Pederson Bartholomew A, Cope Carlie R, Irimia Jose M, Schroeder Jill M, Thurberg Beth L, Depaoli-Roach Anna A, Roach Peter J
Department of Biochemistry and Molecular Biology and Center for Diabetes Research, Indiana University School of Medicine, Indianapolis, IN 46202-5122, USA.
Biochem Biophys Res Commun. 2005 Jun 3;331(2):491-6. doi: 10.1016/j.bbrc.2005.03.206.
Skeletal muscle glycogen is considered to be an important source of energy for contraction and increasing the level of the glucose polymer is generally thought to improve exercise performance in humans. A genetically modified mouse model (GSL30), which overaccumulates glycogen due to overexpression of a hyperactive form of glycogen synthase, was used to examine whether increasing the level of the polysaccharide enhances the ability of mice to run on a treadmill. The skeletal muscle of the GSL30 mice had large deposits of glycogen. There were no significant increases in the work performed by GSL30 mice as compared to their respective wild type littermates when exercised to exhaustion. The amount of muscle glycogen utilized by GSL30 mice, however, was greater, while the amount of liver glycogen consumed during exhaustive exercise was less than wild type animals. This result suggests that increased muscle glycogen stores do not necessarily improve exercise performance in mice.
骨骼肌糖原被认为是收缩的重要能量来源,提高这种葡萄糖聚合物的水平通常被认为可以改善人类的运动表现。一种转基因小鼠模型(GSL30),由于糖原合酶的高活性形式过表达而使糖原过度积累,被用于研究增加多糖水平是否能增强小鼠在跑步机上跑步的能力。GSL30小鼠的骨骼肌有大量糖原沉积。与各自的野生型同窝小鼠相比,GSL30小鼠运动至疲惫时所完成的工作量没有显著增加。然而,GSL30小鼠利用的肌肉糖原量更大,而在力竭运动期间消耗的肝糖原量比野生型动物少。这一结果表明,增加肌肉糖原储备不一定能改善小鼠的运动表现。