PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Skeletal muscle dysfunction”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources
PubMed1999

Respiratory and limb muscle function in lung allograft recipients.

Lung transplantation recipients have reduced exercise capacity despite normal resting pulmonary and hemodynamic function. The limiting factor may be contractile dysfunction of skeletal muscle. To test this postulate, we measured limb and respiratory muscle function in nine clinically stable lung allograft recipients (six men and three women, aged 30 to 65 yr, at 5 to 102 mo after transplantation) with reduced exercise capacity. Respiratory muscle strength was tested by measuring maximal inspiratory and expiratory pressure (MIP and MEP, respectively). Ankle dorsiflexor muscle strength was measured during maximal voluntary contraction (MVC). In a subset of six recipients, we also measured contractile properties and fatigue characteristics of the tibialis anterior muscle, using electrical stimulation of the motor point. Data were compared with values from age- and sex-matched control subjects. MIP values of transplant recipients did not differ from control values; however, MEP was blunted by 30% relative to control (p < 0.05), and MVC was decreased by 39% (p < 0.05). The force-frequency relationships and fatigue characteristics of the tibialis anterior were not different between the patient and control groups. We conclude that stable lung allograft recipients experience expiratory and lower limb weakness that may contribute to exercise intolerance.

Adult↗
PubMed2005

Emphysema-induced reductions in locomotory skeletal muscle contractile function.

Patients with COPD suffer from locomotory skeletal muscle contractile dysfunction. This may be due to the disease per se or as a result of some confounding factor. Therefore, the purpose of this investigation was to determine whether emphysema: (1) reduces force production; (2) increases fatigability; and (3) impairs the speed of recovery in locomotory skeletal muscle in an accepted animal model in which many confounding variables can be controlled. To explore this issue, in situ mechanical properties of gastrocnemius were measured in Syrian Golden hamsters 8 months after intratracheal instillation of either saline (control, n = 5) or elastase (emphysema, n = 7). Emphysema increased excised lung volume (80%; P < 0.01), increased fatigability (control, 25% reduction in maximal strength after 4 min of repeated contractions; emphysema, 55% reduction; P < 0.05) and decreased the recovery rate (half-times of recovery: control, 7 +/- 7 s; emphysema, 92 +/- 92 s; P < 0.05) of gastrocnemius muscle. In contrast, emphysema had no effect on maximal force, whether related to body mass or muscle mass, or force-velocity characteristics of gastrocnemius muscle. These data demonstrate that emphysema, independent of physical activity levels, pharmacological intervention, and/or nutritional status, can increase fatigability and impair the speed of recovery of locomotory skeletal muscle contractile function which may contribute to exercise intolerance of COPD patients.

Animals↗
PubMed2006

Skeletal muscle ultrasonography in children with a dysfunction in the oxidative phosphorylation system.

OBJECTIVE: The aim of this prospective study was to investigate the diagnostic value of quantitative skeletal muscle ultrasonography in children suspected of having a mitochondrial disorder. METHODS: Muscle thickness and quantitatively determined echo intensity of four muscles were established in 53 children with symptoms indicative of a mitochondrial disorder. RESULTS: A sensitivity of 25 to 46 % was found, depending on the chosen cut-off point (abnormal or borderline abnormal), with a specificity of 85 to 100 %. Except for one, all abnormal ultrasound scans were found in children over five years of age. Within the group of patients with a mitochondrial disorder, a significant correlation was found between muscle echo intensity and age (r = 0.38; p = 0.047). CONCLUSIONS: We conclude that skeletal muscle ultrasound can be of additional value in the diagnosis of children with suspected mitochondrial disorders, especially in children over five years of age. With its low sensitivity, it is not suitable for screening purposes. However, since all abnormal ultrasound scans were found in children with a mitochondrial disorder, and no significant correlation with the MDC score was found, muscle ultrasound can be used complementary to this scoring system to facilitate the decision-making in pursuing further invasive diagnostics.

Adolescent↗
PubMed2003

Changes in Ca2+ handling in adult MG29-deficient skeletal muscle.

