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PubMed2004

Exercise rehabilitation and skeletal muscle benefits in hemodialysis patients.

End-stage renal disease patients on hemodialysis (HD) are characterized by poor exercise tolerance and debilitation symptoms, despite advances in dialysis procedures and erythropoietin use. Specifically, the muscle strength and endurance are diminished, as result of skeletal muscle dysfunction and atrophy. These changes are presumed to be secondary to uremic toxins, anemia, malnutrition, deconditioning, neurohormonal insults and other disorders. Previous studies have shown that exercise training limits the pathophysiological changes that occur in HD patients, mainly regarding peripheral skeletal muscle. It is supported that significant peripheral adaptations to training occur, as evidenced by the improvement of muscle function. Especially, morphological and metabolic benefits in the skeletal muscles have been well-documented in HD patients following physical rehabilitation programs. Such beneficial adaptations increase endurance and muscle strength and contribute to improved work capacity. The better understanding of these adaptive mechanisms may allow for improved exercise training strategies in these patients.

Exercise↗

PubMed1996

Protease inhibition attenuates microvascular dysfunction in postischemic skeletal muscle.

Neutrophils accumulate in skeletal muscle subjected to ischemia-reperfusion and appear to contribute to reperfusion-induced microvascular dysfunction. The overall objective of this study was to assess the role of the neutrophilic hydrolytic enzyme elastase in ischemia-reperfusion-induced granulocyte accumulation and microvascular dysfunction in skeletal muscle. We examined the effect of three structurally unrelated elastase inhibitors [eglin C, MeOsuc-Ala-Ala-Val-CH2Cl (MAAPV), or L-658758], administered at the onset of reperfusion, on neutrophil content and the increase in microvascular permeability induced by 4 h of ischemia and 0.5 h of reperfusion in the isolated canine gracilis muscle. Changes in vascular permeability (1 - sigma) were assessed by determining the solvent drag reflection coefficient for total plasma proteins (sigma) in the following groups: 1) 4.5 h of continuous perfusion (nonischemic), 2) ischemia-reperfusion alone, 3) ischemia-reperfusion + eglin C, 4) ischemia-reperfusion + MAAPV, and 5) ischemia-reperfusion + L-658758. Muscle neutrophil content was monitored by assessing tissue myeloperoxidase (MPO) activity in biopsies obtained at the end of the experiments. In nonischemic muscles, 1 - sigma and MPO activity averaged 0.13 +/- 0.03 and 0.7 +/- 0.2 units/g wet wt, respectively. Ischemia-reperfusion was associated with marked increases in microvascular permeability (1 - sigma = 0.39 +/- 0.02) and muscle MPO activity (8.9 +/- 1.2 units/g wet wt) that were attenuated by eglin C, MAAPV, and L-658758 (1 - sigma = 0.21 +/- 0.01, 0.22 +/- 0.02, and 0.21 +/- 0.03, respectively; MPO activity = 2.7 +/- 0.4, 2.1 +/- 0.8, and 2.8 +/- 1.8 units/g wet wt, respectively). These results suggest that granulocyte accumulation in postischemic skeletal muscle is dependent on the release of elastase from activated phagocytic cells. Moreover, neutrophilic elastase appears to play a major role in reperfusion-induced increases in microvascular permeability in skeletal muscle.

Amino Acid Chloromethyl Ketones↗

PubMed2001

Enhanced generation of reactive oxygen species in the limb skeletal muscles from a murine infarct model of heart failure.

BACKGROUND: The generation of reactive oxygen species (ROS) is enhanced in the failing myocardium. We hypothesized that ROS were also increased in the limb skeletal muscles in heart failure. Methods and Results-- Myocardial infarction (MI) was created in mice by ligating the left coronary artery. After 4 weeks, the left ventricle was dilated and contractility was diminished by echocardiography. Left ventricular end-diastolic pressure was elevated after MI in association with an increase in lung weight/body weight and the presence of pleural effusion. The generation of ROS in the limb muscles, including the soleus and gastrocnemius muscles, which were excised after MI, was measured by electron spin resonance spectroscopy with 4-hydroxy-2,2,6,6-tetramethyl-piperidine-N-oxyl (hydroxy-TEMPO). Overall, generation was increased, but it was attenuated in the presence of dimethylthiourea or 4,5-dihydroxy-1,2-benzenedisulfonic disodium salt in the reaction mixture, indicating increased generation of hydroxyl radicals originating from superoxide anion. Thiobarbituric acid-reactive substance formation was also increased in muscles after MI. Mitochondrial complex I and III activities were both decreased after MI, which may have caused the functional uncoupling of the respiratory chain and ROS production. Antioxidant enzyme activities, including superoxide dismutase, catalase, and glutathione peroxidase, were comparable between groups. CONCLUSIONS: Skeletal muscle in post-MI heart failure expressed an increased amount of ROS in association with ROS-mediated lipid peroxidation. This supports the hypothesis that oxidative stress may cause (at least in part) skeletal muscle dysfunction in heart failure.

