In other studies, AMPKα phosphorylation and AMPKα1 and AMPKα2 activities were unaltered during aging at rest, but activation of AMPKα1 was enhanced, while activation of AMPKα2 was suppressed immediately after endurance-type muscle contractions in aged rats, resulting in inactive heterotrimer composition of AMPK and consequently increasing skeletal muscle atrophy sarcopenia [69]. The gene discussed is PRKAA1; the disease is muscular atrophy.