It was reported that a lack of Mitsugumin29 (MG29), a protein expressed at the triad junction, caused morphological changes in sarcoplasmic reticulum and T-tubules, reduced twitch/tetanus ratio, and increased susceptibility to fatigue in adult skeletal muscle and dysfunction of store-operated Ca2+ entry (SOC) in embryonic and neonatal muscles. To deepen our understanding of the role of MG29 in the Ca2+ handling in adult skeletal muscle,Ca2+ stores of wild-type and mutant muscle fibers were depleted by repetitive high-K+ treatments in a Ca2+-free medium. Although wild-type muscle showed only minor caffeine contracture after high-K+ response had disappeared, the mutant muscle showed remarkable caffeine contracture under the conditions used, suggesting functional compartmentalization of the Ca2+-store in the mutant. Activation of SOC in adult mutant muscle was observed upon the voltage-sensitive store depletion as is true with the wild-type muscle. Thus MG29 is not involved in the SOC activation at variance with the previous conclusion with immature muscles.

Animals↗
PubMed2005

Involvement of mitochondria in myasthenia gravis complicated with dermatomyositis and rheumatoid arthritis: a case report.

We report a 57-year-old male with myasthenia gravis complicated with dermatomyositis and rheumatoid arthritis without evidence of thymoma. He showed prominent muscle wasting and weakness in the four extremities and trunk in addition to swallowing disturbance. He showed intolerance to exercise on a bicycle ergometer, and muscle biopsy specimens demonstrated ragged-red fibers. An anti-acetylcholine receptor (AChR) antibody was detected in his serum but no anti-mitochondrial M2 component antibody was found. In contrast, results of immunohistochemical study indicated that his serum sample reacted to muscle mitochondria as well as AChR. These results indicate the presence of an unidentified anti-mitochondrial antibody that may be involved in the development of mitochondrial dysfunction in skeletal muscle of the present patient.

Arthritis, Rheumatoid↗
PubMed2005

Single-institution experience in 110 patients with botulinum toxin A injection into bladder or urethra.

OBJECTIVES: To detail, in a review, one institution's 6-year experience using botulinum toxin A (BTX-A) in the bladder and urethra in 110 patients for a variety of lower urinary tract disorders. METHODS: A total of 110 patients (35 men and 75 women, age range 19 to 82 years) received injections of BTX-A into the bladder (n = 42) or urethra (n = 68). Voiding dysfunction included neurogenic detrusor overactivity and/or detrusor sphincter dyssynergia, overactive bladder, bladder neck obstruction, and interstitial cystitis. Under light sedation in most cases, patients were treated with either 100 to 200 U of BTX-A in 4 mL divided in equal doses into the four quadrants of the external sphincter or by injection into the bladder base using 100 to 300 U of BTX-A diluted in approximately 10 to 30 mL of sterile saline. At last follow-up, 27 patients had received additional injections (up to six) at intervals of 6 months or longer. RESULTS: All patients who underwent bladder BTX-A injection had preoperative evidence of involuntary detrusor contractions during urodynamic testing. Analysis of the 110 patients indicated that 67.3% reported a decrease or absence of incontinence. Diaries indicated a decrease in both daytime and nighttime voiding symptoms. Maximal efficacy occurred between 7 and 30 days and lasted for at least 6 months. Condition-specific quality-of-life symptom scores also demonstrated improvement. No long-term complications had occurred at last follow-up. Two women with multiple sclerosis and mild baseline stress urinary incontinence reported increased leakage with stress after BTX-A external sphincter injection, and one woman with multiple sclerosis noted new onset stress urinary incontinence after external sphincter injection. However, they all reported significant improvement in their detrusor sphincter dyssynergia with decreased postvoid residual urine volume, improved uroflow, decreased urge incontinence, and decreased daytime and nighttime frequency. One woman with multiple sclerosis who underwent bladder injection had increased postvoid residual urine volume from 78 to 155 mL. She did not have to perform intermittent catheterization. CONCLUSIONS: BTX-A injection is a safe and promising treatment modality for a variety of lower urinary tract dysfunctions for both skeletal and smooth muscle dysfunction. In our series, BTX-A is equally effective in women as it is in men. When injected into the sphincter, the risk of stress incontinence is low. Bladder injections with BTX-A are effective for not only neurogenic detrusor overactivity, but also overactive bladder. BTX-A can even be considered for interstitial cystitis.

Adolescent↗
PubMed2006

[Pittsburgh experience with botulinum toxin A injection].

