Vastus Lateralis Muscle Of Patients Research Articles

Mitochondrial respiration in peripheral arterial disease depends on stage severity.

Peripheral arterial disease (PAD) is an increasing cause of morbidity and its severity is graded based on clinical manifestation. To investigate the influence of the different stages on myopathy of ischemic muscle we analysed severity-dependent effects of mitochondrial respiration in PAD. Eighteen patients with severe PAD, defined as chronic limb-threatening ischemia, 47 patients with intermittent claudication (IC) and 22 non-ischemic controls were analysed. High-resolution respirometry (HRR) was performed on muscle biopsies of gastrocnemius and vastus lateralis muscle of patients in different PAD stages to investigate different respiratory states. Results from HRR are given as median and interquartile range and were normalized to citrate synthase activity (CSA), a marker for mitochondrial content. In order to account for inter-individual differences between patients and controls, we calculated the ratio of O₂-flux in gastrocnemius muscle over vastus muscle ('GV ratio'). CSA of the gastrocnemius muscle as a proxy for mitochondrial content was significantly lower in critical ischemia compared to controls. Mitochondrial respiration normalized to CSA was higher in IC compared to controls. Likewise, the GV ratio was significantly higher in IC compared to control. Mitochondrial respiration and CSA of PAD patients showed stage-dependent modifications with greater changes in the mild PAD stage group (IC).

Endoplasmic reticulum stress and unfolded protein response profile in quadriceps of sarcopenic patients with respiratory diseases.

Impaired muscle strength and mass (sarcopenia) are common in patients with respiratory cachexia, namely chronic obstructive pulmonary disease (COPD) and in lung cancer (LC)-cachexia. Misfolded/unfolded proteins in endoplasmic reticulum (ER) induce the compensatory unfolded protein response (UPR). Expression of ER stress and UPR markers may be differentially upregulated in vastus lateralis (VL) of patients with respiratory sarcopenia associated with either a chronic condition (COPD) or subacute (LC)-cachexia. In VL specimens from 40 COPD patients (n = 21, sarcopenic, fat-free mass index [FFMI] 16 kg/m2 and n = 19, nonsarcopenic, FFMI 18 kg/m2 ), 13 patients with LC-cachexia (FFMI 17 kg/m2 ), and 19 healthy controls (FFMI 19 kg/m 2 ), expression markers of ER stress, UPR (protein kinase-like ER kinase [PERK], activating transcription factor [ATF] 6, and inositol-requiring enzyme [IRE] 1-α), oxidative stress, autophagy, proteolysis, and apoptosis (reverse transcription polymerase chain reaction and immunoblotting), and fiber atrophy (histology) were assessed. Atrophy and muscle wasting and weakness were seen in both groups of sarcopenic patients. Compared to healthy controls, in muscles of LC-cachexia patients, expression of ER stress markers and UPR (three arms) was significantly upregulated, while in sarcopenic COPD, expression of a few ER stress markers and IRE1-α arm was upregulated. ER stress and an exaggerated UPR were observed in the VL muscle of patients with respiratory sarcopenia. The three branches of UPR were similarly upregulated in muscles of cancer cachectic patients, whereas in sarcopenic COPD patients, only IRE1 was upregulated. The differential profile of muscle UPR in chronic and subacute respiratory conditions offers a niche for the design of specific novel therapeutic approaches.

Prediction of key genes and miRNAs responsible for loss of muscle force in patients during an acute exacerbation of chronic obstructive pulmonary disease.