Animals↗

PubMed1992

Upper gastrointestinal tract motility in children with progressive muscular dystrophy.

Gastric emptying was evaluated in 15 children (mean age, 8.0 years) with progressive muscular dystrophy to detect early gastrointestinal smooth muscle involvement; 10 of the children also underwent esophageal manometry. Clinical evidence of skeletal muscle dysfunction was minimal in 14 of the 15 patients; 10 of them had no gastrointestinal symptoms. Gastric emptying studies were performed by using 500 muCi of technetium 99m-sulfur colloid bound to a scrambled egg, and scintigraphic measurements were made continuously for 60 to 90 minutes. Gastric emptying studies and manometric tracings were compared with those from 11 children (mean age, 8.4 years) without gastrointestinal or muscular disorders. Mean (+/- SD) percentage retention of gastric isotope was significantly greater in patients with muscular dystrophy than in control subjects. No differences were found between the two groups in distal esophageal motility or in upper and lower esophageal sphincter pressures or relaxation. Contraction amplitudes in the upper portion of the esophagus, however, were significantly lower in patients with myopathy than in control subjects. These data suggest that dysfunction of smooth muscle of the upper gastrointestinal tract is detectable in children with muscular dystrophy early in the course of the disease, even when gastrointestinal symptoms are absent and skeletal muscle symptoms are minimal.

Adolescent↗

PubMed1995

Changes in calmodulin concentration and cyclic 3',5'-nucleotide phosphodiesterase activity in skeletal muscle of hyper- and hypothyroid rats.

Hyper- and hypothyroid states occasionally induce skeletal muscle dysfunction i.e. periodic paralysis and thyroid myopathy. The etiology of these diseases remains unclear, but several findings suggest that the catecholamine-beta-receptor-cAMP system or other messenger systems are disturbed in these diseases. In this context, we evaluated changes in the cyclic 3',5'-nucleotide metabolic enzyme, cyclic 3',5'-nucleotide phosphodiesterase (PDE) and calmodulin concentrations in skeletal muscles of hyper- and hypothyroid rats. Activities of cyclic AMP-PDE were low in skeletal muscle both from hyper- and hypothyroid rats, and calmodulin concentration was high in hyperthyroid and low in hypothyroid rats, as compared with normal rats. DE-52 column chromatographic analysis showed that the cGMP hydrolytic activity in peak I and the cAMP hydrolytic activity in peak II were decreased in hypothyroid rats, whereas cAMP hydrolytic activity in peak III was unchanged. The cAMP hydrolytic activity in peak III was decreased in hyperthyroid rats, but the activities in peaks I and II were unchanged. These findings indicate that cAMP and calmodulin may have some role in skeletal muscle function in the hyperthyroid state, and that cAMP and calmodulin-dependent metabolism may be suppressed in the hypothyroid state.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed2003

Nitric oxide synthases and protein oxidation in the quadriceps femoris of patients with chronic obstructive pulmonary disease.

Skeletal muscle dysfunction contributes to poor exercise performance in patients with chronic obstructive pulmonary disease (COPD). Increased oxygen radicals and nitric oxide (NO) have been proposed as mechanisms. In this study, we assessed the levels of protein oxidation (carbonyl formation), lipid peroxidation (4-hydroxy-2-nonenal formation), catalase and Mn-superoxide dismutase (Mn-SOD) expressions, nitric oxide synthases (NOSs), and protein tyrosine nitration in quadriceps muscles of 12 patients with patients with COPD and 6 control subjects. Lipid peroxidation was elevated in muscles of patients with patients with COPD as compared with control subjects, but protein oxidation was not. Muscle Mn-SOD but not catalase protein expression was significantly higher (200%) in patients with patients with COPDas compared with control subjects. Expression of neuronal NOS and endothelial NOS isoforms did not differ between control subjects and patients with COPD, whereas no inducible NOS protein expression was detected in limb muscles of the two groups of subjects. In patients with COPD, neuronal NOS expression correlated negatively with the degree of the airway obstruction (%FEV1 predicted). 3-Nitrotyrosine levels were significantly elevated in muscles of patients with COPDas compared with control subjects, and correlated positively with nNOS protein levels. These results indicate the development of both oxidative and nitrosative stresses in the quadriceps of patients with COPD, suggesting their involvement in muscle dysfunction.

