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Query: UMLS:C0015672 (fatigue)
51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Muscle ATP loss with exercise has implications both to the causes of fatigue and muscle damage. To study this at the single muscle fibre level, five trained thoroughbred horses performed consecutive 90 second gallops on an inclined treadmill followed by a final gallop to fatigue. Biopsies of the m. gluteus medius were taken at rest, post-exercise and during 24 hour recovery. Blood lactate was 20.0 mmol litre-1 or more, and plasma NH3 300-800 mumol litre-1, following the final gallop. Minimal changes occurred in the plasma markers, CK and AST. ATP loss with exercise was 32.2 (SD 12.2) per cent. Following exercise single fibre ATP contents showed a much broader distribution than at rest, with contents in some close to zero. Following five and 24 hour recovery, however, frequency distribution curves were close to those seen at rest. There was no difference in the ATP contents of types I, IIa and IIb at rest of with exercise or recovery. The results pointed to marked heterogeneity between individual fibres in their biochemical response with exercise, independent of fibre type.
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PMID:ATP loss with exercise in muscle fibres of the gluteus medius of the thoroughbred horse. 949 49

Effects of a serotonin re-uptake inhibitor and oral amino acid supplementations on physical and mental performance as well as neuroendocrine variables were investigated. 10 male subjects cycled in four trials until exhaustion. Participants ingested a placebo in trial (T) I, 20 mg paroxetine in T II, 21 g branched-chain amino acids (BCAA) in T III and 20g tyrosine (TYR) in T IV. Heart rate, capillary lactate, plasma insulin, free fatty acids, glucose, serotonin and beta-endorphin did not differ in trials. Plasma ammonia increments during exercise were higher in T III. Plasma BCAA in T III and plasma TYR in T IV were increased after 30 min of exercise according to the supplemented substances. In contrast to all other trials, the ratio of plasma free TRP/BCAA did not increase in T III. Plasma TYR/BCAA was augmented in T IV and decreased in T III after 30 min of exercise, whereas it did not change in T I and II. Plasma prolactin (PRL), growth hormone, cortisol, adrenocorticotropic hormone, norepinephrine and epinephrine increased during all trials. Plasma PRL increments were higher in T IV. Exhaustion was reached earlier in T II. No significant differences were found between other trials. Drive during psychometric testing subsequent to exercise was improved in T III and IV. The results indicate that fatigue during endurance exercise was increased by pharmacological augmentation of the brain serotonergic activity. However, a reduction of 5-HT synthesis via BCAA supplementation did not affect physical fatigue. TYR administration did not alter physical performance either although plasma PRL increments suggest that changes in the monoaminergic system were induced. Precaution is necessary before assuming an ergogenic value of amino acids.
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PMID:Influence of paroxetine, branched-chain amino acids and tyrosine on neuroendocrine system responses and fatigue in humans. 962 32

Well-trained subjects (n = 6) were studied before and after losing a mean 3.0%-4.3% of body mass to determine whether muscle performance could be maintained or even enhanced by dietary creatine supplementation. During a 5-day period of loss of mass the subjects were randomly assigned to a creatine or placebo supplemented diet. All the subjects were measured before and after loss of mass on both supplements for isokinetic peak torque (PT) and work at peak torque (W(PT)) of knee extensors, also for intermittent high intensity working capacity of the same muscle group. The latter test consisted of submaximal isokinetic knee extensions at an angular velocity of 1.57 rad x s(-1) for 45 s at the rate of 30 contractions each min (submaximal work, Ws max) followed by 15-s maximal effort (maximal work, Wmax). Total duration of the test was 3 min. Haematocrit was measured and haemoglobin, ammonia, lactate, glucose and urea concentrations were analysed in blood samples obtained at rest and after cessation of muscle performance tests. The results indicated that creatine supplementation in comparison with placebo treatment during rapid body mass reduction may help to maintain muscle PT and W(PT)1 at high angular velocities, not influencing Wmax and the rate of fatigue development during Wmax, but affecting adversely Ws max. Within the limitations of the present study the reasons for the partially detrimental effect of creatine administration remain obscure, but it is suggested that impaired creatine uptake in muscle during body mass loss as well as creatine induced changes in muscle glucose and glycogen metabolism may be involved.
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PMID:Effect of creatine supplementation during rapid body mass reduction on metabolism and isokinetic muscle performance capacity. 966 Jan 61