The present study aimed to identify genes and microRNAs (miRNAs or miRs) that were abnormally expressed in the vastus lateralis muscle of patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD). The gene expression profile of GSE10828 was downloaded from the Gene Expression Omnibus database, and this dataset was comprised of 4 samples from patients with AECOPD and 5 samples from patients with stable COPD. Differentially expressed genes (DEGs) were screened using the Limma package in R. A protein-protein interaction (PPI) network of DEGs was built based on the STRING database. Module analysis of the PPI network was performed using the ClusterONE plugin and functional analysis of DEGs was conducted using DAVID. Additionally, key miRNAs were enriched using gene set enrichment analysis (GSEA) software and a miR-gene regulatory network was constructed using Cytoscape software. In total, 166 up- and 129 downregulated DEGs associated with muscle weakness in AECOPD were screened. Among them, NCL, GOT1, TMOD1, TSPO, SOD2, NCL and PA2G4 were observed in the modules consisting of upregulated or downregulated genes. The upregulated DEGs in modules (including KLF6 and XRCC5) were enriched in GO terms associated with immune system development, whereas the downregulated DEGs were enriched in GO terms associated with cell death and muscle contraction. Additionally, 39 key AECOPD-related miRNAs were also predicted, including miR-1, miR-9 and miR-23a, miR-16 and miR-15a. In conclusion, DEGs (NCL, GOT1, SOD2, KLF6, XRCC5, TSPO and TMOD1) and miRNAs (such as miR-1, miR-9 and miR-23a) may be associated with the loss of muscle force in patients during an acute exacerbation of COPD which also may act as therapeutic targets in the treatment of AECOPD.

Effects of 15weeks of resistance exercise on pro-inflammatory cytokine levels in the vastus lateralis muscle of patients with fibromyalgia.

BackgroundThis study aimed at investigating the effect of a resistance exercise intervention on the interstitial muscle levels of pro-inflammatory cytokines in fibromyalgia (FMS) and healthy controls (CON).MethodsTwenty-four female patients with FMS (54 ± 8 years) and 27 female CON (54 ± 9 years) were subjected to intramuscular microdialysis of the most painful vastus lateralis muscle before and after 15 weeks of progressive resistance exercise twice per week. Baseline dialysates were sampled in the resting muscle 140 min after insertion of the microdialysis catheter. The participants then performed repetitive dynamic contractions (knee extension) for 20 min, followed by 60 min rest. Pain intensity was assessed with a 0–100 mm visual analogue scale (VAS), and fatigue was assessed with Borg’s RPE throughout microdialysis. Dialysates were sampled every 20 min and analyzed with Luminex for interleukin (IL)-1β, tumor necrosis factor (TNF) alpha, IL-6, and IL-8.ResultsAt both sessions and for both groups the dynamic contractions increased pain (P < 0.012) and fatigue (P < 0.001). The levels of TNF were lower in the FMS group than the CON group at both sessions (P < 0.05), but none of the other cytokines differed between the groups. IL-6 and IL-8 increased after the dynamic contractions in both groups (P < 0.010), while TNF increased only in CON (P < 0.05) and IL-1β did not change. Overall pain intensity was reduced after the 15 weeks of resistance exercise in FMS (P < 0.05), but there was no changes in fatigue or cytokine levels.ConclusionProgressive resistance exercise for 15 weeks did not affect the interstitial levels of IL-1β, TNF, IL-6, and IL-8 in the vastus lateralis muscle of FMS patients or CON.Trial registrationClinicaltrials.gov NCT01226784, registered 21 October 2010.

Regenerative defect in vastus lateralis muscle of patients with chronic obstructive pulmonary disease.

BackgroundImpaired skeletal muscle regeneration could contribute to the progression of muscle atrophy in patients with chronic obstructive pulmonary disease (COPD).MethodsSatellite cells and myogenesis-related proteins were compared between healthy subjects and patients with COPD, with or without muscle atrophy. Satellite cells were isolated and cultured to assess their proliferative and differentiation aptitudes.ResultsAlthough satellite cell numbers in muscle samples were similar between groups, the proportion of muscle fibers with central nuclei was increased in COPD. In muscle homogenates, increased expression of MyoD and decreased expression of myogenin and MRF4 were observed in COPD. In cultured satellite cells of patients with COPD, increased protein content was observed for Pax7, Myf5 (proliferation phase) and myogenin (differentiation phase) while myosin heavy chain protein content was significantly lower during differentiation.ConclusionIn COPD, the number of central nuclei was increased in muscle fibers suggesting a greater number of attempts to regenerate muscle tissue than in healthy subjects. Myogenesis signaling was also altered in muscle homogenates in patients with COPD and there was a profound reduction in the differentiation potential in this population as indicated by a reduced ability to incorporate myosin heavy chain into newly formed myotubes. Collectively, these results indicate that skeletal muscle regenerative capacity termination is impaired in COPD and could contribute to the progression of muscle atrophy progression in this population.

