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Journal articles on the topic 'Skeletal Muscles'
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1
Lieber, Richard L., and Samuel R. Ward. "Skeletal muscle design to meet functional demands." Philosophical Transactions of the Royal Society B: Biological Sciences 366, no. 1570 (May 27, 2011): 1466–76. http://dx.doi.org/10.1098/rstb.2010.0316.
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Skeletal muscles are length- and velocity-sensitive force producers, constructed of a vast array of sarcomeres. Muscles come in a variety of sizes and shapes to accomplish a wide variety of tasks. How does muscle design match task performance? In this review, we outline muscle's basic properties and strategies that are used to produce movement. Several examples are provided, primarily for human muscles, in which skeletal muscle architecture and moment arms are tailored to a particular performance requirement. In addition, the concept that muscles may have a preferred sarcomere length operating range is also introduced. Taken together, the case is made that muscles can be fine-tuned to perform specific tasks that require actuators with a wide range of properties.
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Kholodnyi, R. D. "MODELING THE SKELETAL MUSCLE INJURY IN RATS." International Journal of Veterinary Medicine, no. 3 (October 18, 2022): 253–57. http://dx.doi.org/10.52419/issn2072-2419.2022.3.253.
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Muscles are the most important executive organs - effectors. Both according to morphological and functional characteristics, muscles are divided into two types - striated and smooth. Striated muscles, in turn, are usually divided into skeletal and cardiac. Striated muscles form the motor apparatus of the skeleton, oculomotor, chewing and other motor systems in animals. The striated muscles, with the exception of the heart muscle, are completely controlled by the central nervous system, they are devoid of automatism.The problem of damage to skeletal muscles is very relevant and widespread. These injuries disrupt the musculoskeletal function of animals, up to its complete loss. To search for methods for restoring the structure and function of muscles, experiments are being carried out on laboratory animals. This article is devoted to the selection of the optimal model of skeletal muscle injury, performed on laboratory rats. The study was conducted on Wistar rats. The choice of the muscle on which the models will be worked out, as well as the surgical access to it, is substantiated. Three options for inflicting damage to muscle tissue (cut wounds directed parallel to muscle fibers; cut wounds directed across muscle fibers; crushed wounds of muscle tissue) and the timing of healing of these injuries are proposed. The result of the study showed that the gastrocnemius muscle is the most suitable for modeling damage to muscle tissue in rats, and a crushed wound has the longest healing time.
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Testa, Marco, Bianca Rocca, Lucia Spath, Franco O. Ranelletti, Giovanna Petrucci, Giovanni Ciabattoni, Fabio Naro, Stefano Schiaffino, Massimo Volpe, and Carlo Reggiani. "Expression and activity of cyclooxygenase isoforms in skeletal muscles and myocardium of humans and rodents." Journal of Applied Physiology 103, no. 4 (October 2007): 1412–18. http://dx.doi.org/10.1152/japplphysiol.00288.2007.
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Conflicting data have been reported on cyclooxygenase (COX)-1 and COX-2 expression and activity in striated muscles, including skeletal muscles and myocardium, in particular it is still unclear whether muscle cells are able to produce prostaglandins (PGs). We characterized the expression and enzymatic activity of COX-1 and COX-2 in the skeletal muscles and in the myocardium of mice, rats and humans. By RT-PCR, COX-1 and COX-2 mRNAs were observed in homogenates of mouse and rat hearts, and in different types of skeletal muscles from all different species. By Western blotting, COX-1 and -2 proteins were detected in skeletal muscles and hearts from rodents, as well as in skeletal muscles from humans. Immunoperoxidase stains showed that COX-1 and -2 were diffusely expressed in the myocytes of different muscles and in the myocardiocytes from all different species. In the presence of arachidonic acid, which is the COX enzymatic substrate, isolated skeletal muscle and heart samples from rodents released predominantly PGE2. The biosynthesis of PGE2 was reduced between 50 and 80% ( P < 0.05 vs. vehicle) in the presence of either COX-1- or COX-2-selective blockers, demonstrating that both isoforms are enzymatically active. Exogenous PGE2 added to isolated skeletal muscle preparations from rodents did not affect contraction, whereas it significantly fastened relaxation of a slow type muscle, such as soleus. In conclusion, COX-1 and COX-2 are expressed and enzymatically active in myocytes of skeletal muscles and hearts of rodents and humans. PGE2 appears to be the main product of COX activity in striated muscles.
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Heo, Jun-Won, Su-Zi Yoo, Mi-Hyun No, Dong-Ho Park, Ju-Hee Kang, Tae-Woon Kim, Chang-Ju Kim, et al. "Exercise Training Attenuates Obesity-Induced Skeletal Muscle Remodeling and Mitochondria-Mediated Apoptosis in the Skeletal Muscle." International Journal of Environmental Research and Public Health 15, no. 10 (October 19, 2018): 2301. http://dx.doi.org/10.3390/ijerph15102301.
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Obesity is characterized by the induction of skeletal muscle remodeling and mitochondria-mediated apoptosis. Exercise has been reported as a positive regulator of skeletal muscle remodeling and apoptosis. However, the effects of exercise on skeletal muscle remodeling and mitochondria-mediated apoptosis in obese skeletal muscles have not been clearly elucidated. Four-week-old C57BL/6 mice were randomly assigned into four groups: control (CON), control plus exercise (CON + EX), high-fat diet (HFD), and HFD plus exercise groups (HFD + EX). After obesity was induced by 20 weeks of 60% HFD feeding, treadmill exercise was performed for 12 weeks. Exercise ameliorated the obesity-induced increase in extramyocyte space and a decrease in the cross-sectional area of the skeletal muscle. In addition, it protected against increases in mitochondria-mediated apoptosis in obese skeletal muscles. These results suggest that exercise as a protective intervention plays an important role in regulating skeletal muscle structure and apoptosis in obese skeletal muscles.
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J Rosochacki, S., T. Sakowski, J. Połoszynowicz, E. Juszczuk-Kubiak, A. Kowalik-Krupa, and J. Oprządek. "Lysosomal proteolysis in skeletal muscles of bulls." Czech Journal of Animal Science 49, No. 8 (December 13, 2011): 340–48. http://dx.doi.org/10.17221/4318-cjas.
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The relationship between lysosomal proteolytic enzyme activities involved in skeletal muscle proteolysis of the longissimus lumborum et thoracis muscle (MLLT) of bulls was described. Samples from the same region were obtained post mortem from 7 Piemontese (P) and 54 Black-and-White bulls (B-W) about 18 months old fed ad libitum. The activity of cathepsin D was determined as pepstatin (cathepsin D inhibitor) sensitive activity (PSCatD) towards 1% haemoglobin. Pepstatin-insensitive acid (PIA) and leupeptin-insensitive (thiol proteinase inhibitor) acid (LIA) autolytic activities were measured in the presence of 1 mM Mg<sup>++</sup>. MLLT was also analysed for RNA, DNA and protein content. The data were processed by analysis of variance and differences between sires were tested by the contrast procedure of general linear model. In the examined muscle RNA decreased by 16% in B-W compared to P, CPS by about 14% and FCS by about 39%. DNA content was higher by 64.5% in B-W compared to P bulls (P ≤ 0.01). Some differences were found between P bulls and B-W groups of sires in the percentage of proteins (P ≤ 0.01), CatD and PSCatD (P ≤ 0.01), but the most pronounced differences were determined in PIA and LIA (P ≤ 0.01), and in the percentage of inhibition by pepstatin and leupeptin (P ≤ 0.01) in AAA. In the Black-and-White group of sires the percentage of protein and percentage of inhibition by pepstatin and leupeptin in AAA were lowered by about 10, 17 and 22%, but PSCatD, PIA and LIA were higher by about 23.7, 41 and 57.7%, respectively, compared to Piemontese bulls. The level of aspartic and thiol proteinases was lower in the muscles of B-W compared to Piemontese. The activity was much higher in B-W compared to P. These results indicate the faster turnover of proteins in the groups after Black-and-White sires and higher anabolic increase in degradation in Piemontese bulls.
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Kostrominova, Tatiana Y., Douglas E. Dow, Robert G. Dennis, Richard A. Miller, and John A. Faulkner. "Comparison of gene expression of 2-mo denervated, 2-mo stimulated-denervated, and control rat skeletal muscles." Physiological Genomics 22, no. 2 (July 14, 2005): 227–43. http://dx.doi.org/10.1152/physiolgenomics.00210.2004.
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Loss of innervation in skeletal muscles leads to degeneration, atrophy, and loss of force. These dramatic changes are reflected in modifications of the mRNA expression of a large number of genes. Our goal was to clarify the broad spectrum of molecular events associated with long-term denervation of skeletal muscles. A microarray study compared gene expression profiles of 2-mo denervated and control extensor digitorum longus (EDL) muscles from 6-mo-old rats. The study identified 121 genes with increased and 7 genes with decreased mRNA expression. The expression of 107 of these genes had not been identified previously as changed after denervation. Many of the genes identified were genes that are highly expressed in skeletal muscles during embryonic development, downregulated in adults, and upregulated after denervation of muscle fibers. Electrical stimulation of denervated muscles preserved muscle mass and maximal force at levels similar to those in the control muscles. To understand the processes underlying the effect of electrical stimulation on denervated skeletal muscles, mRNA and protein expression of a number of genes, identified by the microarray study, was compared. The hypothesis was that loss of nerve action potentials and muscle contractions after denervation play the major roles in upregulation of gene expression in skeletal muscles. With electrical stimulation of denervated muscles, the expression levels for these genes were significantly downregulated, consistent with the hypothesis that loss of action potentials and/or contractions contribute to the alterations in gene expression in denervated skeletal muscles.
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Park, Song-Young, Jayson R. Gifford, Robert H. I. Andtbacka, Joel D. Trinity, John R. Hyngstrom, Ryan S. Garten, Nikolaos A. Diakos, et al. "Cardiac, skeletal, and smooth muscle mitochondrial respiration: are all mitochondria created equal?" American Journal of Physiology-Heart and Circulatory Physiology 307, no. 3 (August 1, 2014): H346—H352. http://dx.doi.org/10.1152/ajpheart.00227.2014.
