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Zhang, Tan, Xin Feng, Bo Feng, Juan Dong, Karen Haas, Barbara M. Nicklas, Osvaldo Delbono e Stephen Kritchevsky. "CARDIAC TROPONIN T MEDIATED AUTOIMMUNE RESPONSE AND ITS ROLE IN SKELETAL MUSCLE AGING". Innovation in Aging 3, Supplement_1 (novembro de 2019): S882. http://dx.doi.org/10.1093/geroni/igz038.3231.
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Abstract Cardiac troponin T (cTnT), a key component of contractile machinery essential for muscle contraction, is also expressed in skeletal muscle under certain conditions (e.g. neuromuscular diseases and aging). We have reported that skeletal muscle cTnT regulates neuromuscular junction denervation preferentially in fast skeletal muscle of old mice. Here, we further report that cTnT is also enriched within some myofibers, and/or along microvascular walls in old mice fast skeletal muscle. Strikingly, immunoglobulin G (IgG), together with markers of complement system activation, cell death (necroptosis or apoptosis), and macrophage infiltration, were all found to be co-localized with cTnT and IgG in those areas. In addition, elevated cTnT and IgG are associated with lower dystrophin expression on muscle fiber membrane, lower muscle capillary density, and reduced muscle performance (wire hanging test). Using purified recombinant TnT proteins, we confirmed that only cTnT, but not slow or fast skeletal muscle TnT1 or TnT3, was detected by immunoblot using sera from old (but not young) mice with pre-determined elevated cTnT and IgG in their skeletal muscle, indicating the existence of anti-cTnT autoantibodies in sera (previously found in human blood) and skeletal muscle of old mice. Immunoblotting further revealed that the age related changes in skeletaI muscle cTnT and IgG are more prominent in fast skeletal muscle than in slow. Importantly, elevated cTnT and IgG were also detected in skeletal muscles from 4 older adults (65-70 yrs, IMFIT). Our finding suggests a novel autoimmune mechanism mediated by cTnT that underlies age related skeletal muscle abnormalities and dysfunction.
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Kholodnyi, R. D. "MODELING THE SKELETAL MUSCLE INJURY IN RATS". International Journal of Veterinary Medicine, n.º 3 (18 de outubro de 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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Azab, Azab. "Skeletal Muscles: Insight into Embryonic Development, Satellite Cells, Histology, Ultrastructure, Innervation, Contraction and Relaxation, Causes, Pathophysiology, and Treatment of Volumetric Muscle I". Biotechnology and Bioprocessing 2, n.º 4 (28 de maio de 2021): 01–17. http://dx.doi.org/10.31579/2766-2314/038.
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Background: Skeletal muscles are attached to bone and are responsible for the axial and appendicular movement of the skeleton and for maintenance of body position and posture. Objectives: The present review aimed to high light on embryonic development of skeletal muscles, histological and ultrastructure, innervation, contraction and relaxation, causes, pathophysiology, and treatment of volumetric muscle injury. The heterogeneity of the muscle fibers is the base of the flexibility which allows the same muscle to be used for various tasks from continuous low-intensity activity, to repeated submaximal contractions, and to fast and strong maximal contractions. The formation of skeletal muscle begins during the fourth week of embryonic development as specialized mesodermal cells, termed myoblasts. As growth of the muscle fibers continues, aggregation into bundles occurs, and by birth, myoblast activity has ceased. Satellite cells (SCs), have single nuclei and act as regenerative cells. Satellite cells are the resident stem cells of skeletal muscle; they are considered to be self-renewing and serve to generate a population of differentiation-competent myoblasts that will participate as needed in muscle growth, repair, and regeneration. Based on various structural and functional characteristics, skeletal muscle fibres are classified into three types: Type I fibres, Type II-B fibres, and type II-A fibres. Skeletal muscle fibres vary in colour depending on their content of myoglobin. Each myofibril exhibits a repeating pattern of cross-striations which is a product of the highly ordered arrangement of the contractile proteins within it. The parallel myofibrils are arranged with their cross-striations in the register, giving rise to the regular striations seen with light microscopy in longitudinal sections of skeletal muscle. Each skeletal muscle receives at least two types of nerve fibers: motor and sensory. Striated muscles and myotendinous junctions contain sensory receptors that are encapsulated proprioceptors. The process of contraction, usually triggered by neural impulses, obeys the all-or-none law. During muscle contraction, the thin filaments slide past the thick filaments, as proposed by Huxley's sliding filament theory. In response to a muscle injury, SCs are activated and start to proliferate; at this stage, they are often referred to as either myogenic precursor cells (MPC) or myoblasts. In vitro, evidence has been presented that satellite cells can be pushed towards the adipogenic and osteogenic lineages, but contamination of such cultures from non-myogenic cells is sometimes hard to dismiss as the underlying cause of this observed multipotency. There are, however, other populations of progenitors isolated from skeletal muscle, including endothelial cells and muscle-derived stem cells (MDSCs), blood-vessel-associated mesoangioblasts, muscle side-population cells, CD133+ve cells, myoendothelial cells, and pericytes. Volumetric muscle loss (VML) is defined as the traumatic or surgical loss of skeletal muscle with resultant functional impairment. It represents a challenging clinical problem for both military and civilian medicine. VML results in severe cosmetic deformities and debilitating functional loss. In response to damage, skeletal muscle goes through a well-defined series of events including; degeneration (1 to 3days), inflammation, and regeneration (3 to 4 weeks), fibrosis, and extracellular matrix remodeling (3 to 6 months).. Mammalian skeletal muscle has an impressive ability to regenerate itself in response to injury. During muscle tissue repair following damage, the degree of damage and the interactions between muscle and the infiltrating inflammatory cells appear to affect the successful outcome of the muscle repair process. The transplantation of stem cells into aberrant or injured tissue has long been a central goal of regenerative medicine and tissue engineering. Conclusion: It can be concluded that the formation of skeletal muscle begins during the fourth week of embryonic development as specialized mesodermal cells, termed myoblasts, by birth myoblast activity has ceased. Satellite cells are considered to be self-renewing, and serve to generate a population of differentiation-competent myoblasts. Skeletal muscle fibres are classified into three types. The process of contraction, usually triggered by neural impulses, obeys the all-or-none law. VML results in severe cosmetic deformities and debilitating functional loss. Mammalian skeletal muscle has an impressive ability to regenerate itself in response to injury. The transplantation of stem cells into aberrant or injured tissue has long been a central goal of regenerative medicine and tissue engineering.
