ABSTRACT
BACKGROUND: High-intensity exercise can induce the depolymerization and/or degradation of tubulin in the skeletal muscle. According to the close relation with the mitochondria, tubulin may influence mitochondrial movement track and molecular motor, thereby varying the movement and distribution of mitochondria. OBJECTIVE: To observe the effect of high-intensity exercise on α-tubulin, MAP4, Miro1 and mitochondrial ultrastructures, analyze their sequential changes and further explore whether tubular depolymerization regulates the movement and distribution of mitochondria via Miro1. METHODS: Fifty-six Sprague-Dawley rats were divided into control (n=8) and exercise (n=48) groups. The rats in the exercise group ran on the treadmill ( -16°, 20 m/minute) for 90 minutes, and the soleus samples were removed immediately, 6, 12, 24, 48 and 72 hours after exercise (n=8 each time point). The expression levels of α-tubulin, MAP4 and Miro1 were detected by western blot assay, and the ultrastructural changes of mitochondria were observed under transmission electron microscope. RESULTS AND CONCLUSION: The expression level of α-tubulin was decreased significantly at 6 and 12 hours after exercise. The expression level of MAP4 was increased significantly at 6, 12, 48 and 72 hours after exercise. The expression level of Miro1 was increased firstly at 6 and 12 hours after exercise, and decreased at 72 hours after exercise. In the control group, the paired mitochondria were arranged on the both sides of Z line, and few appeared in the myolemma. Mitochondria began to accumulate in the myolemma immediately and 6 hours after exercise; the number achieved the peak at 12 hours, reduced at 24 and 48 hours, and returned to normal at 72 hours. These results suggest that high-intensity exercise can induce the depolymerization of microtubules in the skeletal muscle, thus regulating the movement and distribution of mitochondria via Miro1.