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Unlike cardiac and skeletal muscle, little is known about vascular smooth muscle mitochondrial respiration. Therefore, the present study examined mitochondrial respiratory rates in smooth muscle of healthy human feed arteries and compared with that of healthy cardiac and skeletal muscles. Cardiac, skeletal, and smooth muscles were harvested from a total of 22 subjects (53 ± 6 yr), and mitochondrial respiration was assessed in permeabilized fibers. Complex I + II, state 3 respiration, an index of oxidative phosphorylation capacity, fell progressively from cardiac to skeletal to smooth muscles (54 ± 1, 39 ± 4, and 15 ± 1 pmol·s−1·mg−1, P < 0.05, respectively). Citrate synthase (CS) activity, an index of mitochondrial density, also fell progressively from cardiac to skeletal to smooth muscles (222 ± 13, 115 ± 2, and 48 ± 2 μmol·g−1·min−1, P < 0.05, respectively). Thus, when respiration rates were normalized by CS (respiration per mitochondrial content), oxidative phosphorylation capacity was no longer different between the three muscle types. Interestingly, complex I state 2 normalized for CS activity, an index of nonphosphorylating respiration per mitochondrial content, increased progressively from cardiac to skeletal to smooth muscles, such that the respiratory control ratio, state 3/state 2 respiration, fell progressively from cardiac to skeletal to smooth muscles (5.3 ± 0.7, 3.2 ± 0.4, and 1.6 ± 0.3 pmol·s−1·mg−1, P < 0.05, respectively). Thus, although oxidative phosphorylation capacity per mitochondrial content in cardiac, skeletal, and smooth muscles suggest all mitochondria are created equal, the contrasting respiratory control ratio and nonphosphorylating respiration highlight the existence of intrinsic functional differences between these muscle mitochondria. This likely influences the efficiency of oxidative phosphorylation and could potentially alter ROS production.
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Eržen, Ida. "PLASTICITY OF SKELETAL MUSCLE STUDIED BY STEREOLOGY." Image Analysis & Stereology 23, no. 3 (May 3, 2011): 143. http://dx.doi.org/10.5566/ias.v23.p143-152.
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The present contribution provides an overview of stereological methods applied in the skeletal muscle research at the Institute of Anatomy of the Medical Faculty in Ljubljana. Interested in skeletal muscle plasticity we studied three different topics: (i) expression of myosin heavy chain isoforms in slow and fast muscles under experimental conditions, (ii) frequency of satellite cells in young and old human and rat muscles and (iii) capillary supply of rat fast and slow muscles. We analysed the expression of myosin heavy chain isoforms within slow rat soleus and fast extensor digitorum longus muscles after (i) homotopic and heterotopic transplantation of both muscles, (ii) low frequency electrical stimulation of the fast muscle and (iii) transposition of the fast nerve to the slow muscle. The models applied were able to turn the fast muscle into a completely slow muscle, but not vice versa. One of the indicators for the regenerative potential of skeletal muscles is its satellite cell pool. The estimated parameters, number of satellite cells per unit fibre length, corrected to the reference sarcomere length (Nsc/Lfib) and number of satellite cells per number of nuclei (myonuclei and satellite cell nuclei) (Nsc/Nnucl) indicated that the frequency of M-cadherin stained satellite cells declines in healthy old human and rat muscles compared to young muscles. To access differences in capillary densities among slow and fast muscles and slow and fast muscle fibres, we have introduced Slicer and Fakir methods, and tested them on predominantly slow and fast rat muscles. Discussing three different topics that require different approach, the present paper reflects the three decades of the development of stereological methods: 2D analysis by simple point counting in the 70's, the disector in the 80's and virtual spatial probes in the 90's. In all methods the interactive computer assisted approach was utilised.
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Gomez-Cabrera, M. C., G. L. Close, A. Kayani, A. McArdle, J. Viña, and M. J. Jackson. "Effect of xanthine oxidase-generated extracellular superoxide on skeletal muscle force generation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 1 (January 2010): R2—R8. http://dx.doi.org/10.1152/ajpregu.00142.2009.
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Skeletal muscle contractions increase superoxide anion in skeletal muscle extracellular space. We tested the hypotheses that 1) after an isometric contraction protocol, xanthine oxidase (XO) activity is a source of superoxide anion in the extracellular space of skeletal muscle and 2) the increase in XO-derived extracellular superoxide anion during contractions affects skeletal muscle contractile function. Superoxide anion was monitored in the extracellular space of mouse gastrocnemius muscles by following the reduction of cytochrome c in muscle microdialysates. A 15-min protocol of nondamaging isometric contractions increased the reduction of cytochrome c in microdialysates, indicating an increase in superoxide anion. Mice treated with the XO inhibitor oxypurinol showed a smaller increase in superoxide anions in muscle microdialysates following contractions than in microdialysates from muscles of vehicle-treated mice. Intact extensor digitorum longus (EDL) and soleus muscles from mice were also incubated in vitro with oxypurinol or polyethylene glycol-tagged Cu,Zn-SOD. Oxypurinol decreased the maximum tetanic force produced by EDL and soleus muscles, and polyethylene glycol-tagged Cu,Zn-SOD decreased the maximum force production by the EDL muscles. Neither agent influenced the rate of decline in force production when EDL or soleus muscles were repeatedly electrically stimulated using a 5-min fatiguing protocol (stimulation at 40 Hz for 0.1 s every 5 s). Thus these studies indicate that XO activity contributes to the increased superoxide anion detected within the extracellular space of skeletal muscles during nondamaging contractile activity and that XO-derived superoxide anion or derivatives of this radical have a positive effect on muscle force generation during isometric contractions of mouse skeletal muscles.
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Wu, G. Y., and J. R. Thompson. "Is methionine transaminated in skeletal muscle?" Biochemical Journal 257, no. 1 (January 1, 1989): 281–84. http://dx.doi.org/10.1042/bj2570281.
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Methionine transamination is extensive in rat and chick skeletal-muscle homogenates, but is barely detectable in intact rat, but not chick, skeletal muscles. Branched-chain amino acids essentially block methionine transamination in intact muscles and homogenates from both species. The physiological significance of methionine transamination in skeletal muscle is questioned.
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Pistilli, Emidio E., Parco M. Siu, and Stephen E. Alway. "Interleukin-15 responses to aging and unloading-induced skeletal muscle atrophy." American Journal of Physiology-Cell Physiology 292, no. 4 (April 2007): C1298—C1304. http://dx.doi.org/10.1152/ajpcell.00496.2006.
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Interleukin-15 (IL-15) mRNA is constitutively expressed in skeletal muscle. Although IL-15 has proposed hypertrophic and anti-apoptotic roles in vitro, its role in skeletal muscle cells in vivo is less clear. The purpose of this study was to determine if skeletal muscle aging and unloading, two conditions known to promote muscle atrophy, would alter basal IL-15 expression in skeletal muscle. We hypothesized that IL-15 mRNA expression would increase as a result of both aging and muscle unloading and that muscle would express the mRNA for a functional trimeric IL-15 receptor (IL-15R). Two models of unloading were used in this study: hindlimb suspension (HS) in rats and wing unloading in quail. The absolute muscle wet weight of plantaris and soleus muscles from aged rats was significantly less when compared with muscles from young adult rats. Although 14 days of HS resulted in reduced muscle mass of plantaris and soleus muscles from young adult animals, this effect was not observed in muscles from aged animals. A significant aging times unloading interaction was observed for IL-15 mRNA in both rat soleus and plantaris muscles. Patagialis (PAT) muscles from aged quail retained a significant 12 and 6% of stretch-induced hypertrophy after 7 and 14 days of unloading, respectively. PAT muscles from young quail retained 15% hypertrophy at 7 days of unloading but regressed to control levels following 14 days of unloading. A main effect of age was observed on IL-15 mRNA expression in PAT muscles at 14 days of overload, 7 days of unloading, and 14 days of unloading. Skeletal muscle also expressed the mRNAs for a functional IL-15R composed of IL-15Rα, IL-2/15R-β, and -γc. Based on these data, we speculate that increases in IL-15 mRNA in response to atrophic stimuli may be an attempt to counteract muscle mass loss in skeletal muscles of old animals. Additional research is warranted to determine the importance of the IL-15/IL-15R system to counter muscle wasting.
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Maas, Huub, and Thomas G. Sandercock. "Force Transmission between Synergistic Skeletal Muscles through Connective Tissue Linkages." Journal of Biomedicine and Biotechnology 2010 (2010): 1–9. http://dx.doi.org/10.1155/2010/575672.
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The classic view of skeletal muscle is that force is generated within its muscle fibers and then directly transmitted in-series, usually via tendon, onto the skeleton. In contrast, recent results suggest that muscles are mechanically connected to surrounding structures and cannot be considered as independent actuators. This article will review experiments on mechanical interactions between muscles mediated by such epimuscular myofascial force transmission in physiological and pathological muscle conditions. In a reduced preparation, involving supraphysiological muscle conditions, it is shown that connective tissues surrounding muscles are capable of transmitting substantial force. In more physiologically relevant conditions of intact muscles, however, it appears that the role of this myofascial pathway is small. In addition, it is hypothesized that connective tissues can serve as a safety net for traumatic events in muscle or tendon. Future studies are needed to investigate the importance of intermuscular force transmission during movement in health and disease.
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CONTI, Antonio, L. GORZA, and Vincenzo SORRENTINO. "Differential distribution of ryanodine receptor type 3 (RyR3) gene product in mammalian skeletal muscles." Biochemical Journal 316, no. 1 (May 15, 1996): 19–23. http://dx.doi.org/10.1042/bj3160019.
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Activation of intracellular Ca2+-release channels/ryanodine receptors (RyRs) is a fundamental step in the regulation of muscle contraction. In mammalian skeletal muscle, Ca2+-release channels containing the type 1 isoform of RyR (RyR1) open to release Ca2+ from the sarcoplasmic reticulum (SR) upon stimulation by the voltage-activated dihydropyridine receptor on the T-tubule/plasma membrane. In addition to RyR1, low levels of the mRNA of the RyR3 isoform have been recently detected in mammalian skeletal muscles. Here we report data on the distribution of the RyR3 gene product in mammalian skeletal muscles. Western-blot analysis of SR of individual muscles indicated that, at variance with the even distribution of the RyR1 isoform, the RyR3 content varies among different muscles, with relatively higher amounts being detected in diaphragm and soleus, and lower levels in abdominal muscles and tibialis anterior. In these muscles RyR3 was localized in the terminal cisternae of the SR. No detectable levels of RyR3 were observed in the extensor digitorum longus. Preferential high content of RyR3 in the diaphragm muscle was observed in several mammalian species. In situ hybridization analysis demonstrated that RyR3 transcripts are not restricted to a specific subset of skeletal-muscle fibres. Differential utilization of the RyR3 isoform in skeletal muscle may be relevant to the modulation of Ca2+ release with respect to specific muscle-contraction properties.
