Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Important aspects of the excitation-contraction (EC) coupling process in skeletal muscle have been revealed using mechanically-skinned fibers in which the transverse-tubular system can be depolarized by ion substitution or electrical stimulation, activating the voltage-sensors which in turn open the Ca2+ release channels in the adjacent sarcoplasmic reticulum (SR). Twitch and tetanic force responses elicited in skinned fibers closely resemble those in intact fibers, showing that the coupling mechanism is entirely functional. It was found that ATP has to be bound to the Ca2+ release channels for them to be activated by the voltage-sensors and that the coupling mechanism likely involves the voltage-sensors removing the inhibitory effects of cytoplasmic Mg2+ on the release channels; such findings are relevant to the basis of muscle fatigue and to certain diseases such as malignant hyperthermia (MH). EC coupling is evidently not mediated by upmodulation of Ca2+-induced Ca2+ release (CICR) or by an oxidation or phosphorylation reaction. The Ca2+ load in the SR of skinned fibers can be set at the endogenous level or otherwise. The normal coupling mechanism functions well in mammalian fast-twitch fibers even when the SR is only partially loaded, whereas CICR is highly dependent on SR luminal Ca2+ and caffeine is poorly effective at inducing release at the endogenous SR Ca2+ load level.
 ...
PMID:Voltage-sensor control of Ca2+ release in skeletal muscle: insights from skinned fibers. 1189 57

Twitch transdiaphragmatic pressure (Pdi,tw), measured following magnetic stimulation of the phrenic nerves, is used to assess diaphragm strength, contractility and fatigue. Although the effects of posture, lung volume and potentiation on Pdi,tw are well described, it is not known whether the degree of gastric filling affects the measurement. Pdi,tw was recorded in seven healthy volunteers on two occasions with antero-lateral magnetic stimulation of the phrenic nerves. On the first occasion, the subjects had fasted for at least 8 h, whilst on the second occasion, measurements were made after each subject had eaten a substantial meal sufficient to produce a feeling of satiation. Mean postprandial unpotentiated and potentiated Pdi,tw were significantly greater than corresponding fasting Pdi,tw in all seven volunteers (29.8 versus 25.7 cmH2O and 38.9 versus 34.4 cmH2O, respectively). This was due to a significantly increased gastric pressure component (1.10 versus 0.84 and 0.94 versus 0.78, respectively), and reduced abdominal compliance (36 versus 62 mL x cmH2O(-1)). Twitch oesophageal pressure was preserved (15.0 versus 15.4 cmH2O). The postprandial state increases twitch transdiaphragmatic pressure, and this should be taken into account when using twitch transdiaphragmatic pressure to follow-up patients or to assess the effects of interventions on diaphragm contractility.
 ...
PMID:Postprandial effects on twitch transdiaphragmatic pressure. 1235 31

Because patients who fail a trial of weaning from mechanical ventilation experience a marked increase in respiratory load, we hypothesized that these patients develop diaphragmatic fatigue. Accordingly, we measured twitch transdiaphragmatic pressure using phrenic nerve stimulation in 11 weaning failure and 8 weaning success patients. Measurements were made before and 30 minutes after spontaneous breathing trials that lasted up to 60 minutes. Twitch transdiaphragmatic pressure was 8.9 +/- 2.2 cm H2O before the trials and 9.4 +/- 2.4 cm H2O after their completion in the weaning failure patients (p = 0.17); the corresponding values in the weaning success patients were 10.3 +/- 1.5 and 11.2 +/- 1.8 cm H2O (p = 0.18). Despite greater load (p = 0.04) and diaphragmatic effort (p = 0.01), the weaning failure patients did not develop low-frequency fatigue probably because of greater recruitment of rib cage and expiratory muscles (p = 0.004) and because clinical signs of distress mandating the reinstitution of mechanical ventilation arose before the development of fatigue. Twitch pressure revealed considerable diaphragmatic weakness in many weaning failure patients. In conclusion, in contrast to our hypothesis, weaning failure was not accompanied by low-frequency fatigue of the diaphragm, although many weaning failure patients displayed diaphragmatic weakness.
 ...
PMID:Is weaning failure caused by low-frequency fatigue of the diaphragm? 1466 58

