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

This report describes changes of the rate of ATP hydrolysis in single, intact muscle fibres during the development of fatigue induced by intermittent tetanic stimulation. High (type 3) and low (type 1) oxidative muscle fibres dissected from the iliofibularis muscle of Xenopus laevis were studied at 20 degrees C. The rate of ATP hydrolysis was calculated during different time intervals from changes in the content of nucleotides, creatine compounds and lactate, as well as lactate efflux and oxygen uptake. During the first phase of intermittent stimulation, phosphocreatine is fully reduced while the rate of oxygen consumption increases to its maximum, the lactate content increases to a maximum level, and a small amount of IMP is formed; the rate of ATP hydrolysis in type 3 fibres is constant while force decreases, whereas the rate decreases approximately in proportion to force in type 1 fibres. After the first phase, the rate of ATP hydrolysis in type 3 fibres decreases slightly and the fibres reach a steady metabolic state in which the rates of ATP formation and hydrolysis are equal; in type 1 fibres a drastic change of the rate of ATP hydrolysis occurs and a steady metabolic state is not reached. On the basis of the time courses of the metabolic changes, it is concluded that the rate of ATP hydrolysis in type 3 fibres is reduced by acidification and/or a reduced calcium efflux from the sarcoplasmic reticulum, whereas in type 1 fibres inorganic phosphate and/or acidification inhibit the rate initially and ADP is a likely candidate to explain the drastic fall of the rate of ATP hydrolysis during late phases of fatiguing stimulation.
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PMID:ATP formation and ATP hydrolysis during fatiguing, intermittent stimulation of different types of single muscle fibres from Xenopus laevis. 812 21

The role of prolonged electrical stimulation on sarcoplasmic reticulum (SR) Ca2+ sequestration measured in vitro and muscle energy status in fast white and red skeletal muscle was investigated. Fatigue was induced by 90 min intermittent 10-Hz stimulation of rat gastrocnemius muscle, which led to reductions (p < 0.05) in ATP, creatine phosphate, and glycogen of 16, 55, and 49%, respectively, compared with non-stimulated muscle. Stimulation also resulted in increases (p < 0.05) in muscle lactate, creatine, Pi, total ADP, total AMP, IMP, and inosine. Calculated free ADP (ADPf) and free AMP (AMPf) were elevated 3- and 15-fold, respectively. No differences were found in the metabolic response between tissues obtained from the white (WG) and red (RG) regions of the gastrocnemius. No significant reductions is SR Ca2+ ATPase activity were observed in homogenate (HOM) or a crude SR fraction (CM) from WG or RG muscle following exercise. Maximum Ca2+ uptake in HOM and CM preparations was similar in control (C) and stimulated (St) muscles. However, Ca2+ uptake at 400 nM free Ca2+ was significantly reduced in CM from RG (0.108 +/- 0.04 to 0.076 +/- 0.02 mumol.mg-1 protein.min-1 in RG - C and RG - St, respectively). Collectively, these data suggest that reductions in muscle energy status are dissociated from changes in SR Ca2+ ATPase activity in vitro but are related to Ca2+ uptake at physiological free [Ca2+ bd in fractionated SR from highly oxidative muscle. Dissociation of SR Ca2+ ATPase activity from Ca2+ uptake may reflect differences in the mechanisms evaluated by these techniques.
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PMID:Effects of prolonged low frequency stimulation on skeletal muscle sarcoplasmic reticulum. 856 84