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Acevedo, Luz M., Ana I. Raya, Rafael Ríos, Escolástico Aguilera-Tejero, and José-Luis L. Rivero. "Obesity-induced discrepancy between contractile and metabolic phenotypes in slow- and fast-twitch skeletal muscles of female obese Zucker rats." Journal of Applied Physiology 123, no. 1 (July 1, 2017): 249–59. http://dx.doi.org/10.1152/japplphysiol.00282.2017.
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A clear picture of skeletal muscle adaptations to obesity and related comorbidities remains elusive. This study describes fiber-type characteristics (size, proportions, and oxidative enzyme activity) in two typical hindlimb muscles with opposite structure and function in an animal model of genetic obesity. Lesser fiber diameter, fiber-type composition, and histochemical succinic dehydrogenase activity (an oxidative marker) of muscle fiber types were assessed in slow (soleus)- and fast (tibialis cranialis)-twitch muscles of obese Zucker rats and compared with age (16 wk)- and sex (females)-matched lean Zucker rats ( n = 16/group). Muscle mass and lesser fiber diameter were lower in both muscle types of obese compared with lean animals even though body weights were increased in the obese cohort. A faster fiber-type phenotype also occurred in slow- and fast-twitch muscles of obese rats compared with lean rats. These adaptations were accompanied by a significant increment in histochemical succinic dehydrogenase activity of slow-twitch fibers in the soleus muscle and fast-twitch fiber types in the tibialis cranialis muscle. Obesity significantly increased plasma levels of proinflammatory cytokines but did not significantly affect protein levels of peroxisome proliferator-activated receptors PPARγ or PGC1α in either muscle. These data demonstrate that, in female Zucker rats, obesity induces a reduction of muscle mass in which skeletal muscles show a diminished fiber size and a faster and more oxidative phenotype. It was noteworthy that this discrepancy in muscle's contractile and metabolic features was of comparable nature and extent in muscles with different fiber-type composition and antagonist functions. NEW & NOTEWORTHY This study demonstrates a discrepancy between morphological (reduced muscle mass), contractile (shift toward a faster phenotype), and metabolic (increased mitochondrial oxidative enzyme activity) characteristics in skeletal muscles of female Zucker fatty rats. It is noteworthy that this inconsistency was comparable (in nature and extent) in muscles with different structure and function.
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Vernooij, Carlijn A., Raymond F. Reynolds, and Martin Lakie. "Physiological tremor reveals how thixotropy adapts skeletal muscle for posture and movement." Royal Society Open Science 3, no. 5 (May 2016): 160065. http://dx.doi.org/10.1098/rsos.160065.
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People and animals can move freely, but they must also be able to stay still. How do skeletal muscles economically produce both movement and posture? Humans are well known to have motor units with relatively homogeneous mechanical properties. Thixotropic muscle properties can provide a solution by providing a temporary stiffening of all skeletal muscles in postural conditions. This stiffening is alleviated almost instantly when muscles start to move. In this paper, we probe this behaviour. We monitor both the neural input to a muscle, measured here as extensor muscle electromyography (EMG), and its output, measured as tremor (finger acceleration). Both signals were analysed continuously as the subject made smooth transitions between posture and movement. The results showed that there were marked changes in tremor which systematically increased in size and decreased in frequency as the subject moved faster. By contrast, the EMG changed little and reflected muscle force requirement rather than movement speed. The altered tremor reflects naturally occurring thixotropic changes in muscle behaviour. Our results suggest that physiological tremor provides useful and hitherto unrecognized insights into skeletal muscle's role in posture and movement.
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Laughlin, M. H., T. Simpson, W. L. Sexton, O. R. Brown, J. K. Smith, and R. J. Korthuis. "Skeletal muscle oxidative capacity, antioxidant enzymes, and exercise training." Journal of Applied Physiology 68, no. 6 (June 1, 1990): 2337–43. http://dx.doi.org/10.1152/jappl.1990.68.6.2337.
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The purposes of this study were to determine whether exercise training induces increases in skeletal muscle antioxidant enzymes and to further characterize the relationship between oxidative capacity and antioxidant enzyme levels in skeletal muscle. Male Sprague-Dawley rats were exercise trained (ET) on a treadmill 2 h/day at 32 m/min (8% incline) 5 days/wk or were cage confined (sedentary control, S) for 12 wk. In both S and ET rats, catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPX) activities were directly correlated with the percentages of oxidative fibers in the six skeletal muscle samples studied. Muscles of ET rats had increased oxidative capacity and increased GPX activity compared with the same muscles of S rats. However, SOD activities were not different between ET and S rats, but CAT activities were lower in skeletal muscles of ET rats than in S rats. Exposure to 60 min of ischemia and 60 min of reperfusion (I/R) resulted in decreased GPX and increased CAT activities but had little or no effect on SOD activities in muscles from both S and ET rats. The I/R-induced increase in CAT activity was greater in muscles of ET than in muscles of S rats. Xanthine oxidase (XO), xanthine dehydrogenase (XD), and XO + XD activities after I/R were not related to muscle oxidative capacity and were similar in muscles of ET and S rats. It is concluded that although antioxidant enzyme activities are related to skeletal muscle oxidative capacity, the effects of exercise training on antioxidant enzymes in skeletal muscle cannot be predicted by measured changes in oxidative capacity.
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Bickel, C. Scott, Jill M. Slade, Gordon L. Warren, and Gary A. Dudley. "Fatigability and Variable-Frequency Train Stimulation of Human Skeletal Muscles." Physical Therapy 83, no. 4 (April 1, 2003): 366–73. http://dx.doi.org/10.1093/ptj/83.4.366.
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Abstract Background and Purpose. The quadriceps femoris (QF) and tibialis anterior (TA) muscles are often activated through the use of electrical stimulation by physical therapists. These 2 muscles are fundamentally different in regard to their fiber-type composition. Whether protocols developed using a given muscle can be applied to another muscle has seldom been questioned, even if they differ in fiber type. The purpose of this study was to test the hypothesis that torque augmentation during variable-frequency train (VFT) stimulation as compared with constant-frequency train (CFT) stimulation in the fatigued state would not differ between these muscles, even though the TA muscle has 50% relatively more slow fibers than the QF muscle relative to each muscle's overall composition. Subjects. Ten recreationally active men with no history of lower-extremity pathology participated in the study (mean age=25 years, SD=4, range=19–31; mean height=179 cm, SD=5, range=170–188; mean body mass=80 kg, SD=15, range=63–111). Methods. The subjects' TA and QF muscles were stimulated with CFTs (six 200-microsecond square waves separated by 70 milliseconds) or VFTs (first interpulse interval=5 milliseconds) that evoked an isometric contraction. Results. After potentiation, the torque-time integral and peak torque were not different for the VFT and CFT stimulation. Rise time was longer for the TA muscle than for the QF muscle and for CFT stimulation versus VFT stimulation (both approximately 40%). After 180 CFTs (50% duty cycle), peak torque decreased 56% overall, with no differences between muscles. Enhancement of the torque-time integral (25%) by VFT stimulation was not different between fatigued QF and TA muscles. Torque augmentation was due to the VFT stimulation evoking 27% greater peak torque and less slowing of rise time than the CFT stimulation (15% versus 30%). Discussion and Conclusion. The results indicate that the QF muscle may not necessarily fatigue more than the TA muscle. The results suggest that VFTs augment the force of fatigued, human skeletal muscle irrespective of fiber type.
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Shi, Wanchun, Siping Hu, Wenhua Wang, Xiaohui Zhou, and Wei Qiu. "Skeletal Muscle-Specific CPT1 Deficiency Elevates Lipotoxic Intermediates but Preserves Insulin Sensitivity." Journal of Diabetes Research 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/163062.
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Objective. By specific knockout of carnitine palmitoyl transferase 1b (CPT1b) in skeletal muscles, we explored the effect of CPT1b deficiency on lipids and insulin sensitivity.Methods. Mice with specific knockout of CPT1b in skeletal muscles (CPT1b M−/−) were used for the experiment group, with littermate C57BL/6 as controls (CPT1b). General and metabolic profiles were measured and compared between groups. mRNA expression and CPT1 activity were measured in skeletal muscle tissues and compared between groups. Mitochondrial fatty acid oxidation (FAO), triglycerides (TAGs), diglycerides (DAGs), and ceramides were examined in skeletal muscles in two groups. Phosphorylated AKT (pAkt) and glucose transporter 4 (Glut4) were determined with real-time polymerase chain reaction (RT-PCR). Insulin tolerance test, glucose tolerance test, and pyruvate oxidation were performed in both groups.Results. CPT1b M−/− model was successfully established, with impaired muscle CPT1 activity. Compared with CPT1b mice, CPT1b M−/− mice had similar food intake but lower body weight or fat mass and higher lipids but similar glucose or insulin levels. Their mitochondrial FAO of skeletal muscles was impaired. There were lipids accumulations (TAGs, DAGs, and ceramides) in skeletal muscle. However, pAkt and Glut4, insulin sensitivity, glucose tolerance, and pyruvate oxidation were preserved.Conclusion. Skeletal muscle-specific CPT1 deficiency elevates lipotoxic intermediates but preserves insulin sensitivity.
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Meng, H., T. B. Bentley, and R. N. Pittman. "Myoglobin content of hamster skeletal muscles." Journal of Applied Physiology 74, no. 5 (May 1, 1993): 2194–97. http://dx.doi.org/10.1152/jappl.1993.74.5.2194.
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Myoglobin (Mb) may facilitate O2 diffusion in muscle tissue, yet models of O2 transport are often simplified by ignoring the role of Mb. A recent analysis of O2 transport in hamster retractor muscle revealed a large discrepancy between the observed O2 diffusion from arterioles and that predicted by a mathematical model that did not include Mb. To establish whether this simplification was justified, we measured Mb content ([Mb]) in three hamster muscles that vary markedly in histochemical fiber type composition. [Mb] was determined spectrophotometrically using freshly excised tissues from hamsters of different ages (5–34 wk). [Mb] increased rapidly up to 15 wk of age and then rose more slowly. [Mb] in hamster muscles paralleled oxidative capacity. Our measurements of rat and dog muscles also show that [Mb] varies greatly among species and among muscles of a given species. The results indicate that in the hamster the variability in [Mb] with age and muscle should be taken into account when the potential role of Mb in studies on O2 transport is interpreted.
