Department of Physiological Sciences I, Institut d'Investigacions Biomediques August Pi i Sunyer, Universitat de Barcelona, Barcelona, Spain.
PLoS One. 2012;7(7):e42453. doi: 10.1371/journal.pone.0042453. Epub 2012 Jul 31.
Glycogen-depleting exercise can lead to supercompensation of muscle glycogen stores, but the biochemical mechanisms of this phenomenon are still not completely understood.
Using chronic low-frequency stimulation (CLFS) as an exercise model, the tibialis anterior muscle of rabbits was stimulated for either 1 or 24 hours, inducing a reduction in glycogen of 90% and 50% respectively. Glycogen recovery was subsequently monitored during 24 hours of rest.
In muscles stimulated for 1 hour, glycogen recovered basal levels during the rest period. However, in those stimulated for 24 hours, glycogen was supercompensated and its levels remained 50% higher than basal levels after 6 hours of rest, although the newly synthesized glycogen had fewer branches. This increase in glycogen correlated with an increase in hexokinase-2 expression and activity, a reduction in the glycogen phosphorylase activity ratio and an increase in the glycogen synthase activity ratio, due to dephosphorylation of site 3a, even in the presence of elevated glycogen stores. During supercompensation there was also an increase in 5'-AMP-activated protein kinase phosphorylation, correlating with a stable reduction in ATP and total purine nucleotide levels.
Glycogen supercompensation requires a coordinated chain of events at two levels in the context of decreased cell energy balance: First, an increase in the glucose phosphorylation capacity of the muscle and secondly, control of the enzymes directly involved in the synthesis and degradation of the glycogen molecule. However, supercompensated glycogen has fewer branches.
糖原耗竭运动可导致肌肉糖原储存的超代偿，但这一现象的生化机制仍不完全清楚。
使用慢性低频刺激（CLFS）作为运动模型，分别刺激兔的胫骨前肌 1 小时或 24 小时，导致糖原减少 90%和 50%。随后在 24 小时的休息时间内监测糖原的恢复情况。
在刺激 1 小时的肌肉中，糖原在休息期间恢复到基础水平。然而，在刺激 24 小时的肌肉中，糖原发生了超代偿，其水平在休息 6 小时后仍保持在基础水平的 50%以上，尽管新合成的糖原分支较少。糖原的增加与己糖激酶-2表达和活性的增加、糖原磷酸化酶活性比的降低以及糖原合酶活性比的增加相关，这是由于 3a 位的去磷酸化，即使在升高的糖原储存情况下也是如此。在超代偿期间，5'-AMP 激活的蛋白激酶磷酸化也增加，与 ATP 和总嘌呤核苷酸水平的稳定降低相关。
在细胞能量平衡降低的情况下，糖原超代偿需要在两个水平上协调一系列事件：首先，增加肌肉的葡萄糖磷酸化能力，其次，控制直接参与糖原分子合成和降解的酶。然而，超代偿的糖原分支较少。
