Abstract:

BACKGROUND: Studies have shown that cell apoptosis can increase free radical, elevate Ca2+ concentration, and decrease mitochondrial membrane potential, ultimately reducing motor function. Therefore, understanding of relationship between apoptosis and exercise training is very important.
OBJECTIVE: To summarize questions recording muscle exercise and apoptosis in skeletal muscle.
METHODS: A computer-based online search of CNKI (http://dlib.cnki.net/kns50/index.aspx), and PubMed (http://www.ncbi.nlm.nih.gov/pubmed/) was performed to collect articles published between January 1990 and June 2009 with the key words “muscle exercise, apoptosis in the skeletal muscle” in Chinese and English, respectively. Articles highly correlated with current status and development of muscle exercise and apoptosis in the skeletal muscle were included: ①studies on apoptosis in the skeletal muscle; ②studies concerning exercise and apoptosis in the skeletal muscle; ③studies involving gene regulation of exercise-induced apoptosis in the skeletal muscle; ④studies on molecular mechanism of apoptosis in the skeletal muscle; ⑤studies published in latest journal or similar field. Repetitive studies were excluded.
RESULTS AND CONCLUSION: After exercise, apoptosis occurs in normal muscle or muscle under pathologic state. The apoptosis of skeletal muscle cells is similar to common cell apoptosis, including karyopyknosis, plasma membrane vacuole, cell organ shrinking, and apoptotic body formation. The apoptosis process is classified into three stages: initial, effector, and degradation stages. The increased apoptosis in the skeletal muscle is the primary reason for sports fatigue. Currently, studies of gene regulation of apoptosis in the skeletal muscle focus on apoptosis regulatory factor Bcl-2 protein, tumor necrosis α and death protease cysteine aspartase. The bcl-2 inhibits opening of mitochondrial permeability transition pore, suppresses proapoptosis protein release from mitochondria, and prevents mitochondrial membrane lipid peroxidation and mitochondrial matrix Ca2+ release to play anti-apoptotic effect. Tumor necrosis family plays an important role in initializing death factor and its receptor pathways, which depends on death ligand binding death receptor to activate cysteine aspartase and lead to cell apoptosis. The exploration of the relationship between exercise intensity and apoptosis and necrosis in skeletal muscle assists better understanding of the movement mechanism of exercise-induced fatigue and effectively reducing fatigue.