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Lin, BL, S. Govindan, S. Sadayappan, L. Zhao, J. Xu, and R. Han. "ID: 77: FAST-SKELETAL MYOSIN BINDING PROTEIN-C REGULATES SKELETAL MUSCLE CALCIUM SENSITIVITY." Journal of Investigative Medicine 64, no. 4 (March 22, 2016): 917.1–917. http://dx.doi.org/10.1136/jim-2016-000120.13.
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Mutations in myosin binding protein-C (MyBP-C) cause both cardiac and skeletal muscle diseases, such as hypertrophic cardiomyopathy and distal arthrogryposis. There are three isoforms of MyBP-C: slow-skeletal, fast-skeletal, and cardiac (ssMyBP-C, fsMyBP-C, and cMyBP-C, respectively). These isoforms reside within the sarcomere, the functional unit of muscle contraction at the molecular level. However, the function of the three major MyBP-C isoforms remains unclear. The present study is the first to focus on the least characterized isoform, fsMyBP-C, which is expressed in fast- and mixed-type skeletal muscles. To determine the necessity of fsMyBP-C for regulation of contraction in the sarcomere, we generated a conventional fast-skeletal MyBP-C knockout (FSKO) mouse model. We analyzed both structural changes and regulatory function of skeletal muscles from heterozygous (FSKO−/+) and homozygous (FSKO−/−), compared to wild-type (WT) mice. Neither heterozygous nor homozygous FSKO mice exhibited changes in morbidity or mortality relative to WT mice. Molecular analyses revealed a complete knockout of fsMyBP-C in the FSKO−/− skeletal muscles compared to FSKO−/+ and WT mice. Histopathological analyses of both Extensor digitorum longus (EDL) and soleus muscles revealed no obvious abnormalities, such as fibrosis or calcification, in either heterozygous or homozygous FSKO mice. Though fiber structure is preserved, we demonstrated that EDL muscles from FSKO−/− mice increases Ca2+-sensitivity of force development, suggesting that fsMyBP-C regulates contraction at the molecular level by decreasing Ca2+-sensitivity. While others have previously proposed the role of cMyBP-C is to increase Ca2+-sensitivity to normalize a Ca2+ gradient imbalance in the heart, we propose that the role of fsMyBP-C in skeletal muscles is to reduce Ca2+-sensitivity of the thin filaments in order to normalize the reversed Ca2+ gradient imbalance. Despite opposite effects on Ca2+-sensitivity, MyBP-C share the same functional role in both cardiac and skeletal muscles. Thus, in addition to elucidating the role of fast-skeletal MyBP-C and its regulation of skeletal muscle contraction, the present study provides insight into the cardiac isoform and its regulation of cardiac contraction.
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Ardhianto, Peter, Jen-Yung Tsai, Chih-Yang Lin, Ben-Yi Liau, Yih-Kuen Jan, Veit Babak Hamun Akbari, and Chi-Wen Lung. "A Review of the Challenges in Deep Learning for Skeletal and Smooth Muscle Ultrasound Images." Applied Sciences 11, no. 9 (April 28, 2021): 4021. http://dx.doi.org/10.3390/app11094021.
Full textAbstract:
Deep learning has aided in the improvement of diagnosis identification, evaluation, and the interpretation of muscle ultrasound images, which may benefit clinical personnel. Muscle ultrasound images presents challenges such as low image quality due to noise, insufficient data, and different characteristics between skeletal and smooth muscles that can affect the effectiveness of deep learning results. From 2018 to 2020, deep learning has the improved solutions used to overcome these challenges; however, deep learning solutions for ultrasound images have not been compared to the conditions and strategies used to comprehend the current state of knowledge for handling skeletal and smooth muscle ultrasound images. This study aims to look at the challenges and trends of deep learning performance, especially in regard to overcoming muscle ultrasound image problems such as low image quality, muscle movement in skeletal muscles, and muscle thickness in smooth muscles. Skeletal muscle segmentation presents difficulties due to the regular movement of muscles and resulting noise, recording data through skipped connections, and modified layers required for upsampling. In skeletal muscle classification, the problems faced are area-specific, thus making a cropping strategy useful. Furthermore, there is no need to add additional layer modifications for smooth muscle segmentation as muscle thickness is the main problem in such cases.
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Macdonald, W. A., N. Ørtenblad, and O. B. Nielsen. "Energy conservation attenuates the loss of skeletal muscle excitability during intense contractions." American Journal of Physiology-Endocrinology and Metabolism 292, no. 3 (March 2007): E771—E778. http://dx.doi.org/10.1152/ajpendo.00378.2006.
Full textAbstract:
High-frequency stimulation of skeletal muscle has long been associated with ionic perturbations, resulting in the loss of membrane excitability, which may prevent action potential propagation and result in skeletal muscle fatigue. Associated with intense skeletal muscle contractions are large changes in muscle metabolites. However, the role of metabolites in the loss of muscle excitability is not clear. The metabolic state of isolated rat extensor digitorum longus muscles at 30°C was manipulated by decreasing energy expenditure and thereby allowed investigation of the effects of energy conservation on skeletal muscle excitability. Muscle ATP utilization was reduced using a combination of the cross-bridge cycling blocker N-benzyl- p-toluene sulfonamide (BTS) and the SR Ca2+ release channel blocker Na-dantrolene, which reduce activity of the myosin ATPase and SR Ca2+-ATPase. Compared with control muscles, the resting metabolites ATP, phosphocreatine, creatine, and lactate, as well as the resting muscle excitability as measured by M-waves, were unaffected by treatment with BTS plus dantrolene. Following 20 or 30 s of continuous 60-Hz stimulation, BTS-plus-dantrolene-treated muscles showed a 25% lower ATP utilization compared with control muscles. Furthermore, the ability of muscles to maintain excitability during high-frequency stimulation was significantly improved in BTS-plus-dantrolene-treated muscles, indicating a strong link between metabolites, energetic state, and the excitability of the muscle.
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HOLNESS, Mark J., Karen BULMER, Geoffrey F. GIBBONS, and Mary C. SUGDEN. "Up-regulation of pyruvate dehydrogenase kinase isoform 4 (PDK4) protein expression in oxidative skeletal muscle does not require the obligatory participation of peroxisome-proliferator-activated receptor α (PPARα)." Biochemical Journal 366, no. 3 (September 15, 2002): 839–46. http://dx.doi.org/10.1042/bj20020754.
Full textAbstract:
In insulin deficiency, increased lipid delivery and oxidation suppress skeletal-muscle glucose oxidation by inhibiting pyruvate dehydrogenase complex (PDC) activity via enhanced protein expression of pyruvate dehydrogenase kinase (PDK) isoform 4, which phosphorylates (and inactivates) PDC. Signalling via peroxisome-proliferator-activated receptor α (PPARα) is an important component of the mechanism enhancing hepatic and renal PDK4 protein expression. Activation of PPARα in gastrocnemius, a predominantly fast glycolytic (FG) muscle, also increases PDK4 expression, an effect that, if extended to all muscles, would be predicted to drastically restrict whole-body glucose disposal. Paradoxically, chronic activation of PPARα by WY14,643 treatment improves glucose utilization by muscles of insulin-resistant high-fat-fed rats. In the resting state, oxidative skeletal muscles are quantitatively more important for glucose disposal than FG muscles. We evaluated the participation of PPARα in regulating PDK4 protein expression in slow oxidative (SO) skeletal muscle (soleus) and fast oxidative-glycolytic (FOG) skeletal muscle (anterior tibialis) containing a high proportion of oxidative fibres. In the fed state, acute (24h) activation of PPARα by WY14,643 in vivo failed to modify PDK4 protein expression in soleus, but modestly enhanced PDK4 protein expression in anterior tibialis. Starvation enhanced PDK4 protein expression in both muscles, with the greater response in anterior tibialis. WY14,643 treatment in vivo during starvation did not further enhance upregulation of PDK4 protein expression in either muscle type. Enhanced PDK4 protein expression after starvation was retained in SO and FOG skeletal muscles of PPARα-deficient mice. Our data indicate that PDK4 protein expression in oxidative skeletal muscle is regulated by a lipid-dependent mechanism that is not obligatorily dependent on signalling via PPARα.
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Hitachi, Keisuke, Masashi Nakatani, and Kunihiro Tsuchida. "Long Non-Coding RNA Myoparr Regulates GDF5 Expression in Denervated Mouse Skeletal Muscle." Non-Coding RNA 5, no. 2 (April 8, 2019): 33. http://dx.doi.org/10.3390/ncrna5020033.
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Skeletal muscle is a highly plastic tissue and decreased skeletal muscle mass (muscle atrophy) results in deteriorated motor function and perturbed body homeostasis. Myogenin promoter-associated long non-coding RNA (lncRNA) Myoparr promotes skeletal muscle atrophy caused by surgical denervation; however, the precise molecular mechanism remains unclear. Here, we examined the downstream genes of Myoparr during muscle atrophy following denervation of tibialis anterior (TA) muscles in C57BL/6J mice. Myoparr knockdown affected the expression of 848 genes. Sixty-five of the genes differentially regulated by Myoparr knockdown coded secretory proteins. Among these 65 genes identified in Myoparr-depleted skeletal muscles after denervation, we focused on the increased expression of growth/differentiation factor 5 (GDF5), an inhibitor of muscle atrophy. Myoparr knockdown led to activated bone morphogenetic protein (BMP) signaling in denervated muscles, as indicated by the increased levels of phosphorylated Smad1/5/8. Our detailed evaluation of downstream genes of Myoparr also revealed that Myoparr regulated differential gene expression between myogenic differentiation and muscle atrophy. This is the first report demonstrating the in vivo role of Myoparr in regulating BMP signaling in denervated muscles. Therefore, lncRNAs that have inhibitory activity on BMP signaling may be putative therapeutic targets for skeletal muscle atrophy.
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Fujii, Nobuharu, Marni D. Boppart, Scott D. Dufresne, Patricia F. Crowley, Alison C. Jozsi, Kei Sakamoto, Haiyan Yu, et al. "Overexpression or ablation of JNK in skeletal muscle has no effect on glycogen synthase activity." American Journal of Physiology-Cell Physiology 287, no. 1 (July 2004): C200—C208. http://dx.doi.org/10.1152/ajpcell.00415.2003.
