Hormonal
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.
If you have a disease involving inflammation (like cancer or sepsis), your muscle loss is driven by both increased breakdown and decreased synthesis due to inflammatory signals. Preventing loss requires addressing the underlying disease and inflammation, not just rest or exercise.
Contrasting with periods of muscle disuse in the absence of disease, both a diminished MPS and an elevated MPB can contribute to muscle atrophy during infections and disease states characterized by an inflammatory burden.
Why this rating
Based on review of clinical studies in sepsis, cancer, and critical illness.
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 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.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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