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Relevant bibliographies by topics / Skeletal muscle

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Academic literature on the topic 'Skeletal muscle'

Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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Journal articles on the topic "Skeletal muscle"

1

Zhang, Tan, Xin Feng, Bo Feng, Juan Dong, Karen Haas, Barbara M. Nicklas, Osvaldo Delbono, and Stephen Kritchevsky. "CARDIAC TROPONIN T MEDIATED AUTOIMMUNE RESPONSE AND ITS ROLE IN SKELETAL MUSCLE AGING." Innovation in Aging 3, Supplement_1 (November 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, 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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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, no. 4 (May 28, 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, 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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Sandage, Mary J., and Audrey G. Smith. "Muscle Bioenergetic Considerations for Intrinsic Laryngeal Skeletal Muscle Physiology." Journal of Speech, Language, and Hearing Research 60, no. 5 (May 24, 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, and 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, no. 4 (February 20, 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 (May 2006): 63. http://dx.doi.org/10.1249/00005768-200605001-00585.

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Koroteyev, Alexis, Alberto Pochettino, Hiroshi Niinami, and Larry W. Stephenson. "Skeletal Muscle." AORN Journal 53, no. 4 (April 1991): 1005–20. http://dx.doi.org/10.1016/s0001-2092(07)69569-6.

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Ito, Daisuke, Yuji Tokoro, Eiichi Tanaka, and 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, and P. Govindarajulu. "Differential response of rat skeletal muscle glycogen metabolism to testosterone and estradiol." Canadian Journal of Physiology and Pharmacology 77, no. 4 (April 1, 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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Dissertations / Theses on the topic "Skeletal muscle"

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Foxton, Ruth. "Dysferlin in skeletal muscle and skeletal muscle disease." Thesis, University of Newcastle Upon Tyne, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268429.

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Pathare, Neeti C. "Metabolic adaptations following disuse and their impact on skeletal muscle function." [Gainesville, Fla.] : University of Florida, 2005. http://purl.fcla.edu/fcla/etd/UFE0010024.

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Thesis (Ph.D.)--University of Florida, 2005.
Typescript. Title from title page of source document. Document formatted into pages; contains 171 pages. Includes Vita. Includes bibliographical references.

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Peoples, Gregory Edward. "Skeletal muscle fatigue can omega-3 fatty acids optimise skeletal muscle function? /." Access electronically, 2004. http://www.library.uow.edu.au/adt-NWU/public/adt-NWU20041217.123607.

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Thesis (Ph.D.)--University of Wollongong, 2004.
Typescript. This thesis is subject to a 12 month embargo (06/09/05 - 14/09/05) and may only be viewed and copied with the permission of the author. For further information please contact the Archivist. Includes bibliographical references: leaf 195-216.

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Salman, Mahmoud M. "Preconditioning in skeletal muscle." Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1446109/.

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Ischaemia reperfusion injury of skeletal muscle is a major cause of morbidity and mortality in various surgical specialities. Developing a protective method or pharmacological agent that will limit this damage will be of considerable benefit to both patients and doctors. I have used potassium channel openers and calcium as preconditioning agents. The results show that potassium channel openers are a viable option whereas the use of calcium can exacerbate muscle damage. I looked at various protocols of ischaemic and pharmacological preconditioning. The results from both ischaemic and pharmacological preconditioning have shown a comparable decrease with some pharmacological agents in the extent of skeletal muscle infarction both in the early and late period of reperfusion. This decrease in the extent of muscle infarction is associated with changes in the levels of nitric oxide in the circulation. There was preservation of skeletal muscle oxygenation in preconditioned muscle. I have shown that preconditioning of skeletal muscle is a viable option in trying to reduce the amount of damage caused by ischaemia reperfusion injury.

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Blackwell, Danielle. "The role of Talpid3 in skeletal muscle satellite cells and skeletal muscle regeneration." Thesis, University of East Anglia, 2017. https://ueaeprints.uea.ac.uk/66948/.

