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Bishop, Derron L. "Alterations in Z-line thickness following fast motoneuron transplantation onto slow twitch skeletal muscle fibers." Virtual Press, 1995. http://liblink.bsu.edu/uhtbin/catkey/935926.
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Differentiation of skeletal muscle fibers into fast and slow twitch appears to be under control of the stimulation pattern imparted by motoneurons innervating these muscle fibers. Fast twitch muscle fibers receive intense stimulation for brief periods of time while slow twitch muscle fibers receive less intense stimulation for much longer periods of time. This study examined thickness of Zlines in dually innervated skeletal muscle fibers of slow twitch soleus muscle following transplantation of the fast extensor digitorum longus (EDL) nerve onto the surface of the soleus. Eight individual dually innervated fibers were dissected from four transplanted mouse soleus muscles and examined with a transmission electron microscope. Z-lines in these dually innervated fibers were thinner (mean = 83 nm) than control soleus (mean = 123 nm) and thicker than control EDL (mean = 57 nm). A significant difference (p< .002) was also found between Z-line thickness near the foreign EDL endplate (mean = 81 nm) versus the original soleus endplate (mean = 85 nm). These results suggest the factors controlling protein synthesis in skeletal muscle fibers have both a global and localized effect.Department of Physiology and Health Science
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Nishimura, Daigo. "Roles of ADAM8 in elimination of injured muscle fibers prior to skeletal muscle regeneration." Kyoto University, 2015. http://hdl.handle.net/2433/199212.
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Hubatsch, Douglas A. "Passive mechanical stimulation regulates expression of acetylcholinesterase in skeletal muscle fibers." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/mq20923.pdf.
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Ting, Lok Yin. "Calcium dependence of titin-regulated passive force in skeletal muscle fibers." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=110598.
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AbstractRationale: There is evidence that the passive forces produced by titin in skeletal muscles may be regulated by Ca2+. Studies have shown an upwards shift in the passive force-sarcomere length (SL) relation when muscle fibres are tested with a high concentration of Ca2+ and the myosin-actin interaction is abolished.Objective: To test the hypothesis that there is a direct relation between the concentrations of Ca2+ and the cross-bridge independent increase in passive forces.Hypothesis: There is an upward shift in passive force-sarcomere length relation with increase calcium concentration.Methods: Single fibres were isolated from the rabbit psoas muscle and transferred into an experimental chamber, between a force transducer and a motor arm. Fibres were activated in a range of Ca2+ concentrations (pCa2+ between 4.5 and 9.0), before and after administration of the myosin inhibitor blebbistatin. The fibres were submitted to a protocol in which they underwent consecutive step-stretches, starting at an initial SL of 2.5µm (amplitude of stretch: 5% initial SL, duration 300 ms, pauses between stretches: 30 sec).Results: We observed similar passive force-sarcomere length curves in all calcium concentrations. Different pCa2+ did not affect the amount of passive force produced. Conclusions: The results suggest that the passive forces in skeletal muscles are not regulated by calcium concentrations.RésuméPréambule: Il existe des preuves que les forces passives produites par titine des muscles squelettique sont liées avec la concentration de Ca2+. Plusieurs études montrent qu'il existe un lien positif entre la longueur des sarcomères et la force passive générée lorsque les tests sont faits dans des hautes concentrations de Ca2+ et lorsque les interactions actine-myosine sont abolies. Objectifs: Tester l'hypothèse qu'il y a un lien positif entre la concentration de Ca2+ et l'augmentation de la force passive lorsque les pontages croisés sont abolis. Hypothèse: La force passive augmente parallèlement avec l'augmentation de la concentration de calcium.Méthodologie: Les fibres musculaires psoas des lapins sont d'abord isolées et transférées dans une chambre expérimentale fixées entre un transducteur de force et un bras moteur du système. Ces fibres sont activées dans une solution de calcium entre pCa2+4.5 et pCa2+9.0 avant et après l'administration de l'inhibiteur de myosine, blebbistatin. Les fibres sont étirées consécutivement débutant à une longueur de sarcomère 2.5m. (À une amplitude d'étirement de 5% de LS initiale, une durée de 300ms et 30s de pause entre chacun des étirements. Résultats: La force passive est semblable pour chacun des concentrations de calcium, donc il n'y a aucuns effets de calcium sur la production de la force passive.Conclusions: Les résultats nous suggèrent que la force passive n'est pas liée à la concentration de calcium.
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Mligiliche, Nurru Lameck. "Nerve regeneration through basal lamina tubes of detergent treated skeletal muscle fibers." Kyoto University, 2002. http://hdl.handle.net/2433/149700.
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Benigno, Maria Ivone Mendes 1960. "Análise morfométrica e ultraestrutural dos músculos masseter e pterigóideo medial pós exodontia unilateral de molares inferiores : estudo experimental." [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312598.
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Orientadores: Eliane Maria Ingrid Amstalden, Edson Aparecido LibertiTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-26T00:17:07Z (GMT). No. of bitstreams: 1 Benigno_MariaIvoneMendes_D.pdf: 2199405 bytes, checksum: 7460327535443e71e135d559be319402 (MD5) Previous issue date: 2014
Resumo: Introdução: A atividade mastigatória é uma sincronia entre os músculos da mastigação e articulação temporomandibular (ATM). A perda de dentes é um importante fator que contribui para as disfunções do Sistema Estomatognático e consequentes danos aos músculos mastigadores. Considerando os poucos trabalhos sobre o assunto, a necessidade de maior compreensão e detalhamento quanto às alterações das fibras desta musculatura, especialmente na disfunção pela perda dentária, este estudo teve como objetivos: investigar as alterações morfológicas e ultraestruturais do músculo Pterigoideo Medial (PTM) e Masseter, pós exodontia em modelo experimental. Material e Métodos: Foram utilizados 24 ratos wistar para microscopia de luz (ML) e 12 para microscopia eletrônica de transmissão (MET), divididos em três grupos experimentais: GI -15, GII-30 e GIII-60 dias, pós exodontia de molares inferiores esquerdos. Contendo 5 animais experimentais e três controles por grupo para ML e 3 ratos para MET, com 1 controle por grupo. Sob microscopia de luz foram realizados estudos morfométricos e sob luz polarizada, dos músculos PTM e Masseter. A análise morfométrica baseou-se na medida da área das fibras, em cortes transversais, corados pelo H&E (40x.objetiva), com programa digital (software AXION¿vision). Realizadas 240 medidas por animal/ total de 1200 por grupo experimental e 200 medidas por animal/ total de 600 por grupo controle. Análise qualitativa das fibras colágenas foi obtida sob luz polarizada. Também foram observadas, qualitativamente, alterações ultraestruturais destes músculos, ipsilateral às exodontias. Teste ANOVA foi aplicado para a análise dos dados. Resultados: A morfometria da área das fibras do músculo PTM, mostrou redução significante, nos animais submetidos à exodontia, tanto ipsi quanto contralateral. Não foram detectadas diferenças quanto aos quesitos interação entre lados direito e esquerdo e grupos (GI, II e III), nem quando se comparou os lados entre si. Diferenças foram notadas quando se comparou o grupo experimental, nos distintos períodos evolutivos, detectando-se aumento progressivo das áreas das fibras musculares, sendo a média maior no Grupo GIII. Apesar do crescimento progressivo da área das fibras, elas não se tornam hipertróficas nesse estágio avaliatório, uma vez que, a média dos valores obtidos é semelhante à do grupo controle. As fibras do músculo PTM parecem adaptar-se às mudanças. Nenhuma diferença foi detectada quanto à análise morfométrica do músculo Masseter. Ultraestruturalmente, observou-se assimetria e desorganização da linha Z e banda I, apenas no grupo experimental GII, do músculo PTM. A análise das fibras colágenas mostrou que os fascículos musculares são revestidos por uma delicada rede de fibras colágenas do tipo I e do tipo III, com predomínio deste último (fibras reticulares), nos Masseteres, nos diferentes períodos evolutivos. Conclusão: A disfunção temporomandibular, promovida pela exodontia unilateral de molares inferiores em ratos, pode levar a alterações morfométricas ipsi e contralaterais, com redução de áreas de fibras, particularmente no PTM. Entretanto as fibras musculares parecem se adaptar às novas condições, ao longo do experimento. A linha Z e banda I são as mais sensíveis a essa disfunção, no músculo PTM, contudo efêmera, uma vez que foi observada apenas no grupo GII. O músculo PTM mostrou-se mais vulnerável, provavelmente pelas suas características funcionais próprias e maior participação na dinâmica dos movimentos mastigatórios, comparadas às do Masseter. As fibras colágenas do tipo I e do tipo III são os constituintes principais das estruturas fibro conjuntivas desses músculos, com predomínio do tipo III no Masseter e parecem não ser afetadas nesse procedimento
Abstract: The loss of dental elements is an important factor in stomatognathic system dysfunctions and consequential damage to the masticatory muscles. The aim of this study was to analyze the morphometric and ultrastructural changes of the pterygoid medial(PTM) and masseter muscle, under occlusal defects, induced by unilateral left molar extraction, of Wistar rats. Thirty-six male rats were used: 24 for light microscopy (LM) and 12 for transmission electron microscopy analysis (TEM), divided into three experimental groups (GI-15; GII-30 and GIII-60 days), containing 5 animals each for LM with 3 control and 3 for TEM with one animal control for each period. Morphometric studies were made measuring the area of PTM and Masseter muscle fibers ipsi and contralateral to dental extraction, using a digital program. A qualitative analysis was performed to evaluate the ultrastructural findings and of the PTM and Masseter muscle. The results were compared using ANOVA test. There was a reduction of area of PTM of animals undergoing tooth extraction, both ipsi as contralateral. Both sides were similar when compared with each other, as assessed in the various evolutive periods. Differences were observed in the fiber area, especially in the first group and these showed progressive increase, reaching their highest average in GIII. No difference was detected regarding the morphometric analysis of the masseter muscle. For ultrastructure observed asymmetry and disorganization of Z line and I band, only the experimental group GII, muscle PTM. The analysis of the collagen fibers showed that the muscle fascicles are lined by a delicate network of collagen type I and type III, with a predominance of the latter (reticular fibers), in the masseter, in different evolutionary periods. Temporomandibular joint dysfunction, promoted by unilateral molar extraction in wistar rats, can lead to morphometric changes ipsi and contralateral with reduction of areas, particularly in the PTM. However seem to adapt to new conditions throughout the experiment. The band Z and the ith row of the muscle cytoskeleton are the most sensitive to this, dysfunction in muscle PTM, however ephemeral, since it was observed only in the Group (GII) with 30 days of the experiment. The muscle PTM proved to be more vulnerable in this experimental model, probably for its own functional features and greater participation in the dynamics of the masticatory movements, compared to the Masseter. The collagen fibers of type I and type III are the major constituents of the connective fibrous tissue structures of these muscles, with a predominance of type III in the Masseter and doesn't seem to be affected, to this procedure
Doutorado
Ciencias Biomedicas
Doutora em Ciências Médicas
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Mofarrahi, Mahroo. "Regulation of skeletal muscle satellite cell proliferation by NADPH oxidase." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111521.
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Skeletal satellite cells are adult stem cells located among muscle fibers. Proliferation, migration and subsequent differentiation of these cells are critical steps in the repair of muscle injury. We document in this study the roles and mechanisms through which the NAPDH oxidase complex regulates skeletal satellite cell proliferation. The NADPH oxidase subunits Nox2, Nox4, p22phox, p47phox and p67 phox were detected in primary human and murine skeletal muscle satellite cells. In human satellite cells, NADPH oxidase-fusion proteins were localized in the cytosolic and membrane compartments of the cell, except for p47 phox, which was detected in the nucleus. In proliferating subconfluent satellite cells, both Nox2 and Nox4 contributed to O2- production. However, Nox4 expression was significantly attenuated in confluent cells and in differentiated myotubes. Proliferation of satellite cells was significantly reduced by antioxidants (N-acetylcysteine and apocynin), inhibition of p22phox expression using siRNA oligonucleotides, and reduction of Nox4 and p47phox activities with dominant-negative vectors resulted in attenuation of activities of the Erk1/2, PI-3 kinase/AKT and NFkappaB pathways and significant reduction in cyclin D1 levels. We conclude that NADPH oxidase is expressed in skeletal satellite cells and that its activity plays an important role in promoting proliferation of these cells.
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Brault, Jeffrey J. "Creatine uptake and creatine transporter expression among rat skeletal muscle fiber types." free to MU Campus, others may purchase, 2003. http://wwwlib.umi.com/cr/mo/fullcit?p3091902.
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Breitenbach, Simon [Verfasser]. "Reasons for the repolarizing effects of eplerenone on edematous skeletal muscle fibers / Simon Breitenbach." Ulm : Universität Ulm, 2018. http://d-nb.info/1174251891/34.