Aged↗

PubMed2005

Systemic effects of chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) affects various structural and functional domains in the lungs. It also has significant extrapulmonary effects, the so-called systemic effects of COPD. Weight loss, nutritional abnormalities, and skeletal muscle dysfunction are well-recognized systemic effects of COPD. Other less well-known but potentially important systemic effects include an increased risk of cardiovascular disease and several neurologic and skeletal defects. The mechanisms underlying these systemic effects are unclear, but they are probably interrelated and multifactorial, including inactivity, systemic inflammation, tissue hypoxia and oxidative stress among others. These systemic effects add to the respiratory morbidity produced by the underlying pulmonary disease and should be considered in the clinical assessment as well as the treatment of affected patients.

Cardiovascular Diseases↗

PubMed2006

[Physiologic particularities of muscle impairments in the patient with COPD].

Patients with chronic obstructive pulmonary disease (COPD) frequently have skeletal muscle dysfunction, of either respiratory muscles or those located of the limbs. This dysfunction may appear even at relatively early stages and it conditions symptoms and patient's quality of life. In the case of respiratory muscles, factors that seem to determine muscle dysfunction are, particularly, changes in thorax configuration and an unbalance between decreased energy availability and increased energy demands by the muscle. However, respiratory muscles show signs of structural and metabolic adaptation to this situation, partially compensating the above-mentioned deleterious effects. However, at muscles of the limbs, particularly of the lower limbs, dysfunction seems to be essentially due to deconditioning by physical activity reduction. Structural changes in these muscles are involutional in nature. At both respiratory and peripheral muscles, other factors such as nutritional impairments, inflammation, oxidative stress, some drugs, and the presence of comorbidity seem to play a relevant role. All of them will condition both dysfunction and structural changes, which will be heterogeneous for the different muscle groups in each patient.

Humans↗

PubMed2006

Changes in skeletal muscle protein metabolism and myosin heavy chain isoform messenger ribonucleic acid abundance after treatment of hyperthyroidism.

BACKGROUND: Hyperthyroidism causes a hypermetabolic state and skeletal muscle dysfunction, but the underlying mechanism remains incompletely defined. OBJECTIVE: The objective of the study was to determine whether treatment of hyperthyroidism causes changes in amino acid fluxes, synthesis rates of muscle proteins, and expression of muscle myosin heavy chain (MHC) that may impact skeletal muscle function and metabolic rate. METHODS: Eight hyperthyroid patients were studied (TSH 0.008 +/- 0.001 mU/liter) before treatment and at least 9 months after correction of hyperthyroidism (TSH 2.3 +/- 0.4) (P < 0.03). Fluxes of leucine and phenylalanine as well as muscle protein synthesis rates were measured using L[1,2 13C] leucine and L(15N) phenylalanine as tracers. mRNA levels of selected genes were measured in muscle biopsy samples. RESULTS: Treatment decreased resting metabolic rate that paralleled changes in fluxes of leucine and phenylalanine accompanied by improved muscle strength and mass. Synthesis rates of mixed muscle proteins (P = 0.01), sarcoplasmic (P = 0.04), and mitochondrial (P = 0.08) proteins decreased, whereas MHC synthesis was unchanged. Selective increases in mRNA abundance of muscle MHC1 isoform (P = 0.04) and decrease of MHCIIA (P = 0.007) and MHCIIx (P = 024) were observed. Muscle mitochondrial oxidative enzymes and mRNA levels of mitochondrial proteins were unchanged, but uncoupling protein2 and uncoupling protein3 mRNA levels (P = 0.02) decreased. CONCLUSION: Increased amino acid flux, mixed muscle protein synthesis, and synthesis of sarcoplasmic proteins are consistent with the hypermetabolic state in hyperthyroidism. After treatment, MHC synthesis rates were unchanged, but mRNA levels of isoforms of MHC found in slow-twitch and fast-twitch fibers increased and decreased, respectively. These results offer a mechanistic explanation for posttreatment improvement in muscle functions in hyperthyroidism.