The architecture of the ipsilateral quadriceps two years after successful anterior cruciate ligament reconstruction with bone–patellar tendon–bone autograft

BackgroundWe undertook a cross-sectional study to evaluate the pennation angle and muscle thickness of the vastus lateralis muscle in patients undergoing unilateral anterior cruciate ligament (ACL) reconstruction with bone–patellar tendon–bone autograft, and compared these values with the contralateral non-operated limb. MethodsTwenty three consecutive athletic males who underwent ACL reconstruction using the central third of the patellar ligament were evaluated at 25.9±1.5months. The International Knee Documentation Committee (IKDC) score was administered, and angles of pennation and muscle thickness were measured by ultrasonography. ResultsThere was no significant difference in the pennation angle of the operated leg comparing to the contralateral leg (12.5°±1.81° in the operated leg; 13.25°±2.40° after the test; p=0.117). Quadriceps thickness in the operated leg was significantly decreased in all subjects compared to the contralateral leg (28.4±5.3mm in the operated leg; 32.7±4.85mm in the contralateral leg; p=0.007). ConclusionsTwo years after surgery, there is no difference in pennation angle of the vastus lateralis when compared to the contralateral side in patients undergoing unilateral ACL reconstruction with bone–patellar tendon–bone autograft. There is a significant difference in quadriceps muscle thickness, which was less in the operated side on the operated side in all patients. Further studies are required to study the influence of muscle architecture on clinical outcome after ACL reconstruction surgery, and whether there are differences associated with the use of different grafts. Level of evidenceCase–control study; level IV.

Reference values for vastus lateralis fiber type proportions and fiber size

to the editor: Recently Gouzi et al. ([3][1]) reported reference values and lower limits of normal (LLNs) for vastus lateralis fiber size and type in healthy subjects over 40 years old. LLNs are useful to distinguish pathology from physiological variation in high-risk patient groups such as chronic

Mechanisms of striated muscle dysfunction during acute exacerbations of COPD

During acute exacerbations of chronic obstructive pulmonary disease (COPD), limb and respiratory muscle dysfunction develops rapidly and functional recovery is partial and slow. The mechanisms leading to this muscle dysfunction are not yet fully established. However, recent evidence has shown that several pathways involved in muscle catabolism, apoptosis, and oxidative stress are activated in the vastus lateralis muscle of patients during acute exacerbations of COPD, while those implicated in mitochondrial function are downregulated. These pathways may be targeted in different ways by factors related to exacerbations. These factors include enhanced systemic inflammation, oxidative stress, impaired energy balance, hypoxia, hypercapnia and acidosis, corticosteroid treatment, and physical inactivity. Data on the respiratory muscles are limited, but these muscles are undoubtedly overloaded during exacerbations. While they are also subjected to the same systemic elements as the limb muscles (except for inactivity), they also face a specific mechanical disadvantage caused by changes in lung volume during exacerbation. The latter will affect the ability to generate force by the foreshortening of the muscle (especially for the diaphragm), but also by altering rib orientation and motion (especially for the parasternal intercostals and the external intercostals). Because acute exacerbations of COPD are associated with an increase in both prevalence and severity of generalized muscle dysfunction, and both remain present even during recovery, early interventions to minimize muscle dysfunction during exacerbation are warranted. Although rehabilitation may be promising, other therapeutic strategies such as counterbalancing the adverse effects of exacerbations on skeletal muscle pathways may also be used.

