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

Rat slow-twitch muscle, in contrast to fast-twitch muscle, maintains its ATP content near normal during intense stimulation conditions that produce rapid fatigue. An extensive depletion of adenine nucleotide content by the deamination of AMP to IMP + NH3, typical of fast-twitch muscle, does not occur. We evaluated whether this response of slow-twitch muscle could be simply due to failure of synaptic transmission or related to cellular conditions influencing enzyme activity. Stimulation of soleus muscles in situ via the nerve or directly in the presence of curare at 120 tetani/min for 3 min resulted in extensive fatigue but normal ATP contents. Thus the lack of ATP depletion must be related to cellular events distal to neuromuscular transmission. Even nerve and direct muscle stimulation (with curare) during ischemia did not cause a large depletion of ATP or a large elevation of lactate content (12.0 +/- 0.7 mumol/g), even though the decline in tension was essentially complete. However, if the same tension decline during ischemia was prolonged by stimulating for 10 min at 12 tetani/min a large decrease in ATP (2.24 +/- 0.09 mumol/g) and increase in IMP (2.47 +/- 0.16 mumol/g) and lactate (30.4 +/- 2.0 mumol/g) content occurred. Thus adenine nucleotide deamination to IMP can occur in slow-twitch muscle during specific contraction conditions. The cellular events leading to the activation of AMP deaminase require an intense contraction condition and may be related to acidosis caused by a high lactate content.
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PMID:ATP depletion in slow-twitch red muscle of rat. 363 Dec 51

Arginine administration (5 m moles/kg/day) to albino rats for 7 days, revealed that this vital basic amino acid possesses latent potentiality for the accentuation of urea cycle or at least for arginase activity. The mitigation of ammonia toxicity was observed to be more effective in the case of gastrocnemius and red vastus as compared to white vastus. Further, ammonia and lactate levels were also decreased by arginine in blood and thereby delaying the onset of fatigue by preventing ammonotoxemia and lactic acidemia.
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PMID:Arginine protection against ammonia toxicity in exhausted rat. 366 75

Data from 23 normal men and women were used to derive 95% confidence limits for maximum changes in ammonia and lactate values following ischemic forearm exercise. Most normal subjects raised serum lactate and ammonia concentrations more than 20 mg/dl and 100 micrograms/dl, respectively, over baseline values. No significant correlations were found among age, sex, duration of exercise, or estimate of work performed and the maximum ammonia and lactate values achieved. When 70 patients with complaints of weakness, fatigue, or cramps were evaluated, the ischemic exercise test identified 5 patients who proved to have defects in glycolysis or purine metabolism. The test also distinguished those patients with type III glycogen storage disease who lacked debrancher enzyme activity in muscle.
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PMID:The ischemic exercise test in normal adults and in patients with weakness and cramps. 370 11

The effect of dynamic exercise on muscle and blood ammonia (NH3) and amino acid contents has been investigated. Eight healthy men cycled at 50% and 97% of maximal oxygen uptake for 10 min and 5.2 min (to fatigue), respectively. Biopsies (quadriceps femoris muscle), arterial and femoral venous blood samples were obtained at rest and during exercise. Muscle NH3 at rest and after submaximal exercise was (means +/- SE) 0.5 +/- 0.1 mmol/kg dry muscle (d.m.) and increased to 4.1 +/- 0.5 mmol/kg d.m. at fatigue (P less than 0.001). The total adenine nucleotide (TAN) pool (TAN = ATP + ADP + AMP) did not change after submaximal exercise but decreased significantly at fatigue (P less than 0.001). The decrease in TAN was similar to the increase in NH3. Muscle lactate was 3 +/- 1 mmol/kg d.m. at rest and increased to 104 +/- 5 mmol/kg d.m. at fatigue. Whole blood and plasma NH3 did not change significantly during submaximal but both increased significantly during maximal exercise (P less than 0.001). During maximal exercise the leg released 7,120 mumol/min of lactate, whereas only 89 mumol/min of NH3 were released. NH3 accumulation in muscle could buffer only 3% of the hydrogen ions released from lactate, and NH3 release could account for only 1% of the net hydrogen ion transport out of the cell. Muscle glutamine was constant throughout the study, whereas glutamate decreased and alanine increased during exercise (P less than 0.001). No significant changes in either arterial whole blood glutamine or glutamate were observed. Arterial plasma glutamine and glutamate concentrations, however, increased and decreased (P less than 0.001), respectively, during exercise. It is concluded that (1) muscle and blood NH3 levels increase only during strenuous exercise and (2) NH3 accumulation is of minor importance for regulating acid-base balance in body fluids during exercise.
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PMID:Muscle ammonia and amino acid metabolism during dynamic exercise in man. 374 56

Eight horses exercised to fatigue were used to characterize the resulting changes in blood pH, in blood lactate, free fatty acid, bicarbonate, and ammonia concentrations, and in muscle glycogen concentrations. The exercise test was conducted at a speed of 4.5 m/s on a motorized equine treadmill set at a 9% grade. At fatigue, all variables differed significantly (P less than 0.05) from base-line values. Heart rate averaged 191.1 +/- 6.5 beats/min at fatigue, and the plasma lactate concentrations increased from 7.8 +/- 0.95 mg/dl to 94.3 +/- 19.2 mg/dl. Ammonia concentrations increased from 66.7 +/- 6.9 mumol/L before exercise to 136.9 +/- 18.6 mumol/L at fatigue. Bicarbonate concentrations decreased from 31.3 +/- 0.4 mM to 21.1 +/- 1.8 mM, and pH decreased from 7.37 +/- 0.01 to 7.28 +/- 0.04. Free fatty acid concentrations were higher at fatigue and increased throughout the recovery period. Exercise resulted in a 25% decrease of muscle glycogen concentration in gluteus medius specimens.
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PMID:Changes in equine metabolic characteristics due to exercise fatigue. 377 43