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c-Jun NH2-terminal kinase (JNK) is highly expressed in skeletal muscle and is robustly activated in response to muscle contraction. Little is known about the biological functions of JNK signaling in terminally differentiated muscle cells, although this protein has been proposed to regulate insulin-stimulated glycogen synthase activity in mouse skeletal muscle. To determine whether JNK signaling regulates contraction-stimulated glycogen synthase activation, we applied an electroporation technique to induce JNK overexpression (O/E) in mouse skeletal muscle. Ten days after electroporation, in situ muscle contraction increased JNK activity 2.6-fold in control muscles and 15-fold in the JNK O/E muscles. Despite the enormous activation of JNK activity in JNK O/E muscles, contraction resulted in similar increases in glycogen synthase activity in control and JNK O/E muscles. Consistent with these findings, basal and contraction-induced glycogen synthase activity was normal in muscles of both JNK1- and JNK2-deficient mice. JNK overexpression in muscle resulted in significant alterations in the basal phosphorylation state of several signaling proteins, such as extracellular signal-regulated kinase 1/2, p90 S6 kinase, glycogen synthase kinase 3, protein kinase B/Akt, and p70 S6 kinase, in the absence of changes in the expression of these proteins. These data suggest that JNK signaling regulates the phosphorylation state of several kinases in skeletal muscle. JNK activation is unlikely to be the major mechanism by which contractile activity increases glycogen synthase activity in skeletal muscle.
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Geers, C., D. Krüger, W. Siffert, A. Schmid, W. Bruns, and G. Gros. "Carbonic anhydrase in skeletal and cardiac muscle from rabbit and rat." Biochemical Journal 282, no. 1 (February 15, 1992): 165–71. http://dx.doi.org/10.1042/bj2820165.
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We have studied the distribution of carbonic anhydrases (CA) in several skeletal muscles of the hindlimb of rabbits and rats and in cardiac muscle of the rabbit. To remove erythrocyte CA, hindlimbs and hearts were thoroughly perfused with dextran solution, and the effectiveness of the perfusion was in most cases assessed by determining the contamination of the muscles with radioisotopes that had been used to label the erythrocytes before the perfusion was started. We observed three forms of CA: (1) cytosolic (sulphonamide-resistant) CA III; (2) a cytosolic sulphonamide-sensitive CA, probably isoenzyme II; (3) a membrane-bound form that was extracted from the particulate fraction using Triton X-100. These CA isoforms were distributed as follows. (1) CA III is located in the cytoplasm of slow, oxidative skeletal muscles and is absent from or low in fast skeletal and cardiac muscle; this holds for rabbits and rats and is identical with the pattern previously described for several other species. (2) The cytosolic sulphonamide-sensitive CA is present in fast rabbit muscles and absent from slow muscles of this species. In contrast, all skeletal muscles of the rat studied here lack, or possess only very low, activity of this isoenzyme. (3) The membrane-bound form of CA is present in all rabbit muscles studied; its activity appears somewhat higher in fast than in slow skeletal muscles. (4) Cardiac muscle constitutes an exception among all striated muscles of the rabbit as it possesses no form of cytosolic CA but a high activity of the membrane-bound form.
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Holness, M. J., and M. C. Sugden. "Changes in rates of glucose utilization and regulation of glucose disposal by fast-twitch skeletal muscles in late pregnancy." Biochemical Journal 292, no. 2 (June 1, 1993): 431–38. http://dx.doi.org/10.1042/bj2920431.
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Glucose utilization indices (GUI) were measured in vivo in conjunction with active pyruvate dehydrogenase complex (PDH(a) and glycogen synthase (GS) activities in fast-twitch skeletal muscles [extensor digitorum longus (EDL), tibialis anterior and gastrocnemius] of late-pregnant rats and age-matched virgin control rats in the fed state, after 24 h starvation and at 2 h after re-feeding with standard laboratory chow ad libitum after 24 h starvation. As demonstrated previously [Holness and Sugden (1990) Biochem. J 277, 429-433], GUI values of fast-twitch skeletal muscles of virgin rats were low in the fed ad libitum and the 24 h-starved states, but dramatically increased after subsequent chow re-feeding. GUI values of fast-twitch skeletal muscles of late-pregnant rats were also low in the fed and starved states and were increased by re-feeding, but the increase in GUI values elicited by re-feeding was greatly attenuated. PDHa activities in EDL, tibialis anterior and gastrocnemius in the fed state were unaffected by late pregnancy, and skeletal-muscle PDHa activities were decreased after 24 h of starvation in both groups. Whereas re-feeding of virgin rats with standard diet for 2 h restored PDHa activities in fast-twitch skeletal muscles to values for rats continuously fed ad libitum, PDHa activities in fast-twitch skeletal muscles of late-pregnant rats, although increased in response to re-feeding, remained considerably less than the corresponding fed ad libitum values after 2 h of re-feeding. In contrast, neither skeletal-muscle GS re-activation nor rates of skeletal-muscle glycogen deposition after re-feeding were markedly affected by late pregnancy. The results are discussed in relation to the specific targeting of individual pathways of glucose disposal in fast-twitch skeletal muscles during re-feeding in late pregnancy.
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Ryall, James G., Paul Gregorevic, David R. Plant, Martin N. Sillence, and Gordon S. Lynch. "β2-Agonist fenoterol has greater effects on contractile function of rat skeletal muscles than clenbuterol." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, no. 6 (December 1, 2002): R1386—R1394. http://dx.doi.org/10.1152/ajpregu.00324.2002.
Full textAbstract:
Potential treatments for skeletal muscle wasting and weakness ideally possess both anabolic and ergogenic properties. Although the β2-adrenoceptor agonist clenbuterol has well-characterized effects on skeletal muscle, less is known about the therapeutic potential of the related β2-adrenoceptor agonist fenoterol. We administered an equimolar dose of either clenbuterol or fenoterol to rats for 4 wk to compare their effects on skeletal muscle and tested the hypothesis that fenoterol would produce more powerful anabolic and ergogenic effects. Clenbuterol treatment increased fiber cross-sectional area (CSA) by 6% and maximal isometric force (Po) by 20% in extensor digitorum longus (EDL) muscles, whereas fiber CSA in soleus muscles decreased by 3% and Po was unchanged, compared with untreated controls. In the EDL muscles, fenoterol treatment increased fiber CSA by 20% and increased Po by 12% above values achieved after clenbuterol treatment. Soleus muscles of fenoterol-treated rats exhibited a 13% increase in fiber CSA and a 17% increase in Po above that of clenbuterol-treated rats. These data indicate that fenoterol has greater effects on the functional properties of rat skeletal muscles than clenbuterol.
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Herzog, Walter, Timothy Koh, Evelyne Hasler, and Tim Leonard. "Specificity and Plasticity of Mammalian Skeletal Muscles." Journal of Applied Biomechanics 16, no. 1 (February 2000): 98–109. http://dx.doi.org/10.1123/jab.16.1.98.
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We hypothesize that the neuromuscular system is designed to function effectively in accomplishing everyday movement tasks. Since everyday movement tasks may vary substantially in terms of speed and resistance, we speculate that agonistic muscles contribute differently to varying movement tasks such that the mechanical, structural, and physiological properties of the system are optimized at all times. We further hypothesize that a mechanical perturbation to the musculoskeletal system, such as the loss of an important joint ligament or the change of a muscle’s line of action, causes an adaptation of the system aimed at reestablishing effective function. Here. we demonstrate how the specificity of the cat ankle extensors is used to accommodate different locomotor tasks. We then illustrate how the loss of an important ligament in the cat knee leads to neuromuscular adaptation. Finally, we discuss the adaptability of skeletal muscle following an intervention that changes a muscle’s line of action, moment arm, and excursion.
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Vignaud, A., C. Hourde, F. Medja, O. Agbulut, G. Butler-Browne, and A. Ferry. "Impaired Skeletal Muscle Repair after Ischemia-Reperfusion Injury in Mice." Journal of Biomedicine and Biotechnology 2010 (2010): 1–10. http://dx.doi.org/10.1155/2010/724914.
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Ischemia/reperfusion (IR) injury can induce skeletal muscle fibre death and subsequent regeneration. By 14 days, absolute and specific maximal forces and fatigue resistance in ischemic/reperfused soleus muscles were still reduced (−89%, −81%, and −75%, resp.) as compared to control muscles (P<.05). The decrease of these parameters in ischemic/reperfused muscle was much greater than that of myotoxic injured muscles (−12%, −11%, and −19%;P<.05). In addition, at 14 days ischemic/reperfused muscle structure was still abnormal, showing small muscle fibres expressing neonatal myosin heavy chain and large necrotic muscle fibres that were not observed in myotoxin treated muscles. By 56 days, in contrast to myotoxin treated muscles, specific maximal force and muscle weight of the ischemic/reperfused muscles did not fully recover (P<.05). This differential recovery between ischemic/reperfused and myotoxin treated muscles was not related to the differences in the initial cell death, loss of satellite cells after injury, expression of growth factors (IGF1, IGF2..), or capillary density in regenerating muscles. In conclusion, our results demonstrate that IR injury in mice induces long term detrimental effects in skeletal muscles and that the recovery following IR injury was delayed for yet unknown reasons as compared to myotoxic injury.
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Frueh, Bartley R., Paul Gregorevic, David A. Williams, and Gordon S. Lynch. "Specific Force of the Rat Extraocular Muscles, Levator and Superior Rectus, Measured In Situ." Journal of Neurophysiology 85, no. 3 (March 1, 2001): 1027–32. http://dx.doi.org/10.1152/jn.2001.85.3.1027.
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Extraocular muscles are characterized by their faster rates of contraction and their higher resistance to fatigue relative to limb skeletal muscles. Another often reported characteristic of extraocular muscles is that they generate lower specific forces ( sP o, force per muscle cross-sectional area, kN/m2) than limb skeletal muscles. To investigate this perplexing issue, the isometric contractile properties of the levator palpebrae superioris (levator) and superior rectus muscles of the rat were examined in situ with nerve and blood supply intact. The extraocular muscles were attached to a force transducer, and the cranial nerves exposed for direct stimulation. After determination of optimal muscle length ( L o) and stimulation voltage, a full frequency-force relationship was established for each muscle. Maximum isometric tetanic force ( P o) for the levator and superior rectus muscles was 177 ± 13 and 280 ± 10 mN (mean ± SE), respectively. For the calculation of specific force, a number of rat levator and superior rectus muscles were stored in a 20% nitric acid-based solution to isolate individual muscle fibers. Muscle fiber lengths ( L f) were expressed as a percentage of overall muscle length, allowing a mean L f to L o ratio to be used in the estimation of muscle cross-sectional area. Mean L f: L owas determined to be 0.38 for the levator muscle and 0.45 for the superior rectus muscle. The sP o for the rat levator and superior rectus muscles measured in situ was 275 and 280 kN/m2, respectively. These values are within the range of sP o values commonly reported for rat skeletal muscles. Furthermore P o and sP o for the rat levator and superior rectus muscles measured in situ were significantly higher ( P < 0.001) than P oand sP o for these muscles measured in vitro. The results indicate that the force output of intact extraocular muscles differs greatly depending on the mode of testing. Although in vitro evaluation of extraocular muscle contractility will continue to reveal important information about this group of understudied muscles, the lower sP o values of these preparations should be recognized as being significantly less than their true potential. We conclude that extraocular muscles are not intrinsically weaker than skeletal muscles.
