrient supplementation (e.g., amino acids) may enhance this. The response varies by fiber type and the severity/duration of disuse.
Skeletal muscle wasting with disuse atrophy is multi-dimensional: the response and interaction of myonuclei, satellite cells and signaling pathways... Apoptosis as a mechanism for myonuclear loss with atrophy is controversial, whereas cell death of satellite cells has not been considered. Molecular signals such as myostatin/SMAD pathway, MAFbx, and MuRF1 E3 ligases of the ubiquitin proteasome pathway and IGF1-AKT-mTOR pathway are 3 distinctly different contributors to skeletal muscle protein adaptation to disuse.
Why this rating
High-quality review article synthesizing multiple human and animal studies, though it highlights controversies and lack of consensus on some mechanisms.
Source
Skeletal muscle wasting with disuse atrophy is multi-dimensional: the response and interaction of myonuclei, satellite cells and signaling pathways
Naomi Elisabeth Brooks et al. · Frontiers in Physiology · 2014
DOI 10.3389/fphys.2014.00099
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