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

In this study we investigated the roles of cytoplasmic ATP as both an energy source and a regulatory molecule in various steps of the excitation-contraction (E-C) coupling process in fast-twitch skeletal muscle fibres of the rat. Using mechanically skinned fibres with functional E-C coupling, it was possible to independently alter cytoplasmic [ATP] and free [Mg2+]. Electrical field stimulation was used to elicit action potentials (APs) within the sealed transverse tubular (T-) system, producing either twitch or tetanic (50 Hz) force responses. Measurements were also made of the amount of Ca2+ released by an AP in different cytoplasmic conditions. The rate of force development and relaxation of the contractile apparatus was measured using rapid step changes in [Ca2+]. Twitch force decreased substantially (approximately 30%) at 2 mm ATP compared to the level at 8 mm ATP, whereas peak tetanic force only declined by approximately 10% at 0.5 mm ATP. The rate of force development of the twitch and tetanus was slowed only slightly at [ATP] > or = 0.5 mm, but was slowed greatly (> 6-fold) at 0.1 mm ATP, the latter being due primarily to slowing of force development by the contractile apparatus. AP-induced Ca2+ release was decreased by approximately 10 and 20% at 1 and 0.5 mm ATP, respectively, and by approximately 40% by raising the [Mg2+] to 3 mm. Adenosine inhibited Ca2+ release and twitch responses in a manner consistent with its action as a competitive weak agonist for the ATP regulatory site on the ryanodine receptor (RyR). These findings show that (a) ATP is a limiting factor for normal voltage-sensor activation of the RyRs, and (b) large reductions in cytoplasmic [ATP], and concomitant elevation of [Mg2+], substantially inhibit E-C coupling and possibly contribute to muscle fatigue in fast-twitch fibres in some circumstances.
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PMID:Effect of low cytoplasmic [ATP] on excitation-contraction coupling in fast-twitch muscle fibres of the rat. 1530 82

Monodelphis domestica (Didelphidae: Marsupialia) lacks brown adipose tissue and thus relies on skeletal muscle as its primary thermogenic organ. Following cold exposure, the aerobic capacity of skeletal muscle in these animals is greatly increased. We investigated the effects of this plastic response to thermogenesis on locomotion and muscle mechanics. In cold-exposed animals, cost of transport was 15% higher than in controls but was unaffected by exercise training. Twitch kinetics in isolated semitendinosus muscles of cold-exposed animals were characteristic of slow-oxidative fiber types. Both time-to-peak tension and half-relaxation time were longer and maximal shortening velocity was slower following cold exposure compared to either thermoneutral controls or exercise-trained animals. Further, muscles from the cold-exposed animals had greater fatigue resistance than either control or exercise-trained animals, indicating greater oxidative capacity. Finally, we identified an uncoupling protein 3 homologue, whose gene expression was upregulated in skeletal muscle of cold-exposed Monodelphis domestica. Cold exposure provided a potent stimulus for muscle plasticity, driving a fast-to-slow transition more effectively than exercise training. However, linked to the dramatic shift in muscle properties is an equally dramatic increase in whole animal muscle energetics during locomotion, suggesting an uncoupled state, or 'training for inefficiency'.
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PMID:Cost of transport is increased after cold exposure in Monodelphis domestica: training for inefficiency. 1608 13

Few studies have analyzed activity-induced changes in EMG activity in individual human motor units. We studied the changes in human thenar motor unit EMG that accompany the potentiation of twitch force and fatigue of tetanic force. Single motor unit EMG and force were recorded in healthy subjects in response to selective stimulation of their motor axons within the median nerve just above the elbow. Twitches were recorded before and after a series of pulse trains delivered at frequencies that varied between 5 and 100 Hz. This stimulation induced significant increases in EMG amplitude, duration, and area. However, in relative terms, all of these EMG changes were substantially smaller than the potentiation of twitch force. Another 2 min of stimulation (13 pulses at 40 Hz each second) induced additional potentiation of EMG amplitude, duration, and area, but the tetanic force from every unit declined. Thus activity-induced changes in human thenar motor unit EMG do not indicate the alterations in force or vice versa. These data suggest that different processes underlie the changes in EMG and force that occur during human thenar motor unit activity.
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PMID:EMG changes in human thenar motor units with force potentiation and fatigue. 1626 10

