MYOSIN ISOZYMES IN OVERLOADED SKELETAL MUSCLE

以前的研究已经提供了一些证据表明，不同的 骨骼肌中存在的肌球蛋白类型可以通过以下方式进行酶修饰 反复的体力活动。然而，到目前为止，还没有研究表明 旨在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 运动中对步态速度和力量的功能要求 重复常规运动(跑步)。我们建议对此进行测试 通过使用正常动物模型和过载模型进行假设，其中 手术分离腓肠肌内侧肌和股直肌 主要负责涉及后肢的肌肉活动 肌肉学。这一干预措施将限制快速抽搐的总数 和参与运动的慢抽动马达单元，从而迫使任何 潜在的适应将变得高度集中。在8周的手术后 诱导的超负荷，超负荷的动物和正常的对照组将 接受确定的慢性运动计划中的变量 (1)速度和(2)动物的倾斜或体重增加将是 有选择地改变。一些动物将被用仪器测量 肌电记录以监测细胞的相对激活 运动时的肌肉。在给定的锻炼计划结束时， 将从以下几个方面分析节块：(1)收缩和疲劳性能； (2)钙离子调节的肌原纤维ATPase；(3)组织化学检测 纤维分型；(4)柠檬酸合成酶活性；(5)肌球蛋白分析 由ATPase(包括碱性和酸性失活)组成，轻 链状电泳型和天然肌球蛋白电泳法 确定特定的快同工酶和慢同工酶。通过这种组合 运动模型，我们应该能够评估生理刺激如何 从收缩角度改变骨骼肌的基因表达 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.