Adrenergic beta-Antagonists↗

PubMed2024

Age-induced changes in skeletal muscle mitochondrial DNA synthesis, quantity, and quality in genetically unique rats.

Mitochondrial genomic integrity is a key element of physiological processes and health. Changes in the half-life of the mitochondrial genome are implicated in the generation and accumulation of age-induced mitochondrial DNA (mtDNA) mutations, which are implicated in skeletal muscle aging and sarcopenia. There are conflicting data on the half-life of mtDNA, and there is limited information on how aging affects half-life in skeletal muscle. We hypothesized that skeletal muscle mtDNA synthesis rates would decrease with age in both female and male rats concomitant with changes in mtDNA integrity reflected in mtDNA copy number and mutation frequency. We measured mitochondrial genome half-life using stable isotope labeling over a period of 14 days and assessed mtDNA copy number and deletion mutation frequency using digital PCR in the quadriceps muscle of 9-month-old and 26-month-old male and female OKC-HET rats. We found a significant age-related increase in mtDNA half-life, from 132 days at 9 months to 216 days at 26 months of age in OKC-HET quadriceps. Concomitant with the increase in mtDNA half-life, we found an age-related increase in mtDNA deletion mutation frequency in both male and female rats. Notably, 26-month-old female rats had a lower mutation frequency than male rats, and there were no changes in mtDNA copy number with sex, age, or mitochondrial genotype. These data reveal several key findings: (1) mtDNA turnover in rat skeletal muscle decreases with age, (2) mtDNA half-lives in skeletal muscle are approximately an order of magnitude longer than what is reported for other tissues, and (3) muscle mtDNA turnover differs significantly from the turnover of other mitochondrial macromolecules including components of the mitochondrial nucleoid. These findings provide insight into the factors driving age-induced mtDNA mutation accumulation, which contribute to losses of mitochondrial genomic integrity and may play a role in skeletal muscle dysfunction.

Animals↗

PubMed2005

Insulin-like growth factor-1 and muscle wasting in chronic heart failure.

Chronic heart failure is a clinical syndrome of cardiac origin, which affects various organ systems. It is associated with metabolic abnormalities leading to a catabolic syndrome in advanced stages of the disease. As in several other chronic diseases, skeletal muscle dysfunction and structural muscle abnormalities result in progressive muscle wasting and cachexia. These changes are accompanied by increased expression of proinflammatory cytokines, increased rate of apoptosis and activation of the proteolytic ubiquitin-proteasome pathway. Further, reduced expression of the local anabolic insulin-like growth factor-1 has been demonstrated in skeletal muscle of animals and patients with chronic heart failure. This suppression occurs in the presence of normal serum levels of insulin-like growth factor-1. In addition to catabolic effects of proinflammatory cytokines, these recent findings are consistent with reduced anabolism involving altered local insulin-like growth factor-1 levels in progressive muscle atrophy in chronic heart failure. This article describes local effects of insulin-like growth factor-1 on skeletal muscle function and morphology, its role in stem cell recruitment and muscle regeneration as well as its regulation in circumstances of muscle inflammation and wasting.

Apoptosis↗

PubMed1996

Interaction of lipopolysaccharide endotoxin produced from Escherichia coli with D-tubocurarine at the nicotinic2 receptor and adenosine 3':5' cyclic monophosphate during physiological contraction in skeletal muscle.

In this report the murine model of endotoxicosis was used to evaluate hyposensitivity to the neuromuscular relaxant D-tubocurarine (dTC). This hyposensitivity was expressed in terms of a decreased potency to dTC. A rightward shift of the dose-response curve due to endotoxin was observed. Mice were subjected to cumulative intraperitoneal doses of Escherichia coli endotoxin over a 2-wk period. The interaction between endotoxin and dTC was examined during an acute (1 wk) and chronic (2 wk) period of endotoxicosis. Muscle twitch analyses were performed and samples of gastrocnemius muscle were assayed for adenosine 3':5' cyclic monophosphate (cAMP) by [125I]radioimmunoassay. A parallel shift in the dose-response curve occurred in the endotoxin group subjected to doses corresponding to one-third the dose evoking 50% lethality for 2 wk. Both skeletal muscle tension and cAMP levels decreased as cumulative endotoxin doses increased. A relationship between decreasing cAMP levels and increasing dTC and effective dose required to achieve 50% muscle paralysis values was thought to be evoked by the agonistic activity of E. coli endotoxin leading to desensitizing of adenylate cyclase. The perturbations of the classical second messenger cAMP system by endotoxin may be responsible for skeletal muscle dysfunction observed in immunocompromised patients.