The manifestations of fatigue, as observed by reductions in the ability to produce a given force or power, are readily apparent soon after the initiation of intense activity. Moreover, following the activity, a sustained weakness may persist for days or even weeks. The mechanisms responsible for the impairment in performance are various, given the severe strain imposed on the multiple organ systems, tissues and cells by the activity. At the level of the muscle cell, ATP utilization is dramatically accelerated in an attempt to satisfy the energy requirements of the major processes involved in excitation and contraction namely sarcolemmal Na+/K+ exchange, sarcoplasmic reticulum Ca2+ sequestration and actomyosin cycling. In an attempt to maintain ATP levels, high-energy phosphate transfer, glycolysis and oxidative phosphorylation are recruited. With intense activity, ATP production rates are unable to match ATP utilization rates, and reductions in ATP occur accompanied by accumulation of a range of metabolic by-products such as hydrogen ions, inorganic phosphate, AMP, ADP and IMP. Selective by-products are believed to disturb Na+/K+ balance, Ca2+ cycling and actomyosin interaction, resulting in fatigue. Cessation of the activity and normalization of cellular energy potential results in a rapid recovery of force. This type of fatigue is often referred to as metabolic. Repeated bouts of high-intensity activity can also result in depletion of the intracellular substrate, glycogen. Since glycogen is the fundamental fuel used to sustain both glycolysis and oxidative phosphorylation, fatigue is readily apparent as cellular resources are exhausted. Intense activity can also result in non-metabolic fatigue and weakness as a consequence of disruption in internal structures, mediated by the high force levels. This type of impairment is most conspicuous following eccentric muscle activity; it is characterized by myofibrillar disorientation and damage to the cytoskeletal framework in the absence of any metabolic disturbance. The specific mechanisms by which the high force levels promote muscle damage and the degree to which the damage can be exacerbated by the metabolic effects of the exercise remain uncertain. Given the intense nature of the activity and the need for extensive, high-frequency recruitment of muscle fibres and motor units in a range of synergistic muscles, there is limited opportunity for compensatory strategies to enable performance to be sustained. Increased fatigue resistance would appear to depend on carefully planned programmes designed to adapt the excitation and contraction processes, the cytoskeleton and the metabolic systems, not only to tolerate but also to minimize the changes in the intracellular environment that are caused by the intense activity.
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PMID:Mechanisms of muscle fatigue in intense exercise. 923 50

To examine the effect of ambient temperature on metabolism during fatiguing submaximal exercise, eight men cycled to exhaustion at a workload requiring 70% peak pulmonary oxygen uptake on three separate occasions, at least 1 wk apart. These trials were conducted in ambient temperatures of 3 degrees C (CT), 20 degrees C (NT), and 40 degrees C (HT). Although no differences in muscle or rectal temperature were observed before exercise, both muscle and rectal temperature were higher (P < 0.05) at fatigue in HT compared with CT and NT. Exercise time was longer in CT compared with NT, which, in turn, was longer compared with HT (85 +/- 8 vs. 60 +/- 11 vs. 30 +/- 3 min, respectively; P < 0.05). Plasma epinephrine concentration was not different at rest or at the point of fatigue when the three trials were compared, but concentrations of this hormone were higher (P < 0.05) when HT was compared with NT, which in turn was higher (P < 0.05) compared with CT after 20 min of exercise. Muscle glycogen concentration was not different at rest when the three trials were compared but was higher at fatigue in HT compared with NT and CT, which were not different (299 +/- 33 vs. 153 +/- 27 and 116 +/- 28 mmol/kg dry wt, respectively; P < 0.01). Intramuscular lactate concentration was not different at rest when the three trials were compared but was higher (P < 0.05) at fatigue in HT compared with CT. No differences in the concentration of the total intramuscular adenine nucleotide pool (ATP + ADP + AMP), phosphocreatine, or creatine were observed before or after exercise when the trials were compared. Although intramuscular IMP concentrations were not statistically different before or after exercise when the three trials were compared, there was an exercise-induced increase (P < 0.01) in IMP. These results demonstrate that fatigue during prolonged exercise in hot conditions is not related to carbohydrate availability. Furthermore, the increased endurance in CT compared with NT is probably due to a reduced glycogenolytic rate.
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PMID:Effect of ambient temperature on human skeletal muscle metabolism during fatiguing submaximal exercise. 1006 3

To examine the effect of training status on muscle metabolism during exercise, seven endurance-trained [peak oxygen uptake (VO(2 peak)) = 65.8 +/- 2.4 ml. kg(-1). min(-1)] and six untrained (VO(2 peak) = 46. 2 +/- 1.9 ml. kg(-1). min(-1)) men cycled to fatigue at a work rate calculated to require 70% VO(2 peak). Time to exhaustion was 36% longer (P < 0.01) in trained (TR) compared with untrained (UT) men (148 +/- 11 vs. 95 +/- 8 min). Although intramuscular glycogen content was reduced (P < 0.05) in both TR and UT at fatigue, IMP, a marker of a mismatch between ATP supply and demand, was only elevated (P < 0.01) in UT muscle at fatigue and was approximately fourfold higher at this point in UT compared with TR. These data demonstrate that fatiguing submaximal exercise was associated with a similar low level of intramuscular glycogen in both TR and UT men, but a mismatch between ATP supply and demand only occurred in UT individuals.
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PMID:Muscle IMP accumulation during fatiguing submaximal exercise in endurance trained and untrained men. 1040 85

