Amino acid metabolism, branched-chain amino acid feeding and brain monoamine function
Amino acid metabolism, branched-chain amino acid feeding and brain monoamine function
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DOI：
10.1079/pns19980007
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发表时间：
1998-02-01
影响因子：
7
通讯作者：
Jakeman, PM
中科院分区：
文献类型：
--
作者：
Jakeman, PM
本次研讨会上的几篇论文强调了在不同强度和持续时间的运动中碳水化合物和脂肪代谢的重要性和相互作用。在肌肉中，氨基酸代谢被认为对为工作肌肉提供能量的贡献很小，除了少数例外，被忽略了。同样，所谓的“中枢疲劳”的机制，即与大脑或中枢神经系统（CNS）功能改变相关的疲劳，在很大程度上尚未探索。然而，在过去的几年里，一些论文已经促进了某些氨基酸作为中间代谢底物和脑神经递质前体的吸引人的作用。本论文的重点是外周底物利用，氨基酸代谢，脑神经递质功能和疲劳之间的潜在相互作用。为了本次研讨会的目的，将只考虑从人类受试者获得的实验数据。运动期间的疲劳通常被定义为无法维持所需的力量或功率输出。在本讨论中，疲劳或疲劳的感知被认为与在长时间的次最大动态运动期间功率输出的损失或感知到的不能维持功率输出有关。这种类型的运动中的疲劳可以方便地分为“中央”和“外围”组件（图1）。现在已经知道了很多关于底物耗竭在疲劳病因学中的作用（参见本专题讨论会中的相关论文），但是进行长时间运动的受试者在底物耗竭（或外周疲劳的其他成分）迫使受试者停止或降低所需运动强度的点之前就感知到疲劳的增加。这种疲劳的感觉必须存在于大脑和CNS中，被认为与大脑神经递质如血清素（5-羟色胺）、去甲肾上腺素和多巴胺的变化有关，并且通常被称为“中枢疲劳假说”。本质上，中枢疲劳假说表明，随着其氨基酸前体色氨酸的血液输送增加，大脑血清素能功能的增加，可能会损害中枢神经系统功能的某些方面（可能是通过减少多巴胺能活性），以诱导疲劳在长时间运动期间提前发作。
Several papers in the present symposium emphasize the importance and interplay of carbohydrate and fat metabolism during exercise of varying intensities and duration. In constrast, amino acid metabolism is deemed to make only a minimal contribution to the provision of energy for the working muscle and is, with few exceptions, ignored. Equally, the mechanisms of what is termed ‘central fatigue’, ie fatigue associated with alterations in the functioning of the brain or central nervous system (CNS), are largely unexplored. However, several papers over the past few years have promoted an attractive role for certain amino acids as substrates for intermediary metabolism and precursors of brain neurotransmitters. The focus of the present paper is the potential interplay between peripheral substrate utilization, amino acid metabolism, brain neurotransmitter function and fatigue. For the purpose of the present symposium only experimental data obtained from human subjects will be considered. Fatigue during exercise is commonly defined as the inability to maintain the required force or power output. In the present discussion, fatigue, or the perception of fatigue, is considered to be related to the loss of power output, or the perceived inability to maintain power output, during prolonged submaximal dynamic exercise. Fatigue during this type of exercise can be conveniently partitioned into ‘central’and ‘peripheral’components (Fig. 1). Much is now known of the role of substrate depletion in the aetiology of fatigue (see relevant papers in the present symposium) but subjects performing prolonged exercise perceive an increase in fatigue well in advance of the point where substrate depletion (or other components of peripheral fatigue) forces the subject either to stop or to reduce the required intensity of exercise. This perception of fatigue must reside within the brain and CNS, is thought to be related to a change in brain neurotransmitters such as serotonin (5-hydroxytryptamine), noradrenaline and dopamine, and is generally known as the ‘central fatigue hypothesis’. In essence, the central fatigue hypothesis suggests that an increase in brain serotoninergic function in response to an increase in the blood-borne delivery of its amino acid precursor, tryptophan, can impair certain aspects of CNS function (possibly by reducing dopaminergic activity) in order to induce an early onset of fatigue during prolonged exercise.