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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, n.º 10 (19 de outubro de 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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Sandage, Mary J., e Audrey G. Smith. "Muscle Bioenergetic Considerations for Intrinsic Laryngeal Skeletal Muscle Physiology". Journal of Speech, Language, and Hearing Research 60, n.º 5 (24 de maio de 2017): 1254–63. http://dx.doi.org/10.1044/2016_jslhr-s-16-0192.
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PurposeIntrinsic laryngeal skeletal muscle bioenergetics, the means by which muscles produce fuel for muscle metabolism, is an understudied aspect of laryngeal physiology with direct implications for voice habilitation and rehabilitation. The purpose of this review is to describe bioenergetic pathways identified in limb skeletal muscle and introduce bioenergetic physiology as a necessary parameter for theoretical models of laryngeal skeletal muscle function.MethodA comprehensive review of the human intrinsic laryngeal skeletal muscle physiology literature was conducted. Findings regarding intrinsic laryngeal muscle fiber complement and muscle metabolism in human models are summarized and exercise physiology methodology is applied to identify probable bioenergetic pathways used for voice function.ResultsIntrinsic laryngeal skeletal muscle fibers described in human models support the fast, high-intensity physiological requirements of these muscles for biological functions of airway protection. Inclusion of muscle bioenergetic constructs in theoretical modeling of voice training, detraining, fatigue, and voice loading have been limited.ConclusionsMuscle bioenergetics, a key component for muscle training, detraining, and fatigue models in exercise science, is a little-considered aspect of intrinsic laryngeal skeletal muscle physiology. Partnered with knowledge of occupation-specific voice requirements, application of bioenergetics may inform novel considerations for voice habilitation and rehabilitation.
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Chen, Wan-Jing, I.-Hsuan Lin, Chien-Wei Lee e Yi-Fan Chen. "Aged Skeletal Muscle Retains the Ability to Remodel Extracellular Matrix for Degradation of Collagen Deposition after Muscle Injury". International Journal of Molecular Sciences 22, n.º 4 (20 de fevereiro de 2021): 2123. http://dx.doi.org/10.3390/ijms22042123.
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Aging causes a decline in skeletal muscle function, resulting in a progressive loss of muscle mass, quality, and strength. A weak regenerative capacity is one of the critical causes of dysfunctional skeletal muscle in elderly individuals. The extracellular matrix (ECM) maintains the tissue framework structure in skeletal muscle. As shown by previous reports and our data, the gene expression of ECM components decreases with age, but the accumulation of collagen substantially increases in skeletal muscle. We examined the structural changes in ECM in aged skeletal muscle and found restricted ECM degradation. In aged skeletal muscles, several genes that maintain ECM structure, such as transforming growth factor β (TGF-β), tissue inhibitors of metalloproteinases (TIMPs), matrix metalloproteinases (MMPs), and cathepsins, were downregulated. Muscle injury can induce muscle repair and regeneration in young and adult skeletal muscles. Surprisingly, muscle injury could not only efficiently induce regeneration in aged skeletal muscle, but it could also activate ECM remodeling and the clearance of ECM deposition. These results will help elucidate the mechanisms of muscle fibrosis with age and develop innovative antifibrotic therapies to decrease excessive collagen deposition in aged muscle.
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Lieber, Richard L. "Skeletal Muscle". Medicine & Science in Sports & Exercise 38, Supplement (maio de 2006): 63. http://dx.doi.org/10.1249/00005768-200605001-00585.
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Koroteyev, Alexis, Alberto Pochettino, Hiroshi Niinami e Larry W. Stephenson. "Skeletal Muscle". AORN Journal 53, n.º 4 (abril de 1991): 1005–20. http://dx.doi.org/10.1016/s0001-2092(07)69569-6.
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Ito, Daisuke, Yuji Tokoro, Eiichi Tanaka e Sota Yamamoto. "A Constitutive Model for Skeletal Muscle Taking Account of Anisotropic Damage and Viscoelasticity(2C1 Musculo-Skeletal Biomechanics IV)". Proceedings of the Asian Pacific Conference on Biomechanics : emerging science and technology in biomechanics 2007.3 (2007): S152. http://dx.doi.org/10.1299/jsmeapbio.2007.3.s152.
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Ramamani, A., M. M. Aruldhas e P. Govindarajulu. "Differential response of rat skeletal muscle glycogen metabolism to testosterone and estradiol". Canadian Journal of Physiology and Pharmacology 77, n.º 4 (1 de abril de 1999): 300–304. http://dx.doi.org/10.1139/y99-016.
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Although reports on sex steroids have implicated them as promoting protein synthesis and also providing extra strength to the skeletal muscle, it remains unclear whether sex steroids affect glycogen metabolism to provide energy for skeletal muscle functions, since glycogen metabolism is one of the pathways that provides energy for the skeletal muscle contraction and relaxation cycle. The purpose of the current study was to show that testosterone and estradiol act differentially on skeletal muscles from different regions, differentially with reference to glycogen metabolism. To study this hypothesis, healthy mature male Wistar rats (90-120 days of age, weighing about 180-200 g) were castrated (a bilateral orchidectomy was performed to test the significance of skeletal muscle glycogen metabolism in the absence of testosterone). One group of castrated rats was supplemented with testosterone (100 µg/100 g body weight, i.m., for 30 days from day 31 postcastration onwards). To test whether estradiol has any effect on male skeletal muscle glycogen metabolism 17beta-estradiol (5 µg/100 g body weight, i.m., for 30 days from day 31 postcastration onwards) was administered to orchidectomized rats. To test whether these sex steroids have any differential effect on skeletal muscles from different regions, skeletal muscles from the temporal region (temporalis), muscle of mastication (masseter), forearm muscle (triceps and biceps), thigh muscle (vastus lateralis and gracilis), and calf muscle (gastrocnemius and soleus) were considered. Castration enhanced blood glucose levels and decreased glycogen stores in skeletal muscle from head, jaw, forearm, thigh, and leg regions. This was accompanied by diminished activity of glycogen synthetase and enhanced activity of muscle phosphorylase. Following testosterone supplementation to castrated rats, a normal pattern of all these parameters was maintained. Estradiol administration to castrated rats did not bring about any significant alteration in any of the parameters. The data obtained suggest a stimulatory effect of testosterone on skeletal muscle glycogenesis and an inhibitory effect on glycogenolysis. Estradiol did not play any significant role in the skeletal muscle glycogen metabolism of male rats.Key words: testosterone, estradiol, skeletal muscle, glycogen metabolism.
