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)

In myotonic dystrophy alteration in membrane excitability characterizes, in addition to the dystrophic process, modifications of contractile function detectable after fatigue. To verify in which extent sarcolemmal activation or contractility mechanisms are involved in fatigue, some electrophysiological and dynamometer parameters have been studied in tibialis anterior of 5 myotonic dystrophy patients. Evaluation has been performed basally and after protocol consisting of intermittent isometric voluntary contractions lasting 15', at two different muscle lengths, optimal and short. Administration at several recovery times of 20 and 50 Hz tetanizing sequences shows how processes distal to membrane excitability are mainly responsible for fatigue at optimal length, while relative potentiation of excitability preserves the muscle from excessive force loss at short length.
 ...
PMID:[Fatigue at various muscular lengths in myotonic dystrophy]. 180 79

To study effects of fatigue on muscle excitability and contractility in myotonic dystrophy (MyD), we evaluated, by ulnar nerve supramaximal stimulation, both single shock and 40 Hz tetanus, M wave and force parameters from adductor pollicis. In 8 MyD patients and in 6 controls amplitude of M wave, electromechanical delay, single twitch and tetanus tension, contraction and half-relaxation times were recorded in basal condition and at different times after 75 sec. of maximal voluntary contraction. Reduction of force related to fatigue was per cent lesser in MyD compared to controls. Electro-mechanical delay, basally longer in MyD, showed after fatigue 15% increment compared to 47% in controls. Half-relaxation time increased in both groups, but in MyD recovery was faster. Peculiar alterations of excitation-contraction coupling and contractility occurring in MyD can explain the observed modifications of fatigue phenomena in this disease.
 ...
PMID:[Changes in muscular excitability and contractility caused by fatigue in Steinert's disease]. 210 52

The study of skeletal muscle disorders is providing potentially important insights into regulatory mechanisms in human exercise and fatigue and information useful for diagnostic and treatment purposes. This review primarily concerned the general metabolic and physiological factors which set upper limits to performance of various types of exercise in patients with a variety of muscle disorders. From the standpoint of exercise performance, skeletal muscle diseases can be classified into three major groups. One group consists of primary disorders of muscle energy metabolism, including defects in muscle carbohydrate and lipid metabolism, disorders of mitochondrial electron transport, and abnormalities of purine nucleotide metabolism. Exercise performance largely reflects the capacity for ATP resynthesis. Oxidative phosphorylation is the dominant quantitative source of energy for ATP resynthesis under most exercise conditions. Consequently, patients with disordered oxidative metabolism (i.e., patients with defects in the availability or utilization of oxidizable substrate, such as those with phosphorylase or PFK deficiency or those with defects in mitochondrial electron transport) typically demonstrate severely impaired exercise performance. Intolerance to sustained exercise and premature fatigability are salient features of muscle oxidative disorders. Maximal oxygen uptake and maximal a-v O2 difference are markedly subnormal related to an attenuated muscle oxygen extraction. Muscle weakness and atrophy are less common. Anaerobic muscle performance is dramatically limited in patients with virtually complete defects of glycogenolysis/glycolysis but appears relatively normal in those with electron transport defects. A second major group of disorders includes patients with decreased muscle mass due to muscle necrosis, atrophy, and replacement of muscle by fat and connective tissue. These disorders are exemplified by the various muscular dystrophies (Duchenne's dystrophy, Becker's dystrophy, LG dystrophy, FSH dystrophy, and myotonic dystrophy) in which exercise performance is severely impaired due to muscle wasting and weakness in spite of largely normal pathways for muscle ATP resynthesis. In muscular dystrophy patients, the degree to which maximal oxygen uptake and anaerobic muscle performance are impaired appears to be a function of the severity of muscle weakness and atrophy. A third group of disorders includes patients with impaired activation of muscle contraction or relaxation. These disorders may be considered in two subcategories. In the first, impaired activation or relaxation of contractile activity is due to intrinsic muscle dysfunction (e.g., diseases associated with myotonia or periodic paralysis). In the second subcategory, there is impaired muscle activation due to a primary abnormality in the central nervous system, motor nerves, or neuromuscular junction.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Skeletal muscle disorders and associated factors that limit exercise performance. 267 57

