Myology Laboratory, Institute of Biomedical Problems RAS, Moscow, Russia.
Federal State Budgetary Educational Institution of Higher Education, Bauman Moscow State Technical University, Russia.
Arch Biochem Biophys. 2023 Jul 15;743:109647. doi: 10.1016/j.abb.2023.109647. Epub 2023 May 24.
Unloading of slow-twitch muscles results in increased muscle fatigue and the mechanisms of this effect are poorly studied. We aimed to analyze the role of high-energy phosphates accumulation during the first week of rat hindlimb suspension plays in a fiber-type phenotype shift towards fast-type fatigable muscle fibers. Male Wistar rats were divided into 3 groups (n = 8): C - vivarium control; 7HS - 7-day hindlimb suspension; 7HB - 7-day hindlimb suspension with intraperitoneal injection of beta-guanidine propionic acid (β-GPA, 400 mg/kg b w). β-GPA is a competitive inhibitor of creatine kinase and it reduces concentrations of ATP and phosphocreatine. In the 7HB group, β-GPA treatment protected a slow-type signaling network in an unloaded soleus muscle, including MOTS-C, AMPK, PGC1 α and micro-RNA-499. These signaling effects resulted in a preserved soleus muscle fatigue resistance, slow-type muscle fibers percentage and mitochondrial DNA copy number under muscle unloading.
慢肌纤维的卸载会导致肌肉疲劳增加，但其作用机制尚未得到充分研究。我们旨在分析大鼠后肢悬吊第 1 周高能磷酸化合物积累在向快型易疲劳肌纤维纤维型表型转变中的作用。雄性 Wistar 大鼠分为 3 组（n=8）：C-饲养对照；7HS-7 天后肢悬吊；7HB-7 天后肢悬吊加腹腔注射β-胍基丙酸（β-GPA，400mg/kg b w）。β-GPA 是肌酸激酶的竞争性抑制剂，可降低 ATP 和磷酸肌酸的浓度。在 7HB 组中，β-GPA 处理保护了未加载的比目鱼肌中的慢型信号网络，包括 MOTS-C、AMPK、PGC1α 和 micro-RNA-499。这些信号作用导致在肌肉卸载下比目鱼肌疲劳抵抗、慢型肌纤维百分比和线粒体 DNA 拷贝数得以维持。
