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

The composition and structure were studied in the cast and in the solder of bridges which had failed clinically. Both materials were gold alloys but with different contents of Pt, Ag and Zn. The metallographic investigation revealed defects mostly in the solder, situated in the subsurface layer. SEM studied of the fracture surface revealed large porosites and a structure of dense parallel lines--striations--, indicating that the material had failed from fatigue. The materials in the fractured bridges were identified by micro-probe measurements. It was stated that cast material and solder material used together, were of different composition.
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PMID:Microstructure of the solder-casting zone in bridges of dental gold alloys. 1 May 39

Electron probe analysis, cryo-ultramicrotomy, and freeze-substitution were used to determine the nature of vacuolation and the subcellular composition in fatigued frog skeletal muscle fibers. The vacuoles caused by fatigue were part of the T-tubule system and contained high concentrations of NaCl. The calcium concentration in the terminal cisternae was higher than previously measured normal resting values. Mitochondrial calcium content was relatively low (mean +/- SEM, 2 +/- 2 mmol/kg dry weight). Fiber NaCl was increased. It is concluded that fatigue is not due to the depletion of calcium stores from the terminal cisternae or to uncoupling of mitochondria due to calcium loading but may be caused by multiple mechanisms including failure of the T-tubule action potential.
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PMID:Composition of vacuoles and sarcoplasmic reticulum in fatigued muscle: electron probe analysis. 2 54

Fatigue and recovery from fatigue were related to metabolism in single fibers of the frog semitendinosus muscle. The fibers were held at a sarcomere length of 2.3 microm in oxygenated Ringer solution at 15 degrees C and were stimulated for up to 150 s by a schedule of 10-s, 20-Hz tetanic trains that were interrupted by 1-s rest periods, after which they were rapidly frozen for biochemical analysis. Two kinds of fatigue were produced in relation to stimulus duration. A rapidly reversed fatigue occurred with stimulation for under 40 s and was evidenced by a decline in tetanic tension that could be overcome by 1 s of rest. A prolonged fatigue was caused by stimulation for 100-150 s. It was evidenced during stimulation by a fall in tetanic tension that could not be overcome by 1 s of rest, and after stimulation by a reduction, lasting for up to 82 min, in the peak tension of a 200-ms test tetanus. Fiber phosphocreatine (PCr) fell logarithmically in relation to stimulus duration, from a mean of 121 +/- 8 nmol/mg protein (SEM, n = 12) to 10% of this value after 150 s of stimulation. PCr returned to normal levels after 90-120 min of rest. Stimulation for 150 s did not significantly affect fiber glycogen and reduced fiber ATP by at most 15%. It is suggested that the prolonged fatigue caused by 100-150 s of tetanic stimulation was caused by long-lasting failure of excitation-contraction coupling, as it was not accompanied by depletion of energy stores in the form of ATP. One possibility is that H+ accumulated in fatigued fibers so as to interfere with the action of Ca2+ in the coupling process.
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PMID:Metabolic correlates of fatigue and of recovery from fatigue in single frog muscle fibers. 31 Aug 67

Recent work has shown that alterations in the dynamic atrioventricular (AV) nodal response to changes in heart rate can significantly modify AV nodal function. The present study was designed to evaluate the nature and potential importance of sympathetic regulation of the rate-dependent properties of the AV node. Selective stimulation protocols and mathematical formulations were used to independently quantify AV nodal recovery, facilitation, and fatigue in 12 morphine-chloralose-anesthetized dogs. Vagal effects were prevented by bilateral vagal transection and intravenous atropine, and the sinus node was crushed to allow a broader range of pacing cycle lengths. In seven dogs with sympathetic nerves intact, beta-adrenergic receptor blockade increased the recovery time constant (tau rec) for the conduction of premature test beats from 47 +/- 2 (mean +/- SEM) msec (control) to 62 +/- 1 msec (p less than 0.001), whereas isoproterenol decreased tau rec to 38 +/- 1 msec (p less than 0.001). In addition, beta-blockade increased the maximum amount of rate-dependent AV nodal fatigue from 7 +/- 1 msec (at a cycle length of 198 +/- 9 msec [control]) to 17 +/- 2 msec (p less than 0.001). In five dogs with decentralized stellate ganglia, tau rec was decreased from 71 +/- 3 msec (control) to 57 +/- 4 msec and 48 +/- 2 msec (p less than 0.001 for each) by left stellate ganglion stimulation at 5 and 10 Hz, respectively. Maximum fatigue was similarly reduced from 16 +/- 1 msec (control) to 12 +/- 2 msec (p = NS) and 8 +/- 1 msec (p less than 0.01), respectively. Stellate ganglion stimulation, isoproterenol, and beta-blockade did not alter AV nodal facilitation. A mathematical model incorporating quantitative indexes of AV nodal function accurately accounted for tachycardia-dependent increases in the atrial-His activation interval, which were enhanced by beta-adrenergic receptor blockade and reduced by isoproterenol. Furthermore, this model showed that beta-adrenergic effects were increased by increasing heart rate, with the majority of the rate-dependent action being due to changes in the time course of AV nodal recovery. We conclude that beta-adrenergic receptor stimulation alters functional properties that govern the AV nodal response to changes in heart rate. These changes in functional properties alter the ability of the AV node to conduct impulses during tachycardia and, as such, could play a major role in the ability of sympathetic stimulation to promote and beta-adrenergic receptor blockade to prevent the occurrence of AV nodal reentrant arrhythmias.
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PMID:Effects of beta-adrenergic receptor stimulation and blockade on rate-dependent atrioventricular nodal properties. 134 76

