Cell apoptosis and expression of malondialdehyde in the skeletal muscle in a model rat undergoing long-term and high-intensity exercise / 中国组织工程研究

ABSTRACT

BACKGROUND: Apoptosis in the skeletal muscle leads to a variety of skeletal muscle diseases, but there are ideal no therapies so far. OBJECTIVE: To analyze the effects of different intensities of exercises on the morphology and apoptosis of the skeletal muscle in rats. METHODS: Thirty healthy male 3-month-old Sprague-Dawley rats were randomly allocated into three groups (n=10 per group) control group (no swimming), aerobic exercise and high-intensity exercise groups. The rats in the exercise groups underwent swimming for consecutive 10 weeks. Then, the gastrocnemius muscle was isolated from all rats under anesthesia. The morphology and cell apoptosis were detected by hematoxylin-eosin staining and TUNEL test. At the same time, the levels of superoxide dismutase and malondialdehyde in skeletal muscle tissue were tested and the correlation of malondialdehyde with integrated optical density (IOD) was analyzed. RESULTS AND CONCLUSION: The results of hematoxylin-eosin staining showed that the muscle fibers were in disorder arrangement with obscure structure in the high-intensity exercise group. Compared with the control group, the content of malondialdehyde was increased in the exercise groups, especially in the aerobic exercise group (P < 0.05). The level of superoxide dismutase in the high-intensity exercise group was significantly lower than that in the aerobic exercise group (P < 0.05). The results of TUNEL test showed that the IOD values in the high-intensity exercise group were significantly higher than those in the aerobic exercise and control groups (P < 0.05). There was a positive correlation of malondialdehyde with IOD. These results indicate that the long-term and high-intensity exercise can increase the content of malondialdehyde in the skeletal muscle, resulting in an aggravation of fatigue. Aerobic exercise can obtain the adaptation of the skeletal muscle, but damage the morphology and structure of the skeletal muscle because of excessive exercise load, thus accelarating the cell apoptosis. With the exercise intensity increasing, the balance between malondialdehyde production and clearance is broken, and the IOD value is increased.