Six amino acids are metabolized in resting muscle. They are leucine, isoleucine, valine, asparagine, aspartate, and glutamate. These amino acids provide the amino groups and probably the ammonia required for synthesis of glutamine and alanine, which are released in excessive amounts in the postabsorptive state and during ingestion of a protein-containing meal. Only leucine and part of the isolecine molecule can be oxidized in muscle as they are converted to acetyl-CoA. The other carbon skeletons are used solely for de novo synthesis of TCA-cycle intermediates and glutamine. The carbon atoms of the released alanine originate primarily from glycolysis of blood glucose and from muscle glycogen (about half each in resting conditions). After consumption of a protein-containing meal, BCAA and glutamate are taken up by muscle and their carbon skeletons are used for de novo synthesis of glutamine. About half of the glutamine released from muscle originates from glutamate taken up from the blood, both after overnight starvation, after prolonged starvation, and after consumption of a mixed meal. Glutamine produced by muscle is an important fuel and regulator of DNA and RNA synthesis in mucosal cells and immune system cells, and fulfils several other important functions in human metabolism. The alanine aminotransferase reaction functions to establish and maintain high concentrations of TCA-cycle intermediates in muscle during the first 10 min of exercise. The increase in concentration of TCA-cycle intermediates probably is needed to increase the flux of the TCA-cycle and meet the increased energy demand of exercise. A gradual increase in leucine oxidation subsequently leads to a carbon drain on the TCA-cycle in glycogen-depleted muscles, and may thus reduce the maximal flux in the TCA-cycle and lead to fatigue. Deamination of amino acids and glutamine synthesis present alternative anaplerotic mechanisms in glycogen-depleted muscles, but only allow exercise at 40-50% of Wmax. One-leg exercise leads to the net breakdown of muscle protein. The liberated amino acids are used for synthesis of TCA-cycle intermediates and glutamine. Today, the importance of this process in endurance exercise in the field (running or cycling) in athletes who ingest carbohydrates is not clear. It is proposed that the maximal flux in the TCA-cycle is reduced in glycogen-depleted muscles due to insufficient TCA-cycle anaplerosis, and that this presents a limitation for the maximal rate of fatty acid oxidation. Interactions between the amino acid pool and the TCA-cycle are suggested to play a central role in the energy metabolism of the exercising muscle.
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PMID:Muscle amino acid metabolism at rest and during exercise: role in human physiology and metabolism. 969 93

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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PMID:Effects of prolonged exercise on brain ammonia and amino acids. 972 Oct 55

Muscle proteins turn over slowly and there are minimal diurnal changes in the size of the muscle protein pool in response to feeding and fasting. Nitrogen balance and tracer studies indicate that protein oxidation and net protein breakdown (degradation--synthesis) is not increased during dynamic exercise at intensities of < or = 70% VO2max. An imbalance between muscle protein synthesis and degradation does exist during one leg knee extensor exercise and during two legged cycling in patients with glycogen phosphorylase deficiency. In these latter cases amino acids liberated from the protein pool are used for synthesis of TCA-cycle intermediates and glutamine. Six amino acids are metabolized in resting muscle: leucine, isoleucine, valine, asparagine, aspartate and glutamate. Only leucine and part of the isoleucine molecule can be converted to acetylCoA and oxidized. The carbon skeleton of the other amino acids is used for synthesis of TCA-cycle intermediates and glutamine. The six amino acids provide the amino groups and the ammonia for synthesis of glutamine and alanine, which are released by muscle in excessive amounts. About half of the glutamine release from muscle originates from glutamate taken up from the blood. Glutamine produced by muscle is an important fuel and regulator of DNA and RNA synthesis in mucosal cells and immune system cells and fulfils several other important functions in human metabolism. The alanine aminotransferase reaction functions to establish and maintain high concentrations of TCA-cycle intermediates and a high TCA cycle flux in the first minutes of exercise. A gradual increase in leucine oxidation subsequently leads to a carbon drain on the TCA-cycle in glycogen depleted muscles and may thus reduce the maximal flux in the TCA-cycle and lead to fatigue. Deamination of amino acids and glutamine synthesis present alternative anaplerotic mechanisms in glycogen depleted muscles but only allow exercise at 40-50% of Wmax. It is proposed that the maximal flux in the TCA-cycle is reduced in glycogen depleted muscles due to insufficient TCA-cycle anaplerosis and that this presents a limitation for the maximal rate of fatty acid oxidation. Interactions between the amino acid pool and the TCA-cycle thus seem to play a central role in the energy metabolism of the exercising muscle.
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PMID:Protein and amino acid metabolism in human muscle. 978 36

