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

This study investigated the histochemical and morphometric properties of fibres in laryngeal, hyoid, tongue and pharyngeal muscles which contribute in maintaining patency of the upper airway. Muscle specimens from adult female goats were stained for nicotinamide adenine dinucleotide dehydrogenase-tetrazolium reductase and myosin adenosine triphosphatase activities, and the composition and size of the fibre types determined. These muscles contained types 1, 2A, 2B and 2C fibres with type 2 fibres predominating and the fibres possessed oxidative enzyme activity suggesting fast contraction speed and yet moderate resistance to fatigue. Abductor laryngeal muscles contained more type 1 fibres than the adductors. Among pharyngeal muscles fibre size and type 1 fibre composition increased progressively from the hyopharyngeus caudally. Upper airway muscles contained relatively small fibres (range of mean diameter: 25.7 to 46.1 microns) with the pharyngeal and lingualis proprius muscles containing the smallest fibres. These properties might influence the response of upper airway muscles to neuromuscular blocking drugs.
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PMID:Histochemical and morphometric properties of muscles of the upper airway of goats. 823 90

With the advent of functional electrical stimulation (FES) there is the possibility of paraplegic patients regaining some degree of locomotor activity. It is of interest to document the changes in composition histochemistry and size of muscle fibres in such patients both before and after such therapy. We have examined biopsy specimens from quadriceps muscles obtained from 7 male patients, age range 24-47 years, who had been paraplegic for times ranging from 11 months to 9 years and we report the histochemical appearance of the muscle the fibre type composition and the mean fibre areas. In 5 of the 7 subjects there was a marked or complete predominance of fibres which stained as type 2 with the ATPase reaction at pH 9.4. At acid pH these fibres were seen to be predominantly 2B (fast fatigable). The 2 subjects who had been paralysed for the shortest periods had proportions of type 1 fibres which were relatively well preserved. The mean fibre areas of type 2 fibres were below the normal range (2500-7500 microns 2) in every case as were the type 1 fibres in the 4 patients in which these were still present. There was no relationship between the length of time the patient had been paralysed and the mean fibre areas which suggests that atrophy occurs fairly quickly following loss of voluntary control and precedes the loss of type 1 characteristics. Our findings provide an explanation for the rapid onset of fatigue in paraplegic patients taking part in FES programmes since muscles deficient in type 1 fibres will be unable to maintain force for any length of time.
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PMID:Fibre areas and histochemical fibre types in the quadriceps muscle of paraplegic subjects. 833 67

In this study we tested the hypothesis that the ryanodine-binding Ca-release channel activity and density of the sarcoplasmic reticulum (SR) terminal cisternae were decreased in congestive heart failure (CHF) that occurs spontaneously in doberman pinschers or experimentally with rapid ventricular pacing of mongrels. We used a novel, sensitive, and easy-to-perform microassay and demonstrated a 50% decrease in activity of the myocardial SR Ca pump and a 75% reduction in SR Ca-release channel activity in CHF. Decreases in Ca channel content were associated with increases in net Ca sequestration. 45Ca-release experiments from passively loaded SR terminal cisternae and ryanodine-binding studies confirmed a 53-68% downregulation of the Ca-release channel activity. As a consequence of release channel downregulation, there was partial restoration of net Ca sequestration activity in dogs with CHF and complete compensation in dogs with mild cardiac dysfunction. Deterioration of Ca cycling correlated with deterioration of myocardial performance, apparently due to decreased Ca-adenosinetriphosphatase (ATPase) pump and not Ca channel content. One-half the reduction in Ca-release activity could be attributed to decreased Ca sequestration and one-half to decreased Ca channel density. Downregulation of Ca channel content decreases the amplitude of the Ca cycle and maximizes the downregulation of Ca pumps that may occur. Although these adaptations may reduce cellular energy expenditure, they are likely to render the myocardium more susceptible to fatigue and failure.
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PMID:Compensatory downregulation of myocardial Ca channel in SR from dogs with heart failure. 838 26