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Wu, G. Y., e J. R. Thompson. "Is methionine transaminated in skeletal muscle?" Biochemical Journal 257, n.º 1 (1 de janeiro de 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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Shiina, Takahiko, Takeshi Shima, Kazuaki Masuda, Haruko Hirayama, Momoe Iwami, Tadashi Takewaki, Hirofumi Kuramoto e Yasutake Shimizu. "Contractile Properties of Esophageal Striated Muscle: Comparison with Cardiac and Skeletal Muscles in Rats". Journal of Biomedicine and Biotechnology 2010 (2010): 1–7. http://dx.doi.org/10.1155/2010/459789.
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The external muscle layer of the mammalian esophagus consists of striated muscles. We investigated the contractile properties of esophageal striated muscle by comparison with those of skeletal and cardiac muscles. Electrical field stimulation with single pulses evoked twitch-like contractile responses in esophageal muscle, similar to those in skeletal muscle in duration and similar to those in cardiac muscle in amplitude. The contractions of esophageal muscle were not affected by an inhibitor of gap junctions. Contractile responses induced by high potassium or caffeine in esophageal muscle were analogous to those in skeletal muscle. High-frequency stimulation induced a transient summation of contractions followed by sustained contractions with amplitudes similar to those of twitch-like contractions, although a large summation was observed in skeletal muscle. The results demonstrate that esophageal muscle has properties similar but not identical to those of skeletal muscle and that some specific properties may be beneficial for esophageal peristalsis.
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Bilston, Lynne E., Bart Bolsterlee, Antoine Nordez e Shantanu Sinha. "Contemporary image-based methods for measuring passive mechanical properties of skeletal muscles in vivo". Journal of Applied Physiology 126, n.º 5 (1 de maio de 2019): 1454–64. http://dx.doi.org/10.1152/japplphysiol.00672.2018.
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Skeletal muscles’ primary function in the body is mechanical: to move and stabilize the skeleton. As such, their mechanical behavior is a key aspect of their physiology. Recent developments in medical imaging technology have enabled quantitative studies of passive muscle mechanics, ranging from measurements of intrinsic muscle mechanical properties, such as elasticity and viscosity, to three-dimensional muscle architecture and dynamic muscle deformation and kinematics. In this review we summarize the principles and applications of contemporary imaging methods that have been used to study the passive mechanical behavior of skeletal muscles. Elastography measurements can provide in vivo maps of passive muscle mechanical parameters, and both MRI and ultrasound methods are available (magnetic resonance elastography and ultrasound shear wave elastography, respectively). Both have been shown to differentiate between healthy muscle and muscles affected by a broad range of clinical conditions. Detailed muscle architecture can now be depicted using diffusion tensor imaging, which not only is particularly useful for computational modeling of muscle but also has potential in assessing architectural changes in muscle disorders. More dynamic information about muscle mechanics can be obtained using a range of dynamic MRI methods, which characterize the detailed internal muscle deformations during motion. There are several MRI techniques available (e.g., phase-contrast MRI, displacement-encoded MRI, and “tagged” MRI), each of which can be collected in synchrony with muscle motion and postprocessed to quantify muscle deformation. Together, these modern imaging techniques can characterize muscle motion, deformation, mechanical properties, and architecture, providing complementary insights into skeletal muscle function.
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Brooks, Susan V. "CURRENT TOPICS FOR TEACHING SKELETAL MUSCLE PHYSIOLOGY". Advances in Physiology Education 27, n.º 4 (dezembro de 2003): 171–82. http://dx.doi.org/10.1152/advan.2003.27.4.171.
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Contractions of skeletal muscles provide the stability and power for all body movements. Consequently, any impairment in skeletal muscle function results in some degree of instability or immobility. Factors that influence skeletal muscle structure and function are therefore of great interest both scientifically and clinically. Injury, disease, and old age are among the factors that commonly contribute to impairment in skeletal muscle function. The goal of this article is to update current concepts of skeletal muscle physiology. Particular emphasis is placed on mechanisms of injury, repair, and adaptation in skeletal muscle as well as mechanisms underlying the declining skeletal muscle structure and function associated with aging. For additional materials please refer to the “Skeletal Muscle Physiology” presentation located on the American Physiological Society Archive of Teaching Resources Web site ( https://www.lifescitrc.org ).
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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 e 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, n.º 5 (1 de março de 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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Barry, DT. "Acoustic Signals from Skeletal Muscle". Physiology 5, n.º 1 (1 de fevereiro de 1990): 17–21. http://dx.doi.org/10.1152/physiologyonline.1990.5.1.17.
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Contracting skeletal muscles emit pressure waves that are audible at the skin surface and are easily recorded with standard microphones both in vivo and in vitro. These muscle sounds are an intrinsic component of the contractile mechanism and are produced by mechanical vibrations at the resonant frequency of the muscle. The sounds are useful in measuring force, fatigue, and mechanical properties of muscle.
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Shirakawa, Tomohiko, Aki Miyawaki, Tatsuo Kawamoto e Shoichiro Kokabu. "Natural Compounds Attenuate Denervation-Induced Skeletal Muscle Atrophy". International Journal of Molecular Sciences 22, n.º 15 (2 de agosto de 2021): 8310. http://dx.doi.org/10.3390/ijms22158310.
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The weight of skeletal muscle accounts for approximately 40% of the whole weight in a healthy individual, and the normal metabolism and motor function of the muscle are indispensable for healthy life. In addition, the skeletal muscle of the maxillofacial region plays an important role not only in eating and swallowing, but also in communication, such as facial expressions and conversations. In recent years, skeletal muscle atrophy has received worldwide attention as a serious health problem. However, the mechanism of skeletal muscle atrophy that has been clarified at present is insufficient, and a therapeutic method against skeletal muscle atrophy has not been established. This review provides views on the importance of skeletal muscle in the maxillofacial region and explains the differences between skeletal muscles in the maxillofacial region and other regions. We summarize the findings to change in gene expression in muscle remodeling and emphasize the advantages and disadvantages of denervation-induced skeletal muscle atrophy model. Finally, we discuss the newly discovered beneficial effects of natural compounds on skeletal muscle atrophy.
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Potthoff, Matthew J., Michael A. Arnold, John McAnally, James A. Richardson, Rhonda Bassel-Duby e Eric N. Olson. "Regulation of Skeletal Muscle Sarcomere Integrity and Postnatal Muscle Function by Mef2c". Molecular and Cellular Biology 27, n.º 23 (17 de setembro de 2007): 8143–51. http://dx.doi.org/10.1128/mcb.01187-07.
