Muscle atrophy following anterior cruciate ligament reconstruction: A narrative review

Muscle weakness is a common issue following anterior cruciate ligament (ACL) reconstruction and is closely linked to muscle atrophy. Preventing or reducing this atrophy is a key goal of rehabilitation. This review summarizes current knowledge on muscle atrophy after ACL reconstruction, including its spatial distribution, time course, underlying mechanisms, and potential interventions. Atrophy affects multiple lower limb muscles and may be influenced by the type of graft used. Tendon harvesting appears to negatively impact the muscle belly of the donor muscle, while atrophy may also occur in the contralateral limb independently of graft harvesting. Muscle atrophy is often already present before surgery and tends to worsen postoperatively. Although partial recovery may occur, long-term deficits are frequently observed. At the muscle fiber level, evidence is inconsistent regarding which fiber types are more vulnerable to atrophy. A transient shift toward faster fiber types has been reported after surgery. On the cellular and molecular level, satellite cell depletion via apoptosis may hinder muscle regrowth and thereby contribute to persistent muscle atrophy. Concurrently, increased expression of myostatin, atrogin-1, and muscle RING-finger-1, along with postoperative inflammation, may promote protein degradation, further exacerbating muscle atrophy. Rehabilitation strategies that involve early immobilization or non-weight bearing may exacerbate atrophy. Interventions such as eccentric training, neuromuscular electrical stimulation, blood flow restriction training, pharmacological agents, and nutritional support demonstrate potential, but no definitive treatment has been established. Future studies using appropriate animal models to clarify the molecular mechanisms of muscle atrophy will be crucial for developing effective therapies.