This study investigated the effects of sprint training on muscle Na(+)-K(+)-adenosinetriphosphatase (ATPase) concentration, plasma [K+] regulation, muscle performance, and fatigue during severe intermittent exercise. Six untrained male subjects underwent intensive cycle-sprint training for 7 wk. Muscle biopsies were taken at rest from the vastus lateralis muscle before and after 7 wk of training and were assayed for Na(+)-K(+)-ATPase concentration using vanadate-facilitated [3H]ouabain binding to intact samples. Before and after the training period, subjects performed four maximal 30-s exercise bouts (EB) on a cycle ergometer, each separated by a 4-min recovery. Arterialized venous blood samples were drawn immediately before and after each sprint bout and were analyzed for plasma [K+]. The work output was significantly elevated (11%) across all four EBs after training. The muscle [3H]ouabain binding site concentration was significantly increased (16%) from 333 +/- 19 to 387 +/- 15 (SE) pmol/g wet wt after training but was unchanged in muscle obtained from three control subjects. Plasma [K+] rose by 1-2 mmol/l with each EB and declined rapidly by the end of each recovery period. The increases in plasma [K+] resulting from each EB were significantly lower (19%) after training. The ratios of rise in plasma [K+] relative to work output during each EB were also significantly lower (27%) after training. The increased muscle [3H]ouabain binding site concentration and the reduced ratio of rise in [K+] relative to work output with exercise are both consistent with improved plasma and skeletal muscle K+ regulation after sprint training.
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PMID:Sprint training increases human skeletal muscle Na(+)-K(+)-ATPase concentration and improves K+ regulation. 839 76

In order to use functional electrical stimulation effectively in paralyzed muscle treatment, changes in the maximal muscle force, muscle fatigue, and histological changes were evaluated in electrically stimulated muscles. Study 1. Tissue damage by percutaneous intramuscular electrodes implanted into the quadriceps muscle was examined in rat. Stimulation was conducted at various output voltages, and for various durations of time, in order to assess the histological changes in the muscle around the electrodes. Study 2. Electrodes were implanted into the bilateral quadriceps and gastrocnemius muscles of adult cat, and the unilateral muscles were then stimulated from 3 weeks following the transection of the spinal cord at the T9 level. Stimulus parameters were divided into two groups; as "A" stimulation: at -8V for 15min twice/week, and as "B" stimulation: at -16V for 30 min 4 times/week. The histological changes were examined using the myofibrillar ATPase method to determine the diameters and occupation ratios for each muscle fiber type. RESULTS. Study 1. Significant tissue damage began to occur when the voltage output created the maximum muscle contraction force. Until that critical voltage point was reached, tissue damage was not significant, regardless of the duration of the stimulation. Study 2. The maximum muscle force decreased until 4 weeks after the transection, then increased regardless of the presence of electrical stimulation. The muscle fatigability of the non-stimulated muscle was greater than that of the stimulated muscle. High voltage, long duration, and frequent stimulation was effective in controlling fatigue. The ratio of type I fibers was higher in the stimulated muscle. There was no evidence, however, of suppressing muscle fiber atrophy after electrical stimulation. These results suggested that electrically stimulating paralyzed muscles was effective for suppressing muscle fatigue, and for reducing the ratio of type I fibers. In clinical use, the output voltage should be kept below the voltage that induces the maximum muscle contraction to prevent tissue damage.
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PMID:[Histological changes, muscle force and fatigability after electrical stimulation to experimentally paralyzed muscles]. 853 Aug 86

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

In the rat diaphragm muscle, the histochemical classification of type I, IIa, IIb, or IIx fibers was correlated with myosin heavy chain (MHC) immunoreactivity. Expression of MHC isoforms in single dissected fibers was also assessed electrophoretically. Most fibers (approximately 86%) expressed a single MHC isoform, and when present, coexpression of MHC-2X and MHC-2B isoforms was most prevalent. Type I and IIa fibers were the smallest, type IIb fibers were the largest, and type IIx fibers were intermediate. Succinate dehydrogenase (SDH) and calcium-activated myosin adenosinetriphosphatase (actomyosin ATPase) activities were measured with quantitative histochemical procedures. Type I and IIa fibers had the highest SDH activities, followed in rank order by type IIx and IIb fibers. Type I fibers had the lowest actomyosin ATPase activity, followed in rank order by type IIa, IIx, and IIb fibers. Across all fibers, there was an inverse relationship between fiber SDH activity and cross-sectional area and a positive correlation between fiber actomyosin ATPase activity and cross-sectional area. The SDH and actomyosin ATPase activities of muscle fibers were also inversely correlated. These phenotypic differences in SDH and ATPase activities may be important in determining the contractile and fatigue properties of different fiber types in the rat diaphragm muscle.
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PMID:SDH and actomyosin ATPase activities of different fiber types in rat diaphragm muscle. 859 23