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ABSTRACT Myocyte enhancer factor 2 (MEF2) transcription factors cooperate with the MyoD family of basic helix-loop-helix (bHLH) transcription factors to drive skeletal muscle development during embryogenesis, but little is known about the potential functions of MEF2 factors in postnatal skeletal muscle. Here we show that skeletal muscle-specific deletion of Mef2c in mice results in disorganized myofibers and perinatal lethality. In contrast, neither Mef2a nor Mef2d is required for normal skeletal muscle development in vivo. Skeletal muscle deficient in Mef2c differentiates and forms normal myofibers during embryogenesis, but myofibers rapidly deteriorate after birth due to disorganized sarcomeres and a loss of integrity of the M line. Microarray analysis of Mef2c null muscles identified several muscle structural genes that depend on MEF2C, including those encoding the M-line-specific proteins myomesin and M protein. We show that MEF2C directly regulates myomesin gene transcription and that loss of Mef2c in skeletal muscle results in improper sarcomere organization. These results reveal a key role for Mef2c in maintenance of sarcomere integrity and postnatal maturation of skeletal muscle.
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Ardhianto, Peter, Jen-Yung Tsai, Chih-Yang Lin, Ben-Yi Liau, Yih-Kuen Jan, Veit Babak Hamun Akbari e Chi-Wen Lung. "A Review of the Challenges in Deep Learning for Skeletal and Smooth Muscle Ultrasound Images". Applied Sciences 11, n.º 9 (28 de abril de 2021): 4021. http://dx.doi.org/10.3390/app11094021.
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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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Hinkle, Richard T., Elizabeth Donnelly, David B. Cody, Russell J. Sheldon e Robert J. Isfort. "Activation of the vasoactive intestinal peptide 2 receptor modulates normal and atrophying skeletal muscle mass and force". Journal of Applied Physiology 98, n.º 2 (fevereiro de 2005): 655–62. http://dx.doi.org/10.1152/japplphysiol.00736.2004.
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Of the two known vasoactive intestinal peptide receptors (VPAC1R and VPAC2R), the VPAC2R is expressed in skeletal muscle. To evaluate the function of the VPAC2R in the physiological control of skeletal muscle mass, we utilized the VPAC1R selective agonist [K15,R16,L27]VIP(1-7) GRF(8-27)-NH2 and the VPAC2R selective agonist Ro-25-1553 to treat mice and rats undergoing either nerve damage-, corticosteroid-, or disuse-induced skeletal muscle atrophy. These analyses demonstrated that activation of VPAC2R, but not VPAC1R, reduced the loss of skeletal muscle mass and force during conditions of skeletal muscle atrophy resulting from corticosteroid administration, denervation, casting-induced disuse, increased skeletal muscle mass, and force of nonatrophying muscles. These studies indicate that VPAC2R agonists may have utility for the treatment of skeletal muscle-wasting diseases.
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Norheim, Frode, Truls Raastad, Bernd Thiede, Arild C. Rustan, Christian A. Drevon e 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, n.º 5 (novembro de 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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Herring, B. P., M. H. Nunnally, P. J. Gallagher e J. T. Stull. "Molecular characterization of rat skeletal muscle myosin light chain kinase". American Journal of Physiology-Cell Physiology 256, n.º 2 (1 de fevereiro de 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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DU, Jian-tong, Wei LI, Jin-yan YANG, Chao-shu TANG, Qi LI e Hong-fang JIN. "Hydrogen sulfide is endogenously generated in rat skeletal muscle and exerts a protective effect against oxidative stress". Chinese Medical Journal 126, n.º 5 (5 de março de 2013): 930–36. http://dx.doi.org/10.3760/cma.j.issn.0366-6999.20122485.
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Background Skeletal muscle has recently been recognized as an endocrine organ that can express, synthesize and secrete a variety of bioactive molecules which exert significant regulatory effects. Hydrogen sulfide (H2S) is endogenously produced in mammalian tissues and participates in a number of physiological and pathophysiological processes. We aimed to verify whether H2S could be endogenously generated and released by rat skeletal muscle, and determine the biological effects of H2S in rat skeletal muscle. Methods The study was divided into two parts: detection of endogenous H2S generation and release in rat skeletal muscle and determination of antioxidative activity of skeletal muscle-derived H2S. H2S content and production in tissues were detected by sensitive sulfur electrode method. The expressions of H2S producing enzymes cystathionine β-synthase, cystathionine γ-lyase and mercaptopyruvate sulfurtransferase were detected by real-time PCR and western blotting and their tissue distributions were observed by immunohistochemical and immunofluorescent analysis. Rat skeletal muscular ischemia-reperfusion (I-R) injury model was created and evaluated by histological analysis under microscope. The malondialdehyde (MDA) contents, hydrogen peroxide levels, superoxide anion and superoxide dismutase (SOD) activities were detected using spectrophotometer. Results H2S could be endogenously generated and released by skeletal muscle of Sprague-Dawley rats (H2S content: (2.06±0.43) nmol/mg; H2S production: (0.17±0.06) nmol·min-1·mg-1). Gene and protein expressions of the three H2S producing enzymes were detected in skeletal muscle, as well as the liver and kidney. Endogenous H2S content and production were decreased in skeletal muscles of rats with I-R skeletal muscle injury (P <0.05). Furthermore, H2S significantly protected rat skeletal muscle against I-R injury and resulted in decreased MDA content, reduced hydrogen peroxide and superoxide anion levels, but increased SOD activity and protein expression in skeletal muscles (all P <0.01). Conclusion H2S generation pathway exists in rat skeletal muscle and it acts as an antioxidant in skeletal muscle.
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Gao, Jinghui, Elijah Sterling, Rachel Hankin, Aria Sikal e Yao Yao. "Therapeutics Targeting Skeletal Muscle in Amyotrophic Lateral Sclerosis". Biomolecules 14, n.º 7 (22 de julho de 2024): 878. http://dx.doi.org/10.3390/biom14070878.
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Amyotrophic lateral sclerosis (ALS) is a complex neuromuscular disease characterized by progressive motor neuron degeneration, neuromuscular junction dismantling, and muscle wasting. The pathological and therapeutic studies of ALS have long been neurocentric. However, recent insights have highlighted the significance of peripheral tissue, particularly skeletal muscle, in disease pathology and treatment. This is evidenced by restricted ALS-like muscle atrophy, which can retrogradely induce neuromuscular junction and motor neuron degeneration. Moreover, therapeutics targeting skeletal muscles can effectively decelerate disease progression by modulating muscle satellite cells for muscle repair, suppressing inflammation, and promoting the recovery or regeneration of the neuromuscular junction. This review summarizes and discusses therapeutic strategies targeting skeletal muscles for ALS treatment. It aims to provide a comprehensive reference for the development of novel therapeutics targeting skeletal muscles, potentially ameliorating the progression of ALS.