Clentiazem, 8-chloro diltiazem, is a calcium channel blocker currently undergoing evaluation for the treatment of stable angina and hypertension. As patients with ischaemic disorders often present some degree of heart failure, the aim of this study was to investigate the effect of congestive heart failure on clentiazem (200 micrograms kg-1, i.v. bolus) pharmacokinetics in a canine model. Congestive heart failure was induced in six dogs by rapid ventricular pacing (240 beats min-1) for 3-5 weeks. Clentiazem pharmacokinetics was studied in each dog under the control condition and after the development of clinical signs of heart failure (ascites, dyspnea, fatigue). Blood samples were collected up to 480 min post-dose. Clentiazem plasma concentrations were determined by high performance liquid chromatography. The area under the plasma concentration versus time curves (AUC0-infinity) was significantly increased in congestive heart failure dogs (8.8 +/- 1.6 vs 21.8 +/- 1.4 micrograms min ml-1) (mean +/- SEM). These changes were related to a reduction of the volume of distribution of the central compartment (0.9 +/- 0.1 vs 0.2 +/- 0.11 kg-1) and total body clearance (1.9 +/- 0.4 vs 0.7 +/- 0.21 h-1 kg-1). It is concluded that, in our model, congestive heart failure significantly modifies clentiazem disposition. These results suggest that caution should be exercised when clentiazem is given to patients with a low ejection fraction and a compromised cardiac function. Reduced loading and maintenance doses might be recommended in patients with severe congestive heart failure.
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PMID:Effect of congestive heart failure on clentiazem pharmacokinetics in a dog model. 148 42

The effects of increasing the extracellular K+ concentration on the capacity to generate action potentials and to contract were tested on unfatigued muscle fibers isolated from frog sartorius muscle. The goal of this study was to investigate further the role of K+ in muscle fatigue by testing whether an increased extracellular K+ concentration in unfatigued muscle fibers causes a decrease in force similar to the decrease observed during fatigue. Resting and action potentials were measured with conventional microelectrodes. Twitch and tetanic force was elicited by field stimulation. At pHo (extracellular pH) 7.8 and 3 mmol K+.L-1 (control), the mean resting potential was -86.6 +/- 1.7 mV (mean +/- SEM) and the mean overshoot of the action potential was 5.6 +/- 2.5 mV. An increased K+ concentration from 3 to 8.0 mmol.L-1 depolarized the sarcolemma to -72.2 +/- 1.4 mV, abolished the overshoot as the peak potential during an action potential was -12.0 +/- 3.9 mV, potentiated the twitch force by 48.0 +/- 5.7%, but did not affect the tetanic force (maximum force) and the ability to maintain a constant force during the plateau phase of a tetanus. An increase to 10 mmol K+.L-1 depolarized the sarcolemma to -70.1 +/- 1.7 mV and caused large decreases in twitch (31.6 +/- 26.1%) and tetanic (74.6 +/- 12.1%) force. Between 3 and 9 mmol K+.L-1, the effects of K+ at pHo 7.2 (a pHo mimicking the change in interstitial pH during fatigue) and 6.4 (a pHo known to inhibit force recovery following fatigue) on resting and action potentials as well as on the twitch and tetanic force were similar to those at pHo 7.8. Above 9 mmol K+.L-1 significant differences were found in the effect of K+ between pHo 7.8 and 7.2 or 6.4. In general, the decrease in peak action potential and twitch and tetanic force occurred at higher K+ concentrations as the pHo was more acidic. The results obtained in this study do not support the hypothesis that an accumulation of K+ at the surface of the sarcolemma is sufficiently large to suppress force development during fatigue. The possibility that the K+ concentration in the T tubules reaches the critical K+ concentration necessary to cause a failure of the excitation-contraction coupling mechanism is discussed.
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PMID:Effects of K+ on the twitch and tetanic contraction in the sartorius muscle of the frog, Rana pipiens. Implication for fatigue in vivo. 149 91

The self-glazing technique provides an esthetic and hygienic surface for crowns and fixed partial dentures that use porcelain veneers. A study of the biaxial flexure strengths of polished vs. glazed specimens is needed to verify that current laboratory methods are appropriate for planned fatigue studies. Four groups of 50 porcelain disk specimens each were subjected to the following polishing and firing procedures: group one was fired, glazed-no hold, and polished; group two was fired, polished, and glazed-no hold; group three was fired, polished and glazed-1 min. hold; group four was fired, polished, and not glazed. The piston-on-three-ball method was used for testing biaxial flexure strengths. Significantly lower differences in biaxial flexure strengths were noted when group two values were compared with values from groups one, three and four. The results show that the Weibull distribution is an appropriate model for our studies. Differences in glaze thickness among the groups were noted in SEM examination; however, bulk (interior) microcrack density differences were absent. The specimens that were fired, polished to a 1 micron surface finish, and not glazed (group four) were significantly higher in flexure strength than groups one and three at the p less than 0.001 level. The hypothesis that glazing of porcelain surfaces improves the biaxial flexure strength of test specimens was rejected.
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PMID:The effect of glaze on porcelain strength. 152 11

