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To determine if there is muscle mass reduction in patients with ankylosing spondylitis (AS) compared to the general population and to examine the relationship between skeletal muscle mass, quality of life (QOL), strength, and mobility in patients with AS.
A total of 30 AS patients were enrolled in this study. Skeletal muscle mass was measured by bioelectrical impedance analysis, and it was expressed as the skeletal muscle mass index (SMI). QOL was assessed using the EuroQOL (EQ-5D). To measure mobility, the modified Schöber test and chest expansion test were used. To measure grip strength as a measure of muscle strength, we used the hydraulic hand dynamometer. Additionally, we divided the patients into two groups according to the degree of X-ray finding and compared the differences between the two groups.
There was no significant reduction in skeletal muscle mass in patients with AS compared to the general population. Also, there was no significant correlation between SMI and QOL. On the other hand, there was a significant positive correlation between SMI and mobility, and grip strength. A significant positive correlation was found between mobility and QOL. Additionally, there was a statistically significant difference in mobility between the two groups according to the degree of X-ray finding.
Maintaining muscle mass in AS patients may not be helpful for improving QOL, but it may contribute to achieving adequate mobility and strength.
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To evaluate sarcopenic indices in relation to respiratory muscle strength (RMS) in elderly people.
This study included 65 volunteers over the age of 60 (30 men and 35 women). The skeletal muscle mass index (SMI) was measured using bioimpedance analysis. Limb muscle function was assessed by handgrip strength (HGS), the Short Physical Performance Battery (SPPB), and gait speed. RMS was addressed by maximal inspiratory pressure (MIP) and maximal expiratory pressure (MEP) using a spirometer. The relationships between RMS and other sarcopenic indices were investigated using the Pearson correlation coefficients and multiple regression analysis adjusted for age, HGS, and SPPB.
Both MIP and MEP were positively correlated with SMI (r=0.451 and r=0.388, respectively, p<0.05 in both). HGS showed a significant correlation with both MIP and MEP (r=0.560, p<0.01 and r=0.393, p<0.05, respectively). There was no significant correlation between gait speed and either MIP or MEP. The SPPB was positively correlated with MEP (r=0.436, p<0.05). In the multiple regression analysis, MIP was significantly associated with HGS and SMI (p<0.001 and p<0.05, respectively), while MEP was related only with HGS (p<0.05).
This study suggests that respiratory muscles, especially inspiratory muscles, are significantly related to limb muscle strength and skeletal muscle mass. The clinical significance of MIP and MEP should be further investigated with prospective studies.
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To investigate the relationships between respiratory muscle strength and conventional sarcopenic indices such as skeletal muscle mass and limb muscle strength.
Eighty-nine young adult volunteers who had no history of medical or musculoskeletal disease were enrolled. Skeletal muscle mass was measured by bioelectrical impedance analysis and expressed as a skeletal muscle mass index (SMI). Upper and lower limb muscle strength were evaluated by hand grip strength (HGS) and isometric knee extensor muscle strength, respectively. Peak expiratory flow (PEF), maximal inspiratory pressure (MIP), and maximal expiratory pressure (MEP) were evaluated using a spirometer to demonstrate respiratory muscle strength. The relationships between respiratory muscle strength and sarcopenic indices were investigated using Pearson correlation coefficients and multiple linear regression analysis adjusted by age, height, and body mass index.
MIP showed positive correlations with SMI (r=0.457 in men, r=0.646 in women; both p<0.01). MIP also correlated with knee extensor strength (p<0.01 in both sexes) and HGS (p<0.05 in men, p<0.01 in women). However, PEF and MEP had no significant correlations with these sarcopenic variables. In multivariate regression analysis, MIP was the only independent factor related to SMI (p<0.01).
Among the respiratory muscle strength variables, MIP was the only value associated with skeletal muscle mass.
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To observe the changes in protein expression induced by botulinum toxin A (BoNT-A) injection and to characterize the molecular and cellular action of mechanisms of BoNT-A injection on skeletal muscles using proteomic elements as biomarkers.
BoNT-A was injected into left gastrocnemius muscles of 12 Sprague-Dawley rats (2 months of age) at a dosage of 5 units/kg body weight. For the controls same volume of normal saline was injected to right gastrocnemius muscle of each rat. Muscle samples were obtained at 4 time points (3 rats per time point): 3, 7, 14, and 56 day post-injection. To reveal the alterations in muscle protein, we performed 2-dimensional electrophoresis (2DE) and compared Botox group and normal saline group at each time point. Altered protein spots in 2DE were identified using matrix-assisted laser desorption/ionization-time-of-flight mass spectrometer (MALDI-TOF MS) proteomics analysis.