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The primary cilium has recently been recognised as an essential regulator of the Sonic hedgehog (Shh) signalling pathway. Mutations that disrupt cilia function in humans can cause conditions known as ciliopathies. A wide range of phenotypes is observed in chick and mouse ciliopathy models,including polydactyly, craniofacial defects and polycystic kidneys. The Shh pathway and therefore primary cilia are vital for many developmental processes, including embryonic muscle development, with recent evidence suggesting they may also play a role in adult muscle regeneration. Our studies focus on the Talpid3 gene, which encodes a centrosomal protein required for primary cilia formation and Shh signalling. The Talpid3 loss-of-function mutant has perturbed ciliogenesis and displays many of the phenotypes that are typically associated with developmental Shh mutants and with ciliopathies. Talpid3 mutants have defects in Shh signalling, and processing of Gli transcription factors is affected in structures such as the developing limb buds and the neural tube. However, the role of Talpid3 in muscle development and regeneration remains unknown. The role of Talpid3 in adult muscle regeneration was investigated using a tamoxifen inducible, satellite cell specific knock-out of Talpid3 in mice. This mouse model was generated by crossing Talpid3 floxed mice to a mouse carrying an inducible Pax7-CreERT2 allele. To determine whether loss of Talpid3 affects muscle regeneration a cardiotoxin injury model was used. This showed that loss of Talpid3 in satellite cells results in a regeneration defect as fibres were smaller after 5, 10, 15 and 25 days of regeneration compared to control mice. This defect may be due to a reduced ability of Talpid3 mutant satellite cells to differentiate. We also show that Talpid3 plays a role in satellite cell self-renewal as we observe a complete loss of regeneration in some areas of the muscle following repeat injuries. We provide the first evidence that Talpid3 is critical for the regeneration of skeletal muscle following injury.

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Baker, Brent A. "Characterization of skeletal muscle performance and morphology following acute and chronic mechanical loading paradigms." Morgantown, W. Va. : [West Virginia University Libraries], 2007. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=5325.

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Thesis (Ph. D.)--West Virginia University, 2007.
Title from document title page. Document formatted into pages; contains xii, 270 p. : ill. (some col.). Includes abstract. Includes bibliographical references.

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Zhang, Yan. "Cytokines and skeletal muscle wasting." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ47124.pdf.

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Oude, Vrielink Hubertus Hermanus Egbert. "Vasomotion and skeletal muscle perfusion." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1988. http://arno.unimaas.nl/show.cgi?fid=5409.

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Walsh, Garrett Lyndon. "Skeletal muscle powered cardiac assist." Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=63879.

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Kochamba, Gary. "Skeletal muscle powered cardiac assist." Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61746.

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Books on the topic "Skeletal muscle"

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L, Mastaglia Frank, and Walton John Nicholas, eds. Skeletal muscle pathology. 2nd ed. Edinburgh: Churchill Livingstone, 1992.

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2

Schmalbruch, Henning. Skeletal muscle. Berlin: Springer-Verlag, 1985.

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Schmalbruch, Henning. Skeletal Muscle. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-82551-4.

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Walton, John N. Skeletal muscle pathology. 2nd ed. Edinburgh: Churchill Livingstone, 1992.

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1957-, Prilutsky Boris I., ed. Biomechanics of skeletal muscle. Champaign, IL: Human Kinetics, 2012.

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Ryall, James G., ed. Skeletal Muscle Development. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7283-8.

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Myers, Christopher, ed. Skeletal Muscle Physiology. Cham: Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-47065-3.

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Robert, Wortmann, ed. Diseases of the skeletal muscle. Philadelphia: Lippincott Williams & Wilkins, 2000.

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Asakura, Atsushi, ed. Skeletal Muscle Stem Cells. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3036-5.

