Our findings suggest that the following actions could be taken to avoid such an impairment: (i) inhibition of the activity of XO could reduce the initial induction of nonmitochondrial ROS; (ii) restoration of the function of SIRT1 and PGC-1β could rescue mitochondrial function and inhibition of NOX2; (iii) antioxidant treatment could further reduce the muscle atrophy; and (iv) as muscle proteins are impacted by the 2-AA-mediated inhibition of ubiquitin ligases, maintenance of these important sarcomeric proteins could prove to be beneficial in the context of infection. The gene discussed is SIRT1; the disease is infection.