Human Skeletal Muscle Disuse Atrophy: Effects on Muscle Protein Synthesis, Breakdown, and Insulin Resistance-A Qualitative Review.
Level 5 - mechanism / opinion, no new human data
Narrative qualitative review without systematic search or meta-analysis
PubMed 27610086 · doi:10.3389/fphys.2016.00361
What was done
This qualitative review synthesized existing human literature examining the relationships between muscle protein synthesis (MPS), muscle protein breakdown (MPB), insulin resistance, and disuse skeletal muscle atrophy resulting from immobilization or sedentary behavior.
What was found
The abstract provides no quantitative effect sizes or numerical values. Qualitatively, immobilization decreases fasted-state MPS and induces fed-state anabolic resistance alongside muscle insulin resistance. The exact role of MPB remains undefined due to a lack of dynamic human measurements, though gene marker studies suggest potential early proteolytic elevation. The rate of disuse atrophy appears accelerated in chronic insulin-resistant states like type 2 diabetes.
Why it matters
It highlights that impaired anabolic signaling and reduced protein synthesis, rather than established surges in breakdown alone, are primary drivers of disuse-related muscle loss and metabolic decline.
Limits
The review relies on qualitative synthesis rather than systematic methods or meta-analysis. Dynamic measurements of human MPB are lacking across the summarized literature, and the contribution of baseline insulin sensitivity variations across different muscle groups remains uncharacterized.
Cited by
- supports Disuse muscle atrophy occurs primarily because of a reduction in muscle protein synthesis rates in both the fasted state and in response to amino acid feeding.