This study was undertaken to investigate the mechanisms underlying fatigue of chronically overused motor units (MUs). The force of the tibialis anterior muscle (TA) and the firing properties of single MUs were studied during prolonged maximum voluntary effort in 10 prior polio patients selected such that daily living required all residual TA power. Almost all TA fibers were hypertrophic type I. Activities of intermyofibrillar succinate dehydrogenase (SDH) and calcium-stimulated myofibrillar adenosine triphosphatase (ATPase) were measured in single TA fibers from a representative patient. Neither insufficient motoneuron activation nor peripheral blocking of the electrical impulse played a major role in the loss of force during prolonged contraction or for slow recovery after contraction. The ratio of SDH to calcium-stimulated ATPase, representing the relation between energy resynthesis and energy utilization, was significantly (P < 0.001) lower in prior polio patients (0.230 +/- 0.096) compared to control (0.515 +/- 0.097) type I fibers.
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PMID:Fatigue of chronically overused motor units in prior polio patients. 860 23

Ionic regulation is critical to muscle excitation, contraction and metabolism, and thus for muscle function during exercise. This review focuses on the effects of training upon K+, Ca2+ and H+ ion regulation in muscle and K+ regulation in blood during exercise. Training enhances K+ regulation in muscle and blood and reduces muscular fatiguability. Endurance, sprint and strength training in humans induce an increased muscle Na+, K+ pump concentration, usually associated with a reduced rise in plasma [K+] during exercise. Although impaired muscle Ca2+ regulation plays a vital role in fatigue, little is known about possible training effects. In rat fast-twitch muscle, overload-induced hypertrophy and endurance training were associated with reduced sarcoplasmic reticulum Ca2+ uptake, consistent with fast-to-slow fibre transition. In human muscle, endurance and strength training had no effect on muscle Ca2+ ATPase concentration. Whilst muscle Ca2+ uptake, release and Ca2+ ATPase activity were depressed by fatigue, no differences were found between strength athletes and untrained individuals. Muscle H+ accumulation may contribute to fatigue during intense exercise and is also modified by sprint training. Sprint training may increase muscle Lac- and work output with exhaustive exercise, but the rise in muscle [H+] is unchanged or attenuated, indicating a reduced rise in muscle [H+] relative to work performed. Muscle buffering capacity can be dissociated from this improved H+ regulatory capacity after training. Thus, training enhances muscle and blood K+ and muscle H+ regulation during exercise, consistent with improved muscular performance and reduced fatiguability; however, little is known about training effects on muscle Ca2+ regulation during contraction.
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PMID:Effects of training on potassium, calcium and hydrogen ion regulation in skeletal muscle and blood during exercise. 872 94

The proportion of slow-twitch, fatigue-resistant type 1 skeletal muscle (SM) fibers is often reduced in heart failure (HF), while the proportion of fatigue-sensitive type-II fibers increases. This maladaptation may be partially responsible for the exercise intolerance that characterize HF. In this study, we examined the effects of early monotherapy with the angiotensin-converting enzyme inhibor, enalapril, and the beta-blocker, metoprolol, on SM fiber type composition in 18 dogs with moderate HF produced by intracoronary microembolizations. HF dogs were randomized to 3 mo therapy with enalapril (10 mg twice daily), metoprolol (25 mg twice daily), or no treatment. Triceps muscle biopsies were obtained at baseline, before randomization, and at the end of 30 mo of therapy. Type I and type II SM fibers were differentiated by myofibrillar adenosinetriphosphatase (pH 9.4). In untreated dogs, the proportion of type I fibers was 27 +/- 1% before randomization and decreased to 23 +/- 1% (P < 0.05) at the end of 3 mo of follow up. In dogs treated with enalapril or metoprolol, the proportion of type I fibers was 30 +/- 4 and 28 +/- 2% before randomization and 33 +/- 4 and 33 +/- 1%, respectively, after 3 mo of therapy. In conclusion, in dogs with moderate HF, early therapy with enalapril or metoprolol prevents the progressive decline in the proportion of type I SM fibers.
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PMID:Effects of ACE inhibition and beta-blockade on skeletal muscle fiber types in dogs with moderate heart failure. 876 41


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