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Quarta, Marco. "Calcium signals in myogenics cells and muscle fibers: an integrated study." Doctoral thesis, Università degli studi di Padova, 2008. http://hdl.handle.net/11577/3425176.
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Calcium release during skeletal muscle excitation-contraction (EC) coupling occurs at the junctions between the sarcoplasmic reticulum (SR) and either the plasma membrane or T-Tubule. These Ca2+ release units are characterized by a specific molecular composition and their specific structural organization, both of which are important for the tissue-specific mode of skeletal muscle EC coupling. Though EC coupling has been known for over half a century, it is still an active area of biomedical research. The general scheme is that an action potential arrives to depolarise the cell membrane. By mechanisms specific to the muscle type, this depolarisation results in an increase in cytosolic calcium that is called calcium transient. This increase in calcium activates calcium-sensitive myofibrillar proteins that then trigger ATP hydrolysis by myosin causing cell shortening. However, the exact mechanism if EC coupling and the role of related Ca2+ singnaling in regulating intracellular skeletal muscle ptthways is far to be clear. To higlight some of these unclear and dark points, we realized two null-mice for SR proteins. The first lacks of a sarcoplasmic reticulum Ca2+-binding protein, termed Calsequestrin (Csq), which plays an important role in buffering [Ca2+]SR and modulating Ca2+ release and reuptake during EC coupling. Our findings reveal the essential role of Csq1 in reorganizing stores and an impaired calcium handling in mice lacking Csq1.
an essential role of Cs as presented in chapter 1. Our data suggest that Csq1 deficency may result in a myopathy similar to that caused by mutations of RyR1 in skeletal muscle, leading to fulminant malignant hyperthermia (MH) episodes, as presented in chapter 2.
To investigate the structural role of SR we realized a second model, Ank1.5-null mice. The highly regulated nature of the arrangement of the SR around myofibrils is such that specific domains of the SR involved in the mechanisms of Ca2+ release and uptake (i.e., terminal cisternae and longitudinal tubules, respectively) are positioned at regular intervals in correspondence of specific regions of the sarcomere. However, the molecular mechanisms responsible of the interactions between these two cellular structures are not known. The small Ankirin 1.5 locates at SR level and participate in positioning SR and myofibrils. In chapter 3 we present evidence of contractile response impairment in skeletal muscles and altered animal performances of Ank1.5 deficient mices, without structural and ultrastructural morphological changes. The Ank1.5 could play a specific role not restricted to a correct positioning of the SR at specific sarcomere regions and its deficency may contribute to the generation of myopathies, and EC coupling dysfunctions.
To perform a deeper study of the development of the skeletal muscle cells, and in particular to better explore calcium signals in the context of EC coupling, we developed a muscle-cell / semiconductor chip device to induce EC coupling with non invasive long termed electric capacitive stimulation. We present in chapter 4 for the first time a new technique to study live EC coupling and Calcium signals in long term experiments and with high resolution, down to single cells, to induce muscle plasticity and synaptogenesis effects. The same approach is used for muscle fibers dissociated from mouse FDB muscle. To conclude, our hybrid device put an innovative base for new approaches aimed to better understand the muscle development and regeneration in normal and pathogenic conditions.
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Nascimento, Tábata Leal. "Papel da proteína de choque térmico 70 induzível (HSP70) na atrofia muscular e subsequente recuperação." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/42/42131/tde-17042013-085753/.
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As proteínas de choque térmico exercem um papel regulatório chave na defesa celular. Com o intuito de investigar o papel da proteína de choque térmico 70 kDa induzível (HSP70) na atrofia muscular e subsequente recuperação, os músculos extensor longo dos dedos e sóleo de camundongos transgênicos hiperexpressantes de HSP70 foram imobilizados durante 7 dias e subsequentemente liberados da imobilização e avaliados após 7 dias. Houve redução da área de secção transversal (AST) das fibras musculares após imobilização nos animais selvagens e HSP70 porém, apenas os animais HSP70 recuperaram a AST. O número de células satélites bem com a contração tetânica máxima permaneceram inalterados somente nos animais HSP70. O aumento da expressão dos genes atrogin-1 e MuRF-1 induzido pela imobilização foi atenuado nos animais HSP70. Nosso trabalho sugere que a HSP70 é importante para a melhor recuperação estrutural e funcional do músculo após imobilização, e este resultado pode estar relacionado à preservação da quantidade de células satélites e regulação de atrogenes.Heat shock proteins play a key regulatory role in cellular defense. In order to investigate the role of the inducible 70-kDa heat shock protein (HSP70) in skeletal muscle atrophy and subsequent recovery, extensor digitorum longus and soleus muscles from overexpressing HSP70 transgenic mice were immobilized during 7 days and subsequently released from immobilization and evaluated after 7 days. There was a decrease in myofiber cross-sectional area after immobilization in both wild type and HSP70 mice, but only myofibers from HSP70 mice recovered their size. The number of satellite cells and the muscle tetanic contraction were unchanged only in the muscles from HSP70 mice. In addition, the increase of atrogin-1 and MuRF-1 gene expression was attenuated in HSP70 mice. Therefore, our study suggests that the HSP70 is important for structural and functional recovery of muscles after immobilization and this effect might be associated with preservation of satellite cell amount and regulation of atrogenes.
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Stary, Creed Michael. "Contraction-induced elevation of heat shock protein 72 mRNA content in isolated single skeletal muscle fibers." Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2006. http://wwwlib.umi.com/cr/ucsd/fullcit?p3211911.
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Thesis (Ph. D.)--University of California, San Diego, 2006.Title from first page of PDF file (viewed Jul 10, 2006). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
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Wang, Mengxi. "Role of Map4k4 in Skeletal Muscle Differentiation: A Dissertation." eScholarship@UMMS, 2013. http://escholarship.umassmed.edu/gsbs_diss/675.
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Skeletal muscle is a complicated and heterogeneous striated muscle tissue that serves critical mechanical and metabolic functions in the organism. The process of generating skeletal muscle, myogenesis, is elaborately coordinated by members of the protein kinase family, which transmit diverse signals initiated by extracellular stimuli to myogenic transcriptional hierarchy in muscle cells. Mitogen-activated protein kinases (MAPKs) including p38 MAPK, c-Jun N terminal kinase (JNK) and extracellular signal-regulated protein kinase (ERK) are components of serine/threonine protein kinase cascades that play important roles in skeletal muscle differentiation. The exploration of MAPK upstream kinases identified mitogen activated protein kinase kinase kinase kinase 4 (MAP4K4), a serine/threonine protein kinase that modulates p38 MAPK, JNK and ERK activities in multiple cell lines. Our lab further discovered that Map4k4 regulates peroxisome proliferator-activated receptor γ (PPARγ) translation in cultured adipocytes through inactivating mammalian target of rapamycin (mTOR), which controls skeletal muscle differentiation and hypotrophy in kinase-dependent and -independent manners. These findings suggest potential involvement of Map4k4 in skeletal myogenesis.
Therefore, for the first part of my thesis, I characterize the role of Map4k4 in skeletal muscle differentiation in cultured muscle cells. Here I show that Map4k4 functions as a myogenic suppressor mainly at the early stage of skeletal myogenesis with a moderate effect on myoblast fusion during late-stage muscle differentiation. In agreement, Map4k4 expression and protein kinase activity are declined with myogenic differentiation. The inhibitory effect of Map4k4 on skeletal myogenesis requires its kinase activity. Surprisingly, none of the identified Map4k4 downstream effectors including p38 MAPK, JNK and ERK is involved in the Map4k4-mediated myogenic differentiation. Instead, expression of myogenic regulatory factor Myf5, a positive mediator of skeletal muscle differentiation is transiently regulated by Map4k4 to partially control skeletal myogenesis. Mechanisms by which Map4k4 modulates Myf5 amount have yet to be determined.
In the second part of my thesis, I assess the relationship between Map4k4 and IGF-mediated signaling pathways. Although siRNA-mediated silencing of Map4k4 results in markedly enhanced myotube formation that is identical to the IGF-induced muscle hypertrophic phenotype, and Map4k4 regulates IGF/Akt signaling downstream effector mTOR in cultured adipocytes, Map4k4 appears not to be involved in the IGF-mediated ERK1/2 signaling axis and the IGF-mediated Akt signaling axis in C2C12 myoblasts. Furthermore, Map4k4 does not affect endogenous Akt signaling or mTOR activity during C2C12 myogenic differentiation.
The results presented here not only identify Map4k4 as a novel suppressor of skeletal muscle differentiation, but also add to our knowledge of Map4k4 action on multiple signaling pathways in muscle cells during skeletal myogenesis. The effects that Map4k4 exerts on myoblast differentiation, fusion and Myf5 expression implicate Map4k4 as a potential drug target for muscle mass growth, skeletal muscle regeneration and muscular dystrophy.
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Wåhlin, Larsson Britta. "Skeletal muscle in Restless legs syndrome (RLS) and Obstructive sleep apnoea syndrome (OSAS)." Doctoral thesis, Örebro universitet, Hälsoakademin, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-6245.
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Restless legs syndrome (RLS) and Obstructive sleep apnoea syndrome (OSAS) are two sleep disorders that affect daily life with symptoms such as sleepiness and fatigue. It was therefore hypothesised that the skeletal muscle could be affected as symptoms from skeletal muscle are common. The overall aim of the thesis was to investigate aerobic capacity and structure of skeletal muscle in patients with OSAS and RLS and an age matched control group to provide information regarding the underlying mechanisms. The specific aims were to investigate muscle fibre composition, capillary network, capillary proliferation and sings of local inflammation in musculus tibialis anterior of RLS and OSAS.OSAS and RLS patients had a significantly lower predicted VO2 max expressed in ml/min/kg compared with the control group and in the OSAS group apnoes-hyponea index (AHI) was inversely correlated to maximal oxygen uptake Fibre type composition and muscle fibre cross sectional area in the tibialis anterior muscle was equal in all groups with a predominant proportion of slow type I fibres and a smaller fibre area in slow type I fibres compared to fast type II fibres. The distribution of fast fibres (I/IIA, IIA) did not differ except for the group IIX and IIA/IIX where OSAS and RLS had a significantly higher percentage. OSAS patients had a significantly higher number of capillaries per fibre (CAF) for slow type I fibres and CAF per fibre area (CAFA) for fast type II fibres. CFPE- index (capillary to fibre perimeter exchange) and LC/PF-index (length of capillary/perimeter of fibre) were higher in both patient groups. Vascular endothelial growth factor (VEGF) and proliferating endothelial cells were analysed by double-immunofluorescence staining and were presented to a greater extent in the patient groups compared with the healthy controls. Based on normal amounts of T-cells and macrophages in the histological picture it was also demonstrated that local inflammation was not present in the tibialis anterior muscle of RLS and OSAS whish was also supported by the absence of expression of major histocompatibility complex class I molecules (MHC class I) on the surface of the tibialis anterior muscle fibres.In conclusion, the low predicted VO2 max together with higher percentage of type IIX and IIA/IIX muscle fibres indicates a low central capacity in the patient groups. The increased capillary network and the absence of inflammation indicate the occurrence of local hypoxia in tibialis anterior muscle in patients OSAS and RLS.
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Amoasii, Leonela. "In vivo functional studies of myotubularin in mouse skeletal muscle." Thesis, Strasbourg, 2012. http://www.theses.fr/2012STRAJ037.
