These structural changes were accompanied by the down‐regulation of genes associated with the development of muscular atrophy during aging (myostatin, atrogin‐1, foxo‐1, dystrophin) (Figure 5I).[66, 67, 68, 69] Moreover, CHP substantially increased the expression of nrf‐2, a well‐known master regulator of redox homeostasis and antioxidant capacity[70] (Figure 5I). This evidence concerns the gene MSTN and muscular atrophy.