In order to study transient paresis, force and surface electromyograms (EMG) were recorded from the biceps brachii in 3 patients with recessive myotonia congenita, in 8 with myotonic dystrophy and in 3 controls. Epochs of 0.34 s EMG signal were stored every 0.44 s and processed to determine the integrated EMG (IEMG), the power spectrum and the average muscle fibre conduction velocity (MFCV). The protocol consisted of 5 maximal voluntary contractions lasting 10.3 s and 13 s recovery. During the first 1-1.5 s the MFCV and median frequency (Fmed) of the power spectra of the controls increased (mean increase 12.5% and 14%, respectively) in all 5 consecutive contractions. Subsequently, MFCV, Fmed and force declined as a consequence of fatigue. Both the initial force and MFCV declined with successive contractions. The results in myotonic dystrophy were not different from the controls, except that the changes during fatigue were far less pronounced. These events are the reverse of the changes found in myotonia congenita in which an initial loss of force (maximal by 61-79%) and a decline of the IEMG (maximal by 79-92%) was found during the first contraction. This transient paresis was accompanied by a dramatic fall in the MFCV concomitant with a shift of the power spectrum to the lower frequencies. The first MFCV measurement of the 5 contractions was always normal. The decline in MFCV was maximal after 1.5-2.5 s and varied for the 3 patients from 32-52%. In general, the decline in force, IEMG and MFCV lessened with each successive contraction (warming-up phenomenon), though sudden deteriorations were sometimes observed during later contractions. The same results were found for brachioradialis and abductor digiti minimi. The results provide evidence that transient paresis is of clinical relevance in myotonia congenita and that it is caused by alterations in the muscle membrane. These membrane changes result in a strong decline of the muscle action potential conduction velocity and consequent depolarization block of the muscle fibres. Our method did not show the presence of transient paresis during voluntary contraction in myotonic dystrophy.
 ...
PMID:Transient paresis in myotonic syndromes. A surface EMG study. 273 Oct 26

We have previously shown that the chemosensitivity of the respiratory centers is well preserved in myotonic dystrophy but that the ventilatory output is reduced. The present study was designed to determine at which degree of ventilatory performance weakness and fatigability of the respiratory muscles are interfering with ventilation and which mechanical factors contribute to the tachypnea of patients with myotonic dystrophy at rest and during low ventilatory output. We studied 10 patients with the disease and 10 normal control subjects. The strength of respiratory muscles was assessed by measurements of maximal pressure-volume diagrams generated against airway occlusion. Performance was evaluated during 1-min maximal voluntary ventilation (1-min MVV) test, during 7-min 7% CO2 breathing and during quiet breathing. Occlusion pressure (P0.1) in patients at rest was slightly higher than in control subjects, and during CO2 breathing, it was similar to that of control subjects. Maximal static pressure was reduced in patients to an average of 35% of that of control subjects. During the 1-min MVV test, there was a 50% reduction in esophageal and transdiaphragmatic pressure output (Pes, Pdi) in patients, resulting in similar reduction in ventilation (VE) and patients had rapid cycles of alternating dominant thoracic and abdominal volume displacements (Vrc/Vabd) suggesting respiratory muscle fatigue. During the 3- to 4-fold increase in breathing drive induced by hypercapnia, pressure output and the Vrc/Vabd were identical in both groups. However, ventilation was reduced in patients who had tachypneic respiration. In patients, tachypnea was also observed during quiet breathing. This tachypnea was associated with higher impedance of the respiratory system (Zrs) in patients and identical impedance of the lung (ZL) in both groups. In addition, Pdi during tidal volume was significantly higher in patients. These data demonstrate that the ventilatory output in out patients was altered predominantly by weakness and fatigability of the respiratory muscles during high ventilatory performance and by increased impedance of the respiratory system at lower degrees of ventilation.
 ...
PMID:Pathogenesis of respiratory insufficiency in myotonic dystrophy: the mechanical factors. 680 50

An electrically calibrated, isometric hand dynamometer was used to quantitate maximum voluntary contraction (MVC(, relaxation time and fatigue time (at 50% MVC) in 18 normal and 10 myotonic dystrophy subjects. Precise measurements of MVC and fatigue time were obtained in normals and myotonic dystrophy patients. Relaxation times were markedly prolonged and were quite variable in all patients with myotonic dystrophy in contrast to the highly reproducible times in normals. Neither "warm-up" activity nor acetazolamide treatment altered relaxation time.
 ...
PMID:Quantitative testing of handgrip strength, myotonia, and fatigue in myotonic dystrophy. 687 12