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La Myotubularine (MTM1) est une 3-phosphatase à phosphoinositides (PI) mutée dans la myopathie centronucléaire liée au chromosome X (XLCNM), caractérisée par une faiblesse musculaire et un positionnement anormal des noyaux dans les fibres musculaires. MTM1 définit une grande famille de phosphatases, exprimées dans tous les tissus, et qui englobent des phosphatases catalytiquement actives et inactives. Les myotubularines actives dephosphorylent le phosphatidylinositol 3 monophosphate [PtdIns3P] et le 3,5-bisphosphate [PtdIns(3,5)P2] en PtdIns et PtdIns5P, respectivement. Le rôle de MTM1 et son activité phosphatase à lipide dans le muscle restaient peu connus. L’étude approfondie de la protéine a révélé une association de MTM1 au réticulum sarcoplasmique des triades, un sous-compartiment impliqué dans la régulation calcique. La caractérisation de la souris Mtm1 KO, qui reproduit la XLCNM, a témoigné d’une anomalie de l’organisation et de la forme du réticulum sarcoplasmique. Afin d’explorer l’implicationde l’activité phosphatase de MTM1 dans l’organisation de réticulum sarcoplasmique, j’ai utilisé une approche in vivo avec des virus adéno-associé (AAV) pour moduler l’activité phosphatase en sur-exprimant MTM1 et sa forme phosphatase-inactive (MTM1-C375S) dans un muscle sauvage. L’observation des muscles transduits a dévoilé une implication de MTM1 dans le remodelage du réticulum sarcoplasmique et un rôle potentiel de PtdIns3P avec MTM1 dans la courbure des membranes du réticulum sarcoplasmique. Afin de comprendre l’importance de l’activité phosphatase dans le maintien du phénotype XLCNM, les muscles de souris Mtm1 KO ont été injectés avec ces AAVs contenant la forme active et inactive de MTM1 au moment de l’apparition des premiers signes de XLCNM. Étonnamment, la forme phosphatase-inactive(MTM1-C375S) a sauvé le phénotype de la souris Mtm1 KO de la même façon que la forme active, suggérant que l'activité de phosphatase de MTM1 n’est pas nécessaire pour le maintien de la structure intracellulaire des fibres du muscle adulte. Ces données suggèrent que MTM1 exerce une fonction phosphatase-indépendante dans le maintien de la structure musculaire, certainement via des interactions protéine-protéine, et une fonction phosphatase-dépendente dans le remodelage de la forme du réticulum sarcoplasmique dans le muscle squelettiqueMyotubularin (MTM1) is a phosphoinositide (PI) 3-phosphatase mutated in X-linked centronuclear myopathy (XLCNM), a rare congenital myopathy characterized by muscle weakness and abnormal positioning of nuclei in muscle fibers. MTM1 defines a large family of ubiquitously expressed catalytically active and inactive phosphatases. Active myotubularins dephosphorylate both phosphatidylinositol 3-phosphate [PtdIns3P] and 3,5-bisphosphate [PtdIns(3,5)P2] to PtdIns andPtdIns5P, respectively. The specific role of MTM1 and its PI phosphatase activity in muscle remains unknown. Comprehensive analysis of the protein unveiled the association of MTM1 with the sarcoplasmic reticulum (SR) at the triads. Characterization of Mtm1-KO mouse, which reproduce the XLCNM phenotype, revealed a defect of SR organization and shape. In order to gain insight into the involvement of MTM1 phosphatase activity on SR shape and organization, we employed an in vivo approach using Adeno-Associated Virus (AAV) to modulate the phosphatase activity by overexpressingMTM1 and its phosphatase inactive mutant in wild type muscle. The analysis of transduced muscle revealed the involvement of MTM1 in the SR remodeling and its potential role together with PtdIns3P in modulating membrane curvature. In order to understand the importance of the phosphatase activity in the generation of the XLCNM phenotype, Mtm1 KO mice were injected with AAV expressing the active form and the phosphatase inactive form. Surprisingly, both, the phosphatase active and the phosphatase inactive mutant corrected the Mtm1-KO mouse phenotype to a similar extent, thus suggesting that the PI-phosphatase activity of MTM1 is not essential for adult skeletal muscle maintenance. Our data indicates that MTM1 has a phosphatase-independent function in adult muscle structure maintenance and a phosphatase-dependent function in sarcoplasmic reticulum remodeling and shape in skeletal muscle
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Eriksson, Anders. "Strenght training and anabolic steroids : a comparative study of the trapezius, a shoulder muscle and the vastus lateralis, a thigh muscle, of strength trained athletes." Doctoral thesis, Umeå : Umeå universitet, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-869.
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Nishizaka, Takahiro. "Effects of Exposure to Mild Hyperbaric Oxygen on Skeletal Muscle Fibers, Epidermal Basal Cells, and Skin Pigmentation." Kyoto University, 2014. http://hdl.handle.net/2433/193555.
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Kyoto University (京都大学)0048
新制・論文博士
博士(人間・環境学)
乙第12883号
論人博第40号
新制||人||169(附属図書館)
26||論人博||40(吉田南総合図書館)
31601
(主査)教授 石原 昭彦, 教授 船橋 新太郎, 教授 林 達也, 准教授 神﨑 素樹, 准教授 久代 恵介
学位規則第4条第2項該当
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Viau, Francois M. "The role of Ca§+² and calcineurin in regulating the myofibrillar and metabolic properties of individual skeletal muscle fibers." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ61315.pdf.
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Nahirney, Patrick Charles. "Morphological quantitative and ultracytochemical studies on the internal membrane systems of normal and mdx-dystrophic murine skeletal muscle fibers." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0020/NQ48681.pdf.
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Nowacka, Lidia. "Muscle gene transfer studies of a 27-BP segment of the troponin I fast gene IRE enhancer." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111563.
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The fast-skeletal-muscle-fiber-specific expression of the troponin I(fast) (TnIfast) gene is driven by an Intronic Regulatory Element (IRE) located within the first intron of the gene. The IRE is a 148 bp transcriptional enhancer that contains several known and suspected cis-regulatory elements. These include the E-box, the closely-spaced MEF2 site and CACT box, the CACC site, and the CAGG element. Previous loss-of-function studies performed using the quail TnIfast IRE suggest that its activity depended on the MEF2 and CACT elements. The goal of my thesis research was to determine whether the MEF2 and CACT sites were not only necessary, but also sufficient, to support IRE activity. I prepared head-to-tail multimers of a 27-bp IRE segment that consisted largely of the near-adjacent MEF2 and CACT elements and did not contain any other known/suspected elements. These multimers were cloned upstream of a reporter gene consisting of the minimal promoter of the quail TnIfast gene linked to sequences encoding human placental alkaline phosphatase. The transcriptional capabilities of the constructs were assessed by gene transfer into the mouse soleus muscle in vivo by intramuscular injection/electroporation, and histochemical analysis of reporter enzyme plap expression including quantitative microdensitometry. I found that expression of these constructs was readily detectable and that it was markedly reduced by prior mutation of the CACT and, especially, of the MEF2 sites. These data indicate that the short DNA segment containing MEF2 and CACT elements is sufficient to drive expression in skeletal muscle and confirms the functional importance of these specific elements.Although constructs containing the wild-type IRE 27-bp region were expressed, there was little preferential expression in fast fibers, in contrast to expression driven by the complete 148-bp IRE. Thus my results indicate that the MEF2 and CACT elements are not sufficient to drive fast fiber-type-specific expression, and suggest that additional elements outside of the 27-bp region tested are also necessary for fiber-type-specificity.
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Santos, Marcelo Rodrigues dos. "Efeito do treinamento físico isolado ou associado à reposição de testosterona em pacientes com insuficiência cardíaca." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-17012014-122243/.
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Introdução. A insuficiência cardíaca (IC) é caracterizada por exacerbação da atividade nervosa simpática muscular (ANSM), baixa tolerância ao esforço e dispneia. Além disso, é característico nessa população o desequilíbrio entre o anabolismo e catabolismo, favorecendo dessa maneira uma acentuada perda da massa magra muscular, o que agrava ainda mais a qualidade de vida nos pacientes com IC. Dentre as alterações anabólicas observadas na IC avançada destaca-se a diminuição dos hormônios GH, IGF-1 e testosterona. A testosterona, um importante hormônio para as características masculinizantes e na manutenção da massa muscular, apresenta acentuada redução com o avançar da doença. Esta perda da massa magra, leva ao processo de caquexia muscular e consequente atrofia, com diminuição da força e da capacidade funcional do paciente com IC. A reposição de testosterona nesses pacientes tem sido estudada e se mostra uma importante terapêutica para melhorar a capacidade funcional e força muscular. Porém, não se conhece claramente o papel deste tratamento medicamentoso sobre o processo anabólico muscular, bem como na melhora da composição corporal. O exercício físico como tratamento não medicamentoso tem sido amplamente recomendado na IC por reduzir a ANSM, melhorar o fluxo sanguíneo periférico, aumentar a força muscular e melhorar a qualidade de vida. Entretanto, a combinação das estratégias do exercício físico associado à terapia de reposição de testosterona, não é conhecido em pacientes com IC. Métodos. 24 pacientes com IC foram randomizados em 3 grupos: Treinamento (TR, n=9), Testosterona (T, n=8) e Treino+Testosterona (TRT, n=7). A ANSM foi avaliada pela técnica de Microneurografia. O fluxo sanguíneo do antebraço foi avaliado pela pletismografia de oclusão venosa. A composição corporal foi avaliada pela densitometria (DEXA). A biópsia do músculo vasto-lateral foi feita para avaliarmos a área de secção transversa da fibra e a tipagem de fibras musculares. A qualidade de vida foi avaliada pelo questionário de Minnesota. O treinamento físico aeróbio em bicicleta foi realizado 3 vezes por semana, com 40 minutos de exercício por sessão, pelo período de 4 meses. A reposição de testosterona foi realizada pela administração intramuscular de undecilato de testosterona pelo período de 4 meses. Resultados. Após 4 meses de intervenção, observamos restauração dos níveis de testosterona em todos os grupos. A ANSM reduziu nos grupos TR e TRT. Não houve aumento do fluxo sanguíneo entre os grupos. O consumo de oxigênio aumentou em todos os grupos, porém apenas o grupo TRT aumentou a potência máxima ao exercício. A massa magra apresentou aumento significativo apenas no grupo TRT. Não observamos mudança no conteúdo mineral ósseo entre os grupos. Apenas o grupo TRT aumentou de maneira significativa a área de secção transversa das fibras tipo I (oxidativas). A qualidade de vida melhorou apenas nos grupos TR e TRT. Conclusões. O exercício físico associado à terapia de reposição de testosterona se mostrou mais eficaz em reduzir a ANSM, aumentar a capacidade funcional, a força muscular, a massa magra com um importante aumento das fibras do tipo I. Nossos resultados enfatizam a importância do exercício físico em pacientes com IC e traz uma nova perspectiva com a associação da testosterona para pacientes com hipogonadismoIntroduction. Heart failure (HF) is characterized by exacerbation of muscle sympathetic nerve activity (MSNA), exercise intolerance and dyspnea. Furthermore, is characteristic in this population the imbalance between anabolism and catabolism which lead to loss of skeletal muscle mass worsening quality of life in HF patients. Prior studies have demonstrated decrease in anabolic hormones such as GH, IGF-1 and testosterone. Testosterone, an important hormone for masculinization feature and maintenance of muscle mass, shows sharp decline in advanced HF. Loss muscle mass leads to cachexia and atrophy which decrease strength and functional capacity in HF patients. Testosterone replacement in these patients has been studied and shows an important therapeutic to enhance functional capacity and muscle strength. However it is not known the role of this medical treatment on muscle anabolic process as well as on body composition. Physical exercise as a non-medication treatment has been widely recommended to reduce MSNA, enhance peripheral blood flow, increase muscle strength and improve quality of life. However, the combination of the strategies of physical exercise associated with testosterone replacement therapy is not known in HF patients. Methods. 24 HF patients were randomized in 3 groups: Training (TR, n=9), Testosterone (T, n=8) and Training+Testosterone (TRT, n=7). MSNA was recorded by microneurography technic. Forearm blood flow was evaluated by venous occlusion plethysmography. Body composition was measured by densitometry (DEXA). Muscle biopsy was done in vastus lateralis to evaluate the cross-sectional area and type of fibers. Quality of life was assessed by Minnesota living with heart failure questionnaire. Aerobic exercise training on a bicycle was performed 3 times per week, with 40 minutes of exercise per session, for a period of 4 months. Testosterone replacement was performed by intramuscular administration of testosterone undecylate for a period of 4 months. Results. After 4 months testosterone levels were restored in all groups. MSNA decreased in TR and TRT groups. There was no increase in blood flow between groups. Oxygen consumption increased in all groups, but only the TRT group showed increase in maximum power to exercise. Lean body mass increased significantly only in the TRT group. We did not observe changes in bone mineral content between groups. Only TRT group significantly increased the cross-sectional area of type I fibers (oxidative). The quality of life improved only in TR and TRT groups. Conclusions. Exercise training associated with testosterone replacement therapy was more effective in reducing MSNA, increase functional capacity, muscle strength, lean mass with a significant increase in type I fibers. Our results emphasize the importance of physical exercise in patients with HF and bring a new perspective to association testosterone for patients with hypogonadism
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Butugan, Marco Kenji. "Influência da progressão do diabetes nos padrões dinâmicos de recrutamento de fibras musculares analisados através de eletromiografia de alta densidade." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5170/tde-24062014-113902/.