We report one institution's six-year experience using botulinum toxin A (BONT-A) in the bladder and urethra in 110 patients for a variety of lower urinary tract dysfunction. 110 patients (age 19-82) were injected with BONT-A into the bladder (n=42) or urethra (n=68), 35 M, 75 F. Voiding dysfunction included: neurogenic detrusor overactivity and/or detrusor sphincter dyssynergia, overactive bladder (OAB), benign prostatic hyperplasia (BPH), bladder neck obstruction (BNO) and interstitial cystitis (IC). Currently, 27 patients have undergone further injections (up to 6) at intervals > 6 months. All the patients with bladder BONT-A injection had preoperative evidence of involuntary detrusor contractions during urodynamic testing. Analysis of the 110 patients indicates that 67.3% reported a decrease or absence of incontinence. Diaries indicate a decrease in both day and night voiding symptoms. Efficacy occurred within 7 days and lasted for at least 6 months. Condition specific QOL symptom scores also demonstrated improvement. There have been no long-term complications. Two MS women with mild baseline stress urinary incontinence reported increased leakage with stress after BONT-A external sphincter injection. One MS woman who had a bladder injection had an increased residual urine from 78 to 155 ml. She did not have to perform intermittent catheterization. BONT-A injection is a safe and promising treatment modality for a variety of lower urinary tract dysfunctions for both skeletal and smooth muscle dysfunction. In our series, BONT-A is equally effective in women as it is in men. Bladder injections with BONT-A are effective for not only neurogenic detrusor overactivity but also overactive bladder. BONT-A can even be considered for IC.

Adult↗
PubMed2000

Does muscle function and metabolism affect exercise performance in the heat?

It has been suggested that exercise performance in the heat is limited by the degree of hyperthermia, which, in some circumstances, compromises cardiovascular function and/or the central nervous system. However, this review presents evidence that a temperature-induced dysfunction to skeletal muscle contraction may contribute to a reduction in performance during exercise in the heat.

Animals↗
PubMed2000

Skeletal muscle perfusion during exercise using Gd-DTPA bolus detection.

The study was performed to evaluate if skeletal muscle perfusion can be determined during exercise using an IV bolus injection of Gd-DTPA. A fast spoiled gradient echo sequence (T1 weighted) was used with intermittent imaging during one-legged plantar flexion at different workloads. Between repetitive flexions, a 2-sec rest allowed magnetic resonance imaging (MRI) of the lower legs and measurements of the blood flow in the popliteal artery by ultrasonography for subsequent calculation of muscle perfusion. Maximal signal intensity, upslope and downslope of the bolus, mean transit time, and integrated curve area were measured within regions of interest bilaterally. The skeletal muscle perfusion estimated by ultrasonography increased in the exercising leg from 4 ml x 100 g(-1) x min(-1) at rest to 38 ml at low, 86 ml at medium, and 110 ml x 100 g(-1) x min(-1) at high workload. The SImax increased from 1.38 +/- 0.12 to 1.58 +/- 0.15 and the negative slope of the peak nonsignificantly from - 2.38 +/- 1.75 to - 12.05 +/- 9. 71. All obtained MRI parameters could visually separate the muscles into exercising, nonexercising, and presumably low active muscles. It is concluded that the signal intensity curve using a fast spoiled gradient echo sequence did not overall quantitatively mirror the perfusion, evaluated as the blood flow measured by ultrasonography. However, the signal intensity seemed to follow the blood flow velocity within a limited range of 15-60 cm x sec(-1), corresponding to 35-90 ml x 100 g(-1) x min(-1). Nonetheless, it might be useful when studying ischemia or endothelial dysfunction in skeletal muscles during exercise.

Adult↗
PubMed2000

Protective effect of TA-993, a novel therapeutic agent for peripheral circulatory insufficiency, on skeletal muscle fatigue in a rat model of hindlimb ischemia.

TA-993 (cis-(-)-2-(4-methylphenyl)-3-acetoxy-2,3-dihydro-5-(2-dimethylaminoethy l)-8-methyl1,5-benzothiazepine-4(5H)-one maleate), a new 1,5-benzothiazepine derivative, has a selective increasing action on limb blood flow in addition to an antiplatelet action. In this report we studied the effect of TA-993 on a time dependent decrease in developed tension of electrically-induced contraction of tibialis anterior muscle in a rat model of peripheral circulatory insufficiency induced by occlusion of abdominal aorta. In our preparation, the developed tension decreased by 20-30% in a sham-operated group and 30-40% in an abdominal aorta-occluded group at the end of the experimental period of 60 min. Intraduodenal administration (i.d.) of TA-993 (10 mg/kg) to the abdominal aorta-occluded rats ameliorated the decrease in developed tension to the level of the sham-operated group. Moreover, TA-993 at 10 mg/kg, i.d. significantly increased femoral arterial blood flow supplied through collateral circulation and decreased the whole blood viscosity in this model. These results suggest that TA-993 improves dysfunction of skeletal muscle contraction due to peripheral circulating insufficiency through an increase in collateral blood flow and an improvement of red blood cell deformability.