The role of ammonia in exercise-induced fatigue is reviewed. Implications for integrated activity of developing hyperammoneic states, caused by various precipitating conditions such as exercise, liver dysfunction, hypoxia, hyperoxia, and chemical poisoning are described. The central role of ammonia in diverse important metabolic pathways indicates its ubiquitous role in a spectrum of activity ranging from elite exhaustive performance of sportsmen and -women to life-threatening organ dysfunction. The action of ammonia and metabolites from associated pathways in producing seemingly dangerous short term conditions, but inducing possible long term protection against degenerative processes associated with ageing (free radical-induced cellular damage) indicate the paradoxical position of ammonia and its associated metabolic pathways for health and disease processes.
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PMID:Ammonia as an indicator of exercise stress implications of recent findings to sports medicine. 388 58

Within working muscle, development of conditions that directly influence exercise performance is dependent on many factors, including: intensity and duration of exercise, type of skeletal muscle fibres recruited, cardiovascular support to the working fibres and the inherent metabolic characteristics of the contracting fibres. In general, it is possible to identify factors that seem to alter exercise performance only at relatively intense exercise conditions. During prolonged moderately intense exercise (e.g. 70-80% maximal oxygen consumption for at least 60-90 min) decline in performance is related to the depletion of glycogen within the working muscle. Although the cause of muscle performance decline during very intense exercise is not known, an extreme acidosis is found, especially in fast-twitch muscle, which could significantly disrupt normal metabolic and contractile processes. During fatigue caused by intense contraction conditions, ATP content decreases (by approx. 50%) and there is a stoichiometric production of IMP and ammonia in fast-twitch muscle. This loss in adenine nucleotide content is dependent on the severity of the contraction conditions relative to the functional aerobic capacity of the muscle fibre, since fast-twitch red (high mitochondria, high blood flow) and fast-twitch white (low mitochondria, low blood flow) muscles respond differently. In contrast, during similarly intense contraction conditions, rat slow-twitch muscle fibres maintain their ATP content and do not produce significant amounts of IMP. Indirect evidence suggests that a similar contrast between fibres occurs in humans during maximal exercise. Thus, there seems to be a fundamental difference between fast- and slow-twitch muscles in the management of their adenine nucleotide contents during intense contraction conditions. Whether this is related to the known differences in the fatigue process between these fibre types is not known.
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PMID:Metabolic and circulatory limitations to muscular performance at the organ level. 403 72

Ozone, a lower-airway irritant, produces fatigue, lethargy, and increased respiratory rates in several species, including man. Ammonia, an upper-airway irritant, produces burning of the eyes, nose, and throat, and a decrease in respiratory rate. The effects of exposure to these two prototypical irritants were examined to see if behavioral changes during and after exposure occurred at concentrations comparable to those that produce symptoms in humans. Long-Evans rats and Swiss mice, individually housed in running wheels, were exposed either to ozone (0.08, 0.12, 0.25, or 0.5 ppm) or to ammonia (100 or 300 ppm) for 6 hr. Each animal's behavior was compared with its own control performance. Running in both species decreased in a concentration-related manner during exposure to either irritant. The decrease in running activity produced by high concentrations of ozone persisted for several hours after exposure. Concentrations of ammonia that eliminated running during exposure led to an increase in activity following exposure. At comparable concentrations of both compounds, activity in rats decreased more than in mice.
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PMID:Alterations in behavior produced by inhaled ozone or ammonia. 409 73

Although fatigue is a well-known phenomenon and the phrase "exercised until exhaustion" is commonly understood, there is no unequivocal agreement on the fundamental nature of the fatigue process. Ammonia was linked to the development of fatigue as early as 1922, when ammonia production was observed from stimulated nerve and the question whether there could be a relationship between ammonia production and the muscle activity was raised. The immediate source of ammonia from muscle appears to be a result of the deamination of AMP and is more apparent in fast-twitch than in slow-twitch fibers. More recently, increases in blood ammonia levels have been reported in rats after swimming and in humans after arm work, maximal cycle ergometry, and treadmill exercise. Elevated blood ammonia has also been linked to a surprising variety of functional and metabolic neurological disturbances other than exercise and fatigue, including the development of hepatic coma, convulsions from ammonia toxicity precipitated by high-pressure oxygen breathing, epileptic seizures, and decreased neuronal excitability. In addition, a number of genetic disorders (inborn errors in metabolism, or IEMs) are characterized by elevated blood ammonia concentrations. Symptoms of neural disability in all of the above conditions have been related to the concentration of ammonia in blood. Although these studies do not relate to exercise or fatigue directly, it is conceivable that our understanding of the effect of high concentrations of blood ammonia in these clinical conditions may provide valuable insight into the effect of ammonia during exercise. This paper reviews the effect of ammonia production during exercise and other conditions upon purposeful activity and the development of fatigued states.
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PMID:Ammonia metabolism in exercise and fatigue: a review. 634 52

Development of the fatigue state in rats, subjected to prolonged alcohol intoxication, after swimming with might led to dissimilar alterations in the system of ammonia formation and binding in brain and spinal cord as compared with control animals under the same conditions of loading. Within the first minutes of the heavy loading the faster and more distinct accumulation of ammonia was observed, then the rapid exhaustion of the reaction occurred and the ammonia production was markedly decreased in the state of fatigue. Impairments in brain protein deamidation and decrease in content of urea were found. At the same time, dynamics of gamma-aminobutyric acid, dicarboxylic amino acids and their amides was altered.
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PMID:[Brain and spinal cord nitrogen metabolism in chronic alcoholism following strenuous physical exertion]. 719 7


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