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Este estudo teve como objetivo investigar a influência de diferentes estágios de severidade da neuropatia diabética na velocidade de condução das fibras musculares estimada em quatro músculos do membro inferior durante contrações isométricas, utilizando-se eletromiografia de superfície. Oitenta e cinco adultos foram estudados: 16 indivíduos não diabéticos e 69 diabéticos classificados em quatro estágios de neuropatia definidos por um sistema fuzzy: ausente (n=26), leve (n=21), moderada (n=11) e grave (n=11). As velocidades de condução médias das fibras musculares do tibial anterior, gastrocnêmico medial, vasto lateral e bíceps femoral foram avaliadas utilizando uma matriz linear de eletrodos de superfície e foram comparadas entre os grupos estudados por meio de ANOVAs (p < 0,05). As velocidades de condução diminuíram significativamente no grupo com neuropatia moderada para o vasto lateral em relação aos outros grupos (18 a 21% de decréscimo), e foram menores em todos os grupos com diabetes para o tibial anterior em relação ao grupo controle (15 a 20% de decréscimo). Não só a localização anatômica distal do músculo afetou a velocidade de condução, mas também a proporção do tipo de fibras musculares, uma vez que o tibial anterior, com maior proporção de fibras do tipo I, estava com sua velocidade de condução alterada já no grupo ausente, enquanto o vasto lateral, com maior proporção de fibras do tipo II, estava com sua velocidade de condução alterada em estágios mais tardios da doença. De forma geral, os músculos do membro inferior têm diferentes suscetibilidades aos efeitos do diabetes mellitus e da neuropatia e mostram uma redução da velocidade de condução conforme a neuropatia progrideThis study aimed at investigating the influence of different stages of diabetic neuropathy in the muscle fiber conduction velocities estimated in four lower limb mucles during isometric maximal voluntary contraction using surface electromyography. Eighty-five adults were studied: 16 non-diabetic individuals and 69 diabetic patients classified into four neuropathy stages, defined by a fuzzy system: absent (n=26), mild (n=21), moderate (n=11) and severe (n=11). Average muscle fiber conduction velocities of gastrocnemius medialis, tibialis anterior, vastus lateralis and biceps femoris were assessed using linear array electrodes, and the studied groups were compared by ANOVAs (p < 0.05). Conduction velocities were significantly decreased in the moderate neuropathy group for the vastus lateralis compared to other groups (from 18 to 21% decrease), and were decreased in all diabetic groups for the tibialis anterior (from 15 to 20% from control group). Not only the distal anatomical localization of the muscle affects the conduction velocity, but also the proportion of muscle fiber type, where the tibialis anterior, with greater type I fiber proportion, is affected already at the absent group while the vastus lateralis with greater type II fiber proportion is affected in later stages of the disease. Generally, the muscles of the lower limb have different responsiveness to the effects of diabetes mellitus and neuropathy and show a reduction in the conduction velocity as the neuropathy progresses
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Kuhn, Camila. "Estudo morfológico do músculo extensor longo dos dedos da prole de ratas obesas submetidas ou não à cirurgia de derivação gástrica em Y de Roux." Universidade Estadual do Oeste do Paraná, 2018. http://tede.unioeste.br/handle/tede/4166.
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Studies show that maternal obesity can affect fetal development, resulting in diseases in adult life, such as diabetes mellitus type 2, cardiovascular disease, obesity itslef. To reduce the effects of obesity and its comorbidities, bariatric surgeries stand out among the most effective interventions, with Roux-en-Y gastric bypass (RYGB) being the most frequently performed type of bariatric procedure. However, there are still few studies in the literature that evaluate the effects of obesity and bariatric surgeries on the morphology of skeletal muscle tissue in adult offspring. Thus, the objective of this study was to evaluate microscopic parameters of muscle fibers and neuromuscular junctions (NMJs) of the extensor digitorum longus muscle (EDL) in obese rats’ offspring submitted or not to RYGB surgery. Three-week Wistar rats were randomly divided into three groups: Control Group (CTL) which received a standard diet; 2) Cafeteria False Operated (CAF FO) and 3) Cafeteria RYGB (CAF RYGB), the latter two received a cafeteria diet before and after the surgical procedure until the weaning of the offspring. In the 18th of life, the surgical procedure and false operation were performed in the CAF RYGB and CAF FO groups, respectively. The mating of the animals occurred five weeks after the surgical procedure. The birth of the offspring was postnatal day 0, and weaning occurred at three weeks of age, and only the male offspring were separated for the experiment. The offspring of the first generation (F1) were named CTL-F1, OB-F1, CAF FO-F1 and CAF RYGB and received standard diet. At 17 weeks the animals were euthanized and the EDL muscle collected for analysis of fiber muscles and NMJs. When the CTL-F1 and OB-F1 groups were analyzed, the latter had an increase in body weight, retroperitoneal and periepididymal fats, and capillary/fiber ratio. Reduction in the number of nuclei, conjunctive and morphological changes in the parameters evaluated in the ultrastructure. The area and larger diameter of NMJs also showed reduction. The analysis between CAF RYGB-F1 and CAF FO-F1 groups showed reduction of body weight, ELD muscle weight, retroperitoneal and periepididimal fat, nasoanal length, fiber area and nuclei/fiber ratio in the CAF RYGB-F1 group. This group also presented increase in the number of fibers of type I and IIa and number of capillaries, as well as reduction in the area of the NMJs and morphological alterations in the ultrastructure. These results demonstrate that both obesity and bariatric surgery expose the offspring, through metabolic programming, to effects on the morphology of skeletal muscle tissue, being found greater aggravations in the muscular fiber of the offspring of mothers submitted to RYGB.
Estudos apontam que a obesidade materna pode afetar o desenvolvimento fetal, resultando em doenças na vida adulta, tais como diabetes mellitus tipo 2, doenças cardiovasculares e a própria obesidade. Para reduzir os efeitos da obesidade e as suas comorbidades, as cirurgias bariátricas destacam-se entre as intervenções mais eficazes, sendo a derivação gástrica em Y de Roux (DGYR) o tipo de procedimento bariátrico mais frequentemente realizado. No entanto, ainda são escassos na literatura estudos que avaliem os efeitos da obesidade e das cirurgias bariátricas na morfologia do tecido muscular esquelético da prole adulta. Diante disso, o objetivo deste estudo foi avaliar a morfologia e a morfometria das fibras musculares e as junções neuromusculares (JNMs) do músculo extensor longo dos dedos (ELD) da prole de ratas obesas submetidas ou não à cirurgia de DGYR. Para tanto, ratas Wistar de três semanas de vida foram separadas aleatoriamente em três grupos: 1) Controle (CTL), que recebeu dieta padrão; 2) Cafeteria Falso operado (CAF FO) e 3) Cafeteria DGYR (CAF DGYR); esses dois últimos receberam dieta de cafeteria antes e após o procedimento cirúrgico, até o desmame da prole. Na 18ª semana de vida, foi realizado o procedimento cirúrgico e a falsa operação nos grupos CAF DGYR e CAF FO, respectivamente. O cruzamento dos animais ocorreu cinco semanas após o procedimento cirúrgico. O nascimento dos animais foi considerado o dia zero pós-natal e o desmame se deu na terceira semana vida, quando somente os machos foram separados para o experimento. A prole da primeira geração (F1) foi nomeada em CTL-F1, OB-F1, CAF FO-F1 e CAF DGYR-F1 e todos os animais receberam dieta padrão. Na 17ª semana, os animais foram eutanasiados e o músculo ELD coletado para análise das fibras musculares e JNMs. Quando analisado os grupos CTL-F1 e OB-F1, esse último apresentou aumento do peso corpóreo, das gorduras retroperitoneal e periepididimal, e relação capilar/fibra. Além disso, houve a redução do número de núcleos, conjuntivo e alterações morfológica nos parâmetros avaliados na ultraestrutura. A área e diâmetro maior das JNMs também apresentaram redução. A análise entre os grupos CAF DGYR-F1 e CAF FO-F1 evidenciou redução do peso corporal, do peso do músculo ELD, da gordura retroperitoneal e periepididimal, don comprimento nasoanal, da área das fibras e relação núcleo/fibra no grupo CAF DGYR-F1. Esse grupo também apresentou aumento no número de fibras do tipo I e IIa e no número de capilares, assim como redução na área das JNMs e alterações morfológicas na ultraestrutura. Esses resultados demonstram que tanto a obesidade como a cirurgia bariátrica expõem a prole, por meio da programação metabólica, com efeitos na morfologia do tecido muscular esquelético, sendo encontrado maiores agravos na fibra muscular da prole de mães submetidas à DGYR.
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Banas, Krystyna Anna. "K(ATP) channel Kir62 subunit distribution differs between muscles and between fiber types in skeletal muscle." Thesis, University of Ottawa (Canada), 2010. http://hdl.handle.net/10393/28483.
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The activity of the ATP-sensitive potassium (KATP) channel, whose sensitivity to ATP and ability to permit K+ flux together allow the channel to couple the metabolic state of a cell to its membrane excitability, is important in several tissues for the maintenance of glucose homeostasis and cytoprotection. In skeletal muscle specifically, the channel has been shown to be involved in cell volume regulation, modulation of glucose uptake, and the prevention of fiber damage and contractile dysfunction during fatigue. The extent of the cytoprotective capabilities of the KATP channel vary tremendously between muscles with different muscle fiber type composition. Semi-quantitative measurement of Kir6.2 subunit content showed that variances exist in KATP channel content between fiber types and between different muscles. These differences may be related to the extent of importance of the channel's function in a specific muscle. The highest Kir6.2 content was observed in the most glycolytic fiber types and in the more glycolytic muscles studied, and it is these muscles and fiber types which appear to be most dependent on functional KATP channels for their cytoprotective role.
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Sattiraju, Sandhya Ramani. "Apoptosis and necrosis drive muscle fiber loss in lipin1 deficient skeletal muscle." Wright State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=wright1598626794423032.
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Matsumoto, Akiko. "Skeletal muscle fiber characteristics and plasticity to hyperbaric oxygen." Kyoto University, 2011. http://hdl.handle.net/2433/142292.
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Kyoto University (京都大学)0048
新制・課程博士
博士(人間・環境学)
甲第16164号
人博第547号
新制||人||132(附属図書館)
22||人博||547(吉田南総合図書館)
28743
京都大学大学院人間・環境学研究科共生人間学専攻
(主査)教授 石原 昭彦, 教授 津田 謹輔, 准教授 神﨑 素樹
学位規則第4条第1項該当
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Mankal, Fawzi Ahmad. "Assembly, stability and secretion of acetylcholinesterase in skeletal muscle fibres." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ48170.pdf.
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Zhao, Wanfeng. "Development and differentiation of oesophageal muscle in mouse." Thesis, Royal Veterinary College (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367759.
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Boss, Matthew John. "Analysis-ready isogeometric model of skeletal muscles." Thesis, University of Iowa, 2012. https://ir.uiowa.edu/etd/2827.
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New methods are employed to develop an anatomically accurate, analysis-ready isogeometric model of skeletal muscles. Current modeling techniques for the analysis of skeletal muscles include the utilization of finite element meshing, which inherently poses a few well-known problems that provide motivation for isogeometric analysis. In addition to those issues, standard FEA meshing cannot preserve smooth geometries, therefore the accuracy of the foregoing model and analysis is reduced. Moreover, there is no easy means to characterize fiber direction in the FEA framework due to discontinuities at element boundaries. Additionally, material property distributions such as the transition of the muscle-tendon complex along the longitudinal axis through FEA are prescribed on an element by element basis, leading to abrupt, unrealistic property changes at element boundaries. The current research builds on the idea of an isogeometric tensor-product rod using harmonic coordinates and NURBS [1]. Through a direct comparison between a meshed, FEA model and the tensor-product rod model, it can be shown that the tensor-product rod model preserves smoothness, enhancing the geometric representation passed through to analysis while reducing the total DOF of the model. Muscle fibers can be easily implemented as parametric lines with muscle-specific orientations along the muscles' longitudinal axis that match distinct fiber orientations existent within common skeletal muscles. This technique not only allows for the representation of perfectly parallel-fibered structures, but also those that do not directly follow the longitudinal axis such as a helical twist. Utilizing this geometric method also provides the framework for implementing material properties using an interpolative-style scheme. Varying properties at specific longitudinal control point cross-sections near muscle termination areas can be designated to more accurately represent the muscle-tendon complex. These new techniques allow for the creation of an analysis-ready, realistic skeletal muscle model of the male human arm. The model contains 28 muscles complete with muscle-specific geometric, fiber, and heterogeneous property characterizations all compiled into a complete "digital muscle library."
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Butera, Gaia. "Mitochondrial adaptation in parvalbumin knockout muscle fibres." Doctoral thesis, Università degli studi di Padova, 2019. http://hdl.handle.net/11577/3422345.