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Pistilli, Emidio E., Parco M. Siu e Stephen E. Alway. "Interleukin-15 responses to aging and unloading-induced skeletal muscle atrophy". American Journal of Physiology-Cell Physiology 292, n.º 4 (abril de 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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Hitachi, Keisuke, Masashi Nakatani e Kunihiro Tsuchida. "Long Non-Coding RNA Myoparr Regulates GDF5 Expression in Denervated Mouse Skeletal Muscle". Non-Coding RNA 5, n.º 2 (8 de abril de 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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Maas, Huub, e 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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Chen, Ting, Timothy M. Moore, Mark T. W. Ebbert, Natalie L. McVey, Steven R. Madsen, David M. Hallowell, Alexander M. Harris et al. "Liver kinase B1 inhibits the expression of inflammation-related genes postcontraction in skeletal muscle". Journal of Applied Physiology 120, n.º 8 (15 de abril de 2016): 876–88. http://dx.doi.org/10.1152/japplphysiol.00727.2015.
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Skeletal muscle-specific liver kinase B1 (LKB1) knockout mice (skmLKB1-KO) exhibit elevated mitogen-activated protein kinase (MAPK) signaling after treadmill running. MAPK activation is also associated with inflammation-related signaling in skeletal muscle. Since exercise can induce muscle damage, and inflammation is a response triggered by damaged tissue, we therefore hypothesized that LKB1 plays an important role in dampening the inflammatory response to muscle contraction, and that this may be due in part to increased susceptibility to muscle damage with contractions in LKB1-deficient muscle. Here we studied the inflammatory response and muscle damage with in situ muscle contraction or downhill running. After in situ muscle contractions, the phosphorylation of both NF-κB and STAT3 was increased more in skmLKB1-KO vs. wild-type (WT) muscles. Analysis of gene expression via microarray and RT-PCR shows that expression of many inflammation-related genes increased after contraction only in skmLKB1-KO muscles. This was associated with mild skeletal muscle fiber membrane damage in skmLKB1-KO muscles. Gene markers of oxidative stress were also elevated in skmLKB1-KO muscles after contraction. Using the downhill running model, we observed significantly more muscle damage after running in skmLKB1-KO mice, and this was associated with greater phosphorylation of both Jnk and STAT3 and increased expression of SOCS3 and Fos. In conclusion, we have shown that the lack of LKB1 in skeletal muscle leads to an increased inflammatory state in skeletal muscle that is exacerbated by muscle contraction. Increased susceptibility of the muscle to damage may underlie part of this response.
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Pedersen, Thomas H., Frank de Paoli e Ole B. Nielsen. "Increased Excitability of Acidified Skeletal Muscle". Journal of General Physiology 125, n.º 2 (31 de janeiro de 2005): 237–46. http://dx.doi.org/10.1085/jgp.200409173.
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Generation of the action potentials (AP) necessary to activate skeletal muscle fibers requires that inward membrane currents exceed outward currents and thereby depolarize the fibers to the voltage threshold for AP generation. Excitability therefore depends on both excitatory Na+ currents and inhibitory K+ and Cl− currents. During intensive exercise, active muscle loses K+ and extracellular K+ ([K+]o) increases. Since high [K+]o leads to depolarization and ensuing inactivation of voltage-gated Na+ channels and loss of excitability in isolated muscles, exercise-induced loss of K+ is likely to reduce muscle excitability and thereby contribute to muscle fatigue in vivo. Intensive exercise, however, also leads to muscle acidification, which recently was shown to recover excitability in isolated K+-depressed muscles of the rat. Here we show that in rat soleus muscles at 11 mM K+, the almost complete recovery of compound action potentials and force with muscle acidification (CO2 changed from 5 to 24%) was associated with reduced chloride conductance (1731 ± 151 to 938 ± 64 μS/cm2, P < 0.01) but not with changes in potassium conductance (405 ± 20 to 455 ± 30 μS/cm2, P < 0.16). Furthermore, acidification reduced the rheobase current by 26% at 4 mM K+ and increased the number of excitable fibers at elevated [K+]o. At 11 mM K+ and normal pH, a recovery of excitability and force similar to the observations with muscle acidification could be induced by reducing extracellular Cl− or by blocking the major muscle Cl− channel, ClC-1, with 30 μM 9-AC. It is concluded that recovery of excitability in K+-depressed muscles induced by muscle acidification is related to reduction in the inhibitory Cl− currents, possibly through inhibition of ClC-1 channels, and acidosis thereby reduces the Na+ current needed to generate and propagate an AP. Thus short term regulation of Cl− channels is important for maintenance of excitability in working muscle.
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Snyder, G. K., C. Farrelly e J. R. Coelho. "Capillary perfusion in skeletal muscle". American Journal of Physiology-Heart and Circulatory Physiology 262, n.º 3 (1 de março de 1992): H828—H832. http://dx.doi.org/10.1152/ajpheart.1992.262.3.h828.
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Timed perfusions of capillaries in soleus, vastus lateralis, and diaphragm of rats were determined by injecting a fluorescent dye into the aorta or right atrium. At preselected time intervals after dye injection, the circulation was interrupted, skeletal muscles were excised and frozen, and numerical counts of capillaries were made from transverse sections of the muscles. When fluorescent dye was injected into the right atrium or injected relatively slowly into the aorta, 100% of the capillaries contained dye by 3 s in vastus lateralis, 5 s in diaphragm, and 7 s in soleus. Rapid injection into the aorta delayed capillary filling. The rapid appearance of dye in skeletal muscle microvasculature suggests that either all capillaries are open to plasma flow all of the time or that the time constant for reopening of closed capillaries is very short. Furthermore, the patterns of capillary filling in skeletal muscle appear to be independent of muscle fiber type.
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Eržen, Ida. "PLASTICITY OF SKELETAL MUSCLE STUDIED BY STEREOLOGY". Image Analysis & Stereology 23, n.º 3 (3 de maio de 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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Dao, Tien Tuan, e Marie-Christine Ho Ba Tho. "A Systematic Review of Continuum Modeling of Skeletal Muscles: Current Trends, Limitations, and Recommendations". Applied Bionics and Biomechanics 2018 (6 de dezembro de 2018): 1–17. http://dx.doi.org/10.1155/2018/7631818.