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Ito, Masato, Sadayuki Ujihashi, and Hyung Yun Choi. "E4 Biofidelic modeling of skeletal muscles(English session)." Proceedings of the Symposium on sports and human dynamics 2010 (2010): 464–69. http://dx.doi.org/10.1299/jsmeshd.2010.464.
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Vasileiadou, Olga, George G. Nastos, Panagiotis N. Chatzinikolaou, Dimitrios Papoutsis, Dimitra I. Vrampa, Spyridon Methenitis, and Nikos V. Margaritelis. "Redox Profile of Skeletal Muscles: Implications for Research Design and Interpretation." Antioxidants 12, no. 9 (September 7, 2023): 1738. http://dx.doi.org/10.3390/antiox12091738.
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Mammalian skeletal muscles contain varying proportions of Type I and II fibers, which feature different structural, metabolic and functional properties. According to these properties, skeletal muscles are labeled as ‘red’ or ‘white’, ‘oxidative’ or ‘glycolytic’, ‘slow-twitch’ or ‘fast-twitch’, respectively. Redox processes (i.e., redox signaling and oxidative stress) are increasingly recognized as a fundamental part of skeletal muscle metabolism at rest, during and after exercise. The aim of the present review was to investigate the potential redox differences between slow- (composed mainly of Type I fibers) and fast-twitch (composed mainly of Type IIa and IIb fibers) muscles at rest and after a training protocol. Slow-twitch muscles were almost exclusively represented in the literature by the soleus muscle, whereas a wide variety of fast-twitch muscles were used. Based on our analysis, we argue that slow-twitch muscles exhibit higher antioxidant enzyme activity compared to fast-twitch muscles in both pre- and post-exercise training. This is also the case between heads or regions of fast-twitch muscles that belong to different subcategories, namely Type IIa (oxidative) versus Type IIb (glycolytic), in favor of the former. No safe conclusion could be drawn regarding the mRNA levels of antioxidant enzymes either pre- or post-training. Moreover, slow-twitch skeletal muscles presented higher glutathione and thiol content as well as higher lipid peroxidation levels compared to fast-twitch. Finally, mitochondrial hydrogen peroxide production was higher in fast-twitch muscles compared to slow-twitch muscles at rest. This redox heterogeneity between different muscle types may have ramifications in the analysis of muscle function and health and should be taken into account when designing exercise studies using specific muscle groups (e.g., on an isokinetic dynamometer) or isolated muscle fibers (e.g., electrical stimulation) and may deliver a plausible explanation for the conflicting results about the ergogenic potential of antioxidant supplements.
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Koerker, D. J., I. R. Sweet, and D. G. Baskin. "Insulin binding to individual rat skeletal muscles." American Journal of Physiology-Endocrinology and Metabolism 259, no. 4 (October 1, 1990): E517—E523. http://dx.doi.org/10.1152/ajpendo.1990.259.4.e517.
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Studies of insulin binding to skeletal muscle, performed using sarcolemmal membrane preparations or whole muscle incubations of mixed muscle or typical red (soleus, psoas) or white [extensor digitorum longus (EDL), gastrocnemius] muscle, have suggested that red muscle binds more insulin than white muscle. We have evaluated this hypothesis using cryostat sections of unfixed tissue to measure insulin binding in a broad range of skeletal muscles; many were of similar fiber-type profiles. Insulin binding per square millimeter of skeletal muscle slice was measured by autoradiography and computer-assisted densitometry. We found a 4.5-fold range in specific insulin tracer binding, with heart and predominantly slow-twitch oxidative muscles (SO) at the high end and the predominantly fast-twitch glycolytic (FG) muscles at the low end of the range. This pattern reflects insulin sensitivity. Evaluation of displacement curves for insulin binding yielded linear Scatchard plots. The dissociation constants varied over a ninefold range (0.26-2.06 nM). Binding capacity varied from 12.2 to 82.7 fmol/mm2. Neither binding parameter was correlated with fiber type or insulin sensitivity; e.g., among three muscles of similar fiber-type profile, the EDL had high numbers of low-affinity binding sites, whereas the quadriceps had low numbers of high-affinity sites. In summary, considerable heterogeneity in insulin binding was found among hindlimb muscles of the rat, which can be attributed to heterogeneity in binding affinities and the numbers of binding sites. It can be concluded that a given fiber type is not uniquely associated with a set of insulin binding parameters that result in high or low binding.
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Norheim, Frode, Truls Raastad, Bernd Thiede, Arild C. Rustan, Christian A. Drevon, and Fred Haugen. "Proteomic identification of secreted proteins from human skeletal muscle cells and expression in response to strength training." American Journal of Physiology-Endocrinology and Metabolism 301, no. 5 (November 2011): E1013—E1021. http://dx.doi.org/10.1152/ajpendo.00326.2011.
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Regular physical activity protects against several types of diseases. This may involve altered secretion of signaling proteins from skeletal muscle. Our aim was to identify the most abundantly secreted proteins in cultures of human skeletal muscle cells and to monitor their expression in muscles of strength-training individuals. A total of 236 proteins were detected by proteome analysis in medium conditioned by cultured human myotubes, which was narrowed down to identification of 18 classically secreted proteins expressed in skeletal muscle, using the SignalP 3.0 and Human Genome Expression Profile databases together with a published mRNA-based reconstruction of the human skeletal muscle secretome. For 17 of the secreted proteins, expression was confirmed at the mRNA level in cultured human myotubes as well as in biopsies of human skeletal muscles. RT-PCR analyses showed that 15 of the secreted muscle proteins had significantly enhanced mRNA expression in m. vastus lateralis and/or m. trapezius after 11 wk of strength training among healthy volunteers. For example, secreted protein acidic and rich in cysteine, a secretory protein in the membrane fraction of skeletal muscle fibers, was increased 3- and 10-fold in m. vastus lateralis and m. trapezius, respectively. Identification of proteins secreted by skeletal muscle cells in vitro facilitated the discovery of novel responses in skeletal muscles of strength-training individuals.
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Høeg, Louise D., Kim A. Sjøberg, Anne-Marie Lundsgaard, Andreas B. Jordy, Natalie Hiscock, Jørgen F. P. Wojtaszewski, Erik A. Richter, and Bente Kiens. "Adiponectin concentration is associated with muscle insulin sensitivity, AMPK phosphorylation, and ceramide content in skeletal muscles of men but not women." Journal of Applied Physiology 114, no. 5 (March 1, 2013): 592–601. http://dx.doi.org/10.1152/japplphysiol.01046.2012.
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Adiponectin is an adipokine that regulates metabolism and increases insulin sensitivity. Mechanisms behind this insulin-sensitizing effect have been investigated in rodents, but little is known in humans, especially in skeletal muscle. Women have higher serum concentrations of adiponectin than men and are generally more insulin sensitive in skeletal muscle than men. We show here that large differences exist between men and women with regard to apparent adiponectin regulation of insulin-stimulated glucose uptake in skeletal muscle. Serum adiponectin was significantly associated with leg glucose uptake in healthy, young, lean men, but the association was absent in women. In addition, serum adiponectin was significantly associated with AMP-activated protein kinase (AMPK) phosphorylation in skeletal muscles of men but not in women. Serum adiponectin was also significantly, negatively associated with skeletal muscle ceramide content in men only, and interestingly, ceramide content was negatively associated with adiponectin receptor 1 (AdipoR1) expression in skeletal muscles of men. Women had lower AdipoR1 expression in skeletal muscle and a lower percentage of glycolytic adiponectin-sensitive type 2 muscle fibers than men. These associations suggest that the insulin-sensitizing effect of adiponectin on human male skeletal muscles may be mediated via AdipoR1 to activation of AMPK, leading to lowering of ceramide content. The lower skeletal muscle AdipoR1 protein expression and lower expression of adiponectin-sensitive type 2 muscle fibers in women than in men may explain the apparent lesser sensitivity to adiponectin in women.
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Laughlin, M. H., R. E. Klabunde, M. D. Delp, and R. B. Armstrong. "Effects of dipyridamole on muscle blood flow in exercising miniature swine." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 5 (November 1, 1989): H1507—H1515. http://dx.doi.org/10.1152/ajpheart.1989.257.5.h1507.
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The purpose of this study was to determine whether a vasodilator reserve exists in respiratory muscles and forelimb skeletal muscles in miniature swine during treadmill exercise. Blood flow (BF) was measured with radiolabeled microspheres during preexercise and before and after dipyridamole (DYP; 1 mg/kg iv) at 2 min of treadmill exercise at 11.2 (70% Vo2 max) and 17.6 km/h (Vo2 max). Muscle BFs were increased during exercise, and the relationship between exercise intensity and BF varied among the muscles. The high-oxidative extensor muscles and the flexor muscles attained peak BFs at 11.2 km/h, whereas the more superficial, lower oxidative extensor muscles showed increases in BF up to maximal exercise. During running at 11.2 km/h, DYP produced increases in BF only in cardiac muscle, respiratory muscle and the medial head of the triceps muscle (MHT), which is composed of 91% slow-twitch oxidative (SO) fibers. During maximal exercise (17.6 km/h), DYP produced a 31-mmHg decrease in mean arterial pressure (MAP) and increases in vascular conductance in all muscles studied. BF was only increased in MHT and cardiac muscle. We conclude that vasodilator reserve remains in skeletal muscle and respiratory muscle even during maximal exercise in swine. If it is assumed that DYP-induced vasodilation in a muscle sample is indicative of adenosine production, these results suggest that SO skeletal muscle (MHT) and respiratory muscle are similar to cardiac muscle in that they produce adenosine even when adequately perfused. Furthermore, during maximal exercise, all skeletal muscle appears to produce adenosine, suggesting that muscle BF is restricted under these conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
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Caiozzo, Vincent J., Michael J. Baker, Karen Huang, Harvey Chou, Ya Zhen Wu, and Kenneth M. Baldwin. "Single-fiber myosin heavy chain polymorphism: how many patterns and what proportions?" American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 285, no. 3 (September 2003): R570—R580. http://dx.doi.org/10.1152/ajpregu.00646.2002.