Animals↗
PubMed2006

Physical therapy management of Pompe disease.

Pompe disease (Glycogen storage disease type II, GSDII, or acid maltase deficiency) is an autosomal recessive disorder characterized by deficiency of acid alpha-glucosidase resulting in intra-lysosomal accumulation of glycogen and leading to progressive muscle dysfunction. The natural history of infantile-onset Pompe disease is characterized by hypertrophic cardiomyopathy and profound generalized weakness presenting in the first few months of life, with rapid progression and death usually occurring by one year of age. Late-onset Pompe disease is characterized by onset of symptoms after one year of age, less severe or absence of cardiac involvement and slower progression, with symptoms primarily related to progressive dysfunction of skeletal muscles and respiratory muscle involvement. Recent clinical trials of enzyme replacement therapy have begun to allow greater opportunity for potential improvement in motor status, function, and survival than ever before, with hopes of moving toward maximizing physical function for individuals with Pompe disease. Children are living longer with some achieving independent sitting, creeping, and walking-milestones typically never achieved in the untreated natural history of the disorder. With increased survival, clinical management based on an understanding of the pathology and pathokinesiology of motor function gains importance. This article reviews current knowledge regarding the motor system in Pompe disease and provides an overview of physical therapy management of Pompe disease, including management strategies for individuals on enzyme replacement therapy.

Glycogen Storage Disease Type II↗
PubMed1985

Long-term myoneural function after an induced compartment syndrome in the canine hindlimb.

For evaluation of long-term myoneural function in a compartment syndrome model of the canine hindlimb, five conditioned dogs had injections of autologous plasma into the hindlimb anterolateral muscle compartment, maintaining the pressure at 40 mmHg for eight hours. A newly described technique for measuring muscle function was used before pressurization and at weekly intervals following pressurization for a period of one month. Two days after pressurization, isometric twitch torque and tetanic torque showed a significant decrease (p less than .05) when compared with baseline values. Time to peak tension, one-half relaxation time, and endurance tests showed no significant change throughout the four-week testing. At four weeks following pressurization, no muscle dysfunction was noted, and muscle examined histologically was normal. Therefore, the initial muscle dysfunction present was reversed by skeletal muscle recovery or regeneration. Although no long-term muscle dysfunction occurred in this study of dogs, there may exist a lower tolerance to elevated intramuscular pressure in humans. Since dogs have only fatigue-resistant muscle fibers with higher oxidative capacity than human fibers, dog muscle may have a greater regenerative capacity than human muscle. Therefore, exact extrapolation of these dog studies to clinical compartment syndromes is difficult. Although muscle function was recovered in these animal experiments, human muscle may have less capacity to recover. It is advisable to decompress muscle compartments at a pressure of 30 mmHg as soon as clinical symptoms of a compartment syndrome appear.

Animals↗
PubMed2005

Insulin resistance in the HIV-infected population: the potential role of mitochondrial dysfunction.

Insulin resistance is accepted as the underlying fundamental defect that predates and ultimately leads to the development of type 2 (adult onset) diabetes mellitus in the general non-human immunodeficiency virus (HIV)-infected population. Insulin resistance is also a major component of the metabolic syndrome that, in association with other factors such as hypertension, hypercholesterolemia, and central obesity, defines a pre-diabetic atherogenic state that leads to adverse cardiovascular events. Growing evidence now suggests that mitochondrial dysfunction in skeletal muscle may be the mechanism whereby insulin resistance is induced. The prevalence of insulin resistance, glucose intolerance, and diabetes in the HIV-infected population has dramatically increased following the common use of highly active antiretroviral therapy (HAART). The development of insulin resistance in the HIV-infected population is likely to be multifactorial reflecting genetic predisposition, direct and indirect effects of both the protease inhibitor (PI) and nucleoside reverse transcriptase inhibitor (NRTI) class of antiretroviral therapy, and a possible contribution from chronic inflammatory changes induced by HIV. Indirect effects of antiretroviral therapy on insulin resistance may be mediated through both the visceral adiposity and peripheral fat depletion components of lipodystrophy as well as through fatty infiltration in liver and muscle. Based on current knowledge, mitochondrial dysfunction can be hypothesized to play a key role in each of these components.

Acquired Immunodeficiency Syndrome↗
PubMed2005

Transgenic overexpression of locally acting insulin-like growth factor-1 inhibits ubiquitin-mediated muscle atrophy in chronic left-ventricular dysfunction.