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Mitochondrial Ca2+ homeostasis plays a fundamental role in the regulation of several biological processes, ranging from the regulation of ATP production to the control of cell death. Recent studies have identified the multimolecular complex responsible for Ca2+ entry into mitochondria: the mitochondrial calcium uniporter (MCU) complex [1]. It is widely accepted that mitochondria actively participate in the regulation of cellular Ca2+ homeostasis by dictating the spatio-temporal properties of [Ca2+]cyt rises [2]. Mitochondrial calcium uptake, in specific cells, contributes to regulate cellular Ca2+ homeostasis acting as high-capacity fixed buffer, sequestering large amounts of Ca2+ from a subcellular domain[2]. Furthermore, one of the most important roles of mitochondrial Ca2+ uptake is the mitochondrial Ca2+-dependent control of the rate of mitochondrial adenosine triphosphate (ATP) production, the main fuel for sustaining cellular functions [3], [4].
This general picture is particularly relevant in skeletal muscle, a tissue where mitochondria produce most of the ATP required to sustain muscle contraction [3], [5]. It is thus not surprising that skeletal muscle mitochondria display the highest mitochondrial Ca2+ transients, as demonstrated by the measurement of the MCU current by patch-clamp from IMM-derived mitoplasts from different tissues [6].
Moreover, pivotal findings have highlighted the role of mitochondria as key players in the dynamic regulation of crucial signalling pathways in skeletal muscle [7], [8], involved not only in muscle contraction but also in skeletal muscle homeostasis [9], [10]. However, whether skeletal muscle mitochondria act also as a possible high capacity Ca2+ buffer remains a fundamental question on muscle physiology and diseases.
Our research investigated the regulatory processes that modulate mitochondrial Ca2+ signalling in skeletal muscle. In detail, to understand the impact of changes in cytosolic Ca2+ concentrations ([Ca2+]cyt) on mitochondrial Ca2+ uptake and muscle physiology, we explored a condition where intra-fiber Ca2+ kinetics have been profoundly altered by removing parvalbumin (PV), one of the crucial cytosolic Ca2+ buffers in skeletal muscle, specifically expressed in fast twitch muscle fibers [11], [12].
To this end, as study tool, we used a PV knockout (KO) mouse model obtained from the laboratory of Prof. Beat Schwaller (Dept. of Medicine, University of Fribourg, Switzerland) [13].
PV plays an important role in skeletal muscle, acting as a temporary Ca2+ buffer (e.g. increasing the relaxation rate of fast twitch muscle contraction) [14]. To investigate the physiological role of PV in muscle fibers and in Ca2+ homeostasis, we investigated cytosolic and mitochondrial Ca2+ transients in PV KO mice compared. We observed that basal [Ca2+]cyt was not affected in PV knockout fibers, but kinetics of Ca2+ transients and Ca2+ clearance were altered. In detail, consistently with the role of PV in buffering cytosolic Ca2+, the time-to-peak and the half-relaxation time was increased in PV KO FDB fibers. Unexpectedly, however, under tetanic stimulation, PV KO FDB muscle fibers showed a decrease in [Ca2+]cyt. To explain this result we asked whether the lack of PV could induce rearrangements of one of the two main Ca2+ stores, the sarcoplasmic reticulum (SR) and mitochondria. SR Ca2+ measurements demonstrated that lack of PV increases SR Ca2+ release during stimulation. Therefore, we concluded that SR is not causative of the effect of PV removal on cytosolic Ca2+ transients. Consistently, we found no difference in the mRNA levels of RyR1, the main Ca2+ releasing channel in muscle, and on the expression of two different isoforms of SERCA in PV KO muscles compared to WT. We then focused our attention on mitochondrial Ca2+ homeostasis. The data obtained demonstrated that the lack of PV induces an increase of mitochondrial Ca2+ uptake and this is accompanied by the induction of the expression of MCU complex components, the channel responsible for Ca2+ entry in mitochondria [1], [2], [15], [16]. In addition, electron microscopy analysis demonstrated that the volume of PV KO mitochondria was doubled compared to WT with an increase of mitochondria associated to the Ca2+ release units (CRUs), suggesting a tight connection of PV expression with mitochondrial morphology and function in muscle cells. Furthermore, to further prove that mitochondria are responsible for cytosolic Ca2+ buffering in fibers lacking PV, we silenced MCU on WT and PV KO FDB fibers and we measured [Ca2+]cyt.. In WT animals, [Ca2+]cyt was not affected by the absence of MCU, while MCU silencing in PV KO fibers resulted in a significant higher [Ca2+]cyt, reinforcing the hypothesis that, while in WT animals mitochondria do not significantly buffer [Ca2+]cyt, mitochondria of fibers lacking PV adapt to buffer [Ca2+]cyt increases.
Moreover, since PV is one of the most downregulated “atrogenes”, the genes commonly up- and down-regulated during both disuse and systemic types of atrophy [17], [18] and that mitochondrial Ca2+ controls skeletal muscle trophism [10], the role of PV in the regulation of muscle mass was investigated through denervation experiments. In PV KO muscles, loss of muscle mass caused by denervation is reduced compared to WT fibers, demonstrating that the lack of PV can partially protect muscles from denervation-induced atrophy. Since the effect of PV ablation on denervated muscle was modest and the effect on innervated muscles was negligible, we decided to perform PV acute silencing and overexpression in adult WT tibialis anterior (TA) muscles and we monitored fiber size. We demonstrated that the acute modulation of PV protein controls skeletal muscle size. In detail, we observed an increase of fiber size in PV silenced muscles and coherently, PV overexpressing muscles displayed an atrophic phenotype. Since the regulation of muscle size involves a precise transcriptional program [18], [19], we focused our attention on PGC-1α4, a splicing variant of the PGC-1α gene, that plays a key role in triggering muscle hypertrophy as adaptive response to exercise [20]. Intriguingly, we found an up-regulation of PGC-1α4 mRNA in PV KO skeletal muscles, suggesting the activation of this hypertrophic pathway. Of note, our data are in accordance with previous studies showing that mitochondrial Ca2+ positively regulates skeletal muscle mass by impinging also on PGC-1α4 pathway [10]. Our results show that the lack of PV in skeletal muscle leads to morphological and functional adaptations of mitochondria. In particular, mitochondria of fibers lacking PV, either constitutively or transiently, adapt to take up more Ca2+ to control [Ca2+]cyt increases. Furthermore, we demonstrated that the absence of PV partially counteracts denervation atrophy by triggering the expression of PGC-1α4. Our hypothesis is that PV ablation, leading to an increase of mitochondrial Ca2+ uptake, activates mitochondrial Ca2+-dependent pathways to control skeletal muscle trophism.
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Correra, Rosa Maria. "Pw1/Peg3 regulates skeletal muscle growth and satellite cell self-renewal." Electronic Thesis or Diss., Paris 6, 2016. http://www.theses.fr/2016PA066339.
Full textAbstract:
Pw1/Peg3 est un gène d’empreinte parental exprimé par l’allèle paternel. Il est exprimé dans l’ensemble des populations de cellules souches, y compris les cellules satellites du tissu musculaire. Nous avons découvert que la perte constitutive de Pw1/Peg3 entraîne une perte de la masse musculaire, résultat d’une diminution du nombre de fibres musculaires. Le nombre de fibres réduit est présent dès la naissance. De plus, les souris double KO ont un nombre de fibres encore inférieur, suggérant que l’allèle maternel est fonctionnel pendant le développement pré-natal, et des analyses de souris hybrides C57BL6J/CAST/Ei révèlent une expression bi-allélique de Pw1/Peg3 d’environ 10%. Pw1/Peg3 est également fortement exprimé après blessure du muscle squelettique. Chez les souris Pw1/Peg3 KO, nous avons observé que les cellules satellites montrent une réduction de leur capacité d’auto-renouvèlement à la suite d’une blessure. Pw1/Peg3 est également exprimé dans une sous-population de cellules souches interstitielles, les PICS. Afin de déterminer le rôle spécifique de Pw1/Peg3 dans les cellules satellites nous avons croisé notre allèle conditionnel Pw1/Peg3 avec la lignée Pax7-Cre-ER. Ces souris ont un phénotype présentant un défaut de régénération prononcé, montrant ainsi un rôle clair et direct de Pw1/Peg3 dans la fonction régénératrice des cellules satellites. En résumé, l’ensemble de ces données montre un rôle de Pw1/Peg3 dans le développement fœtal et la détermination du nombre de fibres musculaires par son action dans l’auto-renouvellement des cellules satellites du tissu musculairePw1/Peg3 is a parentally imprinted gene expressed from the paternal allele. It is expressed in all adult progenitor/stem cell populations examined to date including muscle satellite cells. We examined the impact of loss-of-function of Pw1/Peg3 in skeletal muscle, a tissue that greatly contributes to body mass. We found that constitutive loss of Pw1/Peg3 results in reduced muscle mass resulting from a decrease in muscle fiber number. The reduced fiber number is present at birth. Mice lacking both the paternal and maternal alleles display a lower fiber number as compared to mice carrying the paternal deletion, suggesting that the maternal allele is functional during prenatal development. Hybrid analyses (C57BL6J and Cast/Ei) of muscle tissue reveal a bi-allelic expression of Pw1/Peg3 around 10%. Pw1/Peg3 is strongly up-regulated in response to muscle injury. Using the constitutive Pw1/Peg3 knock out mouse, we observed that satellite cells display a reduced self-renewal capacity following muscle injury. Pw1/Peg3 is expressed in satellite cells as well as a subset of muscle interstitial cells (PICs). To determine the specific role of Pw1/Peg3 in satellite cells, we crossed our conditional Pw1/Peg3 allele with the Pax7-CreER line. Interestingly, these mice displayed a more pronounced phenotype of impaired regeneration revealing a clear and direct role for Pw1/Peg3 in satellite cells. Taken together, our data show that Pw1/Peg3 plays a role during fetal development in the determination of muscle fiber number that is gene-dosage dependent and plays a specific role in muscle satellite cell self-renewal
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Correra, Rosa Maria. "Pw1/Peg3 regulates skeletal muscle growth and satellite cell self-renewal." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066339.
Full textAbstract:
Pw1/Peg3 est un gène d’empreinte parental exprimé par l’allèle paternel. Il est exprimé dans l’ensemble des populations de cellules souches, y compris les cellules satellites du tissu musculaire. Nous avons découvert que la perte constitutive de Pw1/Peg3 entraîne une perte de la masse musculaire, résultat d’une diminution du nombre de fibres musculaires. Le nombre de fibres réduit est présent dès la naissance. De plus, les souris double KO ont un nombre de fibres encore inférieur, suggérant que l’allèle maternel est fonctionnel pendant le développement pré-natal, et des analyses de souris hybrides C57BL6J/CAST/Ei révèlent une expression bi-allélique de Pw1/Peg3 d’environ 10%. Pw1/Peg3 est également fortement exprimé après blessure du muscle squelettique. Chez les souris Pw1/Peg3 KO, nous avons observé que les cellules satellites montrent une réduction de leur capacité d’auto-renouvèlement à la suite d’une blessure. Pw1/Peg3 est également exprimé dans une sous-population de cellules souches interstitielles, les PICS. Afin de déterminer le rôle spécifique de Pw1/Peg3 dans les cellules satellites nous avons croisé notre allèle conditionnel Pw1/Peg3 avec la lignée Pax7-Cre-ER. Ces souris ont un phénotype présentant un défaut de régénération prononcé, montrant ainsi un rôle clair et direct de Pw1/Peg3 dans la fonction régénératrice des cellules satellites. En résumé, l’ensemble de ces données montre un rôle de Pw1/Peg3 dans le développement fœtal et la détermination du nombre de fibres musculaires par son action dans l’auto-renouvellement des cellules satellites du tissu musculairePw1/Peg3 is a parentally imprinted gene expressed from the paternal allele. It is expressed in all adult progenitor/stem cell populations examined to date including muscle satellite cells. We examined the impact of loss-of-function of Pw1/Peg3 in skeletal muscle, a tissue that greatly contributes to body mass. We found that constitutive loss of Pw1/Peg3 results in reduced muscle mass resulting from a decrease in muscle fiber number. The reduced fiber number is present at birth. Mice lacking both the paternal and maternal alleles display a lower fiber number as compared to mice carrying the paternal deletion, suggesting that the maternal allele is functional during prenatal development. Hybrid analyses (C57BL6J and Cast/Ei) of muscle tissue reveal a bi-allelic expression of Pw1/Peg3 around 10%. Pw1/Peg3 is strongly up-regulated in response to muscle injury. Using the constitutive Pw1/Peg3 knock out mouse, we observed that satellite cells display a reduced self-renewal capacity following muscle injury. Pw1/Peg3 is expressed in satellite cells as well as a subset of muscle interstitial cells (PICs). To determine the specific role of Pw1/Peg3 in satellite cells, we crossed our conditional Pw1/Peg3 allele with the Pax7-CreER line. Interestingly, these mice displayed a more pronounced phenotype of impaired regeneration revealing a clear and direct role for Pw1/Peg3 in satellite cells. Taken together, our data show that Pw1/Peg3 plays a role during fetal development in the determination of muscle fiber number that is gene-dosage dependent and plays a specific role in muscle satellite cell self-renewal
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Watson, Rebecca Reiko. "Immunohistochemical fiber typing, ultrastructure, and morphometry of harbor seal skeletal muscle." Diss., Texas A&M University, 2003. http://hdl.handle.net/1969.1/246.