Skeletal muscle powered assist ventricles (SMV) are being investigated in animal studies as a treatment for heart failure. Muscle fatigue is almost always dependent upon muscle capillary blood flow. This study examined the relationship between SMV intrapouch pressure and blood flow to the circumferential muscle in a working SMV with a mock circulation. The unconditioned rectus abdominis muscle was used to create an in situ SMV in five dogs. Muscle blood flow was measured by both the radioactive microsphere and the electromagnetic flow probe method as the pouch pressure was varied between 10 and 70 mmHg and as the SMV was stimulated to contract at a rate of 20 min-1. The correlation coefficient for the two methods was 0.908. At pouch pressures of 10, 40, and 70 mmHg, the respective blood flow values were 22.60 +/- 2.50 (1 SEM), 12.20 +/- 2.10, and 4.40 +/- 0.74 ml min-1 (p less than 0.05). When they were corrected for muscle weight, the mean blood flow values at these same pouch pressures were 0.28 +/- 0.03, 0.15 +/- 0.03, and 0.05 +/- 0.01 ml min-1 g-1, respectively (p less than 0.05). SMV output was measured for each pouch pressure that was tested. Pouch output, expressed as ml min-1, was 458 +/- 20 (1 SEM) at an SMV diastolic pouch pressure of 10 mmHg, 309 +/- 22 at a pouch pressure of 40 mmHg, and 103 +/- 6 at a pouch pressure of 70 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of skeletal muscle ventricle pouch pressure on muscle blood flow. 153 16

1. The maximum rate of relaxation of stimulated twitches (twitch maximum relaxation rate) of the sternomastoid muscle was compared with its frequency-force curve (expressed as the ratio of force produced at a stimulation frequency of 20 Hz to that produced at 50 Hz, the 20:50 ratio) before and after fatiguing exercise of the sternomastoid muscle in 10 normal subjects. The mean (+/- SEM) fresh state twitch maximum relaxation rate was 9.51 (+/- 0.64)% force loss/10 ms and the mean (+/- SEM) 20:50 ratio was 73.4 (+/- 2.6)%. 2. The mean twitch maximum relaxation rate fell to 71.5 (+/- 2.2)% of the pre-fatigue value at 2 min after exercise, recovering to 73.1 (+/- 1.6)% by 5 min, 78.4 (+/- 2.34)% by 10 min and 80.6 (+/- 2.70)% by 60-min. The 20:50 ratio fell to 72.3 (+/- 3.56)% of pre-fatigue levels at 10 min after exercise and recovered to 78.8 (+/- 3.16)% by 60 min. There was no significant difference in the percentage falls between the two techniques. 3. Further studies were performed to determine the response of the twitch maximum relaxation rate to a prior brief tetanic stimulus or a brief maximal voluntary contraction of the muscle. Both tetanic stimulation and maximal voluntary contraction accelerated the twitch maximum relaxation rate to over 140% of the fresh state value. Both manoeuvres temporarily returned the slowed twitch maximum relaxation rate after fatiguing exercise back to the fresh state value. 4. The effect of fatiguing exercise on the time course of recovery of quadriceps twitch maximum relaxation rate was also studied in two subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sternomastoid muscle twitch maximum relaxation rate: prolonged slowing with fatigue and post-tetanic acceleration. 166 54

We investigated whether fatigue of the expiratory muscle, that is, the abdominal muscle, may account for a change in the respiratory effort sensation in normal subjects during expiratory threshold loading. The respiratory effort sensation was scored using a modified Borg scale. Expiratory muscle fatigue was assessed both from changes in the maximal static expiratory pressure and in the centroid frequency (fc) of the abdominal muscle electromyogram (EMG). Expiratory threshold loading (magnitude of threshold; 40 to 60% of the maximal expiratory pressure at FRC, breathing frequency = 15/min, and duty cycle = 0.5) was continued until exhaustion or for 30 min. Loading was repeated following a 15-min recovery period after the end of the first expiratory loading. The maximal static expiratory pressure during loading (Pmmax) decreased initially and then remained decreased. Decreases were smaller with the 40% load (22 +/- 6%, SEM) than with the 60% load (37 +/- 3%) (p less than 0.05). The decrease during the second run of the 60% load was greater than during the first (p less than 0.01 by ANOVA). The maximal expiratory pressure at TLC before the second run of the 60% load was decreased by 9 +/- 3% compared with the control (p less than 0.02) but that with the 40% load was not. The fc with the 60% load decreased initially by 8 +/- 1% and then remained constant, although no change was observed with the 40% load.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relationship of respiratory effort sensation to expiratory muscle fatigue during expiratory threshold loading. 173 58


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