Exercise-induced changes in branched chain amino acid/aromatic amino acid ratio in the rat brain and plasma.

Okamura, Koji; Matsubara, Futoshi; Yoshioka, Yoshiaki; Kikuchi, Noriaki; Kikuchi, Yūko; Kohri, Hideaki

doi:10.1254/jjp.45.243

Cited by 17 publications

(12 citation statements)

References 24 publications

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“…These data confirm the increase in brain ammonia produced by physicat exercise previously observed by Okamura et al (19). In spite of very large differences in exerase time, trained and untrained rats exhibit the same increase in blood ammonia concentration at exhaustion whereas the longer time of running in trained rats is associated with higher brain ammonia.…”

Section: Discussionsupporting

confidence: 91%

Effects of Prolonged Exercise on Brain Ammonia and Amino Acids

Guezennec

Abdelmalki²,

Serrurier³

et al. 1998

Int J Sports Med

104

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The aim of this study was to investigate if enhanced peripheral ammonia production during exhaustive exercise increases ammonia detoxication in brain mediated by glutamine synthesis, and subsequently influences glutamate and gamma-aminobutyric acid (GABA) levels. This neurotransmitter production is related to the metabolism of glutamine. A group of rats was trained for 6 weeks by treadmill running (TR). They were compared to a group of untrained rats (UN). At the end of training, half of TR and UN rats were submitted to one session of treadmill running until exhaustion (288+/-12 min and 62+/-5 min in TR and UN group, respectively). At exhaustion, running and control rats were sacrificed in order to collect blood and to take samples of the following brain structures: cortex, striatum and cerebellum. Treadmill running until exhaustion induced an increase in blood ammonia by 140% without significant differences between TR and UN groups. Brain ammonia increased in both groups. However, TR group exhibited values 50% higher than those observed in UN group. Brain glutamine was increased at exhaustion in all groups of running rats by 30-75% of basal value whereas the glutamate only decreased in TR rats which were able to run for a longer time. In this group, the GABA level decreased in striatum. These data confirm that enhanced brain ammonia level during exercise stimulates glutamine synthesis as a mechanism of detoxication. After several hours of running, a reduction in brain glutamate levels was observed in all brain structures in trained rats but only in the striatum in untrained animals. The reduced availability of this GABA precursor decreases GABA levels only in the striatum of TR group by 45% of the resting value. These results suggest a relation between cerebral changes in neurotransmitters and excitatory amino acids, such as glutamate and GABA, and central fatigue.

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Section: Discussionsupporting

confidence: 91%

Effects of Prolonged Exercise on Brain Ammonia and Amino Acids

Guezennec

Abdelmalki²,

Serrurier³

et al. 1998

Int J Sports Med

104

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“…Currently little information is available on the accessibility of circulating blood ammonia to the brain during exercise in normal healthy individuals. We have found only one paper which reports elevated brain ammonia in rats during EIH (113). While the absolute values reported here in both blood and brain seem somewhat high, the pattern of their elevation is consistent with the observed elevation of blood and brain ammonia in other conditions (encephalopathy, hyperoxia, etc.…”

Section: Hyperammonemia Olexercisesupporting

confidence: 88%

“…Romanowski and Grabiec (128) were first to report an exerciseinduced increase in brain serotonin (for which TRP is the precursor) and were also probably the first to speculate on its potential role in mediating CENTRAL FATIGUE. Several subsequent studies have supported this theory, reporting an exercise-induced decrease in the ratio of BCAA/AAA in blood, or an increase in the brain uptake of AAA and brain serotonin concentration (2,20,28,29,113). Elevated brain serotonin resulting from exercise could trigger such fatigue-related symptoms as lethargy, appetite suppression, and sleep disorders (23,126).…”

Section: Ammonia From Protein Catabolism During Exercise -Its Influenmentioning

confidence: 95%

“…Exercise exerts several important effects on protein metabolism which may be relevant to CNS toxicity. Firstly, it stimulates catabolism of amino acids in muscle (principally BCAAs) and contributes to elevated blood ammonia (90); secondly, the hyperammonemia accompanying exercise increases the permeability of the BBB to NAA relative to other amino acids (26,48,97,138); thirdly, the circulating BCAA fraction of the NAA group is reduced relative to the AAA fraction, which are neurotransmitter precursors, probably due to enhanced BCAA uptake by active skeletal muscle (2,20,28,113). Thus, the AAAs (Phe, TYR, and TRP) are positioned more favorably for uptake across the BBB (79, 80, 81).…”

Section: Ammonia From Protein Catabolism During Exercise -Its Influenmentioning

confidence: 99%

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Exercise-Induced Hyperammonemia: Peripheral and Central Effects

Banister

Cameron²

1990

Int J Sports Med

152

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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.

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“…Circulating ammonia is taken up by the liver and most of it is detoxified in this tissue through the urea cycle. However, accelerated formation of ammonia tends to exceed hepatic detoxification due to reduced hepatic blood flow during moderate (∼30%) and intense (∼50-60%) exercise (Feling and Wahren, 1971;Okamura et al, 1987). This increasing ammonia concentration in blood starts to affect the liver and brain, generating fatigue due to excess cerebral ammonia and the inability of peripheral organs to detoxify ammonia.…”

Section: Discussionmentioning

confidence: 99%