Animals↗

PubMed2005

Enhancing calstabin binding to ryanodine receptors improves cardiac and skeletal muscle function in heart failure.

Abnormalities in intracellular calcium release and reuptake are responsible for decreased contractility in heart failure (HF). We have previously shown that cardiac ryanodine receptors (RyRs) are protein kinase A-hyperphosphorylated and depleted of the regulatory subunit calstabin-2 in HF. Moreover, similar alterations in skeletal muscle RyR have been linked to increased fatigability in HF. To determine whether restoration of calstabin binding to RyR may ameliorate cardiac and skeletal muscle dysfunction in HF, we treated WT and calstabin-2-/- mice subjected to myocardial infarction (MI) with JTV519. JTV519, a 1,4-benzothiazepine, is a member of a class of drugs known as calcium channel stabilizers, previously shown to increase calstabin binding to RyR. Echocardiography at 21 days after MI demonstrated a significant increase in ejection fraction in WT mice treated with JTV519 (45.8 +/- 5.1%) compared with placebo (31.1 +/- 3.1%; P < 0.05). Coimmunoprecipitation experiments revealed increased amounts of calstabin-2 bound to the RyR2 channel in JTV519-treated WT mice. However, JTV519 did not show any of these beneficial effects in calstabin-2-/- mice with MI. Additionally, JTV519 improved skeletal muscle fatigue in WT and calstabin-2-/- mice with HF by increasing the binding of calstabin-1 to RyR1. The observation that treatment with JTV519 improved cardiac function in WT but not calstabin-2-/- mice indicates that calstabin-2 binding to RyR2 is required for the beneficial effects in failing hearts. We conclude that JTV519 may provide a specific way to treat the cardiac and skeletal muscle myopathy in HF by increasing calstabin binding to RyR.

Analysis of Variance↗

PubMed2005

Oxidative stress and nitric oxide synthase in skeletal muscles of rats with post-infarction, compensated chronic heart failure.

AIM: Involvement of oxidative stress and nitric oxide synthase (NOS) isoforms in skeletal muscle cellular adaptations to chronic heart failure (CHF) is controversial, and possible muscle fibre-type heterogeneity in the oxidative stress and NOS responses to CHF have not been examined. Consequently, we hypothesized that the changes in determinants of elevated oxidative and nitrosylative stress associated with CHF would occur in skeletal muscle and would be similar in predominantly type I slow twitch muscle (soleus) and type II fast twitch muscle (plantaris) of rats. METHODS: The purpose of this study was to measure NOS isoforms (endothelial, inducible and neuronal NOS) and antioxidant enzymes (SOD-1, SOD-2, catalase) by protein immunoblot as well as markers of oxidative stress by biochemical assays in soleus and plantaris muscle sections of the rat hind limb. This was performed for control and post-infarction, compensated CHF rats. RESULTS: Twelve weeks after coronary artery ligation-induced moderate CHF, soleus exhibited decreased SOD-1, SOD-2 and eNOS, but increased iNOS and nNOS isoforms assessed by immunoblot. This was associated with elevated lipid and DNA oxidative damage assessed by biochemical assays. In contrast, plantaris muscle exhibited no changes in antioxidant enzymes or NOS isoforms, and had lower lipid and DNA oxidative damage. CONCLUSION: These observations suggest a heretofore unreported muscle fibre-type-specific response of oxidative stress and NOS isoforms to CHF is of importance in understanding the cellular mechanisms of skeletal muscle dysfunction in CHF.

Adaptation, Physiological↗

PubMed1996

Fibrosis and intercellular collagen connections from four weeks of muscle strains.

The effect of repeated cycles of muscle strain was studied in the soleus muscle of female rats. Muscle strains were repeated 3X/week for 1 month using two different strain protocols. Striking changes, including marked variability in fiber size, evidence of degradation and regeneration, and an expanded extracellular matrix were pronounced in the fast-stretched muscles but not in the slow-stretched muscles. However, the slow-stretched muscles did contain struts of connective tissue joining adjacent myofibers. Therefore, repeated muscle strains at high strain rates produced morphological changes similar to many myopathies, including fibrosis, whereas adaptation occurred in response to the same number of strains at slow strain rates. Such diverse tissue responses have relevance to the understanding of the mechanisms of skeletal muscle dysfunction in cumulative trauma disorders and in the design of preventive actions and treatments.

