Banister E W, Cameron B J
School of Kinesiology, Simon Fraser University, Burnaby, B.C., Canada.
Int J Sports Med. 1990 May;11 Suppl 2:S129-42. doi: 10.1055/s-2007-1024864.
The intent of this paper is to review the recent literature on exercise-induced hyperammonemia (EIH) and to compare the current interpretations of ammonia accumulation during exercise with the recognized clinical symptoms of progressive ammonia toxicity. In doing so, we will speculate on possible exercise-induced symptoms of CNS dysfunction which could result from elevated ammonia during intense short-duration or prolonged exercise. Ammonia is a ubiquitous metabolic product producing multiple effects on physiological and biochemical systems. Its concentration in several body compartments is elevated during exercise, predominantly by increased activity of the purine nucleotide cycle (PNC) in skeletal muscle. Depending on the intensity and duration of exercise, muscle ammonia may be elevated to the extent that it leaks (diffuses) from muscle to blood, and thereby can be carried to other organs. The direction of movement of ammonia or the ammonium ion is dependent on concentration and pH gradients between tissues. In this manner, ammonia can also cross the blood-brain barrier (BBB), although the rate of diffusion of ammonia from blood to brain during exercise is unknown. It seems reasonable to assume that exhaustive exercise may induce a state of acute ammonia toxicity which, although transient and reversible relative to disease states, may be severe enough in critical regions of the CNS to affect continuing coordinated activity. Regional differences in brain ammonia content, detoxification capacity, and specific sensitivity may account for the variability of precipitating factors and latency of response in CNS-mediated dysfunction arising from an exercise stimulus, e. g., motor incoordination, ataxia, stupor. There have been numerous suggestions that elevated ammonia is associated with, or perhaps is responsible for, exercise fatigue, although evidence for this relies extensively on temporal relationships. Fatigue may become manifest both as a peripheral organ or central nervous system phenomenon, or combination of both. Thus, we must examine the sequential or concomitant changes in ammonia concentration occurring in the periphery, the central nervous system (CNS), and the cerebrospinal fluid (CSF) induced by any effector, not only exercise, to interpret and rationalize the diverse physical, physiological, biochemical, and clinical symptoms produced by hyperammonemic states. Since more is known about elevated brain ammonia during other diverse conditions such as disease states, chemically induced convulsion, and hyperbaric hyperoxia, some of these relevant data are discussed.
本文旨在回顾近期关于运动性高氨血症（EIH）的文献，并比较当前对运动期间氨积累的解释与公认的进行性氨中毒临床症状。在此过程中，我们将推测在剧烈短时间或长时间运动期间，由于氨水平升高可能导致的中枢神经系统（CNS）功能障碍的运动诱发症状。氨是一种普遍存在的代谢产物，对生理和生化系统产生多种影响。运动期间，其在身体多个腔室中的浓度会升高，主要是由于骨骼肌中嘌呤核苷酸循环（PNC）的活性增加。根据运动的强度和持续时间，肌肉氨可能会升高到从肌肉泄漏（扩散）到血液的程度，从而可以被输送到其他器官。氨或铵离子的移动方向取决于组织之间的浓度和pH梯度。通过这种方式氨也可以穿过血脑屏障（BBB），尽管运动期间氨从血液扩散到大脑的速率尚不清楚。可以合理地假设，力竭运动可能会诱发急性氨中毒状态，尽管相对于疾病状态而言是短暂且可逆的，但在中枢神经系统的关键区域可能严重到足以影响持续的协调活动。脑氨含量、解毒能力和特定敏感性的区域差异可能解释了运动刺激引起的中枢神经系统介导的功能障碍中诱发因素的变异性和反应潜伏期，例如运动不协调、共济失调、昏迷。有许多观点认为氨水平升高与运动疲劳有关，或者可能是运动疲劳的原因，尽管这方面的证据主要依赖于时间关系。疲劳可能表现为外周器官或中枢神经系统现象，或两者兼而有之。因此，我们必须研究任何效应物（不仅是运动）引起的外周、中枢神经系统（CNS）和脑脊液（CSF）中氨浓度的相继或伴随变化，以解释和合理化高氨血症状态产生的各种身体、生理、生化和临床症状。由于在其他各种情况下，如疾病状态、化学诱导惊厥和高压高氧期间，对脑氨升高的了解更多，因此将讨论其中一些相关数据。