Increased inflammatory cytokine expression in the vastus lateralis of patients with knee osteoarthritis

Increased inflammation and pain are inseparable parts of knee osteoarthritis (OA) that may lead to disuse of the affected limb. The aim of this study was to examine the effects of knee OA on inflammation- and atrophy-related genes and proteins in the vastus lateralis muscle of patients with knee OA. Nineteen patients with knee OA and 14 asymptomatic control subjects matched for age and body mass index underwent strength measurements and a muscle biopsy. Muscle was analyzed for the total cellular protein of inflammatory kinases (p65 NF-κB, JNK1/2, STAT-3, and suppressor of cytokine signaling 3 [SOCS-3]) and inflammatory intracellular molecules (interleukin-6 [IL-6], IL-8, monocyte chemoattractant protein 1 [MCP-1], tumor necrosis factor α [TNFα], IL-1β, and atrogin-1). Knee OA resulted in greater levels of IL-6 protein (34%; P = 0.002). The levels of inflammatory kinases, including STAT-3 (187%; P = 0.002), p65 NF-κB (156%; P = 0.002), and JNK1 (179%; P = 0.027), were also elevated. Furthermore, elevated expression of gene transcripts encoding MCP-1 (28%; P = 0.023), TNFα (85%; P < 0.001), and SOCS-3 (38%; P = 0.055) was observed in patients with knee OA compared with control subjects. Patients with knee OA had reduced muscle strength compared with control subjects (mean ± SEM 84.7 ± 8.7 versus 143.1 ± 20.8 Nm; P = 0.005). Negative correlations were observed between muscle strength and MCP-1 protein abundance (r = -0.37 [P = 0.042]) and the gene expression of TNFα and atrogin-1 messenger RNA (r = -0.46 [P = 0.012] and r = -0.36 [P = 0.040], respectively). Gene expression and the protein abundance of numerous muscle markers of inflammation and atrophy were elevated in patients with knee OA, and the increase in muscle inflammation was associated with a reduction in muscle strength. Given the role inflammation markers may play in muscle strength and atrophy, further studies are needed to investigate the effect of exercise intervention on skeletal muscle inflammation.

Altered mitochondrial regulation in quadriceps muscles of patients with COPD

Evidence exists for locomotor muscle impairment in patients with chronic obstructive pulmonary disease (COPD), including fiber type alterations and reduced mitochondrial oxidative capacity. In this study high-resolution respirometry was used to quantify oxygen flux in permeabilized fibres from biopsies of the vastus lateralis muscle in patients with COPD and compared to healthy control subjects. The main findings of this study were that (i) routine state 2 respiration was higher in COPD; (ii) state 3 respiration in the presence of ADP was similar in both groups with substrate supply of electrons to complex I (COPD 38·28 ± 3·58 versus control 42·85 ± 3·10 pmol s(-1) mg tissue(-1) ), but O(2) flux with addition of succinate was lower in COPD patients (COPD 63·72 ± 6·33 versus control 95·73 ± 6·53 pmol s(-1) mg tissue(-1) ); (iii) excess capacity of cytochrome c oxidase in COPD patients was only ~50% that of control subjects. These results indicate that quadriceps muscle mitochondrial function is altered in patients with COPD. The regulatory mechanisms underlying these functional abnormalities remain to be uncovered.

Gene Expression Profiling in Vastus Lateralis Muscle During an Acute Exacerbation of COPD

Background/aims: The molecular mechanisms leading to loss in muscle force during an acute exacerbation in COPD patients are unknown. A cross-sectional study was designed to compare the gene expression profile of the vastus lateralis muscle in patients with an acute COPD exacerbation and in stable COPD patients. Methods: Muscle biopsies were taken in 9 COPD patients with an exacerbation on day 4 of hospitalization and in 15 stable COPD patients. Micro-array was performed on an UniSet Human 20K Bioarray. Results: Gene Ontology and Gene Set Enrichment Analysis of the microarray data revealed enrichment of 1) the ubiquitin-dependent protein catabolism, the induction of apoptosis and anti-apoptosis and the response to reactive oxygen species in the upregulated transcripts, and 2) the aspartate catabolism and the mitochondrial respiratory chain in the downregulated transcripts. Real Time PCR data confirmed 1) increased expression of MuRF1 and MAFbx, markers of the ubiquitin dependent catabolism pathway, and 2) decreased expression levels of COX6C, a marker of mitochondrial respiration. Conclusions: The present study suggests that multiple pathways leading to muscle atrophy and mitochondrial dysfunction are altered in the muscle during an acute exacerbation. Strategies limiting the loss of muscle function during an acute exacerbation need to be developed.