Human muscles paralysed chronically by spinal cord injury (SCI) fatigue excessively. Whether these reductions in force reflect a decrease in the fatigue resistance of the motor units is unknown. Our aim was to determine the fatigability of thenar motor units paralysed chronically (10 +/- 2 years) by cervical SCI. Surface electromyographic activity (EMG) and force were recorded from 17 paralysed motor units (n = 7 subjects) in response to intraneural motor axon stimulation (13 pulses at 40 Hz, 1 s(-1) for 2 min). Unit force decreased progressively, reaching 8-60% of initial after 2 min, whereas both the amplitude and area of the first EMG potentials in the trains increased significantly (both P < 0.05). Thus, transmission of neural signals to the sarcolemma was effective and the reduction in force must reflect impaired processes in the muscle fibres. The median fatigue index for paralysed units (0.31), the ratio of the force at 2 min compared to the initial force, was significantly lower than that for units from control subjects (0.85, P < 0.05), but the distribution of fatigue indices for each population had a similar shape (ranges: 0.08-0.60 and 0.41-0.95, respectively). Hence, chronic paralysis did not limit the range of fatigability typically found for thenar units, only its magnitude. These findings suggest that all paralysed units underwent similar reductions in fatigue resistance. After fatigue, paralysed unit forces were reduced at all frequencies (1-100 Hz, P < 0.05). Twitch contraction and half-relaxation times were increased, as was the frequency needed to produce half maximal force (P < 0.05). Thus, stimulation protocols used to produce functional movements in paralysed muscles need to accommodate the significant and rapid fatigue of the motor units.
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PMID:Fatigue properties of human thenar motor units paralysed by chronic spinal cord injury. 1651 73

Previously, we showed that artificial rearing using the "pup in a cup" model results in decreased tongue activity and caused some minor alterations in the tongue retrusor musculature. However, the artificial rearing time frame previously chosen was brief (11 days). The purpose of the present investigation was to extend the artificial rearing period from postnatal days 3 to 21 (P21) to determine whether significant alterations occur as a result of this reduced tongue use. Several changes in contractile properties due to the artificial rearing process were observed, which fully recovered by postnatal days 41 to 42 (P41-2). These changes included a shorter twitch contraction time, shorter twitch half-relaxation time, and decreased fatigue resistance. Styloglossus muscle exhibited more neonatal myosin heavy chain (MHC) isoform at P21 for the artificially reared (AR) group. Changes that were persistent at P41-2 were also observed. Maximum tetanic tension was lower for the AR group at P21 and P41-2 compared with their dam-reared counterparts. Twitch tension was also lower by P41-2 in the AR group. At P41-2, the AR group exhibited an increase in MHC IIa and a decrease in MHC IIb for the styloglossus muscle. In addition, the AR group exhibited a decreased MHC IIb for the long head of the biceps brachii at P41-2. Our results are similar to other models of hindlimb immobilization and suspension. By extending our artificial rearing period, this reduced tongue activity induced acute changes and alterations in the tongue retrusor musculature that persisted into early adulthood.
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PMID:Contractile properties and myosin heavy chain composition of rat tongue retrusor musculature show changes in early adulthood after 19 days of artificial rearing. 1680 31

High-intensity exercise can induce diaphragm fatigue which can, in turn, limit exercise performance. We investigated whether expiratory muscles fatigue similarly during exhaustive exercise. Eleven healthy male volunteers cycled to exhaustion at 85% maximal power. Before, immediately after exercise, and after 30 and 60 min of recovery, the nerve roots supplying the abdominal muscles were stimulated magnetically at the T10 level in the prone position after full potentiation. Twitch gastric pressure (Pga,tw) was simultaneously recorded. After cycling, Pga,tw was significantly reduced compared to before exercise (40.2 +/- 6.6 vs. 45.3 +/- 7.5 cmH2O; P < 0.001), whereas after 30 and 60 min of recovery differences were no longer significant. The reduction in Pga,tw directly after exercise correlated neither with the fitness level nor with abdominal muscle work, respiratory sensations, or blood lactate concentration during exercise. These results indicate that the ventilatory requirements during intensive exercise can impair abdominal muscle contractility similar to diaphragmatic contractility. Thus, abdominal muscle fatigue may also contribute to exercise limitation, especially when expiratory resistance is increased as in patients with chronic obstructive pulmonary disease.
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PMID:Impaired abdominal muscle contractility after high-intensity exhaustive exercise assessed by magnetic stimulation. 1681 Jun 95

Genetic deficiency of the muscle chloride channel CLC-1 leads to myotonia congenita in humans as well as myotonia in mice and goats. The hallmark of myotonia is delayed muscle relaxation due to persistent electrical discharges in the muscle. The present study tested the hypothesis that performance of CLC-1 deficient diaphragm muscle is also altered during the contractile phase of the contraction-relaxation cycle. Diaphragm of CLC-1 deficient and wild type mice underwent in vitro isometric contractility testing. Myotonia was easily demonstrable during contractions elicited by train stimulation, but was not seen during twitch stimulation or during train stimulation preceded by a series of twitch stimulations. Twitch force was reduced from 16.7+/-2.5 N/cm(2) in normal muscle to 7.2+/-1.9 N/cm(2) in CLC-1 deficient muscle (P<0.002). Isometric twitch contraction time was shortened from 19.6+/-0.9 to 15.7+/-1.0 ms (P<0.002). During repetitive 25 Hz stimulation, force/area was lower for diseased than normal muscle, whereas force as a percent of initial values declined at a faster rate for normal than diseased muscle. The latter could be accounted for by a rightward shift in the force-frequency relationship of CLC-1 deficient relative to normal muscle, as use of stimulation frequencies which elicited comparable force levels as a percentage of maximum 100 Hz tetanic force led to similar rates of fatigue. These findings indicate that genetic CLC-1 deficiency not only affects muscle relaxation (myotonia) but also modulates diaphragm performance during the contractile phase of the contraction-relaxation cycle.
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PMID:Genetic CLC-1 chloride channel deficiency modifies diaphragm muscle isometric contractile properties. 1695 50

