Muscle hypertrophy, atrophy and remodeling !
- Concept
- For completeness
Muscle grows with load and shrinks with disuse, illness or age, because it constantly builds and breaks down its proteins.
Updated 2026-11-01
Also called: Sarcopenia, Disuse atrophy
See it in 3D: Vastus lateralis · Gastrocnemius (inner head)
What it is
Muscle mass reflects the balance between protein synthesis and breakdown. Mechanical load, amino acids, insulin and IGF-1 drive synthesis through the mTOR pathway, enlarging existing fibers (hypertrophy). Disuse, denervation, inflammation, cortisol and aging tip the balance toward breakdown by the ubiquitin–proteasome system and autophagy (atrophy).
Key facts
- Myostatin is a negative regulator of muscle mass; its loss produces marked muscularity in animals.
- Sarcopenia is age-related loss of muscle mass and strength, with preferential loss of type II fibers.
- Critically ill patients can lose a large share of leg muscle within the first week of intensive care.
- In muscular dystrophies, repeated cycles of damage and repair exhaust satellite cells and fibers are replaced by fat and fibrous tissue.
Regulation
- +Mechanical load (resistance exercise): Activates mTORC1 and satellite cells: fiber enlargement
- +Insulin, IGF-1, testosterone, amino acids: Increase protein synthesis
- −Myostatin: Restrains fiber growth and satellite cell activity
- −Cortisol and inflammatory cytokines: Increase proteolysis: catabolic wasting
- −Disuse and denervation: Synthesis falls, ubiquitin–proteasome breakdown rises
Clinical notes
- Duchenne muscular dystrophy: lack of dystrophin causes continuous damage; calf pseudohypertrophy reflects fat and fibrous tissue, not real muscle gain.
- Prolonged glucocorticoid exposure (Cushing syndrome or long-term therapy) causes proximal muscle wasting.
- Early mobilization in hospital limits disuse atrophy and speeds recovery, especially in older adults.
Test yourself
Think of the answer, then tap the question to see it.
Why does resistance training enlarge a muscle mainly through hypertrophy rather than hyperplasia?
Mature fibers are post-mitotic. Load activates mTORC1 to add myofibrils, and satellite cells fuse into existing fibers to supply extra nuclei rather than forming many new fibers.
Why does a denervated muscle waste faster than a muscle in a cast?
Denervation removes all neural activity and neurotrophic signals, so synthesis falls and proteolysis rises more sharply; fibers also become unstable and fibrillate.
Why can a boy with Duchenne muscular dystrophy have large calves yet be weak?
The calves are enlarged by fat and fibrous tissue that replace damaged fibers (pseudohypertrophy), so contractile muscle is actually reduced.
See it in 3D
The structures of Durgical's 3D anatomy where it happens.
Related topics
- Fast and slow fibers, energy and fatigue
- Exercise and training physiology
- Motor units, recruitment and summation
Related conditions
In Biochemistry
Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.
Sources: 10.6 Exercise and Muscle Performance (OpenStax (Rice University), 2022); Duchenne and Becker muscular dystrophy: MedlinePlus Genetics (MedlinePlus, US National Library of Medicine, 2024); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 6). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).
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Representative model, for educational purposes only.