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1945-, Reznick A. Z., ed. Oxidative stress in skeletal muscle. Basel: Birkhäuser Verlag, 1998.

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Book chapters on the topic "Skeletal muscle"

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Schmalbruch, H. "Muscle Fibre Types in Mammalian Muscles." In Skeletal Muscle, 159–204. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-82551-4_4.

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Schmalbruch, H. "General Overview." In Skeletal Muscle, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-82551-4_1.

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Schmalbruch, H. "Microanatomy of Muscle." In Skeletal Muscle, 5–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-82551-4_2.

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Schmalbruch, H. "Skeletal Muscle Fibres." In Skeletal Muscle, 35–158. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-82551-4_3.

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Schmalbruch, H. "Slow Muscle Fibres." In Skeletal Muscle, 205–16. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-82551-4_5.

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Schmalbruch, H. "Non-Skeletal Muscles." In Skeletal Muscle, 217–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-82551-4_6.

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Schmalbruch, H. "Development, Regeneration, Growth." In Skeletal Muscle, 239–303. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-82551-4_7.

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Schmalbruch, H. "Muscle Fibres as Members of Motor Units." In Skeletal Muscle, 304–11. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-82551-4_8.

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Fung, Yuan-Cheng. "Skeletal Muscle." In Biomechanics, 392–426. New York, NY: Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4757-2257-4_9.

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Blottner, Dieter, and Michele Salanova. "Skeletal Muscle." In The NeuroMuscular System: From Earth to Space Life Science, 9–62. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-12298-4_2.

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Conference papers on the topic "Skeletal muscle"

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Odegard, G. M., T. L. Haut Donahue, D. A. Morrow, and K. R. Kaufman. "Constitutive Modeling of Skeletal Muscle Tissue." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-175848.

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The main functions of the human musculoskeletal system are to sustain loads and provide mobility. Bones and joints themselves cannot produce movement; skeletal muscles provide the ability to move. Knowledge of muscle forces during given activities can provide insight into muscle mechanics, muscle physiology, musculoskeletal mechanics, neurophysiology, and motor control. However, clinical examinations or instrumented strength testing only provides information regarding muscle groups. Musculoskeletal models are typically needed to calculate individual muscle forces.

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NAGATOMI, RYOICHI. "SKELETAL MUSCLE AND HEALTH." In Proceedings of the Tohoku University Global Centre of Excellence Programme. IMPERIAL COLLEGE PRESS, 2012. http://dx.doi.org/10.1142/9781848169067_0003.

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Krivoi, Igor. "ENDOGENOUS OUABAIN AND SKELETAL MUSCLE." In XV International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2019. http://dx.doi.org/10.29003/m446.sudak.ns2019-15/245-246.

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Ramirez, Angelica Maria, Begoña Calvo Calzada, and Jorge Grasa. "The Effect of the Fascia on the Stress Distribution in Skeletal Muscle." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19696.

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The human and vertebrate interaction with the environment is done primarily through the movement. This is possible due the skeletal muscle: anatomical structure able to contract voluntarily. The skeletal muscles are made up of contractile proteins which slide one over another allowing the muscle shortening and the body force generation. This protein structure of actin and myosin maintains its organization through the connective tissue that surrounds it (endomysium, perimysium and epimysium), creating arrays of myofibrils, fibre bundles, fascicles until conform the whole muscle. All this connective tissue extends to the ends of the muscle to form the tendon.

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Neal, Devin, Mahmut Selman Sakar, and H. Harry Asada. "Bioengineered Fascicle-Like Skeletal Muscle Tissue Constructs." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80228.

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Tissue engineered skeletal muscle constructs have and will continue to be valuable in treating, and testing various muscle injuries and diseases. However a significant drawback to numerous methods of producing 3D skeletal muscle constructs grown in vitro is that muscle cell density as a fraction of total volume or mass, is often significantly lower than muscle found in vivo. Therefore a method to increase muscle cell density within a construct is needed.