The magnitude of failure in voluntary drive after fatiguing contractions of different intensities in men and women is not known. The purpose of this study was to compare the time to task failure and voluntary activation of men and women for a sustained isometric contraction performed at a low and high intensity with the elbow flexor muscles. Nine men and nine women sustained an isometric contraction at 20% and 80% of maximal voluntary contraction (MVC) force until task failure during separate sessions. The men had a shorter time to failure than women for the 20% but not the 80% MVC task. Voluntary activation was reduced to similar levels for the men and women at the end of the fatiguing contractions but was reduced less after the 80% MVC task than the 20% MVC contraction. Twitch amplitude was reduced similarly at task failure for both sexes and to similar levels at termination of the 20% and 80% MVC tasks. The rate of change in mean arterial pressure was the main predictor of time to failure for the low-force sustained contraction. These results suggest that women experienced greater muscle perfusion, less peripheral fatigue, and a longer time to task failure than men during the low-force fatiguing contraction. However, the low-force task induced greater central fatigue than the high-force contraction for both men and women. Thus, low-force, long-duration fatiguing contractions can be used in rehabilitation to induce significant fatigue within the central nervous system and potentially greater neural adaptations in men and women.
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PMID:Mechanisms of fatigue differ after low- and high-force fatiguing contractions in men and women. 1762 89

The purpose of this study was to investigate the effect of 22 degrees C local muscle temperature of intact human plantar flexors performing fatiguing contractions on evoked and voluntary contractile properties before and after fatigue. Twelve subjects were tested on plantar flexor voluntary torque, percent muscle activation derived from twitch interpolation, integrated electromyographic (iEMG) activity, and evoked torque and temporal characteristics of maximal twitch and tetanic stimulations before fatigue and 1, 5, and 10 min after intermittent, high-intensity, isometric fatigue under both normothermic and hypothermic conditions. Hypothermic and normothermic changes between time points were analysed by repeated-measures analysis of variance. Normothermic fatigue induced small to large effects (Cohen's d: 0.29-3.06) on voluntary and evoked contractile properties, whereas most effects of unfatigued hypothermia were limited to rate-dependent processes (Cohen's d: 0.78-1.70). Most tetanic properties were potentiated 1 min after normothermic fatigue, but remained unchanged by hypothermic fatigue, resulting in significant differences between the two conditions. Soleus iEMG significantly declined 1 min after normothermic fatigue (-29%), but not after hypothermic fatigue. Twitch torque was potentiated by 29% one minute after fatigue while normothermic, but was potentiated by 46% while hypothermic; rate of twitch torque development and time to peak twitch were potentiated by 39% and 10% while normothermic, but 89% and 28% while hypothermic. Although voluntary contractile properties are generally impaired soon after normothermic fatigue, most were not after hypothermic fatigue. Furthermore, evoked contractile properties were generally higher 1 min after hypothermic fatigue. We conclude that the hypothermic condition slows the recovery of potentiated evoked contractile properties back to baseline values.
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PMID:Effects of 22 degrees C muscle temperature on voluntary and evoked muscle properties during and after high-intensity exercise. 1805 76

Based on the "post-exercise diaphragm shielding" hypothesis this study tested whether both diaphragmatic force-generation (DFG) and diaphragmatic fatigue (DF) remain unchanged during consecutive exercise-trials. Twelve subjects (V(O2 max) 58.4+/-6.6 ml kg(-1) min(-1)) performed three consecutive exercise-trials (T(alpha)/T(beta)/T(gamma); workload(max) 85% V(O2 max)) each followed by recovery (6 min). Twitch transdiaphragmatic pressure during supramaximal magnetic phrenic nerve stimulation (TwPdi, every 30s), ratings of perceived exertion (RPE, every 90 s) and ergospirometric data (continuously) were assessed throughout the entire protocol (46.5 min). DFG and DF did not differ among all trials (TwPdi-baseline: 2.2+/-0.7 kPa; TwPdi-peak: T(alpha)/T(beta)/T(gamma) 3.1+/-0.7 kPa vs 3.0+/-0.8 kPa vs 3.2+/-0.8 kPa; TwPdi-bottom: T(alpha)/T(beta)/T(gamma) 1.9+/-0.6 kPa vs 2.0+/-0.7 kPa vs 1.8+/-0.5 kPa, both p>0.4, RM-ANOVA). Furthermore, TwPdi revealed close relationships with RPE (r=0.91, p<0.0001) and oxygen uptake (r=0.94, p<0.0001) during exercise. In conclusion, both DFG (baseline-to-peak) and DF (baseline-to-bottom) achieve similar magnitudes during and after consecutive exercise-trials and are closely linked to RPE and oxygen uptake. This suggests that DF neither reflects impaired diaphragmatic function nor impairs exercise performance; rather it is likely to reflect post-exercise diaphragm shielding.
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PMID:Post-exercise diaphragm shielding: a novel approach to exercise-induced diaphragmatic fatigue. 1872 11


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