Laboratory of Exercise Biochemistry and Neuroendocrinology, University of Tsukuba Graduate School of Comprehensive Human Sciences, Tsukuba, Ibaraki, Japan.
J Physiol. 2011 Jul 1;589(Pt 13):3383-93. doi: 10.1113/jphysiol.2010.203570. Epub 2011 Apr 26.
Brain glycogen could be a critical energy source for brain activity when the glucose supply from the blood is inadequate (hypoglycaemia). Although untested, it is hypothesized that during prolonged exhaustive exercise that induces hypoglycaemia and muscular glycogen depletion, the resultant hypoglycaemia may cause a decrease in brain glycogen. Here,we tested this hypothesis and also investigated the possible involvement of brain monoamines with the reduced levels of brain glycogen. For this purpose,we exercised male Wistar rats on a treadmill for different durations (30-120 min) at moderate intensity (20 m min⁻¹) and measured their brain glycogen levels using high-power microwave irradiation (10 kW). At the end of 30 and 60 min of running, the brain glycogen levels remained unchanged from resting levels, but liver and muscle glycogen decreased. After 120 min of running, the glycogen levels decreased significantly by ∼37-60% in five discrete brain loci (the cerebellum 60%, cortex 48%, hippocampus 43%, brainstem 37% and hypothalamus 34%) compared to those of the sedentary control. The brain glycogen levels in all five regions after running were positively correlated with the respective blood and brain glucose levels. Further, in the cortex, the levels of methoxyhydroxyphenylglycol (MHPG) and 5-hydroxyindoleacetic acid (5-HIAA), potential involved in degradation of the brain glycogen, increased during prolonged exercise and negatively correlated with the glycogen levels. These results support the hypothesis that brain glycogen could decrease with prolonged exhaustive exercise. Increased monoamines together with hypoglycaemia should be associated with the development of decreased brain glycogen, suggesting a new clue towards the understanding of central fatigue during prolonged exercise.
当血液中的葡萄糖供应不足（低血糖）时，大脑中的糖原可能是大脑活动的关键能量来源。虽然尚未经过测试，但人们假设，在导致低血糖和肌肉糖原耗竭的长时间剧烈运动中，由此产生的低血糖可能会导致大脑糖原减少。在这里，我们检验了这一假设，并研究了大脑单胺类物质与大脑糖原水平降低之间可能存在的关系。为此，我们让雄性 Wistar 大鼠在跑步机上以中等强度（20 m min⁻¹）进行不同时间（30-120 分钟）的运动，并使用高功率微波辐射（10 kW）测量其大脑糖原水平。在跑步 30 和 60 分钟结束时，大脑糖原水平与静息水平相比保持不变，但肝糖原和肌肉糖原减少。在跑步 120 分钟后，五个离散脑区（小脑 60%、皮层 48%、海马体 43%、脑干 37%和下丘脑 34%）的糖原水平与久坐不动的对照组相比显著下降了约 37-60%。跑步后所有五个区域的大脑糖原水平与相应的血液和脑葡萄糖水平呈正相关。此外，在皮层中，可能参与大脑糖原降解的甲氧基羟苯乙二醇（MHPG）和 5-羟色胺乙酸（5-HIAA）的水平在长时间运动期间增加，并与糖原水平呈负相关。这些结果支持了大脑糖原可能随着长时间剧烈运动而减少的假设。随着单胺类物质的增加和低血糖的发生，应该与大脑糖原减少有关，这为理解长时间运动期间的中枢疲劳提供了一个新的线索。
