Effects of Prolonged Exercise on Brain Ammonia and Amino Acids

1998 ◽  
Vol 19 (05) ◽  
pp. 323-327 ◽  
Author(s):  
C. Guezennec ◽  
A. Abdelmalki ◽  
B. Seirurier ◽  
D. Merino ◽  
X. Bigard ◽  
...  
1974 ◽  
Vol 32 (2) ◽  
pp. 143-147 ◽  
Author(s):  
J. R. Poortmans ◽  
G. Siest ◽  
M. M. Galteau ◽  
O. Houot

2006 ◽  
Vol 38 (Supplement) ◽  
pp. S404
Author(s):  
Misaki Yoshida ◽  
Hiroko Tanaka ◽  
Takako Niijima ◽  
Masae Miyatani ◽  
Motohiko Miyachi ◽  
...  

1990 ◽  
Vol 259 (2) ◽  
pp. G290-G299 ◽  
Author(s):  
J. R. Pappenheimer

Mice, rats, or rabbits were provided with a liquid diet of 10-12% glucose (Glc), 0.5-1% creatinine, 1-2% mannitol, and mannitol labeled with 3H on a terminal carbon. Average rates of ingestion of Glc were greater than maximum rates of active, carrier-mediated Glc transport reported for the intestines of these species. The discrepancy was small in mice but increased exponentially with body weight (BW). Ingestion-absorption of Glc increased exponentially with the 0.73 power of BW as expected from metabolic rate, whereas active transport, estimated from the literature, varied exponentially with the 0.50 power of BW. It is estimated that in humans the ingestion-absorption rate of Glc may be 10-20 times greater than active transport. In the presence of Glc, 50-65% of the ingested creatinine was recovered in urine compared with 75-85% recovered after intraperitoneal or subcutaneous injections. The amount of creatinine recovered in urine depended on the amount of ingested Glc, as predicted from the effects of Glc on width and permeability of absorptive cell junctions. Eighty percent or more of the 3H label on mannitol was recovered in urine or other body fluids, although most of the [3H]mannitol was oxidized to [3H]water after being absorbed intact from the intestine. It is concluded that in the presence of Glc, creatinine and mannitol (together with Glc, amino acids, and other small nutrients) are absorbed passively by solvent drag between absorptive cells, as found previously in anesthetized rats (J. R. Pappenheimer and K. Z. Reiss. J. Membr. Biol. 100: 123-136, 1987). The ratio of solvent drag to carrier-mediated transport increases exponentially with BW and may account for the capacity of human intestines to absorb large amounts of Glc during prolonged exercise, Glc tolerance tests, or oral Glc-saline therapy for dehydration.


2001 ◽  
Vol 11 (1) ◽  
pp. 87-108 ◽  
Author(s):  
Martin J. Gibala

The contribution of amino acid oxidation to total energy expenditure is negligible during short-term intense exercise and accounts for 3–6% of the total adenosine triphosphate supplied during prolonged exercise in humans. While not quantitatively important in terms of energy supply, the intermediary metabolism of several amino acids—notably glutamate, alanine, and the branched-chain amino acids—afreets other metabolites .including the intermediates within the tricarboxylic acid (TCA) cycle. Glutamate appears to be a key substrate for the rapid increase in muscle TCA cycle intermediates (TCAI) that occurs at the onset of moderate to intense exercise, due to a rightward shift of the reaction catalyzed by alanine aminotransferase (glutamate + pyruvate <-> alanine + 2-oxoglutarate). The pool of muscle TCAI declines during prolonged exercise, and this has been attributed to an increase in leucine oxidation that relies on one of the TCAI. However, this mechanism does not appear to be quantitatively important due of the relatively low maximal activity of branched-chain oxoacid dehydrogenase, the key enzyme involved. It has been suggested that an increase in TCAI is necessary to attain high rates of aerobic energy production and that a decline in TCAI may be a causative factor in local muscle fatigue. These topics remain controversial, but recent evidence suggests that changes in TCAI during exercise are unrelated to oxidative energy provision in skeletal muscle.


1996 ◽  
Vol 81 (6) ◽  
pp. 2644-2650 ◽  
Author(s):  
Klavs Madsen ◽  
Dave A. Maclean ◽  
Bente Kiens ◽  
Dirk Christensen

Madsen, Klavs, Dave A. MacLean, Bente Kiens, and Dirk Christensen. Effects of glucose, glucose plus branched-chain amino acids, or placebo on bike performance over 100 km. J. Appl. Physiol. 81(6): 2644–2650, 1996.—This study was undertaken to determine the effects of ingesting either glucose ( trial G) or glucose plus branched-chain amino acids (BCAA; trial B), compared with placebo ( trial P), during prolonged exercise. Nine well-trained cyclists with a maximal oxygen uptake of 63.1 ± 1.5 ml O2 ⋅ min−1 ⋅ kg−1performed three laboratory trials consisting of 100 km of cycling separated by 7 days between each trial. During these trials, the subjects were encouraged to complete the 100 km as fast as possible on their own bicycles connected to a magnetic brake. No differences in performance times were observed between the three trials (160.1 ± 4.1, 157.2 ± 4.5, and 159.8 ± 3.7 min, respectively). In trial B, plasma BCAA levels increased from 339 ± 28 μM at rest to 1,026 ± 62 μM after exercise ( P < 0.01). Plasma ammonia concentrations increased during the entire exercise period for all three trials and were significantly higher in trial B compared with trials G and P ( P< 0.05). The respiratory exchange ratio was similar in the three trials during the first 90 min of exercise; thereafter, it tended to drop more in trial P than in trials G and B. These data suggest that neither glucose nor glucose plus BCAA ingestion during 100 km of cycling enhance performance in well-trained cyclists.


2007 ◽  
Vol 17 (s1) ◽  
pp. S37-S46 ◽  
Author(s):  
Romain Meeusen ◽  
Phil Watson

It is clear that the cause of fatigue is complex, infuenced 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.


1991 ◽  
Vol 160 (1) ◽  
pp. 149-165
Author(s):  
J. Henriksson

Protein is not normally an important energy fuel for exercising muscle. In spite of this, there is a significant increase in the rate of amino acid catabolism during exercise. This is secondary to the exercise-induced increase in several metabolic processes, such as hepatic gluconeogenesis and the citric acid cycle, where amino acid carbon is utilized. The suppression of protein synthesis during an exercise bout leaves amino acids available for catabolism. There is some evidence that basal amino acid concentrations in plasma and muscle may be higher in trained than in untrained individuals. In the rat, the concentration of free amino acids is higher in slow-twitch than in fast-twitch muscles. With short-term exercise, the transamination of glutamate by alanine aminotransferase leads to increased levels of alanine in muscle and plasma, and an increased release of alanine from the muscle. At the same time, the muscle and plasma glutamate concentrations are markedly decreased. The plasma glutamine level is elevated with short-term exercise, but changes in muscle glutamine concentration are more variable. With prolonged exercise, there is a depletion of the plasma amino acid pool, which may be explained by an increased consumption in organs other than muscle. With the exception of alanine, we found, however, that the muscle levels of free amino acids are kept stable throughout a 3.5-h exercise period. There is a significant activation of branched-chain amino acid metabolism with prolonged exercise, and the current data indicate that this is more pronounced in endurance-trained subjects than in untrained controls.


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