Dept of Human Physiology and Sportsmedicine, Vrije Universiteit Brussels, Brussels, Belgium.
Int J Sport Nutr Exerc Metab. 2007 Aug;17 Suppl:S37-46. doi: 10.1123/ijsnem.17.s1.s37.
It is clear that the cause of fatigue is complex, influenced by both events occurring in the periphery and the central nervous system (CNS). It has been suggested that exercise-induced changes in serotonin (5-HT), dopamine (DA), and noradrenaline (NA) concentrations contribute to the onset of fatigue during prolonged exercise. Serotonin has been linked to fatigue because of its documented role in sleep, feelings of lethargy and drowsiness, and loss of motivation, whereas increased DA and NA neurotransmission favors feelings of motivation, arousal, and reward. 5-HT has been shown to increase during acute exercise in running rats and to remain high at the point of fatigue. DA release is also elevated during exercise but appears to fall at exhaustion, a response that may be important in the fatigue process. The rates of 5-HT and DA/NA synthesis largely depend on the peripheral availability of the amino acids tryptophan (TRP) and tyrosine (TYR), with increased brain delivery increasing serotonergic and DA/NA activity, respectively. TRP, TYR, and the branched-chained amino acids (BCAAs) use the same transporter to pass through the blood-brain barrier, meaning that the plasma concentration ratio of these amino acids is thought to be a very important marker of neurotransmitter synthesis. Pharmacological manipulation of these neurotransmitter systems has provided support for an important role of the CNS in the development of fatigue. Work conducted over the last 20 y has focused on the possibility that manipulation of neurotransmitter precursors may delay the onset of fatigue. Although there is evidence that BCAA (to limit 5-HT synthesis) and TYR (to elevate brain DA/NA) ingestion can influence perceived exertion and some measures of mental performance, the results of several apparently well-controlled laboratory studies have yet to demonstrate a clear positive effect on exercise capacity or performance. There is good evidence that brain neurotransmitters can play a role in the development of fatigue during prolonged exercise, but nutritional manipulation of these systems through the provision of amino acids has proven largely unsuccessful.
很明显，疲劳的原因很复杂，受到外周和中枢神经系统（CNS）中发生的事件的影响。有人认为，运动引起的 5-羟色胺（5-HT）、多巴胺（DA）和去甲肾上腺素（NA）浓度的变化导致长时间运动时疲劳的发生。5-HT 与疲劳有关，因为它在睡眠、昏睡和嗜睡感以及动力丧失中的作用已被记录在案，而增加的 DA 和 NA 神经传递有利于动力、唤醒和奖励的感觉。5-HT 在跑步大鼠的急性运动中显示增加，并且在疲劳点保持高。DA 释放也在运动期间升高，但在疲劳时似乎下降，这种反应可能在疲劳过程中很重要。5-HT 和 DA/NA 合成的速率在很大程度上取决于色氨酸（TRP）和酪氨酸（TYR）的外周可用性，增加脑内输送分别增加 5-羟色胺能和 DA/NA 活性。TRP、TYR 和支链氨基酸（BCAA）使用相同的转运体穿过血脑屏障，这意味着这些氨基酸的血浆浓度比被认为是神经递质合成的一个非常重要的标志物。对这些神经递质系统的药理学操作为中枢神经系统在疲劳发展中的重要作用提供了支持。过去 20 年来的工作集中在操纵神经递质前体是否可能延迟疲劳的发生。尽管有证据表明 BCAA（限制 5-HT 合成）和 TYR（升高脑 DA/NA）摄入可以影响感知的努力和一些心理表现的测量，但几个明显的对照良好的实验室研究的结果尚未证明对运动能力或表现有明显的积极影响。有充分的证据表明，脑神经递质在长时间运动时的疲劳发展中起作用，但通过提供氨基酸对这些系统进行营养操作在很大程度上尚未成功。
