ACTIVITY REGULATION OF SKELETAL ISOMYOSIN EXPRESSION

以前的研究提供了一些证据表明， 存在于骨骼肌中的肌球蛋白的类型可以通过酶促修饰， 反复的体力活动 然而，到目前为止，还没有研究表明， 被设计来充分测试肌球蛋白同工酶的假设， 给定肌肉的模式可以根据肌肉的运动来调节。 功能需求的引导速度和力施加在它的过程中 重复常规运动（跑步）。 我们打算测试一下 假设通过使用正常动物模型和超载模型，其中 通过手术分离内侧腓肠肌和股直肌， 主要负责涉及后肢的肌肉活动 肌肉组织 这种干预措施将限制快速抽搐的总数。 和参与运动的慢收缩运动单位，从而迫使任何 潜在的适应变得高度集中。 手术8周后 诱导超负荷，超负荷动物，沿着正常对照， 进行非常规的慢性运动计划，其中变量 （1）速度和（2）倾斜或增加动物的重量， 选择性地改变。 一些动物将被装备 肌电图记录，以监测相对激活的 运动过程中的肌肉 在给定的锻炼计划结束时， 将分析神经节的：（1）收缩和疲劳特性; (2)Ca ~（++）调节的肌原纤维ATP酶;（3）组织化学检测 纤维分型;（4）柠檬酸合酶活性;（5）肌球蛋白分析 包括ATP酶（包括碱性和酸性失活），光 链电泳模式和天然肌球蛋白电泳， 鉴定特异性快和慢同工酶。 通过这种组合， 我们应该能够评估生理刺激 改变骨骼肌的收缩基因表达 功能

Previous studies have provided some evidence to suggest that the different types of myosin present in skeletal muscle can be modified enzymatically by repeated bouts of physical activity. To date, however, no studies have been designed to adequately test the hypothesis that the myosin isozyme pattern of a given muscle can be regulated in accordance with the functional demands of gaiting speed and of force imposed on it during repeated conventional exercise (running). We propose to test this hypothesis by using a normal animal modeland an overload model in which the medial gastrocnemius and rectus femoris muscles are surgically isolated to be primarily responsible for muscle activity involving the hindlimb musculature. This intervention will limit the total number of fast-twitcha nd slow-twitch motor units participating in locomotion, thereby forcing any potential adaptation to become highly focused. After 8 weeks of surgical induced overload, the overloaded animals, along with normal controls, will be subjected to identicle chronic exercise programs in which the variables of (1) speed and (2) incline or weight addition to animals will be selectively changed. some animals will be instrumented for electromyographic recordings to monitor the relative activation of the muscles during locomotion. At the termination of a given exercise program, the nuscles will be analyzed for: (1) contractile and fatigue properties; (2) Ca++ regulated myofibril ATPase; (3) histochemistry to assess fiber-typing; (4) citrate synthase activity; and (5) myosin analyses consisting of ATPase (including alkaline and acid inactivation), light chain electrophoretic patterns, and native myosin electrophoresis to identify specific fast and slow isozymes. With this combination of exercise models, we should be able to assess how physiological stimuli alter the genetic expression of skeletal muscle in terms of contractile function.