Abstract

One of the main gravity-determined functions of the locomotor system is to maintain an upright posture. According to the views developed in the scientific school of Prof. I.B. Kozlovskaya, these functions are provided by the tonic muscular system. Under the term “tonic system” I.B. Kozlovskaya meant all the structures and regulatory mechanisms able to maintain basal mechanical tension (tone) for a long time. In mammals, she assigned to the tonic system the slow-twitch muscle fibers with a predominant expression of the myosin heavy chain beta slow isoform, MYHC I(β), and all the neural mechanisms of their control. It is quite obvious that the muscle’s ability to maintain tonic tension for a long time depends on the intensity of slow-myosin expression. Therefore, it would not be a great exaggeration if we call the slow myosin gene myh7 the true muscle tone gene. In the recent years, it has generally become clear how, against the background of prolonged increased muscle contractile activity, an increase in the expression of the slow MYHC isoform and a decrease in the expression of fast MYHC isoforms are triggered. Far less is known about the mechanisms behind a decrease in the expression of MYHC I(β) caused by a decrease in muscle contractile activity. This phenomenon was observed after exposure to true (spaceflight) weightlessness, after bed-rest hypokinesia and “dry” immersion, and also when using a standard rodent hindlimb suspension (unloading) model. Numerous studies of the myosin phenotypic plasticity are mainly concentrated on the search for the mechanisms that link changes in the expression of myosin genes with the muscle contractile activity pattern. The data discussed in the review indicate that constant expression of slow myosin is controlled by tonic activity and, in turn, is a prerequisite for maintaining such an activity. When this activity is considerably reduced or stopped, the metabolic and mechanical incentives, which trigger the signaling pathways of myh7 gene expression, disappear. Exactly this phenomenon is in the focus of this work.

中文翻译：

---

肌肉活动如何控制慢肌球蛋白表达

摘要

运动系统的主要重力决定功能之一是保持直立姿势。根据 IB Kozlovskaya 教授科学学院的观点，这些功能是由强直肌肉系统提供的。在术语“强直系统”下，IB Kozlovskaya 意味着能够长时间维持基础机械张力（音调）的所有结构和调节机制。在哺乳动物中，她将主要表达肌球蛋白重链 β 慢同种型 MYHC I(β) 及其控制的所有神经机制的慢肌纤维分配给强直系统。很明显，肌肉长时间维持强直张力的能力取决于慢肌球蛋白表达的强度。因此，将慢肌球蛋白基因称为慢肌球蛋白基因也不过分myh7真正的肌肉张力基因。近年来，在肌肉收缩活动延长的背景下，如何触发慢 MYHC 同种型表达的增加和快速 MYHC 同种型表达的减少已普遍变得清晰。关于由肌肉收缩活动减少引起的 MYHC I(β) 表达减少背后的机制知之甚少。这种现象是在暴露于真正的（太空飞行）失重后，在卧床休息和“干”浸泡后，以及在使用标准啮齿动物后肢悬挂（卸载）模型时观察到的。许多关于肌球蛋白表型可塑性的研究主要集中在寻找将肌球蛋白基因表达变化与肌肉收缩活动模式联系起来的机制。综述中讨论的数据表明，慢肌球蛋白的持续表达受强直活动控制，反过来，这是维持这种活动的先决条件。当这种活动大大减少或停止时，代谢和机械激励会触发myh7基因表达，消失。正是这种现象是这项工作的重点。