Full textAbstract:
There is strong evidence that the skeletal muscles of pinnipeds are adapted for an aerobic, lipid-based metabolism under the hypoxic conditions associated with breath-hold diving. However, regional variations in mitochondrial density are unknown, and the few fiber typing studies performed on pinniped skeletal muscles are not consistent with an aerobic physiological profile. Thus, the objectives of this study were to (1) reexamine the fiber type distribution throughout the primary locomotory muscles of the harbor seal, and (2) to better understand the density and distribution of mitochondria in the locomotory muscles. Multiple samples from transverse sections of the epaxial muscles and a single sample of the pectoralis muscle of wild harbor seals were analyzed using immunohistochemical fiber typing and electron microscopy. Fiber typing results indicated that harbor seal epaxial muscles are composed of 47.4% type I (slow twitch, oxidative) fibers and 52.8%, IIa (fast twitch, oxidative) fibers. No fast twitch, glycolytic (type IIb) fibers were detected in the epaxial muscles or the pectoralis muscle. Mean volume density of mitochondria [Vv(mt,f)] was 5.6%, which is elevated over what would be predicted for a terrestrial mammal of similar mass. The elevated Vv(mt,f) had a high proportion of intermyofibrillar mitochondria, a trait not normally found in the muscles of terrestrial mammals with elevated Vv(mt,f). These results provide further evidence that the elevated mitochondrial volume density in pinniped muscle decreases the oxygen diffusion distance between myoglobin and mitochondria to facilitate aerobic respiration in working muscles. In addition, analyses of heterogeneity revealed that the regions of the epaxial muscles that were located deep within the muscle showed a significantly higher Vv(mt,f) relative to those regions that were superficially-located. In contrast, there was no significant heterogeneity of fiber type detected in either plane of the epaxial muscles. Thus, there was a fine-scale pattern of spatial heterogeneity of Vv(mt,f) within the epaxial muscles that does not manifest in fiber type distribution, indicating that the fibers have similar oxidative capacities.
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Stuart, Charles A., Melanie P. McCurry, Anna Marino, Mark A. South, Mary E. A. Howell, Andrew S. Layne, Michael W. Ramsey, and Michael H. Stone. "Slow-Twitch Fiber Proportion in Skeletal Muscle Correlates With Insulin Responsiveness." Digital Commons @ East Tennessee State University, 2013. https://dc.etsu.edu/etsu-works/4123.
Full textAbstract:
Context: The metabolic syndrome, characterized by central obesity with dyslipidemia, hypertension, and hyperglycemia, identifies people at high risk for type 2 diabetes.
Objective: Our objective was to determine how the insulin resistance of the metabolic syndrome is related to muscle fiber composition.
Design:Thirty-nine sedentary men and women (including 22 with the metabolic syndrome) had insulin responsiveness quantified using euglycemic clamps and underwent biopsies of the vastus lateralis muscle. Expression of insulin receptors, insulin receptor substrate-1, glucose transporter 4, and ATP synthase were quantified with immunoblots and immunohistochemistry.
Participants and Setting: Participants were nondiabetic,metabolic syndrome volunteers and sedentary control subjects studied at an outpatient clinic.
Main Outcome Measures: Insulin responsiveness during an insulin clamp and the fiber composition of a muscle biopsy specimen were evaluated.
Results: There were fewer type I fibers and more mixed (type IIa) fibers in metabolic syndrome subjects.Insulin responsiveness and maximal oxygen uptake correlated with the proportion of type I fibers.Insulin receptor,insulin receptor substrate-1, and glucose transporter 4 expression were not different in whole muscle but all were significantly less in the type I fibers of metabolic syndrome subjects when adjusted for fiber proportion and fiber size.Fat oxidation and muscle mitochondrial expression were not different in the metabolic syndrome subjects.
Conclusion:Lower proportion of type I fibers in metabolic syndrome muscle correlated with the severity of insulin resistance. Even though whole muscle content was normal, key elements of insulin action were consistently less in type I muscle fibers, suggesting their distribution was important in mediating insulin effects
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Barton-Davis, Elisabeth R. "Characterization of a novel model of muscle plasticity : stimulation-induced fiber transformation in an isolated fast skeletal muscle /." Thesis, Connect to this title online; UW restricted, 1996. http://hdl.handle.net/1773/10543.
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Natanek, Samantha Amanda. "Skeletal muscle in chronic obstructive pulmonary disease : Regulation of quadriceps muscle fibre characteristics." Thesis, Imperial College London, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.535008.
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Moretti, Irene. "Role of the transcription factor MRF4 in adult skeletal muscle." Doctoral thesis, Università degli studi di Padova, 2009. http://hdl.handle.net/11577/3426129.
Full textAbstract:
Myogenesis is a dynamic process in which mononucleated undifferentiated myoblasts first proliferate, then withdraw from the cell cycle and finally differentiate and fuse to form the multinucleated mature muscle fibers. This process is controlled by members of a family of muscle-specific basic helix-loop-helix (bHLH) proteins that, in concert with members of the ubiquitous E2A and myocytes enhancers factor 2 (MEF2) families, activate the differentiation program by inducing transcription of regulatory and structural muscle specific gene. The MRF proteins contains one or two transactivation domain, a conserved basic DNA-binding domain essential for sequence-specific DNA binding, and an HLH motif required for heterodimerization.
MRFs specific knockout studies suggest that MyoD and Myf5 are required for commitment to the myogenic lineage, whereas myogenin plays a critical role in the expression of the terminal muscle phenotype; Mrf4 partly subserves both roles.
In the adult skeletal muscle, the expression of MRFs considerably changes: Myf5 is not expressed in adult fibers, MyoD and myogenin are expressed at low levels and respectively in fast muscle and in slow muscle, Mrf4 is the only muscle regulatory factors expresses at high levels in adult skeletal muscle, but its role is still unknown.
The aim of this work is study the expression and the physiological role of Mrf4 in the adult skeletal muscle.
We demonstrate that Mrf4 is similarly expressed at mRNA and protein levels in the slow soleus muscle and in the fast EDL muscle, but this transcription factor has a predominantly nuclear localization in soleus and a predominantly cytosolic localization in EDL. We also demonstrate that Mrf4 expression is activity dependent using two experimental models: elettrostimulation and denervation (inactivity condition). When EDL muscles were stimulates with a slow pattern, Mrf4 translocates to the nucleus, whereas with a fast pattern Mrf4 remains in the cytoplasm. Moreover, after denervation Mrf4 accumulates in to the nucleus. This observation suggests that MRF4 may undergo nucleo-cytoplasmic shuttling, as in the case of other transcription factors, but not describes for the MRFs.
To get further insight about the function of Mrf4 in adult muscle we examined the effect of Mrf4 overexpression and knockdown using an in vivo transfection approach in adult rat skeletal muscles. We evaluated if Mrf4 is involved in the regulation of two features of muscle phenotype: the muscle growth and the fiber type specification.
Muscle growth: we demonstrate that Mrf4 silencing in adult and regenerating muscles induces hypertrophy. On the other hand, the overexpression of Mrf4 cDNA in regenerating muscles, but not in the adult muscles, causes a decrease of cross sectional area of transfected fibers. Moreover the MRF4 knockdown prevents denervation atrophy. This data suggest that Mrf4 acts as a negative regulator of muscle fiber growth.
Fiber type specification: we used two luciferase reporter under control of the MyHC slow (MyHC slow-Luc) and the MyHC 2B (MyHC 2B-Luc) promoter. We demonstrate that Mrf4 knockdown in adult skeletal muscle inhibits the activity of MyHC slow-Luc and induces the activity of MyHC 2B-Luc; on the other hand, this reporter is activated by Mrf4 overexpression. We have also study the effect of Mrf4 silencing on endogenous gene: we demonstrate that Mrf4 knockdown blocks the expression of endogenous MyHC slow. This data suggest that Mrf4 is involved in the induction and in the maintenance of slow gene program.Lo sviluppo del muscolo scheletrico è controllato da una famiglia di fattori trascrizionali, chiamati Muscle Regulatory Factors (MRFs), i cui membri sono MyoD, Myf5, Mrf4 e miogenina. Questi fattori trascrizionali sono in grado di dare inizio al programma miogenico, convertendo cellule non muscolari in derivati miogenici. Gli MRFs appartengono alla famiglia di proteine bHLH (basic helix-loop-helix) e presentano motivi strutturali caratteristici: uno o due domini di transattivazione, un dominio basico di legame al DNA molto conservato e la regione HLH, necessaria per l’eterodimerizzazione. È stato osservato in vitro ed in vivo che i fattori MRF sono in grado di eterodimerizzare con un’altra famiglia di proteine bHLH, le proteine E, e di legarsi al DNA su una sequenza consenso specifica, detta E box (CANNTG). Questo legame permette l’attivazione trascrizionale di specifici geni muscolari, come ?-actina, MCK (Muscle Creatin Kinase) e troponina I. L’analisi di diversi knockout degli MRFs ha permesso di definire ruoli diversi nello sviluppo muscolare per i vari membri della famiglia. In particolare, Myf5 e MyoD sono induttori del programma miogenico, mentre miogenina ha un’azione fondamentale nelle fasi successive del differenziamento dei mioblasti. Mrf4 è l’unico fattore ad essere coinvolto sia nella fase iniziale di induzione, che in stadi avanzati del differenziamento miogenico. Nel muscolo scheletrico adulto l’espressione degli MRFs viene mantenuta, ad eccezione di Myf5. In particolare, MyoD e miogenina sono espressi a livelli bassi, e sono più abbondanti rispettivamente nelle fibre di tipo rapido e di tipo lento. Mrf4 è l’unico dei quattro fattori trascrizionali a mantenere livelli di espressione molto elevati nel muscolo scheletrico adulto, ma la sua distribuzione in diversi tipi di muscoli (rapidi e lenti) ed il suo ruolo fisiologico non sono stati ancora caratterizzati. Questo progetto ha avuto come obiettivo principale quello di definire il profilo di espressione e il ruolo di Mrf4 nel muscolo scheletrico adulto. Abbiamo pertanto analizzato l’espressione di Mrf4 in un muscolo tipicamente lento, il soleo, ed in un muscolo rapido, l’extensor digitorum longus (EDL). I nostri risultati indicano che la sua espressione è paragonabile nei due tipi di muscoli, sia a livello di mRNA che a livello di proteina. Abbiamo invece messo in luce delle differenze nella localizzazione di Mrf4, che risulta essere prevalentemente nucleare nel soleo, mentre l’EDL presenta solo alcuni nuclei positivi ed una marcatura diffusa nel citoplasma. Per chiarire se l’espressione di Mrf4 fosse controllata dall’attività nervosa, ci siamo serviti di due modelli sperimentali in vivo su ratto: l'eletrostimolazione e la denervazione (condizione di inattività). Mrf4, in seguito a stimolazione di tipo lento, trasloca nei nuclei, mentre rimane nel citosol se stimolato con un pattern di tipo rapido. In seguito a denervazione Mrf4 sia accumula nei nuclei sia nel soleo che nell’EDL. Queste osservazioni suggeriscono che Mrf4 possa andare incontro ad un fenomeno di shuttling nucleo-citoplasmatico, fenomeno comune a vari fattori trascrizionali ma non descritto nel caso degli MRFs. Per comprendere il suo ruolo fisiologico nel muscolo scheletrico adulto, abbiamo effettuato esperimenti di iperespressione e di silenziamento genico. Abbiamo valutato se Mrf4 potesse essere coinvolto nella regolazione di due aspetti del fenotipo muscolare: la crescita e la specificazione del tipo di fibre. Regolazione della crescita muscolare: abbiamo dimostrato che il silenziamento genico di Mrf4 in muscoli adulti e rigeneranti induce ipertrofia delle fibre trasfettate; per contro l’iperespressione di Mrf4 in muscoli rigeneranti, ma non adulti, causa una diminuzione dell’area delle fibre trasfettate. Abbiamo inoltre dimostrato che Mrf4 previene l’atrofia indotta da denervazione. Questi dati suggeriscono che Mrf4 agisce come regolatore negativo della crescita. Specificazione del tipo di fibra: abbiamo utilizzato due reporter luciferasi sotto il controllo dei promotori della catena pesante della miosina lenta (MyHC slow-Luc) e della miosina rapida 2B (MyHC 2B-Luc). Abbiamo dimostrato che il silenziamento genico di Mrf4 in muscolo scheletrico adulto inibisce l’attività del reporter MyHC slow-Luc mentre induce quella del reporter MyHC 2B-Luc. Al contrario l’iperespressione di Mrf4 con il promotore della miosina rapida induce diminuzione dell’attività, mentre non modifica l’attività della miosina lenta. Abbiamo inoltre analizzato l’effetto del silenziamento di Mrf4 su geni endogeni in muscolo rigenerante e abbiamo dimostrato che il silenziamento genico di Mrf4 blocca l’espressione della miosina lenta indotta dal nervo. Questi esperimenti dimostrano quindi che Mrf4 attiva il programma genico lento e inibisce quello rapido, contribuendo ai meccanismi di induzione e di mantenimento dei programmi genici coinvolti nella specificazione del tipo di fibra.
