Theoretical studies on the regulation of anaerobic glycolysis and its influence on oxidative phosphorylation in skeletal muscle
Theoretical studies on the regulation of anaerobic glycolysis and its influence on oxidative phosphorylation in skeletal muscle
复制标题
DOI：
10.1016/j.bpc.2004.01.011
复制
发表时间：
2004-07-01
影响因子：
3.8
通讯作者：
Liguzinski, P
中科院分区：
文献类型：
--
作者：
Korzeniewski, B;Liguzinski, P
使用兰贝斯和Kushmerick最近开发的骨骼肌中糖酵解的计算机模型（Ann. Biomed. Bioenerg，30（2001）19-34）并入Korzeniewski等人开发的氧化磷酸化的计算机模型（Biophys. 83（2001）19-34），ADP、AMP和Pi对糖酵解的调节显然不足以解释完整骨骼肌从休息到剧烈运动的过渡期间糖酵解通量的大幅增加。基于糖酵解ATP和H+产生的简单动力学描述的计算机模拟强烈表明，糖酵解必须在肌肉收缩过程中被直接激活。他们还表明，H+抑制糖酵解是必要的，以解释该途径的短暂激活在运动开始以及运动开始后的初始碱化的持续时间和程度。最后，它表明，ATP供应厌氧糖酵解减慢VO 2动力学在休息到工作的过渡。(C)2004 Elsevier B. V.保留所有权利。
It is shown, using the computer model of glycolysis in skeletal muscle developed recently by Lambeth and Kushmerick (Ann. Biomed. Bioenerg, 30 (2001) 19-34) incorporated into the computer model of oxidative phosphorylation developed by Korzeniewski et al. (Biophys. Chem. 83 (2001) 19-34) that the regulation of glycolysis by ADP, AMP and Pi is decidedly insufficient to explain the large increase in the glycolytic flux during transition from rest to intensive exercise in intact skeletal muscle. Computer simulations based on a simple kinetic description of the glycolytic ATP and H+ production strongly suggests that glycolysis must be directly activated during muscle contraction. They also demonstrate that the inhibition of glycolysis by H+ is needed to explain the transient activation of this pathway at the onset of exercise as well as the duration time and extent of the initial alkalization after the onset of exercise. Finally, it is shown that ATP supply from anaerobic glycolysis slows down the VO2 kinetics during rest-to-work transition. (C) 2004 Elsevier B.V. All rights reserved.