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

The plasma ammonia response to exercise in chronic obstructive pulmonary disease (COPD) was examined and the relationship between plasma ammonia concentration and muscle adenine nucleotide metabolism was explored. In total, 25 stable COPD patients and 13 similar-aged controls underwent incremental and constant-work rate cycle exercise tests. Arterialised venous blood was sampled at rest, at 1-min intervals during exercise and <or=5 min after exercise for ammonia and lactate concentration. Peak incremental work rate was significantly less in COPD subjects (67+/-21 W) than similar-aged controls (156+/-46 W). In COPD and control subjects, plasma ammonia concentration increased during incremental exercise until 2 min post-exercise and then declined by 5 min post-exercise. However, two distinct patterns were seen in COPD subjects. In one group (n = 16), ammonia increased (42.8+/-3.3 micromol x L(-1)) by a similar magnitude as the controls (55.5+/-7.0 micromol x L(-1)). In the second COPD group (n = 9), no ammonia increase was observed despite a similar lactate increase. Ammonia change with incremental and constant-work rate exercise strongly correlated in COPD subjects. Plasma ammonia increase correlated with muscle inosine-5'-monophosphate formation after constant-work rate exercise. Plasma ammonia concentration increases during incremental and constant-work rate cycle exercise in chronic obstructive pulmonary disease subjects at lower absolute work rates compared with similar-aged controls. The plasma ammonia response may provide useful information about adenine nucleotide metabolism and, therefore, muscle fatigue during exercise in patients with chronic obstructive pulmonary disease.
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PMID:The plasma ammonia response to cycle exercise in COPD. 1837 78

The aim of this study was to investigate the effects of adding a high-intensity intermittent session twice a week during a 7-week karate training (KT) on markers of aerobic and anaerobic metabolisms in elite class karate athletes. Two groups were studied: a KT group (n=8, age 20.1+/-0.9 years, 70.0+/-8.8 kg) that followed traditional KT, and a group that followed combined traditional karate and a high-intensity intermittent training (HIT group, n=9, age 24.4+/-3.1 years, 67.0+/-7.8 kg). The subjects undertook a supramaximal exercise and a maximal oxygen uptake test before and after the training. Blood lactate, pH and plasma ammonia were determined at rest, immediately at the end of the supramaximal exercise and during the recovery period at 2, 4, 6, 8, 10 and 15 min. After the training period, no changes occurred in the KT group. However, in the HIT group, the time to exhaustion, MAOD and in the maximal oxygen uptake test were significantly improved by 23.6%, 10.3% and 4.6%, respectively. A clear-cut discrepancy was observed in the time course of lactate and pH in the supramaximal test after the training in the HIT group. We observed a significantly higher peak for lactate and a lower extreme value for pH with a shorter delay of appearance. At the end of the test, the lactate concentration increased significantly (+53.7%) and pH declined significantly, when compared with the values obtained after the same test before the training period. Ammonia was not influenced. The addition of high-intensity intermittent sessions twice per week during the period of KT induced beneficial physiological adaptations in athletes, allowing improvement in the duration of intense physical exercise before a state of fatigue is reached.
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PMID:Impressive anaerobic adaptations in elite karate athletes due to few intensive intermittent sessions added to regular karate training. 1869 36

Arginine supplementation has been shown to alleviate endothelial dysfunction and improve exercise performance through increasing nitric oxide production in patients with cardiopulmonary diseases. In addition, arginine supplementation could decrease accumulations of lactate and ammonia, metabolites involved in development of muscular fatigue. The aim of this study was to investigate the effect of short-term arginine supplementation on performance in intermittent anaerobic exercise and the underlying mechanism in well-trained male athletes. Ten elite male college judo athletes participated with a randomized crossover, placebo-controlled design. The subjects consumed 6 g/day arginine (ARG trial) or placebo (CON trial) for 3 days then performed an intermittent anaerobic exercise test on a cycle ergometer. Blood samples were collected before supplementation, before and during exercise and 0, 3, 6, 10, 30 and 60 min after exercise. ARG trial had significantly higher arginine concentrations than CON trial at the same time point before, during and after exercise. In both trials, nitrate and nitrite concentration was significantly higher during and 6 min after exercise comparing to the basal concentration. The increase in nitrate and nitrite concentration during exercise in both trials was parallel to the increase in plasma citrulline concentrations. There was no significant difference between the 2 trials in plasma nitrate and nitrite, lactate and ammonia concentrations and peak and average power in the exercise. The results of this study suggested that short-term arginine supplementation had no effect on nitric oxide production, lactate and ammonia metabolism and performance in intermittent anaerobic exercise in well-trained male athletes.
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PMID:No effect of short-term arginine supplementation on nitric oxide production, metabolism and performance in intermittent exercise in athletes. 1870 87