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Finite elasticity theory has been commonly used to model skeletal muscle. A very large range of heterogeneous constitutive laws has been proposed. In this review, the most widely used continuum models of skeletal muscles were synthetized and discussed. Trends and limitations of these laws were highlighted to propose new recommendations for future researches. A systematic review process was performed using two reliable search engines as PubMed and ScienceDirect. 40 representative studies (13 passive muscle materials and 27 active muscle materials) were included into this review. Note that exclusion criteria include tendon models, analytical models, 1D geometrical models, supplement papers, and indexed conference papers. Trends of current skeletal muscle modeling relate to 3D accurate muscle representation, parameter identification in passive muscle modeling, and the integration of coupled biophysical phenomena. Parameter identification for active materials, assumed fiber distribution, data assumption, and model validation are current drawbacks. New recommendations deal with the incorporation of multimodal data derived from medical imaging, the integration of more biophysical phenomena, and model reproducibility. Accounting for data uncertainty in skeletal muscle modeling will be also a challenging issue. This review provides, for the first time, a holistic view of current continuum models of skeletal muscles to identify potential gaps of current models according to the physiology of skeletal muscle. This opens new avenues for improving skeletal muscle modeling in the framework of in silico medicine.
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Heidlauf, Thomas, e Oliver Röhrle. "Modeling the Chemoelectromechanical Behavior of Skeletal Muscle Using the Parallel Open-Source Software Library OpenCMISS". Computational and Mathematical Methods in Medicine 2013 (2013): 1–14. http://dx.doi.org/10.1155/2013/517287.
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An extensible, flexible, multiscale, and multiphysics model for nonisometric skeletal muscle behavior is presented. The skeletal muscle chemoelectromechanical model is based on a bottom-up approach modeling the entire excitation-contraction pathway by strongly coupling a detailed biophysical model of a half-sarcomere to the propagation of action potentials along skeletal muscle fibers and linking cellular parameters to a transversely isotropic continuum-mechanical constitutive equation describing the overall mechanical behavior of skeletal muscle tissue. Since the multiscale model exhibits separable time scales, a special emphasis is placed on employing computationally efficient staggered solution schemes. Further, the implementation builds on the open-source software library OpenCMISS and uses state-of-the-art parallelization techniques taking advantage of the unique anatomical fiber architecture of skeletal muscles. OpenCMISS utilizes standardized data structures for geometrical aspects (FieldML) and cellular models (CellML). Both standards are designed to allow for a maximum flexibility, reproducibility, and extensibility. The results demonstrate the model’s capability of simulating different aspects of nonisometric muscle contraction and efficiently simulating the chemoelectromechanical behavior in complex skeletal muscles such as the tibialis anterior muscle.
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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, n.º 1 (julho de 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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Zhou, Daixing, Jeanine A. Ursitti e Robert J. Bloch. "Developmental Expression of Spectrins in Rat Skeletal Muscle". Molecular Biology of the Cell 9, n.º 1 (janeiro de 1998): 47–61. http://dx.doi.org/10.1091/mbc.9.1.47.
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Skeletal muscle contains spectrin (or spectrin I) and fodrin (or spectrin II), members of the spectrin supergene family. We used isoform-specific antibodies and cDNA probes to investigate the molecular forms, developmental expression, and subcellular localization of the spectrins in skeletal muscle of the rat. We report that β-spectrin (βI) replaces β-fodrin (βII) at the sarcolemma as skeletal muscle fibers develop. As a result, adult muscle fibers contain only α-fodrin (αII) and the muscle isoform of β-spectrin (βIΣ2). By contrast, other types of cells present in skeletal muscle tissue, including blood vessels and nerves, contain only α- and β-fodrin. During late embryogenesis and early postnatal development, skeletal muscle fibers contain a previously unknown form of spectrin complex, consisting of α-fodrin, β-fodrin, and the muscle isoform of β-spectrin. These complexes associate with the sarcolemma to form linear membrane skeletal structures that otherwise resemble the structures found in the adult. Our results suggest that the spectrin-based membrane skeleton of muscle fibers can exist in three distinct states during development.
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Hussain, Sabah N. A., e Marco Sandri. "Role of autophagy in COPD skeletal muscle dysfunction". Journal of Applied Physiology 114, n.º 9 (1 de maio de 2013): 1273–81. http://dx.doi.org/10.1152/japplphysiol.00893.2012.
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Chronic obstructive pulmonary disease (COPD) is a debilitating disease caused by parenchymal damage and irreversible airflow limitation. In addition to lung dysfunction, patients with COPD develop weight loss, malnutrition, poor exercise performance, and skeletal muscle atrophy. The latter has been attributed to an imbalance between muscle protein synthesis and protein degradation. Several reports have confirmed that enhanced protein degradation and atrophy of limb muscles of COPD patient is mediated in part through activation of the ubiquitin-proteasome pathway and that this activation is triggered by enhanced production of reactive oxygen species. Until recently, the importance of the autophagy-lysosome pathway in protein degradation of skeletal muscles has been largely ignored, however, recent evidence suggests that this pathway is actively involved in recycling of cytosolic proteins, organelles, and protein aggregates in normal skeletal muscles. The protective role of autophagy in the regulation of muscle mass has recently been uncovered in mice with muscle-specific suppression of autophagy. These mice develop severe muscle weakness, atrophy, and decreased muscle contractility. No information is yet available about the involvement of the autophagy in the regulation of skeletal muscle mass in COPD patients. Pilot experiments on vastus lateralis muscle samples suggest that the autophagy-lysosome system is induced in COPD patients compared with control subjects. In this review, we summarize recent progress related to molecular structure, regulation, and roles of the autophagy-lysosome pathway in normal and diseased skeletal muscles. We also speculate about regulation and functional importance of this system in skeletal muscle dysfunction in COPD patients.
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Gomez-Cabrera, M. C., G. L. Close, A. Kayani, A. McArdle, J. Viña e 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, n.º 1 (janeiro de 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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Collins, Asiamah Amponsah, Kun Zou, Zhang Li e Su Ying. "Mechanism and Functions of Identified miRNAs in Poultry Skeletal Muscle Development – A Review". Annals of Animal Science 19, n.º 4 (1 de outubro de 2019): 887–904. http://dx.doi.org/10.2478/aoas-2019-0049.
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AbstractDevelopment of the skeletal muscle goes through several complex processes regulated by numerous genetic factors. Although much efforts have been made to understand the mechanisms involved in increased muscle yield, little work is done about the miRNAs and candidate genes that are involved in the skeletal muscle development in poultry. Comprehensive research of candidate genes and single nucleotide related to poultry muscle growth is yet to be experimentally unraveled. However, over a few periods, studies in miRNA have disclosed that they actively participate in muscle formation, differentiation, and determination in poultry. Specifically, miR-1, miR-133, and miR-206 influence tissue development, and they are highly expressed in the skeletal muscles. Candidate genes such as CEBPB, MUSTN1, MSTN, IGF1, FOXO3, mTOR, and NFKB1, have also been identified to express in the poultry skeletal muscles development. However, further researches, analysis, and comprehensive studies should be made on the various miRNAs and gene regulatory factors that influence the skeletal muscle development in poultry. The objective of this review is to summarize recent knowledge in miRNAs and their mode of action as well as transcription and candidate genes identified to regulate poultry skeletal muscle development.