Respiratory muscle strength and endurance is reduced in patients with congestive heart failure, making these patients susceptible to diaphragmatic fatigue during exercise. In order to determine whether or not contractile fatigue of the diaphragm occurs in patients with congestive heart failure following intense exercise, twitch transdiaphragmatic pressures (twitch Ptdi) were measured during unpotentiated and potentiated cervical magnetic stimulation (CMS) of the phrenic nerves before and at intervals after cycle endurance exercise. Ten patients aged 65.7+/-6.0 yrs (mean+/-SD) with an ejection fraction of 31.2+/-9.8% performed a constant-load symptom-limited exercise test at 60% of their peak work capacity. Twitch Ptdi at baseline were 15.9+/-6.3 cmH2O (unpotentiated CMS) and 28.8+/-10.7 cmH2O (potentiated CMS) and at 10 min postexercise were 16.4+/-4.7 cmH2O (unpotentiated CMS) and 27.6+/-10.1 cmH2O (potentiated CMS). One patient demonstrated a sustained fall in twitch Ptdi of > or = 15%, considered potentially indicative of diaphragmatic fatigue. Contractile diaphragmatic fatigue is uncommon in untrained patients with congestive heart failure following high-intensity constant-workload cycle exercise. Therefore, diaphragmatic fatigue is an unlikely cause of exercise-limitation during activities of daily living in heart failure patients.
 ...
PMID:Diaphragmatic function after intense exercise in congestive heart failure patients. 1250 95

We describe a patient with Kennedy's disease (X-linked bulbospinal neuronopathy) who experienced leg muscle fatigue with long-distance running. The patient also reported muscle twitching involving the face and extremities and long-standing muscle cramps. Aside from mild facial and tongue weakness (and fasciculations), his examination was normal, including completely preserved muscle strength in the extremities. Electrodiagnostic evaluation revealed evidence for a chronic motor axonopathy/neuronopathy and abnormal sensory nerve action potentials. In addition, repetitive nerve stimulation studies were normal, but neuromuscular jitter tested in the same muscle was markedly abnormal. The normal clinical strength and repetitive nerve stimulation studies in a muscle showing markedly increased neuromuscular jitter suggested a mechanism for this patient's symptoms of muscle fatigue, related to failure of neuromuscular transmission at a critical number of endplates during extremes of physical activity.
 ...
PMID:Fatigue and abnormal neuromuscular transmission in Kennedy's disease. 1254 35

The metabolism of high energy phosphates during muscular contraction due to direct electrical stimulation, indirect stimulation via nerve excitation, and magnetic stimulation was studied in isolated muscles (frog sartorius muscles) by (31)P nuclear magnetic resonance ((31)P-NMR). Twitch amplitudes elicited by each stimulus were measured alternatively at 3 mm displacement loading and 5 g weight. Both the creatine/inorganic phosphate (PCr/Pi) and pH changes were more marked in direct electrical stimulation than in magnetic stimulation. The muscular contraction caused by magnetic stimulation showed less fatigue than that caused by direct electrical muscular stimulation.
 ...
PMID:Phosphate metabolites in muscular contraction caused by magnetic stimulation. 1282 Feb 94

The role of muscle potentiation in overcoming low-frequency fatigue (LFF) as it developed during submaximal voluntary exercise was investigated in eight males (age 26.4 +/- 0.7 years, mean +/- SE) performing isometric leg extension at approximately 30% of maximal voluntary contraction for 60 min using a 0.5-duty cycle (1 s contraction, 1 s rest). At 5, 20, 40, and 60 min, exercise was interrupted for 3 min, and the maximum positive rate of force development (+dF/dtmax) and maximal twitch force (Pt) were measured in maximal twitch contractions at 0, 1, 2, and 3 min of rest (R0, R1, R2, R3); they were also measured at 15 min of recovery following the entire 60-min exercise period. These measures were compared with pre-exercise (PRE) as an indicator of potentiation. Force at low frequency (10 Hz) was also measured at R0, R1, R2, and R3, and at 15 min of recovery, while force at high frequency (100 Hz) was measured only at R0 and R3 and in recovery. Voluntary exercise increased twitch +dF/dtmax at R0 following 5, 20, 40, and 60 min of exercise, from 2553 +/- 150 N/s at PRE to 39%, 41%, 42%, and 36% above PRE, respectively (P<0.005). Twitch +dF/dtmax decayed at brief rest (R3) following 20, 40, and 60 min of exercise (P<0.05). Pt at R0 following 5 and 20 min of exercise was above that at PRE (P<0.05), indicating that during the early phase of moderate-intensity repetitive exercise, potentiation occurs in the relative absence of LFF. At 40 and 60 min of exercise, Pt at R0 was unchanged from PRE. The LFF (10 Hz) induced by the protocol was evident at 40 and 60 min (R0-R3; P<0.05) and at 15 min following exercise (P<0.05). High-frequency force was not significantly compromised by the protocol. Since twitch force was maintained, these results suggest that as exercise progresses, LFF develops, which can be compensated for by potentiation.
 ...
PMID:Coexistence of potentiation and low-frequency fatigue during voluntary exercise in human skeletal muscle. 1471 27