This study evaluated the effects of Prunus mume extract on exercise-induced fatigue recovery in a trained rat model. Male Sprague-Dawley rats were raised either on a control diet (EC) or on diets supplemented with 0.15% (0.15EP), 0.3% (0.3EP), or 0.9% (0.9EP) Prunus mume extract for 4 weeks (n = 18). Each dietary group was divided into two subgroups; at the end of the experimental period, one subgroup was sacrificed immediately after a 1-hour exercise, and the other subgroup was sacrificed after a 30-minute rest following the exercise (n = 9). Compared to the values for EC rats, serum ammonia concentration was significantly lower in 0.3EP and 0.9EP rats that were sacrificed immediately after the exercise-loading and in 0.15EP, 0.3EP and 0.9EP rats that were sacrificed after a 30-minute rest following the exercise. Compared to that in EC rats, serum lactate levels were significantly lower in rats fed 0.15% or higher levels of P. mume extract when they were sacrificed after a 30-minute rest following the exercise. Dietary supplementation with the P. mume extract significantly elevated hepatic and muscle glycogen concentrations of the rats sacrificed immediately after the exercise. P. mume extract significantly reduced lactate dehydrogenase activity and increased citrate synthase activity in the skeletal muscles of the rats sacrificed immediately after the exercise-loading. Taken together, these results indicate that the P. mume extract administered during endurance exercise training may enhance the oxidative capacity of exercising skeletal muscle and may induce the muscle to prefer fatty acids for its fuel use rather than amino acids or carbohydrates.
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PMID:Prunus mume extract ameliorates exercise-induced fatigue in trained rats. 1880 Aug 92

Citrin deficiency is a common congenital metabolic defect not only in East Asian populations but also in other populations around the world. It has been shown that although liver transplantation is ultimately required in many patients to prevent neurological decompensation associated with hyperammonaemia, arginine is effective in lowering ammonia in hyperammonaemic patients, and a high-protein low-carbohydrate diet may provide some benefit to infants in improving failure to thrive. In the present study, the clinical symptoms and laboratory findings are reported for a 13-year-old citrin-deficient girl in the early stage of adult-onset type II citrullinaemia (CTLN2), and the therapeutic effect of orally administered arginine and sodium pyruvate was investigated. The patient complained of anorexia, lethargy, fatigue and poor growth, and showed laboratory findings typical of CTLN2; elevated levels of plasma citrulline, threonine-to-serine ratio, and serum pancreatic secretory trypsin inhibitor. Oral administration of arginine and sodium pyruvate for over 3 years improved her clinical symptoms and has almost completely normalized her laboratory findings. It is suggested that the administration of arginine and sodium pyruvate with low-carbohydrate meals may be an effective therapy in patients with citrin deficiency in order either to prolong metabolic normalcy or to provide a safer and more affordable alternative to liver transplantation.
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PMID:Treatment of a citrin-deficient patient at the early stage of adult-onset type II citrullinaemia with arginine and sodium pyruvate. 1895 81

We examined the effects of L-ornithine administration on physical fatigue. In a double-blind, placebo-controlled, 2-way crossover study, 17 healthy volunteers were randomized to L-ornithine (2000 mg/d for 7 days and 6000 mg/d for 1 day as L-ornithine hydrochloride) or placebo for 8 days. The fatigue-inducing physical task consisted of workload trials on a cycle ergometer at fixed workloads for 2 hours on 2 occasions. We found that oral L-ornithine administration promoted lipid metabolism and activated the urea cycle from serum triacylglycerol, ketone bodies, free fatty acids, and blood ammonia level changing. L-ornithine significantly attenuated the subjective feeling of fatigue (measured by visual analog scale at postrecovery) compared with postload (P < .01). Moreover, in female subjects, the subjective feeling of fatigue was significantly lower compared with the placebo group (P < .05). In the physical performance test in female subjects, the decrease in mean speed for 10 seconds maximum pedaling from 0.5- to 3.5-hour trials in the group receiving L-ornithine was smaller than that in the group receiving placebo (P < .05). These results suggest that L-ornithine has an antifatigue effect by increasing the efficiency of energy consumption and promoting the excretion of ammonia. L-ornithine is a free amino acid and is not rich in meats or fish, so it is difficult to obtain amounts of L-ornithine from ordinary meals that would be sufficient to promote the antifatigue effect. We recommend L-ornithine intake as a nutritional supplement in cases of physical fatigue.
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PMID:L-ornithine supplementation attenuates physical fatigue in healthy volunteers by modulating lipid and amino acid metabolism. 1908 82

