Mixed
In preclinical rodent models, disuse atrophy involves both decreased protein synthesis and increased protein degradation, with the extent of degradation being muscle-specific and dependent on fiber type.
While rodent studies show that muscle breakdown increases during disuse, human studies suggest this is not the primary driver. This highlights the importance of not blindly applying animal research to human health advice. For humans, maintaining synthesis (via minimal movement/nutrition) is likely more critical than worrying about breakdown rates.
In summary, changes in muscle mass following unloading in rats are a consequence of the net changes in both protein synthesis and degradation... Predominantly slow oxidative antigravity muscles appear to be the most susceptible to atrophy in response to unloading, exhibiting decreases in protein synthesis and increases in multiple degradation pathways.
Why this rating
Based on detailed preclinical studies in rats with multiple time points and muscle types.
Source
Control of skeletal muscle atrophy in response to disuse: clinical/preclinical contentions and fallacies of evidence
Philip J. Atherton et al. · American Journal of Physiology-Endocrinology and Metabolism · 2016
DOI 10.1152/ajpendo.00257.2016
More from this paper
- Disuse-induced muscle atrophy in humans is primarily driven by a sustained reduction in muscle protein synthesis (MPS) rather than an increase in muscle protein breakdown (MPB).Good
- Immobilization induces rapid muscle insulin resistance (MIR) within 3-5 days, which may contribute to the dysregulation of protein metabolism, although a direct causal link to atrophy is not fully established.Good
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