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Koeppen, Ryan, Meghan E. Huber, Dagmar Sternad, and Neville Hogan. "Controlling Physical Interactions: Humans Do Not Minimize Muscle Effort." In ASME 2017 Dynamic Systems and Control Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dscc2017-5202.

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Physical interaction with tools is ubiquitous in functional activities of daily living. While tool use is considered a hallmark of human behavior, how humans control such physical interactions is still poorly understood. When humans perform a motor task, it is commonly suggested that the central nervous system coordinates the musculo-skeletal system to minimize muscle effort. In this paper, we tested if this notion holds true for motor tasks that involve physical interaction. Specifically, we investigated whether humans minimize muscle forces to control physical interaction with a circular kinematic constraint. Using a simplified arm model, we derived three predictions for how humans should behave if they were minimizing muscular effort to perform the task. First, we predicted that subjects would exert workless, radial forces on the constraint. Second, we predicted that the muscles would be deactivated when they could not contribute to work. Third, we predicted that when moving very slowly along the constraint, the pattern of muscle activity would not differ between clockwise (CW) and counterclockwise (CCW) motions. To test these predictions, we instructed human subjects to move a robot handle around a virtual, circular constraint at a constant tangential velocity. To reduce the effect of forces that might arise from incomplete compensation of neuro-musculo-skeletal dynamics, the target tangential speed was set to an extremely slow pace (∼1 revolution every 13.3 seconds). Ultimately, the results of human experiment did not support the predictions derived from our model of minimizing muscular effort. While subjects did exert workless forces, they did not deactivate muscles as predicted. Furthermore, muscle activation patterns differed between CW and CCW motions about the constraint. These findings demonstrate that minimizing muscle effort is not a significant factor in human performance of this constrained-motion task. Instead, the central nervous system likely prioritizes reducing other costs, such as computational effort, over muscle effort to control physical interactions.

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Burmeister and Lehman. "Force Relaxation In Human Skeletal Muscle." In Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.589829.

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Burmeister, E. E., and S. L. Lehman. "Force relaxation in human skeletal muscle." In 1992 14th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.5761946.

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Pohle, Regina, Ludwig von Rohden, and Dagmar Fisher. "Skeletal muscle sonography with texture analysis." In Medical Imaging 1997, edited by Kenneth M. Hanson. SPIE, 1997. http://dx.doi.org/10.1117/12.274164.

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Jaramillo, Paola, Adam Shoemaker, Alexander Leonessa, and Robert W. Grange. "Skeletal Muscle Contraction in Feedback Control." In ASME 2012 5th Annual Dynamic Systems and Control Conference joint with the JSME 2012 11th Motion and Vibration Conference. ASME, 2012. http://dx.doi.org/10.1115/dscc2012-movic2012-8592.

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Reports on the topic "Skeletal muscle"

1

Walters, Thomas. Engineered Skeletal Muscle for Craniofacial Reconstruction. Fort Belvoir, VA: Defense Technical Information Center, November 2011. http://dx.doi.org/10.21236/ada601864.

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C. Uy, Genevieve, Raymond L. Rosales, and Satish Khadilkar. Myopathies in Clinical Care: A Focus on Treatable Causes. Progress in Neurobiology, February 2024. http://dx.doi.org/10.60124/j.pneuro.2024.10.01.

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Myopathies present a wide range of clinical symptoms that affect the skeletal muscles, including weakness, fatigue, and pain. While acquired myopathies receive significant attention due to the availability of treatment options, it is important to note that some inherited myopathies can also be effectively managed. These myopathies can be classified based on their underlying causes, such as infectious agents, autoimmune disorders leading to muscle inflammation, granulomatous inflammation, metabolic abnormalities within the muscle cells, skeletal muscle channel dysfunctions, prolonged ICU stay, and inherited conditions such as Duchenne muscular dystrophy. In this review, we initially present a clinical approach to neuromuscular diseases and subsequently place specific emphasis on myopathies, particularly to those that have treatment options available.