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Grönlund, Christer. "Spatio-temporal processing of surface electromyographic signals : information on neuromuscular function and control /." Umeå : Umeå universitet, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-958.
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Cong, Xiaofei. "Role of SH3 and Cysteine-Rich Domain 3 (STAC3) in Skeletal Muscle Development, Postnatal Growth and Contraction." Diss., Virginia Tech, 2016. http://hdl.handle.net/10919/78432.
Full textAbstract:
The SH3 and cysteine rich domain 3 (Stac3) gene is expressed specifically in skeletal muscle and essential for skeletal muscle contraction and postnatal life in mice. In this dissertation project, I conducted two studies to further understand the role of STAC3 in skeletal muscle development, growth, and contraction. In the first study, I compared the contractile responses of hindlimb muscles of Stac3 knockout and control mice to electrical stimulation, high [K+]-induced membrane depolarization, and caffeine and 4-chloro-m-cresol (4-CMC) activation of ryanodine receptor (RyR). Frequent electrostimulation-, high [K+]-, 4-CMC- and caffeine-induced maximal tensions in Stac3-deleted muscles were approximately 20%, 29%, 58% and 55% of those in control muscles, respectively. 4-CMC- and caffeine-induced increases in intracellular calcium were not different between Stac3-deleted and control myotubes. Myosin-ATPase and NADH-tetrazolium reductase staining as well as gene expression analyses revealed that Stac3-deleted hindlimb muscles contained more slow type-like fibers than control muscles. These data together confirm a role of STAC3 in EC coupling but also suggest that defective EC coupling is only partially responsible for the significantly reduced contractility in Stac3-deleted hindlimb muscles. In the second study, I determined the potential role of STAC3 in postnatal skeletal muscle growth, fiber composition, and contraction by disrupting Stac3 gene expression in postnatal mice through the Flp-FRT and tamoxifen-inducible Cre-loxP systems. Postnatal Stac3 deletion inhibited body and limb muscle mass gains. Histological staining and gene expression analyses revealed that postnatal Stac3 deletion decreased the size of myofibers and increased the percentage of myofibers containing centralized nuclei without affecting the total myofiber number. Postnatal Stac3 deletion decreased limb muscle strength. Postnatal Stac3 deletion reduced electrostimulation- but not caffeine-induced maximal force output in limb muscles. Similarly, postnatal Stac3 deletion reduced electrostimulation- but not caffeine-induced calcium release from the sarcoplasmic reticulum. These results demonstrate that STAC3 is important to myofiber hypertrophy, myofiber type composition, contraction, and EC coupling in postnatal skeletal muscle.Ph. D.
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PARSONS, STEPHANIE A. "THE ROLE OF CALCINEURIN IN SKELETAL MUSCLE HYPERTROPHY AND FIBER TYPE DIVERSITY." University of Cincinnati / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1078511890.
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Higginson, James Matthew. "Signal transduction pathways involved in skeletal muscle fibre type regulation." Thesis, University of Central Lancashire, 2003. http://clok.uclan.ac.uk/21870/.
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Mature skeletal muscle fibres can be classified as type I, type IIa, type IIx or type IIb fibres according to the myosin heavy chain (MHC) isoform that they express. More broadly, type I fibres are classified as slow fibres and type IIa, IIx and IIb fibres as fast fibres. However, the phenotype of an adult skeletal muscle fibre is not fixed: it displays plasticity being capable of adapting to changing activity and loading levels by either transition towards a slower phenotype or transition towards a faster phenotype. Overall, the aims of these studies were to further investigate and define the signal transduction pathways implicated in the control of skeletal muscle fibre phenotype. The ability of a fast muscle to undergo a transition towards a slower phenotype in response to chronic low-frequency stimulation (CLFS) was assessed, via metabolic enzyme activity assays and NADH-TR staining, following blockade of the calcineurin signalling pathway. Metabolic enzyme assays and northern blots were employed to assess the changes in enzyme activities and MEC isoform expression levels following blockade of the calcineurin and ERK1/2 signalling pathways in primary cultures of rat myotubes. Differences in the levels of various signal transduction proteins/transcription factors between slow and fast muscle were investigated using western blotting. The nuclear translocation kinetics of NFAT and NF-κB in response to treatment with the calcium ionophore A23187 were investigated in L6 myotubes using immunocytochernistry. Calcineurin blockade using cyclosporin A failed to prevent a decrease in lactate dehydrogenase activity and an increase in NADH-TR staining intensity, both characteristics of a transition towards a slower phenotype, following CLFS of the fast rat tibialis anterior muscle. Blockade of the ERK1/2 pathway in primary cultures of rat myotubes using U0126 significantly decreased MHC Iβ mRNA levels and significantly increased MIHC IIx, MEC IIb and perinatal MHC mRNA levels. Calcineurin blockade significantly decreased MHC Iβ and embryonal mRNA levels and significantly increased MHC IIx mRNA levels. Calcineurin blockade also significantly increased the activities of lactate dehydrogenase and creatine kinase while ERK1/2 blockade significantly increased the activities of lactate dehydrogenase, creatine kinase, hexokinase, malate dehydrogenase and β-hydroxyacyl-CoA deydrogenase. ERK1/2 and NF-κB levels were found to be higher in slow muscle compared to fast muscle while calcineurin and p38α,β levels were higher in fast muscle compared to slow muscle. No nuclear translocation of NF-κB and only limited evidence for NFAT nuclear translocation was seen in L6 myotubes following treatment with A23187. Overall these studies further characterize the roles of the ERK1/2 and calcineurin pathways in the regulation of muscle phenotype suggesting that each pathway controls some, but not all, of the genes that are differentially expressed between slow and fast muscle fibres. Western blotting suggests further signal transduction protein/transcription factor targets, the functions of which may be explored in the future.
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de, Freitas Fatima Pestana. "The Importance of Fast Skeletal Regulatory Light Chain in Muscle Contraction." Scholarly Repository, 2008. http://scholarlyrepository.miami.edu/oa_theses/97.
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The aim of this project was to produce and study a murine homozygous knock-in model containing a fast skeletal regulatory light chain (RLC) containing a Asp49toAla point mutation. The D49A mutation is in the functional calcium binding loop of RLC, which is believed to modulate muscle contraction in striated muscle. To introduce the mutation, a reversible knock-out/knock-in system was employed. The Cre/Lox-P strategy was used to conditionally knock-in the RLC D49A mutation. The generation of the knock-in mouse was attempted with two different breeding strategies consisting of two Cre mouse lines with differential expression patterns during development. The proposed animal was never produced because the RLC knock-out recombination event introduced a splicing error resulting in a stop codon in intron 2. Extensive DNA, RNA and protein analysis as well as histological, gross morphology and muscle physiology studies obtained from the animals of the two breeding strategies lead to the identification of the splicing error. Evidence for this outcome is presented. A recommendation for a different strategy in future studies is included.
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Seymour, Kacie Tinnesz. "Examining the Influence of Muscle Fiber Type on Protein Turnover Signaling in Growing Pigs." Thesis, Virginia Tech, 2020. http://hdl.handle.net/10919/98592.
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Postnatal skeletal muscle growth occurs through myonuclear accretion and high protein turnover rate. While fiber type composition of the muscle could affect protein turnover rate, less is known about how fiber type influences the regulation of protein synthesis and degradation signaling pathways. Thus, the hypothesis of this work was that variation in fiber type composition will differentially affect the regulation of signaling pathways related to protein turnover in skeletal muscle hypertrophy in growing pigs. Downregulated protein synthesis signaling and reduced expression of type II MyHC isoforms have been reported in skeletal muscles of low birth weight (LBWT) neonatal pigs. Therefore, we sought to determine whether these changes are sustained until weaning and would explain the reduction in LBWT pig growth compared to their normal birth weight (NBWT) sibling at weaning. Another objective was to determine whether the regulation of protein turnover signaling pathways are correlated to fiber type differences in skeletal muscles. Our data suggest that the longissimus dorsi (LD, glycolytic) muscle of LBWT pigs experienced compensatory growth while the soleus (oxidative) remained proportionally smaller. Growth of the LD was accompanied by upregulation of translation initiation. Additionally, there was no difference in expression of MyHC isoforms between NBWT and LBWT pigs. These data suggest the rapid growth of the LD of LBWT pigs may be attributed to an upregulation of protein synthesis signaling and occurred only in glycolytic muscles. A caveat in LBWT pig model is that the reduction in type II MyHC at birth is not the only factor that could influence muscle growth, and that other factors may have confounded our results. This is why we aimed to use β-adrenergic agonist as a means to induce a shift fiber type in muscles to a more glycolytic phenotype. Our objective was to determine the influence of the β-adrenergic agonist Ractopamine (RAC) induced slow-to-fast fiber type transformation on the regulation of protein synthesis and degradation pathways. Although supplementation improved translational capacity, enhanced S6K1 phosphorylation, and reduced the abundance of calcium-dependent proteases, RAC feeding had no effect on body or muscle weights. These results suggest that a fiber type transformation without other physiological influences does not alter protein turnover signaling in favor of hypertrophy in growing pigs.Master of Science
Skeletal muscles grow by increasing the amount of protein contained within them. The amount of protein deposited is determined by the net balance between the rates at which proteins are synthesized and degraded. However, not all skeletal muscles grow at the same rate. One factor that is thought to influence protein synthesis and degradation rates is the types of muscle fibers that are present within a muscle. These fibers can display a range of contractile and metabolic characteristics, from slow-twitch oxidative fibers to fast-twitch glycolytic fibers. In the presented studies, we sought to determine whether changes in fiber type composition result in difference to the signaling pathways the regulate protein synthesis and degradation, ultimately leading to differences in the muscle growth of young pigs. We have previously shown reduced activation of the protein synthesis pathway in the skeletal muscle of low birth weight (LBWT) newborn pigs. These pigs also had lower expression of glycolytic fibers. In experiment 1, we aimed to compare the signaling pathways regulating protein synthesis and degradation in LBWT and normal birth weight (NBWT) pigs at weaning. We also sought to determine if the regulation of these signaling pathways changed between muscles with differing fiber type compositions. The glycolytic longissimus dorsi (LD) muscle of LBWT pigs grew rapidly between birth and weaning whereas the highly oxidative soleus did not. In addition, the LD of LBWT pigs had greater protein synthesis signaling and similar expression of muscle fibers compared with NBWT pigs, suggesting the improvement in protein synthesis signaling of LBWT pigs between birth and weaning may be related to a shift in fiber type. In experiment 2, we used a compound called ractopamine hydrochloride (RAC) to promote a slow-to-fast fiber type switch in the muscle of young pigs. With this study, we sought to determine the effect of this fiber type transformation, without the influence of birth weight, on the regulation of protein synthesis and degradation pathways. Although RAC-fed pigs showed some minor changes that could improve protein synthesis and decrease protein degradation, RAC feeding had no observable effect on body weight or muscle growth. These results suggest that a fiber type transformation alone is not enough to promote muscle growth in growing pigs.
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Bozkurt, Ozlem. "The Effect Of Diabetes On Rat Skeletal Muscle Tissues At Molecular Level." Master's thesis, METU, 2006. http://etd.lib.metu.edu.tr/upload/12607735/index.pdf.
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In the present study Fourier Transform Infrared Spectroscopy was used to examine the effects of streptozotocin-induced diabetes mellitus on the structural components of slow- and fast-twitch rat skeletal muscles, at molecular level.