Apart from few studies, the majority of the research conducted on the effects of heat stress on energy metabolism during exercise has only been done so in the past two decades. Whilst increasing exercise duration under conditions of heat stress favours the oxidation of carbohydrate (CHO) and appears to increase the rate of muscle glycogenolysis, total CHO oxidation is often less and levels of muscle glycogen remain much higher at the point of fatigue when compared with the same exercise without heat stress. Furthermore, supplementing CHO during exercise in the heat appears to exert an ergogenic effect that is not related to 'peripheral' but rather 'central' factors. However, there may be a role for the excess ammonia (NH3) produced in the exercising muscle during heat stress, as cerebral uptake and subsequent metabolism of NH3 may have detrimental effects on cerebral function. Recent exciting results point toward an increased cerebral CHO uptake relative to that of O2, termed the cerebral metabolic ratio (CMR) during exercise with heat stress, although a causative link between this and reduced exercise performance has yet to be identified. Therefore, it appears that despite a shift towards greater CHO utilisation in both skeletal muscular and cerebral metabolism, these responses have ultimately not proved limiting to exercise with heat stress.
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PMID:Exercise heat stress and metabolism. 1920 3

This study examined the effects of heavy resistance training on dynamic exercise-induced fatigue task (5 x 10RM leg-press) after two loading protocols with the same relative intensity (%) (5 x 10RM(Rel)) and the same absolute load (kg) (5 x 10RM(Abs)) as in pretraining in men (n=12). Maximal strength and muscle power, surface EMG changes [amplitude and spectral indices of muscle fatigue], and metabolic responses (i.e.blood lactate and ammonia concentrations) were measured before and after exercise. After training, when the relative intensity of the fatiguing dynamic protocol was kept the same, the magnitude of exercise-induced loss in maximal strength was greater than that observed before training. The peak power lost after 5 x 10RM(Rel) (58-62%, pre-post training) was greater than the corresponding exercise-induced decline observed in isometric strength (12-17%). Similar neural adjustments, but higher accumulated fatigue and metabolic demand were observed after 5 x 10RM(Rel). This study therefore supports the notion that similar changes are observable in the EMG signal pre- and post-training at fatigue when exercising with the same relative load. However, after training the muscle is relatively able to work more and accumulate more metabolites before task failure. This result may indicate that rate of fatigue development (i.e. power and MVC) was faster and more profound after training despite using the same relative intensity.
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PMID:Neuromuscular fatigue after resistance training. 1938 55

It has been well established that, in addition to the pulmonary involvement, COPD has systemic consequences that can lead to peripheral muscle dysfunction, with greater muscle fatigue, lower exercise tolerance and lower survival in these patients. In view of the negative repercussions of early muscle fatigue in COPD, the objective of this review was to discuss the principal findings in the literature on the metabolic and bioenergy determinants of muscle fatigue, its functional repercussions, as well as the methods for its identification and quantification. The anatomical and functional substrate of higher muscle fatigue in COPD appears to include lower levels of high-energy phosphates, lower mitochondrial density, early lactacidemia, higher serum ammonia and reduced muscle perfusion. These alterations can be revealed by contraction failure, decreased firing rates of motor units and increased recruitment of motor units in a given activity, which can be functionally detected by a reduction in muscle strength, power and endurance. This review article also shows that various types of muscle contraction regimens and protocols have been used in order to detect muscle fatigue in this population. With this understanding, rehabilitation strategies can be developed in order to improve the resistance to muscle fatigue in this population.
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PMID:Methods for the assessment of peripheral muscle fatigue and its energy and metabolic determinants in COPD. 2001 49

Exercise-induced hyperthermia is associated with central fatigue as indicated by an impaired ability to sustain maximal motor activation during prolonged voluntary efforts. Therefore, exercise in hot environments challenges not only to the cardiorespiratory and locomotive systems but also to the brain. However, exercise with superimposed hyperthermia is not only a challenge to the brain it also provides an excellent model for studying factors of importance for central fatigue. Excessive heat storage within the brain appears to be the primary cause for the central fatigue during exercise in the heat, but pharmacological manipulations provide evidence for involvement of the dopaminergic system and other monoamines. Thus, enhanced dopaminergic activity may counteract hyperthermia mediated central fatigue and improve performance in the heat, while noradrenaline re-uptake inhibition appears to aggravate central fatigue and degrade exercise performance. Hyperthermia mediated central fatigue may include other cerebral perturbations such as reduced perfusion of the brain, accumulation of ammonia or depletion of neuronal energy stores, but further research is needed to elucidate their possible contributions.
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PMID:CNS fatigue provoked by prolonged exercise in the heat. 2003 22


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