Muscle atrophy frequently occurs in patients with anterior cruciate ligament (ACL) injury, despite active participation in muscle strengthening programs. Without appropriate countermeasures such as exercise and pharmacological interventions, the atrophy may worsen. At the cellular and molecular levels, various protein synthesis‑related pathways and redox‑dependent molecules regulate processes associated with atrophy by activating or deactivating key signaling pathways. Muscle atrophy and the associated dysfunction can be reversed by physical exercise, which increases protein synthesis, thereby improving muscle strength and function around the ACL. However, the influence of different features of exercise protocols, including exercise type, intensity and duration, as well as the individual capacity of the patient, on the activity of the aforementioned pathways requires further investigation. Additionally, the mechanism by which redox‑sensitive molecules attenuate atrophy in ACL injury remains to be fully understood. The present review discusses exercise, signaling pathways and muscle atrophy in ACL injury, and highlights potential therapeutic strategies. These findings may also have implications for other joint diseases associated with ACL‑related injury.