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Minami, Elina, Hans Reinecke e Charles E. Murry. "Skeletal muscle meets cardiac muscle". Journal of the American College of Cardiology 41, n.º 7 (abril de 2003): 1084–86. http://dx.doi.org/10.1016/s0735-1097(03)00083-4.
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Cabezas Perez, Ricardo Julián, Marco Fidel Ávila Rodríguez e Doris Haydee Rosero Salazar. "Exogenous Antioxidants in Remyelination and Skeletal Muscle Recovery". Biomedicines 10, n.º 10 (13 de outubro de 2022): 2557. http://dx.doi.org/10.3390/biomedicines10102557.
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Inflammatory, oxidative, and autoimmune responses cause severe damage to the nervous system inducing loss of myelin layers or demyelination. Even though demyelination is not considered a direct cause of skeletal muscle disease there is extensive damage in skeletal muscles following demyelination and impaired innervation. In vitro and in vivo evidence using exogenous antioxidants in models of demyelination is showing improvements in myelin formation alongside skeletal muscle recovery. For instance, exogenous antioxidants such as EGCG stimulate nerve structure maintenance, activation of glial cells, and reduction of oxidative stress. Consequently, this evidence is also showing structural and functional recovery of impaired skeletal muscles due to demyelination. Exogenous antioxidants mostly target inflammatory pathways and stimulate remyelinating mechanisms that seem to induce skeletal muscle regeneration. Therefore, the aim of this review is to describe recent evidence related to the molecular mechanisms in nerve and skeletal muscle regeneration induced by exogenous antioxidants. This will be relevant to identifying further targets to improve treatments of neuromuscular demyelinating diseases.
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Kohno, Shohei, Yui Yamashita, Tomoki Abe, Katsuya Hirasaka, Motoko Oarada, Ayako Ohno, Shigetada Teshima-Kondo et al. "Unloading stress disturbs muscle regeneration through perturbed recruitment and function of macrophages". Journal of Applied Physiology 112, n.º 10 (15 de maio de 2012): 1773–82. http://dx.doi.org/10.1152/japplphysiol.00103.2012.
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Skeletal muscle is one of the most sensitive tissues to mechanical loading, and unloading inhibits the regeneration potential of skeletal muscle after injury. This study was designed to elucidate the specific effects of unloading stress on the function of immunocytes during muscle regeneration after injury. We examined immunocyte infiltration and muscle regeneration in cardiotoxin (CTX)-injected soleus muscles of tail-suspended (TS) mice. In CTX-injected TS mice, the cross-sectional area of regenerating myofibers was smaller than that of weight-bearing (WB) mice, indicating that unloading delays muscle regeneration following CTX-induced skeletal muscle damage. Delayed infiltration of macrophages into the injured skeletal muscle was observed in CTX-injected TS mice. Neutrophils and macrophages in CTX-injected TS muscle were presented over a longer period at the injury sites compared with those in CTX-injected WB muscle. Disturbance of activation and differentiation of satellite cells was also observed in CTX-injected TS mice. Further analysis showed that the macrophages in soleus muscles were mainly Ly-6C-positive proinflammatory macrophages, with high expression of tumor necrosis factor-α and interleukin-1β, indicating that unloading causes preferential accumulation and persistence of proinflammatory macrophages in the injured muscle. The phagocytic and myotube formation properties of macrophages from CTX-injected TS skeletal muscle were suppressed compared with those from CTX-injected WB skeletal muscle. We concluded that the disturbed muscle regeneration under unloading is due to impaired macrophage function, inhibition of satellite cell activation, and their cooperation.
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McDonough, Alicia A., Curtis B. Thompson e Jang H. Youn. "Skeletal muscle regulates extracellular potassium". American Journal of Physiology-Renal Physiology 282, n.º 6 (1 de junho de 2002): F967—F974. http://dx.doi.org/10.1152/ajprenal.00360.2001.
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Maintaining extracellular fluid (ECF) K+ concentration ([K+]) within a narrow range is accomplished by the concerted responses of the kidney, which matches K+ excretion to K+ intake, and skeletal muscle, the main intracellular fluid (ICF) store of K+, which can rapidly buffer ECF [K+]. In both systems, homologous P-type ATPase isoforms are key effectors of this homeostasis. During dietary K+ deprivation, these P-type ATPases are regulated in opposite directions: increased abundance of the H,K-ATPase “colonic” isoform in the renal collecting duct drives active K+ conservation while decreased abundance of the plasma membrane Na,K-ATPase α2-isoform leads to the specific shift of K+ from muscle ICF to ECF. The skeletal muscle response is isoform and muscle specific: α2 and β2, not α1 and β1, levels are depressed, and fast glycolytic muscles lose >90% α2, whereas slow oxidative muscles lose ∼50%; however, both muscle types have the same fall in cellular [K+]. To understand the physiological impact, we developed the “K+ clamp” to assess insulin-stimulated cellular K+ uptake in vivo in the conscious rat by measuring the exogenous K+ infusion rate needed to maintain constant plasma [K+] during insulin infusion. Using the K+ clamp, we established that K+deprivation leads to near-complete insulin resistance of cellular K+ uptake and that this insulin resistance can occur before any decrease in plasma [K+] or muscle Na+ pump expression. These studies establish the advantage of combining molecular analyses of P-type ATPase expression with in vivo analyses of cellular K+ uptake and excretion to determine mechanisms in models of disrupted K+ homeostasis.
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Eng, Diana, Hsiao-Yen Ma, Michael K. Gross e Chrissa Kioussi. "Gene Networks during Skeletal Myogenesis". ISRN Developmental Biology 2013 (19 de setembro de 2013): 1–8. http://dx.doi.org/10.1155/2013/348704.
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Mammalian skeletal muscles are derived from mesoderm segments flanking the embryonic midline. Upon receiving inductive cues from the adjacent neural tube, lateral plate mesoderm, and surface ectoderm, muscle precursors start to delaminate, migrate to their final destinations and proliferate. Muscle precursor cells become committed to the myogenic fate, become differentiated muscle cells, and fuse to form myofibers. Myofibers then fuse together to form the muscle groups. Muscle precursor cells have the ability to proliferate, and differentiate during development, while a subset remains capable of regeneration and repair of local injuries in adulthood. When the process of muscle development is perturbed such as in muscular dystrophies and injuries, ways to intervene and allow for proper muscle development or repair are the focus of regenerative medicine. Thus, understanding the developmental program of muscle at the genetic, cellular, and molecular levels has become a major focus of skeletal muscle regeneration research in the last few years.