Human genome comparison of paretic and nonparetic vastus lateralis muscle in patients with hemiparetic stroke

Hemiparetic stroke leads to major skeletal muscle abnormalities, as illustrated by paretic leg atrophy, weakness, and spasticity. Furthermore, the hemiparetic limb muscle shifts to a fast-twitch muscle fiber phenotype with anaerobic metabolism. This study investigated whether skeletal muscle genes were altered in chronic hemiparetic stroke. The nonparetic leg muscle served as an internal control. We used Affymetrix microarray analysis to survey gene expression differences between paretic and nonparetic vastus lateralis muscle punch biopsies from 10 subjects with chronic hemiparetic stroke. Stroke latency was greater than 6 months. We found that 116 genes were significantly altered between the paretic and non paretic vastus lateralis muscles. These gene differences were consistent with reported differences after stroke in areas such as injury and inflammation markers, the myosin heavy chain profile, and high prevalence of impaired glucose tolerance and type 2 diabetes. Furthermore, while many other families of genes were altered, the gene families with the most genes altered included inflammation, cell cycle regulation, signal transduction, metabolism, and muscle contractile protein genes. This study is an early step toward identification of specific gene regulatory pathways that might lead to these differences, propagate disability, and increase vascular disease risk.

Reduced mitochondrial density in the vastus lateralis muscle of patients with COPD

Skeletal muscle dysfunction is a well-recognised hallmark of chronic obstructive pulmonary disease (COPD) leading to exercise intolerance. The vastus lateralis of COPD patients is characterised by reduced mitochondrial enzyme activity; however, this is not the case in the tibialis anterior. It is, however, unclear whether the compromised oxidative capacity in the vastus is due to reduced mitochondrial volume density. Muscle biopsies were obtained from the vastus lateralis of six COPD patients and four healthy age-matched controls, and from the tibialis anterior of another six COPD patients and six controls. Mitochondrial number, fractional area and morphometry, as well as Z-line width (as a surrogate marker of fibre type), were analysed using transmission electron microscopy. Mitochondrial number (0.34 versus 0.63 n.microm(-2)) and fractional area (1.95 versus 4.25%) were reduced in the vastus of COPD patients compared with controls. Despite a reduced mitochondrial number (0.65 versus 0.88 n.microm(-2)), the mitochondrial fractional area was maintained in the tibialis of COPD patients compared with controls. It can be concluded that the reduced mitochondrial fractional area is likely to contribute to the decreased oxidative capacity in the vastus of chronic obstructive pulmonary disease patients, whereas the maintained mitochondrial fractional area in the tibialis may explain the normal oxidative capacity.

Regulation of muscle cathepsin B proteolytic activity in protein-depleted patients with chronic diseases

Background & aims: The lysosomal cathepsin system contributes to degrading cellular skeletal muscle proteins in many catabolic diseases. We have assessed the relationships between cathepsin B mRNA levels and the enzyme activity for this protease in the skeletal muscle of acutely ill patients with severe trauma ( n=7) and in patients with a variety of chronic disease states (hemodialysis, n=3; nervous anorexia, n=1; type 2 diabetes, n=2; prolonged immobilization, n=1). Methods: Muscle biopsies were taken from the vastus lateralis muscle in patients and controls to assess tissue levels of cathepsin B mRNA by competitive–quantitative polymerase chain reaction, cathepsin B proteolytic activity and myofibrillar protein content as alkali-soluble protein to DNA ratio (ASP/DNA). In the trauma patients, muscle protein loss was assessed by the arteriovenous balance technique as rate of phenylalanine release from leg muscle. Results: The acute trauma patients exhibited a significant net phenylalanine release from leg muscle (33±4 nmol phenylalanine/min/100 ml leg volume) despite a continuous nutritional support. The muscle ASP/DNA ratio was lower ( P<0.05) in the patients with chronic diseases (383±33) than in groups of healthy controls (554±41) or of uncomplicated, moderately obese subjects (525±26). Cathepsin B mRNA levels were 6–10 times greater ( P<0.05) in the patients with acute trauma or chronic catabolic diseases than in the healthy subjects. Cathepsin B enzymatic activity were 2–3 times greater ( P<0.05) in the chronic and acute patients than in the group of uncomplicated, moderately obese subjects. Regression analysis between cathepsin B mRNA and cathepsin B enzymatic activity indicates a significant direct correlation ( r=0.84; P<0.05) in the chronic catabolic conditions, but not in the acute trauma patients ( r=−0.05). Conclusions:In skeletal muscle of patients with stable chronic catabolic diseases, cathepsin B activity is directly related to cathepsin B mRNA levels, suggesting that in these patients this enzyme could be mainly regulated at the level of gene transcription.