The gait of five patients with myotonic dystrophy was analyzed using light-emitting diodes and a force plate. When compared with the gait of control subjects, that of myotonics suggested weakness of the tibialis anterior and triceps surae muscles. Although the myotonics showed no evidence of lower-extremity myotonia (delayed muscle relaxation following contraction), or of weakness of the hip or knee musculature, all had striking abnormalities in their hip motion. In contrast to the smooth and consistent extension of the hip throughout stance phase observed during gait in control subjects, the hips of myotonics oscillated irregularly as they progressed through stance phase extension, with considerable variation between legs and during successive strides. Excessive use of hip musculature in an attempt to control the oscillatory hip motion may contribute to the chronic fatigue associated with myotonic dystrophy.
 ...
PMID:Characterization of gait parameters in adult-onset myotonic dystrophy: abnormal hip motion. 781 Nov 71

All individuals in a Swedish county afflicted with any type of hereditary muscular dystrophy (MD) were identified and 57 (85 percent) of eligible individuals in the age range 16 to 64 were included in the study. Respiratory disturbances were estimated by means of spirometry and analysis of arterial blood gases, and 58 percent yielded abnormal results on at least one of these examinations. Elevated PCO2 was found more commonly than reduced forced vital capacity (FVC) and there was a moderate association between these parameters. Respiratory symptoms, most commonly breathlessness, were encountered in 79 percent. Pathologic ECG recordings were found in 21 individuals (37 percent). Conduction disturbances and affection of the myocard were most frequent in myotonic dystrophy. Quality of life was assessed by means of the Sickness Impact Profile instrument and the Kaasa test. The results showed that quality of life was significantly related to FVC and to the symptom of abnormal fatigue. Respiratory and cardiac parameters showed a greater number of significant correlations with measures of functional ability than with subjective well-being.
 ...
PMID:Respiratory function, electrocardiography and quality of life in individuals with muscular dystrophy. 802 Feb 68

Myotonic dystrophy (MyD) patients have been reported to show severe nocturnal desaturation related to sleep respiratory disorders. However, the reason of respiratory failure in MyD has remained unclear. In this study, ten patients with MyD underwent overnight polysomnography to evaluate the mechanisms which would cause respiratory failure, compared with Duchenne muscular dystrophy (DMD) patients in these three views: 1) sleep-related nocturnal desaturation, 2) histopathological evaluation of respiratory muscles, and 3) abnormalities of respiratory center. Nocturnal desaturation was more prominent in MyD rather than DMD. Apnea-hypopnea index (AHI) was higher in MyD than DMD. Type of respiratory disorder during sleep was mainly central apnea-hypopnea pattern, including Cheyne-Stokes respiration. In histopathological findings, central core change in respiratory muscle related to respiratory muscle fatigue was found less frequently in MyD than DMD. In respiratory center function, MyD showed hyporesponse to both alveolar hypercapnic and hypoxic stimulation. However, DMD showed normal response to both stimulations. We concluded that respiratory failure in patients with MyD would be attributed to respiratory center disorder rather than respiratory muscle weakness, which is the main cause of respiratory failure in patients with DMD.
 ...
PMID:[Respiratory failure: respiratory disorder during sleep in patients with myotonic dystrophy]. 875 39

In an effort to find parameters to evaluate patients with neuromuscular disorders, surface electromyography (SEMG) of proximal leg muscles was performed in 33 patients with myotonic dystrophy (MyD), 29 patients with Charcot-Marie-Tooth (CMT) disease and 20 healthy controls. The root mean square (RMS) of the SEMG amplitude (microV) was calculated at different torque levels. Endurance (seconds) and median frequency (Fmed) of the SEMG power spectrum, used as parameters of fatigue, were determined at 80% of MVC. Maximum voluntary contraction (MVC) was found to be decreased in patients; the ratio between RMS values of antagonists and agonists was increased and torque-EMG ratios (Nm/microV) were decreased. These differences with respect to controls were more pronounced in MyD than in CMT. The initial Fmed value was lowest in CMT. The greatest decrease in Fmed was found in MyD. SEMG data in relation to force have not been determined before in groups of MyD or CMT patients. In both disorders, parameters differed from controls, which means that adding SEMG to strength measurements could be useful in studying the progress of the disorder and the effects of interventions.
 ...
PMID:Surface EMG of proximal leg muscles in neuromuscular patients and in healthy controls. Relations to force and fatigue. 1052 11


1 2 3 4 5 6 Next >>