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Yang, Hui, Xi-Xi Wan, Hui Ma, Zhen LI, Li Weng, Ying Xia, and Xiao-Ming Zhang. Prevalence and mortality risk of low skeletal muscle mass in critically ill patients: an updated systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0132.

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Review question / Objective: The PICOS principle was adopted when we confirmed the study eligibility. The inclusion criteria were as follows: (1) patients were critically ill, which was defined as adult patients who were from the ICU department; (2) exposure: patients had a clear definition of LSMM based on CT scans, anthropometric methods and ultrasound; (3) presented the prevalence of LSMM or could be calculated by the available data from the article; and (4) study design: observational study (cohort study or cross-sectional study). Articles that were reviews, case reports, comments, correspondences, letters or only abstracts were excluded. Condition being studied: Critical illness often results in low skeletal muscle mass for multiple reasons. Multiple studies have explored the association between low skeletal muscle mass and mortality. The prevalence of low skeletal muscle mass and its association with mortality are unclear. This systematic review and meta-analysis aim to identify the prevalence and mortality risk of low skeletal muscle mass among critically ill patients.

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Buck, Edmond. Mechanism of Calcium Release from Skeletal Muscle Sarcoplasmic Reticulum. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.1306.

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Kuo, Meng-Hsuan, Chih-Wei Tseng, Ching-Sheng Hsu, Yen-Chun Chen, I.-Ting Kao, and Chen-Yi Wu. Protocol for systematic review and meta-analysis of prognostic value of sarcopenia in advanced HCC patients treating with systemic therapy. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2023. http://dx.doi.org/10.37766/inplasy2023.2.0011.

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Review question / Objective: P: Advanced HCC patients under systemic therapy; I: low skeletal muscle mass (LSMM); C: Non-LSMM; O:overall survival or mortality. Eligibility criteria: (1) cohort studies or cross sectional studies investigations with HCC patients treated with systemic therapy; (2) the articles estimated pretreatment skeletal muscle mass measured by CT-images; (3) studies provided statistical data about the prevalence pretreatment LSMM or influence of LSMM on OS orPFS.

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Holdsworth, Clark, Steven Copp, Tadakatsu Inagaki, Daniel Hirai, Scott Ferguson, Gabrielle Sims, Michael White, David Poole, and Timothy Musch. Chronic (-)-epicatechin administration does not affect contracting skeletal muscle microvascular oxygenation. Peeref, May 2022. http://dx.doi.org/10.54985/peeref.2206p3750191.

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Phillips, Stuart, Kyle Lau, Alysha D'Souza, and Everson Nunes. An umbrella review of systematic reviews of β-hydroxy-β-methyl butyrate (HMB) supplementation in promoting skeletal muscle mass and function in aging and clinical practice. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2021. http://dx.doi.org/10.37766/inplasy2021.10.0072.

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Review question / Objective: An umbrella review of systematic reviews of the use of β-hydroxy-β-methyl butyrate (HMB) supplementation in promoting skeletal muscle mass and function in aging and clinical practice. Condition being studied: Muscle mass (and various proxies thereof), strength, and physical function. Information sources: Pubmed, Web of Science, Embase.

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Koh, Timothy J. Enhancement of Skeletal Muscle Repair by the Urokinase-Type Plasminogen Activator System. Fort Belvoir, VA: Defense Technical Information Center, January 2006. http://dx.doi.org/10.21236/ada448526.

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Xiong, Hui. Modification of the CA²⁺ Release Channel from Sarcoplasmic Reticulum of Skeletal Muscle. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.1303.

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Wilmore, Douglas W. A Program for the Study of Skeletal Muscle Catabolism Following Physical Trauma. Fort Belvoir, VA: Defense Technical Information Center, November 1989. http://dx.doi.org/10.21236/ada216569.

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