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Previous studies have reported the existence of skeletal muscle fibers that coexpress multiple myosin heavy chain isoforms. These surveys have usually been limited to studying the polymorphic profiles of skeletal muscle fibers from a limited number of muscles (i.e., usually <4). Additionally, few studies have considered the functional implications of polymorphism. Hence, the primary objective of this study was to survey a relatively large number of rat skeletal muscle/muscle regions and muscle fibers ( n≈ 5,000) to test the hypothesis that polymorphic fibers represent a larger fraction of the total pool of fibers than do so-called monomorphic fibers, which express only one myosin heavy chain isoform. Additionally, we used Hill's statistical model of the force-velocity relationship to differentiate the functional consequences of single-fiber myosin heavy chain isoform distributions found in these muscles. The results demonstrate that most muscles and regions of rodent skeletal muscles contain large proportions of polymorphic fibers, with the exception of muscles such as the slow soleus muscle and white regions of fast muscles. Several muscles were also found to have polymorphic profiles that are not consistent with the I↔IIA↔IIX↔IIB scheme of muscle plasticity. For instance, it was found that the diaphragm muscle normally contains I/IIX fibers. Functionally, the high degree of polymorphism may 1) represent a strategy for producing a spectrum of contractile properties that far exceeds that simply defined by the presence of four myosin heavy chain isoforms and 2) result in relatively small differences in function as defined by the force-velocity relationship.
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Kenis, V. M., A. V. Sapogovskiy, E. V. Melchenko, O. E. Agranovich, A. I. Shubina, and M. V. Zhurbitskaya. "Ultrasound elastography of muscles in cerebral palsy: systematic review." Neuromuscular Diseases 12, no. 1 (February 14, 2022): 10–20. http://dx.doi.org/10.17650/2222-8721-2022-12-1-10-20.
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Quantitative analysis of skeletal muscles in cerebral palsy is an important but unsolved problem. Ultrasound elastography is a group of diagnostic methods that allow visualizing tissue stiffness, measuring and displaying biomechanical properties of tissues. The aim of our study was to conduct a systematic analysis of literature on ultrasound elastography of skeletal muscles in children with cerebral palsy.A literary search for keywords in the databases PubMed, Google Scholar, eLIBRARY was carried out. The inclusion criteria were nosology (cerebral palsy), age (up to 18 years) and the study design (original study in ultrasound elastography of the skeletal muscler), as well as the availability of detailed information about the technical issues, demographic and clinical data.The final analysis included 20 publications. Patients with hemiplegic cerebral palsy were most often studied, with the healthy side used as a control, shear wave elastography was used more often, in which both share wave velocity and shear modulus were assessed, and linear probes were used more often. The most frequent anatomical objects were the calf muscles. Most often, elastography was used to assess the results of botulinum therapy, and demonstrated an increase in muscle elasticity after treatment.Ultrasound elastography as a method od assessment of the mechanical properties of skeletal muscles in children with cerebral palsy cannot be considered suitable as a routine study at the moment. But the method showed promising results for the research purposes: all the publications we analyzed demonstrated significant difference in elastography indicators both when comparing with unaffected limb or with healthy controls. Positive changes were also detected after various therapeutic interventions aimed to reducing muscle tone and retraction e. g. botulinum toxin injections.The absence of a unified approach to muscle elastography in children with cerebral palsy was demonstrated, both for data obtaining and interpretation. In general, ultrasound elastography of the skeletal muscles in children with cerebral palsy is a promising method for qualitative and quantitative assessment of muscle tissue that requires further development. Improvement of technology, standardization of technique and measurements will further expand the usage of this method.
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Grounds, Miranda D. "Factors Controlling Movement of Skeletal Muscles." Leonardo 48, no. 3 (June 2015): 270–71. http://dx.doi.org/10.1162/leon_a_01028.
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The contraction of specialized skeletal muscle cells results in classic movements of bones and other parts of the body that are vital for life. There is exquisite control over the movement of diverse types of muscles. This paper indicates the way in which skeletal muscles (myofibres) are formed; then factors that contribute to generating the movement are outlined: these include the nerve, sarcomeres, cytoskeleton, cell membrane and the extracellular matrix. The factors controlling the movement of mature myofibres in 3-dimensional tissues in vivo are vastly more complex than for tissue cultured immature muscle cells in an artificial in vitro environment.
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Turinsky, J., D. M. O'Sullivan, and B. P. Bayly. "Modulation of prostaglandin E2 synthesis in rat skeletal muscle." American Journal of Physiology-Endocrinology and Metabolism 262, no. 4 (April 1, 1992): E476—E482. http://dx.doi.org/10.1152/ajpendo.1992.262.4.e476.
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The effect of muscle denervation, inhibitors of protein synthesis, G proteins, and sphingolipids on prostaglandin E2 (PGE2) release by rat soleus muscle in vitro was investigated. To assess the effect of muscle denervation, the sciatic nerve in one hindlimb of rats was interrupted, and soleus muscles from the denervated hindlimb and the contralateral sham (control) hindlimb were excised 1-5 days after surgery. Compared with corresponding sham muscles, PGE2 release by denervated muscles was increased 56, 230, and 435% at 1, 3, and 5 days after denervation, respectively. Protein synthesis inhibitors cycloheximide (10 microM) and puromycin (10 microM) lowered PGE2 release by sham and denervated muscles 62-80%. The release of PGE2 by sham and denervated muscles was not altered by pertussis toxin (1 microgram/ml) but was inhibited 30-51% by AlF4-. Addition of 100 microM guanosine 5'-O-(3-thiotriphosphate) to saponin-permeabilized sham and denervated muscles had only a moderate, if any, stimulatory effect on PGE2 release. This effect was not counteracted by 1 mM guanosine 5'-O-(2-thiodiphosphate). Increasing muscle ceramide concentration by incubation with sphingomyelinase (100 mU/ml) increased PGE2 release by sham and denervated muscles 43 and 157%, respectively. Because degradation of ceramides yields sphingosine, the effect of sphingosine was also tested. Sphingosine (25 microM) increased PGE2 release by sham and denervated muscles 139 and 187%, respectively, without affecting muscle viability, as assessed by the release of lactate dehydrogenase. The data indicate that muscle denervation, treatment with sphingomyelinase, and sphingosine stimulate, whereas inhibitors of protein synthesis inhibit PGE2 synthesis by muscle.
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O'Connell, Grant, Ge Guo, Janelle Stricker, LeBris S. Quinn, Averil Ma, and Emidio E. Pistilli. "Muscle-specific deletion of exons 2 and 3 of theIL15RAgene in mice: effects on contractile properties of fast and slow muscles." Journal of Applied Physiology 118, no. 4 (February 15, 2015): 437–48. http://dx.doi.org/10.1152/japplphysiol.00704.2014.
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Interleukin-15 (IL-15) is a putative myokine hypothesized to induce an oxidative skeletal muscle phenotype. The specific IL-15 receptor alpha subunit (IL-15Rα) has also been implicated in specifying this contractile phenotype. The purposes of this study were to determine the muscle-specific effects of IL-15Rα functional deficiency on skeletal muscle isometric contractile properties, fatigue characteristics, spontaneous cage activity, and circulating IL-15 levels in male and female mice. Muscle creatine kinase (MCK)-driven IL-15Rα knockout mice ( mIl15rafl/fl/Cre+) were generated using the Cre-loxP system. We tested the hypothesis that IL-15Rα functional deficiency in skeletal muscle would increase resistance to contraction-induced fatigue, cage activity, and circulating IL-15 levels. There was a significant effect of genotype on the fatigue curves obtained in extensor digitorum longus (EDL) muscles from female mIl15rafl/fl/Cre+mice, such that force output was greater during the repeated contraction protocol compared with mIl15rafl/fl/Cre−control mice. Muscles from female mIl15rafl/fl/Cre+mice also had a twofold greater amount of the mitochondrial genome-specific COXII gene compared with muscles from mIl15rafl/fl/Cre−control mice, indicating a greater mitochondrial density in these skeletal muscles. There was a significant effect of genotype on the twitch:tetanus ratio in EDL and soleus muscles from mIl15rafl/fl/Cre+mice, such that the ratio was lower in these muscles compared with mIl15rafl/fl/Cre−control mice, indicating a pro-oxidative shift in muscle phenotype. However, spontaneous cage activity was not different and IL-15 protein levels were lower in male and female mIl15rafl/fl/Cre+mice compared with control. Collectively, these data support a direct effect of muscle IL-15Rα deficiency in altering contractile properties and fatigue characteristics in skeletal muscles.
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McCutchan, H. J., J. R. Schwappach, E. G. Enquist, D. L. Walden, L. S. Terada, O. K. Reiss, J. A. Leff, and J. E. Repine. "Xanthine oxidase-derived H2O2 contributes to reperfusion injury of ischemic skeletal muscle." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 5 (May 1, 1990): H1415—H1419. http://dx.doi.org/10.1152/ajpheart.1990.258.5.h1415.
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We hypothesized that xanthine oxidase (XO)-derived hydrogen peroxide (H2O2) contributes to ischemic skeletal muscle injury during reperfusion. We found that after ischemia (3 h) and then reperfusion (4 h) rat gastrocnemius muscles had decreased contractile function following direct stimulation. Three lines of investigation suggested that XO-derived H2O2 contributes to reperfusion injury of ischemic skeletal muscle. First, treatment with dimethylthiurea (DMTU), a highly permeant O2 metabolite scavenger, but not urea, just before reperfusion improved muscle function in legs subjected to ischemia and then reperfusion. Second, gastrocnemius muscles from rats fed tungsten or allopurinol had negligible XO activities and increased muscle function after ischemia and reperfusion. Third, as assessed by measurement of skeletal muscle catalase activity in the presence of aminotriazole, H2O2 was measured during reperfusion of ischemic muscles from untreated or urea-treated rats but not during reperfusion of muscles from rats treated with DMTU, tungsten, or allopurinol.
