Hormonal
In healthy humans, disuse-induced muscle atrophy is primarily driven by a significant reduction in muscle protein synthesis (MPS), while muscle protein breakdown (MPB) remains largely unchanged.
If you are immobilized or inactive but healthy, your muscle loss is not because your body is actively destroying muscle tissue, but because it has stopped building it. The primary lever to prevent loss is to restore the stimulus for muscle protein synthesis (e.g., through resistance exercise or adequate protein intake) rather than focusing solely on preventing breakdown.
It has been recognized that decreased MPS is the primary driving process leading to loss of muscle protein over time in disuse muscle atrophy in humans... declines of 50%–60% in both fasting (hypoaminoacidemia) and fed (hyperaminoacidemia) MPS during unloading support the theses that elevated MPB, and 'bulk' proteolysis has little, if any, contribution to the decrement in muscle mass observed during simple muscle disuse.
Why this rating
Based on a comprehensive review of multiple human trials showing consistent MPS reductions.
Source
Disuse-induced skeletal muscle atrophy in disease and nondisease states in humans: mechanisms, prevention, and recovery strategies
Everson Araújo Nunes et al. · American Journal of Physiology-Cell Physiology · 2022
DOI 10.1152/ajpcell.00425.2021
More from this paper
- In disease states (e.g., sepsis, cancer, critical illness), muscle atrophy is driven by both elevated muscle protein breakdown (MPB) and reduced muscle protein synthesis (MPS), mediated by inflammatory cytokines.Good
- Aging is associated with 'anabolic resistance,' where older adults require more protein to stimulate muscle protein synthesis (MPS) compared to younger adults, contributing to sarcopenia.Good
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