In this study we examined the time course of changes in the plasma concentration of oxypurines [hypoxanthine (Hx), xanthine and urate] during prolonged cycling to fatigue. Ten subjects with an estimated maximum oxygen uptake (VO2(max)) of 54 (range 47-67) ml x kg(-1) x min(-1) cycled at [mean (SEM)] 74 (2)% of VO2(max) until fatigue [79 (8) min]. Plasma levels of oxypurines increased during exercise, but the magnitude and the time course varied considerably between subjects. The plasma concentration of Hx ([Hx]) was 1.3 (0.3) micromol/l at rest and increased eight fold at fatigue. After 60 min of exercise plasma [Hx] was >10 micromol/l in four subjects, whereas in the remaining five subjects it was <5 micromol/l. The muscle contents of total adenine nucleotides (TAN = ATP+ADP+AMP) and inosine monophosphate (IMP) were measured before and after exercise in five subjects. Subjects with a high plasma [Hx] at fatigue also demonstrated a pronounced decrease in muscle TAN and increase in IMP. Plasma [Hx] after 60 min of exercise correlated significantly with plasma concentration of ammonia ([NH(3)], r = 0.90) and blood lactate (r = 0.66). Endurance, measured as time to fatigue, was inversely correlated to plasma [Hx] at 60 min (r = -0.68, P < 0.05) but not to either plasma [NH(3)] or blood lactate. It is concluded that during moderate-intensity exercise, plasma [Hx] increases, but to a variable extent between subjects. The present data suggest that plasma [Hx] is a marker of adenine nucleotide degradation and energetic stress during exercise. The potential use of plasma [Hx] to assess training status and to identify overtraining deserves further attention.
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PMID:Plasma hypoxanthine and ammonia in humans during prolonged exercise. 1050 75

Eight female games players (GP) and eight female endurance athletes (EA) ran intermittently at high-intensity and for prolonged periods in hot (30 degrees C) and moderate (16 degrees C) ambient temperatures. The subjects performed a two-part (A, B) test based on repeated 20-m shuttle runs. Part A comprised 60 m of walking, a maximal 15-m sprint, 60 m of cruising (90% maximal oxygen uptake, VO(2max)) and 60 m of jogging (45% VO(2max)) repeated for 75 min with a 3-min rest every 15 min. Part B involved an exercise and rest pattern of 60-s running at 100% VO(2max) and 60-s rest which was continued until fatigue. Although the GP and EA did not respond differently in terms of distances completed, performance was 25 (SEM 4)% less (main effect trial, P < 0.01) in the hot (HT) compared with the moderate trial (MT). Sprints of 15 m took longer to complete in the heat (main effect, trial, P < 0.01), and sprint performance declined during HT but not MT (interaction, trial x time, P < 0.01). A very high correlation was found between the rate of rise in rectal temperature in HT and the distance completed [GP, r =-0.94, P < 0. 01; EA (n = 7), r = -0.93, P < 0.01]. Blood lactate [La(-) ](b) and plasma ammonia [NH(3)](p1) concentrations were higher for GP than EA, but were similar in HT and MT [La(-) ](b), HT: GP vs EA, 8.0 (SEM 0. 9) vs 4.9 (SEM 1.1) mmol x l(-1); MT: GP vs EA, 8.0 (SEM 1.3) vs 4.4 (SEM 1.2) mmol x l(-1); interaction, group x time, P < 0.01; [NH(3)](p1), HT: GP vs EA, 70.1 (SEM 12.7) vs 43.2 (SEM 6.1) mmol x l(-1); MT: GP vs EA, 76.8 (SEM 8.8) vs 32.5 (SEM 3.8) micromol x l(-1); interaction, group x time, P < 0.01. Ad libitum water consumption was higher in HT [HT: GP vs EA, 18.9 (SEM 2.9) vs 13.5 (SEM 1.7) ml x kg(-1) x h(-1); MT: GP vs EA, 12.7 (SEM 3.7) vs 8.5 (SEM 1.5) ml x kg(-1) x h(-1); main effect, group, n.s.; main effect, trial, P < 0.01]. These results would suggest that elevated body temperature is probably the key factor limiting performance of prolonged, intermittent, high-intensity running when the ambient temperature is high, but not because of its effect on the metabolic responses to exercise.
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PMID:Physiological and metabolic responses of female games and endurance athletes to prolonged, intermittent, high-intensity running at 30 degrees and 16 degrees C ambient temperatures. 1055 71