Lipofuscin accumulation in the vastus lateralis muscle in patients with chronic obstructive pulmonary disease.

Exercise-induced oxidative stress has been reported in patients with chronic obstructive pulmonary disease (COPD) and may play a role in muscle fatigue. It is speculated that oxidative stress during exercise originates from the contracting muscles but this has not been documented. The accumulation of lipofuscin, a marker of cellular oxidative damage, was evaluated in the vastus lateralis muscle in 17 patients with COPD and 10 healthy subjects of similar age. Each subject performed a stepwise exercise test up to maximal capacity during which oxygen uptake (VO(2)) was measured. Resting and peak exercise blood gases were also obtained. Two indices of lipofuscin accumulation were used: lipofuscin inclusions/fiber ratio (LI/F) and lipofuscin inclusions/fiber cross-sectional area ratio (LI/CSA). These ratios were also determined for each specific fiber-type. LI/F (P < 0.01) and LI/CSA (P < 0.01) were greater in COPD compared to healthy subjects. LI/F and LI/CSA for all fiber types were also greater in COPD (P < 0.001). In both groups, LI/F (P < 0.001) and LI/CSA (P < 0.01) were higher in type I than in type II fibers. LI/F and LI/CSA did not correlate significantly with resting PaO(2) and SaO(2), peak VO(2), and DeltaPaO(2) and DeltaSaO(2) during exercise (P > 0.05). Increased lipofuscin accumulation, a marker of oxidative damage, was found in the vastus lateralis muscle in patients with COPD compared to healthy subjects. Oxidative damage of muscle tissue may thus be involved in skeletal muscle dysfunction and wasting in COPD.

Specific oxidative alterations in vastus lateralis muscle of patients with the diagnosis of chronic fatigue syndrome

Chronic fatigue syndrome (CFS) is a poorly understood disease characterized by mental and physical fatigue, most often observed in young white females. Muscle pain at rest, exacerbated by exercise, is a common symptom. Although a specific defect in muscle metabolism has not been clearly defined, yet several studies report altered oxidative metabolism. In this study, we detected oxidative damage to DNA and lipids in muscle specimens of CFS patients as compared to age-matched controls, as well as increased activity of the antioxidant enzymes catalase, glutathione peroxidase, and transferase, and increases in total glutathione plasma levels. From these results we hypothesize that in CFS there is oxidative stress in muscle, which results in an increase in antioxidant defenses. Furthermore, in muscle membranes, fluidity and fatty acid composition are significantly different in specimens from CFS patients as compared to controls and to patients suffering from fibromyalgia. These data support an organic origin of CFS, in which muscle suffers oxidative damage.

Oxidative enzyme activities of the vastus lateralis muscle and the functional status in patients with COPD

BACKGROUNDEnzymatic and histochemical abnormalities of the peripheral muscle may play a role in exercise intolerance in patients with chronic obstructive pulmonary disease (COPD). A study was undertaken to measure the...

Altered expression of myosin heavy chain in the vastus lateralis muscle in patients with COPD.

