The most direct characteristic of muscle atrophy is reduction in muscle mass, which is due to increased protein degradation or reduced protein synthesis in skeletal muscle. The loss of muscle mass can directly affect the quality of daily life, prolong the recovery period, and become the main risk factor for chronic diseases. However, there is currently no effective way to prevent and treat this disease, and therefore it is imperative to explore effective therapeutic approaches for muscle atrophy. It is well known that physical exercise is important for maintaining good health and long-term adherence to exercise can reduce the risk of cardiovascular diseases, obesity, and diabetes. It is also well established that exercise training can promote the synthesis of muscle protein and activate signaling pathways that regulate the metabolism and function of muscle fibers. Therefore, exercise can be used as a method to treat muscle atrophy in many of these conditions. Mitochondria play an important role in skeletal muscle homeostasis and bioenergy metabolism. Mitochondria are sensitive to contractile signals, and hence exercise can improve mitochondrial function and promote biosynthesis, which ultimately maintains the healthy state of cells and the whole body. On the other hand, frequent unaccustomed exercise will change the structure and function of skeletal muscle fibers, which is called exercise-induced muscle damage. When the exercise-induced muscle damage happens, it can cause temporary muscle damage and soreness, giving a negative effect on the muscle function.
Keywords: Excessive exercise; Mitochondria; Muscle atrophy; Physical exercise.