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Song, Taejeong, James W. McNamara, Weikang Ma, Maicon Landim-Vieira, Kyoung Hwan Lee, Lisa A. Martin, Judith A. Heiny et al. "Fast skeletal myosin-binding protein-C regulates fast skeletal muscle contraction". Proceedings of the National Academy of Sciences 118, n.º 17 (22 de abril de 2021): e2003596118. http://dx.doi.org/10.1073/pnas.2003596118.
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Fast skeletal myosin-binding protein-C (fMyBP-C) is one of three MyBP-C paralogs and is predominantly expressed in fast skeletal muscle. Mutations in the gene that encodes fMyBP-C, MYBPC2, are associated with distal arthrogryposis, while loss of fMyBP-C protein is associated with diseased muscle. However, the functional and structural roles of fMyBP-C in skeletal muscle remain unclear. To address this gap, we generated a homozygous fMyBP-C knockout mouse (C2−/−) and characterized it both in vivo and in vitro compared to wild-type mice. Ablation of fMyBP-C was benign in terms of muscle weight, fiber type, cross-sectional area, and sarcomere ultrastructure. However, grip strength and plantar flexor muscle strength were significantly decreased in C2−/− mice. Peak isometric tetanic force and isotonic speed of contraction were significantly reduced in isolated extensor digitorum longus (EDL) from C2−/− mice. Small-angle X-ray diffraction of C2−/− EDL muscle showed significantly increased equatorial intensity ratio during contraction, indicating a greater shift of myosin heads toward actin, while MLL4 layer line intensity was decreased at rest, indicating less ordered myosin heads. Interfilament lattice spacing increased significantly in C2−/− EDL muscle. Consistent with these findings, we observed a significant reduction of steady-state isometric force during Ca2+-activation, decreased myofilament calcium sensitivity, and sinusoidal stiffness in skinned EDL muscle fibers from C2−/− mice. Finally, C2−/− muscles displayed disruption of inflammatory and regenerative pathways, along with increased muscle damage upon mechanical overload. Together, our data suggest that fMyBP-C is essential for maximal speed and force of contraction, sarcomere integrity, and calcium sensitivity in fast-twitch muscle.
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Park, Joo Yeon, Sun Mi Park, Tae Sup Lee, Seo Young Kang, Ji-Young Kim, Hai-Jeon Yoon, Bom Sahn Kim e Byung Seok Moon. "Radiopharmaceuticals for Skeletal Muscle PET Imaging". International Journal of Molecular Sciences 25, n.º 9 (29 de abril de 2024): 4860. http://dx.doi.org/10.3390/ijms25094860.
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The skeletal muscles account for approximately 40% of the body weight and are crucial in movement, nutrient absorption, and energy metabolism. Muscle loss and decline in function cause a decrease in the quality of life of patients and the elderly, leading to complications that require early diagnosis. Positron emission tomography/computed tomography (PET/CT) offers non-invasive, high-resolution visualization of tissues. It has emerged as a promising alternative to invasive diagnostic methods and is attracting attention as a tool for assessing muscle function and imaging muscle diseases. Effective imaging of muscle function and pathology relies on appropriate radiopharmaceuticals that target key aspects of muscle metabolism, such as glucose uptake, adenosine triphosphate (ATP) production, and the oxidation of fat and carbohydrates. In this review, we describe how [18F]fluoro-2-deoxy-D-glucose ([18F]FDG), [18F]fluorocholine ([18F]FCH), [11C]acetate, and [15O]water ([15O]H2O) are suitable radiopharmaceuticals for diagnostic imaging of 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, n.º 3 (1 de agosto de 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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Naruse, Masatoshi, William Fountain, Alex Claiborne, Holmes Finch, Scott Trappe e Todd Trappe. "MUSCLE GROUP SPECIFIC SKELETAL MUSCLE AGING: A FIVE YEAR LONGITUDINAL STUDY IN SEPTUAGENARIANS". Innovation in Aging 6, Supplement_1 (1 de novembro de 2022): 800. http://dx.doi.org/10.1093/geroni/igac059.2887.
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Abstract Most of the scientific literature on human skeletal muscle aging has focused on the quadriceps femoris, with the remaining few hundred skeletal muscles receiving limited specific investigation. This longitudinal investigation compared changes in skeletal muscle size via computed tomography of the quadriceps (rectus femoris, vastus lateralis, vastus medialis, vastus intermedius), hamstrings (biceps femoris short and long heads, semitendinosus, semimembranosus), psoas, rectus abdominis, lateral abdominals (obliques and transversus abdominus), and paraspinal muscles (erector spinae and multifidi) of older individuals from the Health ABC study at baseline and 5.0±0.1 years later (n=469, 73±3y & 78±3y, 49% women, 33% black). Skeletal muscle size decreased (p < 0.05) in quadriceps (-3.3%), hamstrings (-5.9%), psoas (-0.4%), and rectus abdominus (-7.0%). The hamstrings and rectus abdominus atrophied approximately twice as much as the quadriceps (p < 0.05), while the quadriceps atrophied substantially more than the psoas (p < 0.05). The paraspinals (+4.3%) and lateral abdominals (+5.9%) hypertrophied (p < 0.05) to a similar degree (p>0.05) over the 5 years. These data suggest that skeletal muscle mass in older individuals changes in a muscle group specific fashion in the eighth decade, a critical time period in the aging process. A broader understanding of muscle group specific skeletal muscle aging is needed to better guide exercise programs and other interventions that mitigate decrements in physical function with aging.
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Macdonald, W. A., N. Ørtenblad e O. B. Nielsen. "Energy conservation attenuates the loss of skeletal muscle excitability during intense contractions". American Journal of Physiology-Endocrinology and Metabolism 292, n.º 3 (março de 2007): E771—E778. http://dx.doi.org/10.1152/ajpendo.00378.2006.
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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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CONTI, Antonio, L. GORZA e Vincenzo SORRENTINO. "Differential distribution of ryanodine receptor type 3 (RyR3) gene product in mammalian skeletal muscles". Biochemical Journal 316, n.º 1 (15 de maio de 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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Rasmussen, Tara, e Haley Tucker. "Loss of SMYD1 Results in Perinatal Lethality via Selective Defects within Myotonic Muscle Descendants". Diseases 7, n.º 1 (20 de dezembro de 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.