This study was designed to further characterize peripheral skeletal muscle alterations in patients with chronic obstructive pulmonary disease (COPD) and to evaluate the possible relationship between myosin heavy chain (MyoHC) isoform expression and exercise tolerance in these individuals. MyoHC composition from biopsy of the vastus lateralis muscle was examined in 12 COPD patients (forced expiratory volume in one second (FEV1)=31+/-9% predicted, peak oxygen consumption (V'O2)=15+/-4 mL x kg(-1) x min(-1)) and 10 age-matched normal male subjects (peak V'O2=20+/-5 mL x kg(-1) x min(-1)). The proportion of MyoHC type I was smaller in COPD than in normals (27+/-17% versus 41+/-9%, p<0.05) with an increase in MyoHC type IIa (51+/-15% versus 39+/-9%, p<0.05) and the proportion of MyoHC type IIx being comparable between both groups. A significant relationship was found between peak V'Oo2 mL x kg(-1) x min(-1) and FEV1 % pred (r=0.91, p<0.0001) and the percentage of MyoHC type I (r=0.61, p=0.016). In stepwise multiple regression, only FEV1 % pred was found to be a significant determinant of peak V'O2 (p<0.0001). This variable explained 83% of the total variance of peak V'O2. In summary, this study showed considerable modifications in the phenotypic expression of the myosin heavy chain in the vastus lateralis muscle in patients with chronic obstructive pulmonary disease. An independent effect of myosin heavy chain expression on exercise capacity was not found. These results suggest that chronic inactivity and muscle deconditioning may not be the sole factors explaining peripheral muscle dysfunction in patients with chronic obstructive pulmonary disease.

EFFECT OF ACTIVITIES OF DAILY LIVING ON FIBER TYPE ATROPHY OF THE VASTUS LATERALIS MUSCLE IN PATIENTS WITH JOINT DISORDERS

The histopathologic study was performed to elucidate whether the fiber type atrophy of the vastus lateralis muscle in patients with hip or knee joint disorders is related to the activities of daily living (ADL) or habitual physical activity. Subjects were 16 female patients, 52.4 +/- 16.0 yr of age (mean +/- standard deviation), who underwent a vastus lateralis muscle biopsy at the time of total hip or knee replacement. At the time of referral to the rehabilitation center, the Functional Independence Measure (FIM) motor score and habitual physical activity at home were evaluated, and the diameter and atrophy factor for each muscle fiber type were measured on the histopathologic preparations of the biopsied muscles. The data were analyzed using ttest, one-way analysis of variance (ANOVA), Kruskal-Wallis one-way ANOVA, Spearman's correlation coefficient, and partial correlation coefficient. The patients showed muscle fiber atrophy and small angular fibers, and the atrophy factor was significantly increased in type 1, 2A, and 2B fibers, in that order (one-way ANOVA, P < 0.05). The patterns of the fiber type atrophy, consisting of normal, type 2B atrophy, type 2AB atrophy, and type 1 and 2AB atrophy, had a significant relationship with the fiber type atrophy (Spearman's correlation coefficient; rho = 0.834, P < 0.001). The FIM motor score showed a significant correlation with the atrophy factor (r = -0.584, P < 0.05), and significant differences were recognized among the four patterns of the fiber type atrophy (Kruskal-Wallis one-way ANOVA, P < 0.05). In conclusion, the muscle atrophy and patterns of the fiber type atrophy of the vastus lateralis muscle in patients with joint disorders may be related to changes in the FIM motor score.

Skeletal muscle damage during tourniquet-induced ischaemia. The initial step towards atrophy after orthopaedic surgery?

Muscle biopsies from the vastus lateralis muscle of patients who had undergone anterior cruciate ligament surgery under conditions of tourniquet-induced ischaemia were examined under the electron microscope at different periods of time up to 90 min of ischaemia. The severity of the alterations in ultrastructure appeared to depend on the period of ischaemia. The pathological changes consisted of accumulation of lysosomes, persistent intrafibre oedema, and some extracellular oedema. Signs of fibre necrosis were found after 90 min of ischaemia. Capillary ultrastructure was only altered with regard to some swelling of the endothelium and marked thickening of the basement membrane. It was concluded that skeletal muscle could be severely affected even during relatively short periods of ischaemia, which might facilitate the development of muscle atrophy during immobilization after orthopaedic surgery.