Diabetes mellitus is a chronic disorder of carbohydrate, fat and protein metabolism, which is characterized by hyperglycemia caused by a defective or deficient insulin secretory response. The effect of diabetes is seen on a variety of tissues leading to important secondary complications
such as kidney failure, liver dysfunction, cardiac disorders, etc. Skeletal muscle is one of the major tissues determining carbohydrate and lipid metabolism in the bodytherefore, is one of the target tissues of diabetes. The two main types of muscle fibers are type I (slow-twitch) and type II (fast-twitch) fibers
having different structural organization and metabolic features. The FTIR spectra revealed a considerable decrease in lipid and protein content of diabetic skeletal muscles, indicating an increased lipolysis and protein breakdown or decreased protein synthesis. Moreover changes in protein structure and conformation were observed. In diabetes, muscle membrane lipids were more ordered and the amount of unsaturated lipids was decreased possibly due to lipid peroxidation. Diabetes caused a decrease in the content of nucleic acids, especially RNA, and hydrogen bonded phospholipids in the membrane structures of skeletal muscles. In all of the spectral parameters investigated slow-twitch muscle was more severely affected from diabetes. Thus, FTIR spectroscopy appears to be a useful method to evaluate the effect of diabetes on skeletal muscle tissues at molecular level.
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Carroll, Kevin M., Caleb D. Bazyler, Jake R. Bernards, Christopher B. Taber, Charles A. Stuart, Brad H. DeWeese, Kimitake Sato, and Michael H. Stone. "Skeletal Muscle Fiber Adaptations Following Resistance Training Using Repetition Maximums or Relative Intensity." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etsu-works/5786.
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The purpose of the study was to compare the physiological responses of skeletal muscle to a resistance training (RT) program using repetition maximum (RM) or relative intensity (RISR). Fifteen well-trained males underwent RT 3 d·wk−1 for 10 weeks in either an RM group (n = 8) or RISR group (n = 7). The RM group achieved a relative maximum each day, while the RISR group trained based on percentages. The RM group exercised until muscular failure on each exercise, while the RISR group did not reach muscular failure throughout the intervention. Percutaneous needle biopsies of the vastus lateralis were obtained pre-post the training intervention, along with ultrasonography measures. Dependent variables were: Fiber type-specific cross-sectional area (CSA); anatomical CSA (ACSA); muscle thickness (MT); mammalian target of rapamycin (mTOR); adenosine monophosphate protein kinase (AMPK); and myosin heavy chains (MHC) specific for type I (MHC1), type IIA (MHC2A), and type IIX (MHC2X). Mixed-design analysis of variance and effect size using Hedge’s g were used to assess within- and between-group alterations. RISR statistically increased type I CSA (p = 0.018, g = 0.56), type II CSA (p = 0.012, g = 0.81), ACSA (p = 0.002, g = 0.53), and MT (p < 0.001, g = 1.47). RISR also yielded a significant mTOR reduction (p = 0.031, g = −1.40). Conversely, RM statistically increased only MT (p = 0.003, g = 0.80). Between-group effect sizes supported RISR for type I CSA (g = 0.48), type II CSA (g = 0.50), ACSA (g = 1.03), MT (g = 0.72), MHC2X (g = 0.31), MHC2A (g = 0.87), and MHC1 (g = 0.59); with all other effects being of trivial magnitude (g < 0.20). Our results demonstrated greater adaptations in fiber size, whole-muscle size, and several key contractile proteins when using RISR compared to RM loading paradigms.
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Parsons, Stephanie A. "The role of the calcineurin in skeletal muscle hypertrophy and fiber type diversity." Cincinnati, Ohio : University of Cincinnati, 2003. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=ucin1078511890.
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Russell, Paul. "Membrane properties and calcium ion activity in skeletal muscle fibres of the dystrophic mouse." Thesis, University of Central Lancashire, 1993. http://clok.uclan.ac.uk/20630/.
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The ReJI29 murine model of muscular dystrophy was employed to investigate the properties of skeletal muscle plasmalemma and calcium ion movements during muscle wastage, with the intention of determining the route of calcium influx, and the efficacy of calcium ion blockers in preventing this influx. Electrophysiological parameters (Resting membrane potential [RMP] and input resistance) reached adult magnitude in normal soleus and extensor digitorum longus (EDL) by 4 weeks and 3 weeks respectively. Electrophysiological parameters in dystrophic soleus developed in a similar maimer to normal muscle, but RMP in dystrophic EDL was reduced and input resistance was elevated suggesting the presence of a population of regenerating fibres. Twitch and contracture tension development reached mature levels by 4 weeks in normal soleus muscle, but development was prolonged to 10 weeks in EDL, due to the slower development of type II fibres. Contracture tension was markedly smaller in EDL possibly due to fibre type-related differences in the concentrations of calcium sequestering proteins. Twitch and contracture tension in dystrophic soleus was identical to normal. In dystrophic EDL, 4 week old muscle did not generate tension from either electrical or chemical stimulation. Older muscles generated tension but smaller than their normal counterparts. Twitch and contracture tomography revealed similarities between dystrophic EDL and immature normal EDL corroborating with the conclusions made from the electrophysiological experiments. Caffeine contractures generated in glycinerated normal soleus muscle, incubated in low calcium saline, and then bathed in high calcium saline reached 115-185% the magnitude of caffeine contractures generated prior to incubation. 4 week dystrophic soleus attained similar sized contractures, but contractures were reduced to 77-90% in older muscles. This technique was found to be inappropriate in the study of EDL. Caffeine contractures generated by normal soleus in normal saline, after incubation in low calcium saline, reached the magnitude of contractures generated in high calcium saline after 30 minutes. Contractures generated by dystrophic soleus remained identical to those generated in high calcium saline suggesting that the sarcoplasmic reticulum in these fibres was unable to cope with a high calcium load. This result gave the first indication that soleus muscle was affected by muscular dystrophy. Membrane bound calcium derived from 45Calcium influx studies was 2nmoles/mg tissue/30 minutes in soleus and 1 Snmoles/mg tissue weight/30 minutes in EDL. Intracellular influx was 0.5-0.6nmoles/mg tissue weight/ 30 minutes in both muscles. Membrane bound calcium was elevated in dystrophic EDL to 2.5-3.8nmoles/mg tissue weight/30 minutes, but influx was normal in both dystrophic soleus and EDL, casting doubt on whether the plasmalemma is more permeable to calcium. The increase in membrane bound calcium may be artefactual. Cadmium blocked influx in both normal and dystrophic muscles. Blot weights showed continual growth in normal muscles although the rate decreased after 10 weeks. In dystrophic muscles growth ceased after 10 weeks. NCP data was limited but did show a decrease in dystrophic muscle, followed by an increase. Tension as a function of tissue mass, revealed that the contractile apparatus in normal soleus matured within 2 weeks, and by 10 weeks in EDL due to the differences in myosin isoforms present in each fibre type. These ratios were elevated in dystrophic muscle indicating calcium accumulation in the sarcoplasmic reticulum. The results showed that EDL muscle was more severely affected by muscular dystrophy. Between 2 and 4 weeks, the muscle underwent degeneration via an unidentified process. There was regeneration, and the regenerating fibres appeared to be normal. Soleus muscle appeared resistant to the disease but succumbed under unusual chemical stresses. Some aspects of development of normal muscle were also considered.
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Jones, Simon W. "Fibre-type specific expression of the calpain proteolytic system in skeletal muscle." Thesis, University of Nottingham, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312237.
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Dickinson, Jared M. "A method to study in vivo protein synthesis in slow and fast twitch muscle fibers and initial measurements in humans." Muncie, Ind. : Ball State University, 2009. http://cardinalscholar.bsu.edu/773.
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Hopwood, Henry J. "The association between skeletal muscle fibre typology external load during elite Australian Football match-play." Thesis, Griffith University, 2021. http://hdl.handle.net/10072/407553.
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Introduction: Skeletal muscle fibre typology (MFT) directly influences a muscle's contraction speed and fatigue profile both during and following exercise. MFT of a given muscle can vary dramatically between individuals and is largely determined hereditarily. Furthermore, MFT is associated with an athlete's suitability to a sport/event and is suggested as a determining factor for separating elite athletes, from their sub-elite counterparts in sprint and endurance sporting disciplines. Despite these important characteristics, there is limited research on the MFT of team-sport athletes and the impact this may have on performance. The invasive nature of the muscle biopsy, the gold standard of MFT determination, has shielded research investigating the MFT of professional team-sport athletes. Recently validated, non-invasive measures to estimate MFT, through the use of magnetic resonance imaging (MRI) and proton magnetic resonance spectroscopy (1H-MRS), may renew the interest of MFT in team-sport athletes. Australian football (AF) is a team sport that requires athletes to cover large distances at varying speeds and intensities. External load is a quantification of the work performed by an athlete (i.e. distance travelled, distance travelled at high speeds, etc.). It is important to quantify external loads achieved during match-play as this will provide relevant data on the specific movement profiles of competition and may assist in the development of AFL-specific conditioning programs, testing protocols as well as team recruitment and selection. Numerous contextual factors have an influence on the external loads a professional AF athlete achieves during match-paly; position, physical characteristics, and conceivably, their MFT. Preliminary findings in elite soccer athletes have suggested that athletes with a higher proportion of type II fibres will achieve reduced distance sprinting (> 6.67 m×s-1), have a reduced peak 1-min sprint period, and display a larger decrement in high-speed running (HSR) (> 4.17 m×s-1) from the first to the second half of match-play. Despite these findings stemming from an elite team-sport cohort, more research is required on a larger cohort, across an entire season, and in the sport of AF, due to the difference in the external loads of match-play. Further investigation may determine whether such findings are true across different team sports, such that a particular MFT may achieve higher external loads during match-play of some variable and therefore may be predictive of success in a sport, be better suited to a position, or require a higher degree of fatigue management during match-play. As such, further investigation is required to determine if similar findings can be made in AF, which can provide novel and impactful information to practitioners and researchers alike.
Aim: The primary aim of this research study was to investigate the association between MFT and different variables pertaining to the external loads achieved during professional AF match-play. Secondary aims include; quantifying the MFT of professional AF athletes and quantify the external-loads of match-play during professional AF.
Methods: Twenty-four professional AF athletes were characterised by position (smalls, talls, and hybrids), differences in anthropometrics (height, body mass, and body composition), and physical (muscular strength, power, and endurance) and physiological characteristics (MFT) were determined. 1H-MRS was used to quantify intramuscular carnosine content in the soleus and gastrocnemius muscles and expressed as a Z-score relative to an age and gender-matched non-athlete population to estimate MFT. A more negative Z-score is predictive of a higher proportion of type I fibres, while a more positive Z-score is predictive of a higher proportion of type II fibres. External load during matchplay was collected using portable global navigational satellite system (GNSS) units (n = 224 matches). Data were extracted following each session from proprietary software, onto a customised statistical software. External load was expressed as a peak period of matchplay, determined using the maximal mean method. Power law was used to calculate the decrement in intensity with time, expressed as intercept (peak value) and slope (decrement over time). R software was used to perform ANOVA and linear mixed model analyses to determine; i) differences in MFT between playing position groups ii) differences in external loads in match-play between positions, and iii) the association between match-play external load and MFT. Microsoft excel was used to collate data and calculate group means, as well as calculate 95 % confidence intervals from linear mixed models results.
Results: MFT of the gastrocnemius and soleus was significantly associated with HSR (>4.17 m×s-1) distance (soleus; p = 0.013, gastrocnemius; p < 0.001), and HSR slope (soleus; p = 0.021, gastrocnemius; p < 0.001). The cohort presented with a large range of Z-scores across both gastrocnemius (min -1.83, max 0.81) and soleus (min -2.06, max 1.88), with a greater affinity for negative Z-scores (gastrocnemius; 17/24, 70.1 %, soleus; 19/24, 79.2 %). Talls spent a greater duration on the ground than both smalls and hybrids (p = 0.027), while hybrids averaged 16 m×min-1 greater speed than talls (p = 0.001) as well as ~800 m more distance covered in HSR (p < 0.001). Hybrids had the largest intercept for speed, HSR, and acceleration, however only significantly greater than talls for speed intercept (p = 0.006).
Conclusion: MFT appears to influence a professional AF athlete's HSR distance achieved within a match, as well as their HSR slope across peak periods of play. A high proportion of negative Z-scores were found within the cohort. These findings are similar to previous research investigating the influence of MFT on variables describing high intensity running in elite soccer athletes. These cross-sport similarities strengthen the rationale to continue investigations on the effect of MFT on team sport athletes. The high proportion of negative Z-scores reflects the high endurance capacity and load tolerance that the sport of AF demands, conceivably suggesting that athletes with high proportions of type II fibres may not fit the ideal phenotype for the sport. As has been established previously, external loads of match-play exhibited positional differences, with hybrids typically achieving the greatest loads. This information highlights the need for practitioners to individualise training prescription on a positional basis for both load and intensity. Future research should investigate the association between MFT and team sport athlete's ability to recover from exercise, which seems to be the likely cause of the difference observed in MFT for HSR. This information will empower practitioners to better manage athletes' recovery within a match and throughout a pre-season period.Thesis (Masters)
Master of Medical Research (MMedRes)
School of Pharmacy & Med Sci
Griffith Health
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