Compared with normal saline group, 46 protein spots showed changed protein expression. Twelve protein spots demonstrated increased volume and 34 protein spots demonstrated decreased volume. Among spots of decreased volume, 17 spots showed statistically significant differences. Thirty-eight identified proteins were associated with alterations in energy metabolism, muscle contractile function, transcription, translation, cell proliferation, and cellular stress response.
BoNT-A gives influences on muscle contractile function and energy metabolism directly or indirectly besides neurotoxic effects. Proteomic expression provides better understanding about the effect of BoNT-A on skeletal muscle.
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Method: Rectus femoris muscles of rats were divided into 4 groups according to conditioned ischemic stresses as followings: sham-operated control group; 2 hour ischemia group by clamping the proximal femoral vessel; ischemia- reperfusion group by 30 minutes of reperfusion following 2 hours of ischemia; ischemia-reperfusion-electrical nerve stimulation group in which current was applied at the femoral nerve during 30 min of reperfusion period to induce repetitive muscle contraction. Either genistein-5% dimethyl sulfoxide (DMSO) or DMSO was injected 2 hours before ischemic induction. NF-κB activities were analysed by electrophoretic mobility shift assay.
Results: NF-κB activities pretreated with DMSO were significantly increased in ischemia, ischemia-reperfusion and ischemia-reperfusion-electrical nerve stimulation group compared with those of control group and in ischemia- reperfusion-electrical nerve stimulation group compared with those of ischemia group. Muscle edema was increased in ischemia- reperfusion-electrical nerve stimulation group. But, NF-κB activities and muscle edema pretreated with genistein were attenuated in ischemia-reperfusion-electrical nerve stimulation group compared with those pretreated with DMSO alone.
Conclusion: NF-κB activities reflect the severity of ischemic stresses. Pretreatment with genistein can attenuate NF-κB activities and muscle edema in ischemic stress of rat skeletal muscle. (J Korean Acad Rehab Med 2003; 27: 990-996)
Method: L6 cell, rat skeletal myoblast, was cultured in the low mitogen medium and caveolin-3 expression was observed both by immunocytochemistry and western blot analysis. Localization of caveolin-3 within the muscle tissue was investigated and compared to that of dystrophin. Results: While caveolin-3 was not expressed in the proliferating myolast, caveolin-3 was expressed in the differentiated myoblast. Caveolin-3 and dystrophin were co-expressed in the membrane of muscle tissue and integrated density of caveolin-3 was elevated in the area of muscle injury. In the Duchenne muscular dystrophy, caveolin-3 was expressed in the membrane of muscle tissue, but dystrophin was not.
Conclusion: Caveolin-3 was induced during the myobalst differentiation and its expression was increased during the muscle regeneration. Caveolin-3 was physically associated with dystrophin as a complex, but not absolutely required for the biogenesis of dystrophin complex. (J Korean Acad Rehab Med 2003; 27: 382-387)
To investigate the skeletal muscle changes, intramuscular injections of local anesthetics were performed using animal, Sprague-Dawley rat.
The experiments were composed of two procedures, experiment I and II. In experi ment I, single injection was performed using 0.4 cc of 1 and 2% of procaine and lidocaine.
In experiment II, repeated injection of 0.4 cc of 2% lidocaine on weekly bases 3 times were performed.
The experimental rats were divided into five groups in experiment I: Four experimental groups 40(10 rats for each local anesthetics) and Control 10 and were divided into two groups in experiment II: Experimental group 8 and Control 4. The muscle biopsies were performed in 15 minutes, 2, 4, 8 and 16 days after injection in two experiments.
No muscle fiber changes were shown in control group, and 1~2 % procaine, and 2% lidocaine injected groups of experiment I and control group of experiment II. In the groups of single and repeated injections of 2% lidocaine, muscular inflammatory changes were shown on 2 and 4 days after injection. The changes were more extensive in the group of repeated injections. The inflammatory reaction was usually abated on 8 days after injection and the muscles appeared to be normal in quality and quantity on 16 days after injection. These histopathologic results indicated reversible muscular changes.
Although the muscular changes are reversible after local anesthetics injection, the concentration of local anesthetics and injection interval should be considered to minimize the muscle fiber changes in the repeated injections.
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