Laboratory of Health and Sports Sciences, Center for Liberal Arts, Meiji Gakuin Univ., 1518 Kamikurata-cho, Totsuka-ku, Yokohama, Kanagawa 244-8539, Japan.
J Appl Physiol (1985). 2010 Feb;108(2):306-13. doi: 10.1152/japplphysiol.00278.2009. Epub 2009 Dec 3.
This study aimed to investigate torque deficit and activation of protein synthesis and/or protein degradation signaling pathways during the early and recovery phase after high- and low-velocity eccentric contractions (ECs). Male Wistar rats (n = 36) were randomly divided into fast angular velocity ECs group (FAST; 180 degrees/s; n = 12), slow ECs group (SLOW; 30 degrees/s; n = 12), and control group (control; n = 12). ECs comprised four sets of five forced dorsiflexions combined with electrical stimulation of the plantar flexors. Isometric tetanic torque was measured before and after ECs. Tissue contents of Akt(P) (P, phosphorylated), mammalian target of rapamycin (mTOR)(P), 70-kDa ribosomal protein S6 kinase (P70S6k), P70S6k(P), forkhead transcription factor 1 of the O class (FOXO1), FOXO1(P), FOXO3, FOXO3(P), myostatin, and activin receptor type IIB (ActRIIB) were measured. The isometric tetanic torque after ECs was significantly lower in FAST than in SLOW (days 1, 3, and 5, P < 0.05; day 2, P < 0.01). The ratio of P70S6k(P) against total P70S6k on days 2 and 7 was significantly higher in SLOW than in the control. The ratio of FOXO1 against total FOXO1, the ratio of FOXO3a against total FOXO3a, and myostatin on days 2 and 7 were significantly higher in FAST than in the control, while that of ActRIIB on day 7 was significantly lower in SLOW than in the other two groups. These results suggest that EC intensity plays a key role in impairment of muscular function and activation of protein synthesis and/or protein degradation signaling pathways.
本研究旨在探讨在高、低角速度离心收缩（EC）后的早期和恢复期，力矩不足以及蛋白质合成和/或蛋白质降解信号通路的激活情况。雄性 Wistar 大鼠（n = 36）被随机分为快速角速度 EC 组（FAST；180°/s；n = 12）、慢速 EC 组（SLOW；30°/s；n = 12）和对照组（control；n = 12）。EC 由四组五次强制背屈运动与足底屈肌电刺激相结合组成。EC 前后分别测量等长强直收缩力矩。测量 Akt(P)（P，磷酸化）、哺乳动物雷帕霉素靶蛋白（mTOR）(P)、70kDa 核糖体蛋白 S6 激酶（P70S6k）、P70S6k(P)、叉头转录因子 O 类 1（FOXO1）、FOXO1(P)、FOXO3、FOXO3(P)、肌肉生长抑制素和激活素受体 IIB（ActRIIB）的组织含量。EC 后，FAST 的等长强直收缩力矩明显低于 SLOW（第 1、3 和 5 天，P < 0.05；第 2 天，P < 0.01）。第 2 和第 7 天，SLOW 的 P70S6k(P)与总 P70S6k 的比值明显高于对照组。第 2 和第 7 天，FAST 的 FOXO1 与总 FOXO1 的比值、FOXO3a 与总 FOXO3a 的比值以及肌肉生长抑制素明显高于对照组，而 SLOW 的 ActRIIB 与第 7 天的对照组相比明显较低。这些结果表明，EC 强度在肌肉功能障碍和蛋白质合成和/或蛋白质降解信号通路的激活中起着关键作用。
