Skeletal muscle injuries are prone to induce fatigue, decrease resistance and imbalances in the body. Although ovalbumin (OVA) has such biological effect as promoting tissue development and immunomodulation, its impact on repairing skeletal muscle injuries has been rarely reported. In this study, a mouse model of muscle injury was constructed and found that OVA significantly increased muscle weight, muscle thickness, and exercise capacity in muscle-injured mice. Meanwhile, OVA improved the morphology of muscle tissues by reducing serum levels of urea nitrogen, creatine kinase, and lactate dehydrogenase, as well as decreasing the levels of inflammatory factors interleukin (IL)-1β, tumor necrosis factor α, and IL-6, respectively. In addition, transcriptomic and metabolomic analyses revealed that OVA could enhance muscle tissue morphology by upregulating the phosphatidylinositol 3-kinase-protein kinase B signaling pathway and improving amino acid metabolism through the upregulation of Col11a2, Ccn2, Thbs1, Tnc, Klf2, Bcl2l1, Adh3a1, and Rsad1. The study provided a theoretical foundation for understanding the molecular mechanisms in OVA-aided muscle injury repair.