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.%背景:大强度运动可诱导骨骼肌微管蛋白的解聚或降解,通过其与线粒体的密切联系,从而影响线粒体的运动轨道以及分子马达,从而改变线粒体的移动和分布.目的:观察一次大强度运动对骨骼肌α-tubulin蛋白、MAP4蛋白和Miro1蛋白的影响,以及对线粒体超微结构的影响,分析它们之间的时序性变化,探讨微管蛋白的解聚是否可以通过与Miro1蛋白的作用,从而对骨骼肌线粒体的移动和分布产生调控作用.方法:56只SD大鼠经适应训练后分为安静对照组(8只)和运动组(48只),运动模型为一次大强度跑台运动,-16°下坡跑,20 m/min,90 min.将运动组大鼠分别在运动后即刻,6 h,12 h,24 h,48 h和72 h(每个时间点8只)取比目鱼肌.Western blotting检测α-tubulin、MAP4和Miro1的蛋白表达,透射电镜观察线粒体的超微结构.结果与结论:①α-tubulin蛋白表达在运动后6 h和12 h显著降低;②MAP4蛋白表达在运动后6,12,48和72 h均显著升高;③Miro1蛋白表达在运动后6 h和12 h有升高趋势,在72 h下降;④电镜下线粒体在安静状态时成对排列于Z线两侧,肌膜下较少;运动后即刻和6 h在肌膜下开始积聚;12 h后在肌膜下积聚和损伤最为严重;24 h和48 h后肌膜下肌膜减弱;72 h后已恢复至安静状态.⑤结果表明,一次大强度运动可能诱导骨骼肌微管的解聚,并可能通过对Miro1的作用,从而调节线粒体的移动和分布.
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