Disuseatrofia

Disuse atrophy, or disuseatrofia, is the loss of skeletal muscle mass and strength that occurs when muscles are not regularly stimulated by movement or are immobilized for a period of time. It is a reversible form of muscle wasting and is distinct from neurogenic atrophy, cachexia, or age-related sarcopenia.

Causes and risk factors include limb immobilization after fractures or surgery, prolonged bed rest due to illness, casting or splinting, and sedentary lifestyle. Situations such as extended spaceflight or chronic illnesses that limit activity can also trigger disuse atrophy. It most commonly affects the muscles of the immobilized limb and nearby muscle groups.

Pathophysiology involves reduced mechanical loading leading to changes in muscle protein turnover. There is decreased protein synthesis and increased proteolysis, mediated in part by pathways such as the ubiquitin–proteasome system and autophagy. Muscle fiber cross-sectional area, especially type II fibers, declines, and there may be accompanying reductions in mitochondrial content and capillary density.

Clinical features include progressive reduction in muscle mass and strength in the affected region, sometimes with visible limb girth loss and decreased endurance. Diagnosis is based on history of reduced activity or immobilization, supported by imaging studies showing muscle thinning. Ultrasound can assess muscle thickness quickly; MRI or CT provides detailed structural information; DXA can estimate lean mass.

Management focuses on removing or reducing disuse through early mobilization and progressive resistance exercise. Physical therapy, functional training, and sometimes electrical stimulation aid recovery. Adequate nutrition, with sufficient protein intake, supports rehabilitation. Prognosis is generally favorable with timely retraining, though recovery may be slower after prolonged or severe disuse. Prevention emphasizes maintaining activity and gradual reconditioning after immobilization.