Metabolic abnormalities develop in various chronic diseases and lead to progressive catabolism with decrements in the skeletal musculature that result in muscle atrophy. We investigated pathways of skeletal muscle proteolysis using an experimental model of chronic left-ventricular dysfunction. Skeletal muscle atrophy developed in wild-type mice 12 weeks following myocardial infarction accompanied by an increase in total protein ubiquitination and enhanced proteasome activity, activation of Foxo transcription factors, and robust induction of the ubiquitin-protein ligase atrogin-1/MAFbx. Further studies identified skeletal muscle myosin as a specific target of ubiquitin-mediated degradation in muscle atrophy. In contrast, transgenic overexpression of a local isoform of insulin-like growth factor-1 prevented muscle atrophy and increased proteasome activity, inhibited skeletal muscle activation primarily of Foxo4, and blocked the expression of atrogin-1/MAFbx. These results suggest that skeletal muscle atrophy occurs through increased activity of the ubiquitin-proteasome pathway. The inhibition of muscle atrophy by local insulin-like growth factor-1 provides a promising therapeutic avenue for the prevention of skeletal muscle wasting in chronic heart failure and potentially other chronic diseases associated with skeletal muscle atrophy.

Animals↗
PubMed1991

Oxidant-mediated, CD18-dependent microvascular dysfunction induced by complement-activated granulocytes.

To determine the mechanisms whereby complement-activated granulocytes induce microvascular dysfunction in skeletal muscle, we examined the effect of antineutrophil serum (ANS), IB4 (a monoclonal antibody that inhibits CD18-dependent neutrophil adherence), xanthine oxidase inhibition or inactivation, deferoxamine, and catalase on the increase in canine gracilis muscle microvascular permeability induced by intravascular administration of zymosan-activated plasma (ZAP). Changes in vascular permeability were assessed by measurement of the solvent drag reflection coefficient (sigma) for total plasma proteins, and the extent of neutrophil infiltration was estimated by assessing muscle myeloperoxidase activity. ZAP infusion was associated with a marked increase in vascular permeability compared with control muscles that received no treatment or to muscles treated with zymosan heat-inactivated plasma (ZIP) (sigma = 0.51 +/- 0.04, 0.89 +/- 0.02, and 0.90 +/- 0.01, respectively). Estimates of sigma in animals rendered neutropenic with ANS, or treated with IB4, deferoxamine, or catalase before ZAP infusion were not significantly different from values obtained in control or ZIP-treated muscles (sigma = 0.96 +/- 0.02, 0.88 +/- 0.03, 0.85 +/- 0.02, and 0.79 +/- 0.01, respectively). However, xanthine oxidase inactivation or inhibition provided no protection from this ZAP-induced microvascular dysfunction (sigma = 0.58 +/- 0.02 and 0.58 +/- 0.01, respectively). In addition, neutropenia and inhibition of neutrophil adherence also prevented ZAP-induced increases in vascular resistance and tissue neutrophil infiltration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

Exercise training and peripheral vascular disease.

BACKGROUND: Conservative management is advocated as a treatment of choice for patients with intermittent claudication. This is a review of the mechanisms behind the improvement following an exercise rehabilitation programme. METHODS: All Medline articles from the National Library of Medicine, USA containing the text words 'claudication' or 'peripheral vascular disease' and 'exercise' were reviewed. Cross-referencing from relevant articles was carried out. RESULTS AND CONCLUSION: The poor physical status of a patient with intermittent claudication is not solely due to a reduction in blood flow to the lower limbs; associated factors, such as metabolic inefficiency, poor cardiorespiratory reserve and exercise-induced inflammation contribute. An exercise programme frequently improves both the physical aspect and quality of life, and the success of such exercise is multifactorial. An increase in the blood flow to the lower extremity is uncommon. Other factors, such as a redistribution of blood flow, changes in oxidative capacity of the skeletal muscles and greater utilization of oxygen, occur and the associated metabolic dysfunction of the skeletal muscles is rectified. Following exercise training, blood rheology improves and exercise-induced inflammation is ameliorated; cardiorespiratory status also benefits and the oxygen cost of exercise decreases.

Biomechanical Phenomena↗
PubMed1991

Mitochondrial dysfunction in multiple symmetrical lipomatosis.

Multiple symmetrical lipomatosis is a striking clinical finding associated with a variety of peripheral and central nervous system abnormalities. We describe 4 unrelated patients with evidence of mitochondrial dysfunction in skeletal muscle. Multiple symmetrical lipomatosis is an additional, albeit unusual, manifestation of the expanding clinical spectrum of mitochondrial diseases.

Adult↗