The aim was to study metabolic response and locomotion pattern in Standardbred trotters during incremental treadmill exercise performed by increasing speed by 1 m/s in 1 min steps (start 7 m/s) until the onset of fatigue. The test protocol included determination of oxygen uptake, heart rate (HR), stride length (SL) and stride frequency (SF). Venous blood samples were collected at rest, at the end of each exercise step and after 30 min of recovery. Muscle biopsies were taken at rest and post exercise and muscle temperature was measured after exercise. As horses fatigued at different speed steps (9-11 m/s), variation was seen in running time (180-300 s), oxygen uptake (109-170 ml/kg bwt min), HR (200-225 beats/min), SL (4.4-5.7 m) and SF (116-130 strides/min) at the last speed step. Increased mean plasma lactate concentration (20.5 mmol/l) was seen at onset of fatigue and increased mean uric acid concentration after 30 min of recovery (112.8 mumol/l). After exercise, a decrease was seen in muscle ATP (7.1 mmol/kg d.w.), creatine phosphate (43.9 mmol/kg d.w.) and glycogen (160 mmol/kg d.w.), and an increase was seen in ADP (0.3 mmol/kg d.w.), AMP (0.18 mmol/kg d.w.), IMP (5.8 mmol/kg d.w.) and lactate (100.8 mmol/kg d.w.). At onset of fatigue, muscle temperature varied from 39.9-41.4 degrees C. Running time correlated with SL (r = 0.86), with an increase in IMP (r = 0.79) and AMP (r = 0.70) post exercise and with plasma uric acid concentration (r = 0.74) at 30 min of recovery. SF correlated negatively with the increase in ADP after exercise (r = 0.85). The results of this study indicate that running time during incremental treadmill exercise until the onset of fatigue is related to locomotion pattern and to a marked degree of anaerobic metabolism, especially adenine nucleotide degradation.
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PMID:Incremental treadmill exercise until onset of fatigue and its relationship to metabolic response and locomotion pattern. 1065 79

The effects of sprint training on muscle metabolism and ion regulation during intense exercise remain controversial. We employed a rigorous methodological approach, contrasting these responses during exercise to exhaustion and during identical work before and after training. Seven untrained men undertook 7 wk of sprint training. Subjects cycled to exhaustion at 130% pretraining peak oxygen uptake before (PreExh) and after training (PostExh), as well as performing another posttraining test identical to PreExh (PostMatch). Biopsies were taken at rest and immediately postexercise. After training in PostMatch, muscle and plasma lactate (Lac(-)) and H(+) concentrations, anaerobic ATP production rate, glycogen and ATP degradation, IMP accumulation, and peak plasma K(+) and norepinephrine concentrations were reduced (P<0.05). In PostExh, time to exhaustion was 21% greater than PreExh (P<0.001); however, muscle Lac(-) accumulation was unchanged; muscle H(+) concentration, ATP degradation, IMP accumulation, and anaerobic ATP production rate were reduced; and plasma Lac(-), norepinephrine, and H(+) concentrations were higher (P<0.05). Sprint training resulted in reduced anaerobic ATP generation during intense exercise, suggesting that aerobic metabolism was enhanced, which may allow increased time to fatigue.
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PMID:Skeletal muscle metabolic and ionic adaptations during intense exercise following sprint training in humans. 1105 28

