Department of Nutrition, Shigakkan University, 55 Nadakayama, Yokone-machi, Ohbu 474-0011, Japan.
Biochem Biophys Res Commun. 2011 Feb 25;405(4):615-9. doi: 10.1016/j.bbrc.2011.01.078. Epub 2011 Jan 25.
An acute bout of exercise induces repression of protein synthesis in skeletal muscle due in part to reduced signaling through the mammalian target of rapamycin complex 1 (mTORC1). Previous studies have shown that upregulated expression of regulated in DNA damage and development (REDD) 1 and 2 is an important mechanism in the regulation of mTORC1 activity in response to a variety of stresses. This study investigated whether induction of REDD1/2 expression occurs in rat skeletal muscle in response to a burst of endurance exercise. In addition, we determined if ingestion of glucose or branched chain amino acids (BCAA) before exercise changes the expression of REDD1/2 in muscle. Rats ran on a motor-driven treadmill at a speed of 28 mmin(-1) for 90 min, and then the gastrocnemius muscle was removed and analyzed for phosphorylation of the eukaryotic initiation factor (eIF) 4E binding protein 1 (4E-BP1) and expression of REDD1/2. Exercise repressed the mTORC1-signaling pathway regardless of the ingestion of nutrients before the exercise, as shown by dephosphorylation of 4E-BP1. In addition, exercise induced the expression of REDD1 mRNA (∼8-fold) and protein (∼3-fold). Exercise-induced expression of REDD1 was not affected by the ingestion of glucose or BCAA. Expression of REDD2 mRNA was not altered by either exercise or nutrients. These findings indicated that enhanced expression of REDD1 may be an important mechanism that could partially explain the downregulation of mTORC1 signaling, and subsequent inhibition of protein synthesis in skeletal muscle during exercise.
急性运动发作会导致骨骼肌蛋白质合成受到抑制，部分原因是哺乳动物雷帕霉素靶蛋白复合物 1（mTORC1）信号通路减少。先前的研究表明，调节 DNA 损伤和发育的蛋白 1（REDD1）和 2（REDD2）的上调表达是调节 mTORC1 活性以响应各种应激的重要机制。本研究探讨了在急性耐力运动后大鼠骨骼肌中是否会诱导 REDD1/2 表达。此外，我们还确定了在运动前摄入葡萄糖或支链氨基酸（BCAA）是否会改变肌肉中 REDD1/2 的表达。大鼠以 28 mmin(-1) 的速度在电动跑步机上跑步 90 分钟，然后取出比目鱼肌并分析真核起始因子（eIF）4E 结合蛋白 1（4E-BP1）的磷酸化和 REDD1/2 的表达。无论在运动前摄入营养物质与否，运动都会抑制 mTORC1 信号通路，这表现为 4E-BP1 的去磷酸化。此外，运动还诱导了 REDD1 mRNA（约 8 倍）和蛋白（约 3 倍）的表达。运动诱导的 REDD1 表达不受葡萄糖或 BCAA 的摄入影响。运动或营养物质均未改变 REDD2 mRNA 的表达。这些发现表明，REDD1 的表达增强可能是部分解释运动时 mTORC1 信号下调和随后骨骼肌蛋白质合成抑制的重要机制。