Animals↗

PubMed2004

Effect of acute hyperoxia during exercise on quadriceps electrical activity in active COPD patients.

AIMS: This study investigated whether acute hyperoxia improves electrical muscle activity in active chronic obstructive pulmonary disease (COPD) patients with mild hypoxemia (rest PaO(2) = 9.1 +/- 0.4 kPa). METHODS: Two identical incremental exercise tests were performed by nine patients while breathing either air or 30% oxygen. Pulmonary gas exchanges, venous concentrations of lactate and pyruvate, and the electromyographic signal of the quadriceps muscle (vastus lateralis and vastus medialis) were sampled each minute. RESULTS: Peak working capacity increased significantly in hyperoxia (94.4 +/- 5.2W) compared with normoxia (85.4 +/- 5.8W, P < 0.01). During hyperoxic exercise and for a given work load, oxygen uptake was increased (P < 0.001) and ventilation decreased (P < 0.05). Lactate concentration was significantly decreased (P < 0.01) at isowork level and during recovery (respectively - 26% and at least - 15%). In the quadriceps muscle, M-wave amplitude (P < 0.05), root mean square (P < 0.01) and root mean square/oxygen uptake ratio (P < 0.001) were significantly increased during hyperoxic exercise compared with room air. Although median frequency values did not differ between conditions, the median frequency was significantly decreased for higher exercise intensity in hyperoxic condition. These modifications reflected better aerobic metabolism, later emergence of muscle fatigue, and greater muscle excitability and activation for the same level of exercise under hyperoxic condition. CONCLUSION: These data suggest that the acute addition of oxygen in active COPD patients improves their muscle electrical activity during dynamic exercise. Hypoxemia-induced skeletal muscle dysfunction most probably acts through mechanisms based on oxygen availability.

Acute Disease↗

PubMed2006

Scaling skeletal muscle function to mass in patients with moderate-to-severe COPD.

Skeletal muscle performance and muscle mass are commonly reduced in patients with advanced chronic obstructive pulmonary disease (COPD). It is currently unclear, however, whether negative changes in muscle structure and function are proportionately related to each other in these patients. In a cross-sectional study, 39 patients (post-bronchodilator FEV1=49.7+/-15.5% pred) and 17 controls were submitted to knee isokinetic dynamometry [peak torque (PT), isometric strength (IS), and total work (TW)] and dual energy X-ray absorptiometry for the evaluation of leg muscle mass (LMM). Muscle function (F) was normalised for LMM by using ratio standards (F.LMM-1), power function ratios (F.LMM-b, where b is usually not equal 1), and analysis of covariance (ANCOVA). Patients with COPD presented with reduced PT, IS, TW, and LMM as compared to controls: there were significant linear correlations among these variables in both groups (P<0.05). Ratio standards of PT.LMM-1 and TW.LMM-1 were, on average, 14% lower in patients than controls (P<0.01). The coefficients for allometric correction of IS and TW were significantly higher in patients as compared to controls (0.975 vs. 0.603 and 1.471 vs. 0.824, respectively, P<0.05), i.e. more LMM was needed to generate a given functional output in patients than normal subjects. In addition, adjusted means of muscle function variables by ANCOVA were 11-18% lower for patients than controls with LMM as the covariate (P<0.05). We conclude that factors other than simple atrophy (i.e. mass-independent mechanisms) might play a role in explaining the COPD-related skeletal muscle dysfunction.

Absorptiometry, Photon↗

PubMed1998

Skeletal muscle abnormalities in patients with COPD: contribution to exercise intolerance.

Exercise intolerance in COPD patients appears to be in part because of skeletal muscle dysfunction. Studies using biopsy techniques and magnetic resonance spectroscopy have demonstrated changes in enzyme activities and metabolism that indicate reduced oxidative capacity in the peripheral muscles of these patients. Regarding the respiratory muscles, the biochemical characteristics have been studied in only a few works and the results seem to depend on the specific muscle group studied. Several factors, such as hypoxemia, nutritional status, pharmacological treatment, and deconditioning, may be responsible for these skeletal muscle abnormalities. This brief review describes the changes in peripheral and respiratory muscles in COPD patients based on data from the literature. The causes of these muscle abnormalities, their contribution to exercise intolerance, and the effects of training are then discussed. We conclude with suggested directions for future investigation using contemporary noninvasive technologies.

Energy Metabolism↗