The aim of the present study was to investigate the effect of creatine (Cr) supplementation on muscle metabolic response in connection with a maximal treadmill exercise test, known to cause a marked anaerobic metabolic response and adenine nucleotide degradation. First, 6 Standardbred trotters performed a standardised maximal exercise test until fatigue (baseline test). The test used was an inclined incremental treadmill test in which the speed was increased by 1 m/s, starting at 7 m/s, every 60 s until the horse could no longer keep pace with the treadmill. After this baseline test, the horses were separated into 2 equal groups. One half received a dose of 25 g creatine monohydrate twice daily, and the other group were given the same dose of lactose (placebo). The supplementation period was 6.5 days, after which the maximal treadmill exercise test was performed again. A washout period of 14 days was allowed before treatments were switched between groups and a new supplementation period started. After this second supplementation period a new maximal exercise test was performed. After supplementation with creatine or placebo, horses were stopped after performing the same number of speed steps and duration of exercise as they had in the baseline test. Blood samples for analysis of plasma lactate, creatine (Cr), creatinine, hypoxanthine, xanthine and uric acid concentrations were collected at rest, during each speed step and during recovery. The total blood volume (TBV) was also determined. Muscle biopsies for analysis of muscle metabolites (adenosine triphosphate [ATP], adenosine diphosphate [ADP], adenosine monophosphate [AMP], inosine monophosphate [IMP], creatine phosphate [CP], lactate [La] and glycogen) were taken at rest, immediately post exercise and after 15 min recovery. The results showed no significant increase in plasma Cr or muscle total creatine concentration (TCr) after supplementation with Cr. At the end of exercise ATP and CP concentrations had decreased and IMP and lactate concentrations increased in muscle in all groups. Plasma lactate concentration increased during exercise and recovery and plasma uric acid concentration increased during recovery in all groups. No influence could be found in TBV after supplementation with creatine. These results show that creatine supplementation in the dosage used in this study had no influence on muscle metabolic response or TBV.
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PMID:Effect of creatine supplementation on muscle metabolic response to a maximal treadmill exercise test in Standardbred horses. 1109 28

Administration of bicarbonate has been shown to cause metabolic alkalosis both in man and in horses and is, therefore, thought to increase the buffering capacity of the body and thereby delay the onset of fatigue. However, results regarding the influence of sodium bicarbonate loading on performance both in human athletes and in horses are conflicting. The aim of this study was, therefore, to investigate the metabolic response to a standardised treadmill exercise test to fatigue, in horses given bicarbonate (0.6 g/kg bwt), in comparison to horses given placebo (water). Five Standardbred trotters performed the test on 2 occasions. Venous blood samples were collected before and after administration of test substance, during exercise and during recovery. Muscle biopsy specimens were taken at rest, postexercise and at 15 min of recovery. The increases in pH and concentration of bicarbonate in the blood and the shift seen in base excess showed that the administration of sodium bicarbonate caused metabolic alkalosis. Exercise caused similar decreases in muscle ATP, CP and glycogen and similar increases in muscle IMP, lactate and plasma lactate and uric acid concentrations both in the placebo- and bicarbonate-treated group. The effect upon postexercise muscle and plasma metabolites was similar with both test treatments. Duration of exercise did not change after sodium bicarbonate intake. In conclusion, sodium bicarbonate caused metabolic alkalosis, but did not affect the metabolic response or duration of exercise.
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PMID:Effect of sodium bicarbonate administration on metabolic responses to maximal exercise. 1240 47

During intense exercise there is an augmented production of ammonia and IMP in the exercised muscle that could be related to the establishment of peripheral fatigue. In order to prevent this accumulation, the urea cycle in the liver eliminates ammonia in the form of urea and the skeletal muscle buffers the increase of ammonia via transamination reactions. In the present study we evaluated the effect of arginine, citrulline and ornithine supplementation, intermediates of the urea cycle, on the performance of sedentary and swimming-trained rats submitted to a single bout of exhaustive exercise. We also measured the glycogen content of the soleus and gastrocnemius muscles and of the liver, as well as the plasma concentrations of ammonia, urea, glutamine, glucose and lactate. The results indicate that arginine, citrulline and ornithine supplementation increased the flux of substrate through the reaction catalysed by glutamine synthetase, leading to increased glutamine production after an exhaustive bout of exercise, and of the mechanism involved in ammonia buffering.
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PMID:Effect of arginine, ornithine and citrulline supplementation upon performance and metabolism of trained rats. 1257 27


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