Milligan C Louise
Department of Biology, The University of Western Ontario, London, ON N6A 5B7 Canada.
J Exp Biol. 2003 Sep;206(Pt 18):3167-73. doi: 10.1242/jeb.00538.
To test the hypothesis that cortisol has a regulatory role in fish muscle glycogenesis post-exercise, rainbow trout were treated 1 h prior to exercise with either saline (control) or metyrapone (2-methyl-1, 2-di-3-pyridyl-1-propanone) to block cortisol synthesis. Following exercise (time 0), half of the metyrapone-treated fish received a single injection of cortisol, to mimic the post-exercise rise usually observed. Muscle glycogen and the relative activities of glycogen phosphorylase a (Phos a) and glycogen synthase I (GSase I), regulatory enzymes for glycogen resynthesis, were monitored 4 h post-exercise. Metyrapone treatment succeeded in blocking the post-exercise rise in plasma cortisol (17+/-2 vs 118+/-13 ng ml(-1) in controls at time 0), and cortisol injection resulted in a larger and more prolonged cortisol increase than in controls (159+/-22 vs 121+/-14 ng ml(-1) in controls at 1 h). Muscle glycogen was completely restored in the metyrapone-treated fish within 2 h after exercise (8.3+/-0.6 vs 8+/-0.7 micromol g(-1) pre-exercise), only partially restored in control fish at 4 h (5.4+/-01.4 vs 8.8+/-1.3 micromol g(-1) pre-exercise), and not at all in cortisol-treated fish (1.0+/-0.5 micromol g(-1) at 4 h). The rapid glycogen resynthesis in the metyrapone-treated fish was associated with a more rapid inactivation of Phos a and stimulation of GSase I compared to controls. In cortisol-treated fish, Phos a activity persisted throughout 4 h post-exercise; there was also a significant stimulation of GSase I activity. As a consequence of dual activation of Phos a and GSase I, glycogen cycling probably occurred, thus preventing net synthesis. This explains why the post-exercise elevation of cortisol inhibits net glycogen synthesis in trout muscle.
为了验证皮质醇在鱼类运动后肌肉糖原生成中具有调节作用这一假设，在运动前1小时，用生理盐水（对照）或美替拉酮（2 - 甲基 - 1,2 - 二 - 3 - 吡啶基 - 1 - 丙酮）处理虹鳟鱼，以阻断皮质醇的合成。运动后（时间0），一半接受美替拉酮处理的鱼单次注射皮质醇，以模拟通常观察到的运动后皮质醇升高。在运动后4小时监测肌肉糖原以及糖原磷酸化酶a（Phos a）和糖原合酶I（GSase I）的相对活性，它们是糖原再合成的调节酶。美替拉酮处理成功阻断了运动后血浆皮质醇的升高（时间0时，对照为118±13 ng/ml，美替拉酮处理组为17±2 ng/ml），并且注射皮质醇导致皮质醇升高幅度更大、持续时间更长，高于对照组（1小时时，对照为121±14 ng/ml，皮质醇处理组为159±22 ng/ml）。运动后2小时内，接受美替拉酮处理的鱼肌肉糖原完全恢复（运动前为8±0.7 μmol/g，运动后为8.3±0.6 μmol/g），对照鱼在4小时时仅部分恢复（运动前为8.8±1.3 μmol/g，运动后为5.4±0.4 μmol/g），而接受皮质醇处理的鱼完全没有恢复（4小时时为1.0±0.5 μmol/g）。与对照组相比，接受美替拉酮处理的鱼糖原快速再合成与Phos a更快失活和GSase I受刺激有关。在接受皮质醇处理的鱼中，运动后4小时内Phos a活性持续存在；GSase I活性也有显著刺激。由于Phos a和GSase I的双重激活，可能发生了糖原循环，从而阻止了净合成。这解释了为什么运动后皮质醇升高会抑制鳟鱼肌肉中的净糖原合成。
