Abstract
Homozygosity for the common ACTN3 null polymorphism (ACTN3 577X) results in α-actinin-3 deficiency in ∼20% of humans worldwide and is associated with reduced sprint and power performance in both elite athletes and the general population. α-Actinin-3 deficiency is also associated with reduced muscle mass and strength, increased sarcopenic risk in the elderly, and modifies disease severity and progression in a number of neuromuscular disorders such as Duchenne muscular dystrophy (DMD). Using an Actn3 knockout mouse model, we now show that α-actinin-3 plays a key role in the regulation of protein synthesis and breakdown in skeletal muscle, and its influence on muscle mass begins during early postnatal muscle development.
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