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Fagan, J. M., E. F. Wajnberg, L. Culbert, and L. Waxman. "ATP depletion stimulates calcium-dependent protein breakdown in chick skeletal muscle." American Journal of Physiology-Endocrinology and Metabolism 262, no. 5 (May 1, 1992): E637—E643. http://dx.doi.org/10.1152/ajpendo.1992.262.5.e637.
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The contribution of metabolic energy to the degradation of intracellular proteins in skeletal muscle was investigated. Isolated chick skeletal muscles deprived of oxygen and muscles incubated in buffer under nonphysiological conditions containing inhibitors of glycolysis and mitochondrial respiration had lower concentrations or undetectable levels of ATP and faster rates of proteolysis. Both total protein breakdown and the breakdown of myofibrillar proteins were stimulated 35-124% in ATP-depleted tissues. However, ATP-depleted muscles incubated in buffer to which no Ca2+ was added showed slower rates of total protein breakdown and no significant change in myofibrillar proteolysis compared with control muscles. Trans-epoxysuccinyl-L-leucylamido(4-guanidino)butane (E-64), a compound that inhibits the calpains and the lysosomal cysteine proteases, completely blocked the Ca(2+)-stimulated breakdown of nonmyofibrillar and myofibrillar proteins in ATP-depleted muscles. However, Ca(2+)-stimulated proteolysis was not inhibited in ATP-depleted muscles incubated with weak bases to prevent lysosome function. These data suggest that intracellular proteins can be degraded in skeletal muscle in the absence of metabolic energy and that the calpains play a major role in the enhanced proteolysis in skeletal muscles depleted of ATP.
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Dong, Gongwu, and Yu Wang. "EFFECT OF PHYSICAL EXERCISE ON INCREASING THE MAXIMUM OXYGEN UPTAKE OF SKELETAL MUSCLE." Revista Brasileira de Medicina do Esporte 27, no. 7 (July 2021): 710–13. http://dx.doi.org/10.1590/1517-8692202127072021_0352.
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ABSTRACT Introduction: Aerobic exercise can improve the physical function of athletes and increase the oxygen content in skeletal muscles. This has a significant reference value for evaluating training effects and judging sports fatigue. Objective: Maximum oxygen uptake is one of the most critical indicators of aerobic work capacity. The thesis analyzes the medical promotion effect of physical exercise on the oxygen content of skeletal muscle. Methods: The thesis performed aerobic exercises on two groups of young rowers. Athletes in group A performed high-load exercise, and athletes in group B performed low-load exercise. At the same time, we placed a detector on the athletes’ skeletal muscle to test the volunteer's muscle oxygen content and other physiological indicators. Results: Comparing high-load exercise and low-load exercise, the maximum oxygen uptake and the utilization rate of the maximum oxygen uptake when reaching the anaerobic net were 10% and 16% higher, respectively. There was no difference in the activity of muscle enzymes between the two groups. Conclusions: After aerobic training, the muscle's oxygen utilization capacity is strengthened. Physical exercise promotes the maximum oxygen uptake of skeletal muscles. Level of evidence II; Therapeutic studies - investigation of treatment results.
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Herring, B. P., M. H. Nunnally, P. J. Gallagher, and J. T. Stull. "Molecular characterization of rat skeletal muscle myosin light chain kinase." American Journal of Physiology-Cell Physiology 256, no. 2 (February 1, 1989): C399—C404. http://dx.doi.org/10.1152/ajpcell.1989.256.2.c399.
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A 1.85-kilobase (kb) cDNA has been isolated that encodes the catalytic and calmodulin binding domains of rat skeletal muscle myosin light chain kinase. The cDNA hybridized to a 3.3-kb RNA present in fast- and slow-twitch skeletal muscles. The reported enzymatic activity (3-fold greater in fast- than slow-twitch skeletal muscles) reflects the relative abundance of this RNA in the two types of skeletal muscle. No hybridization of the cDNA was detected to RNA isolated from smooth or nonmuscle tissues. The clone cross hybridized to a 2.2-kb RNA present in cardiac tissue. Ribonuclease protection analysis of skeletal and cardiac muscle RNA revealed major differences in the two hybridizing RNAs. Thus rat skeletal muscle contains a single myosin light chain kinase isoform, which is distinct from the cardiac, smooth, and nonmuscle forms.
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Sato, Koji, Motoyuki Iemitsu, Katsuji Aizawa, and Ryuichi Ajisaka. "Testosterone and DHEA activate the glucose metabolism-related signaling pathway in skeletal muscle." American Journal of Physiology-Endocrinology and Metabolism 294, no. 5 (May 2008): E961—E968. http://dx.doi.org/10.1152/ajpendo.00678.2007.
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Circulating dehydroepiandrosterone (DHEA) is converted to testosterone or estrogen in the target tissues. Recently, we demonstrated that skeletal muscles are capable of locally synthesizing circulating DHEA to testosterone and estrogen. Furthermore, testosterone is converted to 5α-dihydrotestosterone (DHT) by 5α-reductase and exerts biophysiological actions through binding to androgen receptors. However, it remains unclear whether skeletal muscle can synthesize DHT from testosterone and/or DHEA and whether these hormones affect glucose metabolism-related signaling pathway in skeletal muscles. We hypothesized that locally synthesized DHT from testosterone and/or DHEA activates glucose transporter-4 (GLUT-4)-regulating pathway in skeletal muscles. The aim of the present study was to clarify whether DHT is synthesized from testosterone and/or DHEA in cultured skeletal muscle cells and whether these hormones affect the GLUT-4-related signaling pathway in skeletal muscles. In the present study, the expression of 5α-reductase mRNA was detected in rat cultured skeletal muscle cells, and the addition of testosterone or DHEA increased intramuscular DHT concentrations. Addition of testosterone or DHEA increased GLUT-4 protein expression and its translocation. Furthermore, Akt and protein kinase C-ζ/λ (PKC-ζ/λ) phosphorylations, which are critical in GLUT-4-regulated signaling pathways, were enhanced by testosterone or DHEA addition. Testosterone- and DHEA-induced increases in both GLUT-4 expression and Akt and PKC-ζ/λ phosphorylations were blocked by a DHT inhibitor. Finally, the activities of phosphofructokinase and hexokinase, main glycolytic enzymes, were enhanced by testosterone or DHEA addition. These findings suggest that skeletal muscle is capable of synthesizing DHT from testosterone, and that DHT activates the glucose metabolism-related signaling pathway in skeletal muscle cells.
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Wu, G., J. R. Thompson, and V. E. Baracos. "Glutamine metabolism in skeletal muscles from the broiler chick (Gallus domesticus) and the laboratory rat (Rattus norvegicus)." Biochemical Journal 274, no. 3 (March 15, 1991): 769–74. http://dx.doi.org/10.1042/bj2740769.
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Oxidative decarboxylation of L-[1-14C]glutamine was studied in isolated chick and rat skeletal muscles incubated in the presence of glucose, insulin and plasma concentrations of amino acids. (1) The rate of oxidative decarboxylation of L-[1-14C]glutamine was high, and exceeded that of L-[1-14C]leucine in all muscles. (2) The rate of oxidative decarboxylation of L-[1-14C]glutamine increased with increasing intracellular concentrations of glutamine. (3) The activities of glutamine aminotransferases K and L were more than 10-fold greater in rat than in chick skeletal muscles. (4) Mitochondrial phosphate-activated glutaminase activity was approx. 10-fold greater in chick than in rat skeletal muscles and increased with increasing glutamine concentrations. (5) An inhibitor of glutaminase, 6-diazo-5-oxo-L-norleucine, inhibited the rate of glutamine decarboxylation in chick, but not in rat, skeletal muscle. These findings suggest that glutamine degradation in skeletal muscle may be substantial and may make an important contribution to the regulation of intramuscular glutamine concentrations. A species difference in the pathways and the subcellular location for the conversion of glutamine into 2-oxoglutarate in rat and chick skeletal muscles is implied by the relative activities of glutamine-degrading enzymes.
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Rasmussen, Tara, and Haley Tucker. "Loss of SMYD1 Results in Perinatal Lethality via Selective Defects within Myotonic Muscle Descendants." Diseases 7, no. 1 (December 20, 2018): 1. http://dx.doi.org/10.3390/diseases7010001.
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SET and MYND Domain 1 (SMYD1) is a cardiac and skeletal muscle-specific, histone methyl transferase that is critical for both embryonic and adult heart development and function in both mice and men. We report here that skeletal muscle-specific, myogenin (myoG)-Cre-mediated conditional knockout (CKO) of Smyd1 results in perinatal death. As early as embryonic day 12.5, Smyd1 CKOs exhibit multiple skeletal muscle defects in proliferation, morphology, and gene expression. However, all myotonic descendants are not afflicted equally. Trunk muscles are virtually ablated with excessive accumulation of brown adipose tissue (BAT), forelimb muscles are disorganized and improperly differentiated, but other muscles, such as the masseter, are normal. While expression of major myogenic regulators went unscathed, adaptive and innate immune transcription factors critical for BAT development/physiology were downregulated. Whereas classical mitochondrial BAT accumulation went unscathed following loss of SMYD1, key transcription factors, including PRDM16, UCP-1, and CIDE-a that control skeletal muscle vs. adipose fate, were downregulated. Finally, in rare adults that survive perinatal lethality, SMYD1 controls specification of some, but not all, skeletal muscle fiber-types.
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Sun, Baojun, Hitomi Maruta, Yun Ma, and Hiromi Yamashita. "Taurine Stimulates AMP-Activated Protein Kinase and Modulates the Skeletal Muscle Functions in Rats via the Induction of Intracellular Calcium Influx." International Journal of Molecular Sciences 24, no. 4 (February 18, 2023): 4125. http://dx.doi.org/10.3390/ijms24044125.
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Taurine (2-aminoethanesulfonic acid) is a free amino acid abundantly found in mammalian tissues. Taurine plays a role in the maintenance of skeletal muscle functions and is associated with exercise capacity. However, the mechanism underlying taurine function in skeletal muscles has not yet been elucidated. In this study, to investigate the mechanism of taurine function in the skeletal muscles, the effects of short-term administration of a relatively low dose of taurine on the skeletal muscles of Sprague–Dawley rats and the underlying mechanism of taurine function in cultured L6 myotubes were investigated. The results obtained in this study in rats and L6 cells indicate that taurine modulates the skeletal muscle function by stimulating the expression of genes and proteins associated with mitochondrial and respiratory metabolism through the activation of AMP-activated protein kinase via the calcium signaling pathway.