Muscle fatigue reflects alterations of both activation and cross-bridge function, which will have markedly different affects on steady-state vs. dynamic performance. Such differences offer insight into the specific origins of fatigue, its mechanical manifestation, and its consequences for animal movement. These were inferred using dynamic contractions (twitches and cyclic work as might occur during locomotion) and steady-state performance with maximal, sustained activation (tetani, stiffness, and isokinetic force) during fatigue and then recovery of frog (Rana pipiens) anterior tibialis muscle. Stiffness remained unaltered during early fatigue of force and then declined only 25% as force dropped 50%, suggesting a decline with fatigue in first the force-generating ability and then the number of cross bridges. The relationship between stiffness and force was different during fatigue and recovery; thus the number of cross bridges and force per cross bridge are not intimately linked. Twitch duration increased with fatigue and then recovered, with trajectories that were remarkably similar to and linear with changes in tetanic force, perhaps belying a common mechanism. Twitch force increased and then returned to resting levels during fatigue, reflecting a slowing of activation kinetics and a decline in cross-bridge number and force. Net cyclic work fatigued to the degree of becoming negative when tetanic force had declined only 15%. Steady-state isokinetic force (i.e., shortening work) declined by 75%, while cyclic shortening work declined only 30%. Slowed activation kinetics were again responsible, augmenting cyclic shortening work but greatly augmenting lengthening work (reducing net work). Steady-state measures can thus seriously mislead regarding muscle performance in an animal during fatigue.
 ...
PMID:Fatigue and recovery of dynamic and steady-state performance in frog skeletal muscle. 1472 26

The twitch interpolation technique is commonly employed to assess the completeness of skeletal muscle activation during voluntary contractions. Early applications of twitch interpolation suggested that healthy human subjects could fully activate most of the skeletal muscles to which the technique had been applied. More recently, however, highly sensitive twitch interpolation has revealed that even healthy adults routinely fail to fully activate a number of skeletal muscles despite apparently maximal effort. Unfortunately, some disagreement exists as to how the results of twitch interpolation should be employed to quantify voluntary activation. The negative linear relationship between evoked twitch force and voluntary force that has been observed by some researchers implies that voluntary activation can be quantified by scaling a single interpolated twitch to a control twitch evoked in relaxed muscle. Observations of non-linear evoked-voluntary force relationships have lead to the suggestion that the single interpolated twitch ratio can not accurately estimate voluntary activation. Instead, it has been proposed that muscle activation is better determined by extrapolating the relationship between evoked and voluntary force to provide an estimate of true maximum force. However, criticism of the single interpolated twitch ratio typically fails to take into account the reasons for the non-linearity of the evoked-voluntary force relationship. When these reasons are examined, it appears that most are even more challenging to the validity of extrapolation than they are to the linear equation. Furthermore, several factors that contribute to the observed non-linearity can be minimised or even eliminated with appropriate experimental technique. The detection of small activation deficits requires high resolution measurement of force and careful consideration of numerous experimental details such as the site of stimulation, stimulation intensity and the number of interpolated stimuli. Sensitive twitch interpolation techniques have revealed small to moderate deficits in voluntary activation during brief maximal efforts and progressively increasing activation deficits (central fatigue) during exhausting exercise. A small number of recent studies suggest that resistance training may result in improved voluntary activation of the quadriceps femoris and ankle plantarflexor muscles but not the biceps brachii. A significantly larger body of evidence indicates that voluntary activation declines as a consequence of bed-rest, joint injury and joint degeneration. Twitch interpolation has also been employed to study the mechanisms by which caffeine and pseudoephedrine enhance exercise performance.
 ...
PMID:Assessing voluntary muscle activation with the twitch interpolation technique. 1504 17

Short-term diabetes was induced in male Wistar rats with streptozotocin injection. The effects of diabetes on latissimus dorsi (LD) muscle contractile and biochemical properties and acute cardiomyoplasty (CDM) were assessed and compared with data from 16 control rats. Isometric force, contractile properties, and fatigue were measured in electrically stimulated muscles (0.3 ms, 1-256 Hz), and Na+K+ and Ca2+ATPase activities were quantified in muscle membrane preparations. Systolic arterial pressure and aortic blood flow were recorded at rest and during LD muscle stimulation. Compared with control muscle, diabetic muscle showed smaller maximum specific tetanic tension and lower rates of rise and fall in force. Diabetic LD muscle also showed lower muscle enzyme activities. Twitch tension and fatigue did not differ between groups. Smaller increases in aortic flow and systolic pressure after CDM were found in diabetic rats compared to controls. The marked decrease in CDM effectiveness in diabetic rats likely reflected the alterations in muscle properties associated with diabetes.
 ...
PMID:Diabetes-induced alterations in latissimus dorsi muscle properties impair effectiveness of dynamic cardiomyoplasty in rats. 1508 90


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>