Blunting of protein synthesis during exercise in rat skeletal muscle

工作骨骼肌中的蛋白质合成受到抑制。从目的论来看，肌肉停止消耗 ATP 的构建过程，以在紧急情况下为收缩活动腾出 ATP，这是有道理的。至少到目前为止，已经提出了两种机制来抑制工作肌肉中的蛋白质合成。其中一个故事是 AMPK 抑制 mTORC1，mTORC1 可以说是蛋白质翻译起始步骤的主要调节因子。另一个故事是 eEF2 的 Ca2 依赖性失活，它调节 eEF2 的延伸步骤。文献报道表明，除 AMPK 和/或 eEF2 之外的其他因素也可能参与蛋白质合成的减弱。我们已经证明 REDD1 也可能是抑制工作肌肉中蛋白质合成的候选者。了解这些机制可能会导致开发新的策略和治疗方法，不仅适用于运动员，也适用于患有肌肉萎缩症等肌肉萎缩症的个体。

Protein synthesis is suppressed in working skeletal muscle. Teleologically, it makes sense that the muscle stops an ATP-consuming building process to spare ATP for contractile activity in an emergency. At least so far two mechanisms have been proposed for blunting protein synthesis in working muscle. One of them is a story that AMPK inhibits mTORC1, which is arguably a master regulator of initiation step in protein translation. Another story is that Ca2+-dependent inactivation of eEF2, which regulates elongation step in it. Reports in the literature suggest that other factors rather than AMPK and/or eEF2 would be involved in the blunting of protein synthesis. We have shown that REDD1 might be also a candidate for blunting protein synthesis in working muscle. Understanding of these mechanisms may lead to development of new strategies and treatments not only for athletes but also for individuals with muscle-wasting conditions such as sarcopenia.