In this paper we describe 3 clinical cases of hypothyroidism causing myopathy and hyperammonemia. The patients, all females, aged 32 to 64 years, presented with hoarseness, fatigue, dyspepsia (case I), difficulty speaking secondary to the sensation of tongue swelling and hoarseness (case II), and progressive weight gain and difficulty speaking secondary to tongue swelling after delivery (case III). Laboratory tests showed a marked increase in creatine phosphokinase (up to 4090 U/L; normal values 24-176 U/L) of muscle origin, and an increase in transaminases and ammonia (124 to 150 micrograms/dL; normal values up to 75 micrograms/dL). Hypothyroidism was confirmed by TSH > 100 microIU/mL (normal values 0.3-5 microIU/mL). Treatment only with L-thyroxine determined the complete and persistent recovery of well-being and of biochemical abnormalities. The patients remained in good health after more than 2 years of follow-up. Our finding of hyperammonemia caused by the lack of thyroid hormones in 3 patients with hypothyroid myopathy appears to be of a certain interest as, to our knowledge, this phenomenon has not been previously described. In conclusion our hypothesis is that increased muscle production of ammonia secondary to the hypothyroid myopathy determined an increased ammonia load, resulting in hyperammonemia. Decreased liver ureagenesis induced by the lack of thyroid hormones also contributed to the hyperammonemia.
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PMID:[Hyperammonemia during hypothyroidism: an unusual biohumoral finding normalized by hormonal replacement treatment]. 1063 22

We reported a case of adult-onset citrullinemia associated with hypertrigliceridemia and diabetes mellitus. A 24-year-old female was healthy until recently. She first felt intermittent headaches and nausea. Then she noticed memory loss and tiredness. Abnormal behavior such as getting lost on the way from her company sometimes occurred. She came to our hospital because these symptoms had been getting worse. Neurologically she had a very mild disturbed consciousness. An EEG recording showed diffuse slow wave with high amplitude. MR image of the brain showed hyper-intensity in globus pallidus with T1-weighted image. Plasma citrullin level was very high. Plasma ammonia and triglyceride showed a moderately high level. Using biopsied liver tissues, the enzymes of the urea cycle were analyzed. Argininosuccinate synthetase activity was extremely low. Because of clinical course and the result of liver biopsy, the patient was diagnosed as type 2 citrullinemia. A low protein diet was started, but intermittent nausea and consciousness disturbance did not improve. A partial liver transplantation was performed. The living donor was her father, a 50-year-old male, who had normal liver function. After the liver transplantation, all neurological signs soon disappeared. Plasma citrulline, ammonia and triglyceride normalized rapidly. An EEG recording became normal, and the hyper-intensity in globus pallidus with T1-weighted MR image disappeared two months after surgery. Liver transplantation should be planned as soon as possible in a type 2 citrullinemia patient.
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PMID:[Liver transplantation in type II citrullinemia]. 1065 68

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