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Dissertations / Theses on the topic 'Skeletal Muscle contraction'
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Yeung, Wai Ella, and 楊慧. "Eccentric contraction-induced injury in mammalian skeletal muscle." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29750313.
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Baker, Brent A. "Characterization of skeletal muscle performance and morphology following acute and chronic mechanical loading paradigms." Morgantown, W. Va. : [West Virginia University Libraries], 2007. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=5325.
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Thesis (Ph. D.)--West Virginia University, 2007.Title from document title page. Document formatted into pages; contains xii, 270 p. : ill. (some col.). Includes abstract. Includes bibliographical references.
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Griffiths, R. H. ugh. "Modelling the Regulation of Skeletal Muscle Contraction." Thesis, University of Kent, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499839.
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Spencer, C. I. "Chemomechanical coupling in skeletal muscle." Thesis, Open University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383710.
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Ford, Jonathan M. "Skeletal Muscle Contraction Simulation: A Comparison in Modeling." Scholar Commons, 2013. http://scholarcommons.usf.edu/etd/4814.
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Computer generated three-dimensional (3-D) models are being used at increasing rates in the fields of entertainment, education, research, and engineering. One of the aspects of interest includes the behavior and function of the musculoskeletal system. One such tool used by engineers is the finite element method (FEM) to simulate the physics behind muscle mechanics. There are several ways to represent 3-D muscle geometry, namely a bulk, a central line of action and a spline model. The purpose of this study is to exmine how these three representations affect the overall outcome of muscle movement. This is examined in a series of phases with Phase I using primitive geometry as a simplistic representation of muscle. Phases II and III add anatomical representations of the shoulder joint with increasing complexity. Two methods of contraction focused on an applied maximal force (Fmax) and prescribed displacement. Further analyses tested the variability of material properties as well as simulated injury scenarios. The results were compared based on displacement, von Mises stress and solve time. As expected, more complex models took longer to solve. It was also supported that applied force is a preferred method of contraction as it allows for antagonistic and synergistic interaction between muscles. The most important result found in these studies was the consistency in the levels of displacement and stress distribution across the three different 3-D representations of muscle. This stability allows for the interchangeability between the three different representations of muscles and will permit researchers to choose to use either a bulk, central line of action or a spline model. The determination of which 3-D representation to use lies in what physical phenomenon (motion, injury etc.) is being simulated.
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Mazelet, Lise. "The role of contraction in skeletal muscle development." Thesis, Queen Mary, University of London, 2015. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8960.
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The aim of this project was to determine the role of contraction in skeletal muscle development. The role of the initial spontaneous contractions observed in zebrafish embryos from 17 to 24 hours post fertilisation was examined. Genetic and pharmacologic approaches were used to study paralysis-induced disruption of skeletal muscle structure and function and subsequently determine the role of contraction. The structural and functional characteristics of developing skeletal muscles were found to be regulated by a dual mechanism of both movement-dependent and independent processes, in vivo. Novel data demonstrates that contraction controls sarcomere remodelling, namely regulation of actin length, via movement driven localisation of the actin capping protein, Tropmodulin1. Myofibril length was also shown to be linked to the mechanical passive property, stretch, with lengthening leading to an increase of the muscle’s ability to stretch. In addition, myofibril bundling and the myofilament lattice spacing, responsible for active tension generation via cross-bridge formation, were shown to be unaffected by paralysis and thus, movement-independent processes. Furthermore, the mechanism of the contraction-driven myofibril organisation pathway at the focal adhesion complexes (FAC), was shown to be different in zebrafish compared to mammals, with mechanosensing revolving around the Src protein rather than Fak. In summary, the role of contraction was established as a critical driver of myofibril organisation and passive tension in the developing zebrafish skeletal muscle. Passive tension regulates muscle function by determining its operational range ensuring that the needs of locomotion are met. Furthermore, investigation of FAC’s role in the contractiondriven myofibril organisation pathway led to the discovery of a novel function for Src in zebrafish somitogenesis. These two findings (i) that contraction is a driver of myofibril organisation and (ii) that Src is a key protein of the skeletal muscle development provides the potential for new therapeutic approaches in humans.
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Dunaway, Dwayne Lee. "Nano-mechanics of skeletal muscle structures /." Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/8022.
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Heger, Max. "Ultrasound Based Localization and Quantification of Skeletal Muscle Contraction." Thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for teknisk kybernetikk, 2014. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-26099.
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Earlier experiments indicates that motor unit activity during isometric contractions can be imaged using a high-definition ultrasound scanner. In this study, ultrasound raw-data is analysed in MATLAB to localize and quantify the signal contributions from individual motor units during a muscle twitch. It is believed that imaging of mechanical response of contracting muscles can contribute to a more explicit study of muscle physiology and a more dexterous method for prosthetic control.Two different experiments were executed during this study, one for determining the time delay between ECG electrode and ultrasound response and one for imaging muscle activity during an isometric contraction. Both test setups consisted of a GE-Vingmed Vivid E9 ultrasound scanner and an ML6-15 linear probe, where the scans were executed by using "Strain rate"-mode in the test option "Msc TVI" with a frequency of 15MHz, which resulted in frame rates between 120 and 220, depending on the depth of the scan. To determine the time delay, an ECG electrode was connected to the probe and then submerged in a bucket filled with water and the last two ECG electrodes, where the time delay between the two responses were measured in MATLAB. To image muscle activity in a sequence of ultrasound strain rate images, the probe were placed in a clamped and fixed position over the biceps, giving images perpendicular to muscle fibers. Scans of isometric muscle contractions were recorded, with ECG electrodes placed on each side of the probe to detect associated motor unit action potentials.The measurements of the time delay between EMG and ultrasound response shows that there are an expected time delay between 6.68ms and 15.38ms, depending on the propagation velocity of the motor unit action potentials. This indicates that motor unit activity can be captured in ultrasound strain rate image sequences. Motor unit behaviour in strain rate image sequences can be used for locating individual motor units, but this method struggles to identify overlapping motor units as individual. It was found that PCA for feature extraction in combination with a cluster based classification algorithm would be a more robust and time-saving method for localization of individual motor units.
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Sandström, Marie. "Regulation of carbohydrate metabolism in skeletal muscle during and after contraction /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-969-6/.
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Aydin, Jan. "Skeletal muscle calcium homeostasis during fatigue : modulation by kinases and mitochondria /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-247-7/.
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Archer, Akibi A. A. "Two dimensional spatial coherence of skeletal muscle's natural vibrations during voluntary contractions." Thesis, Georgia Institute of Technology, 2010. http://hdl.handle.net/1853/42803.
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Low frequency mechanical vibrations (<100 Hz) are naturally generated by skeletal muscles during voluntary contractions. Recording of these vibrations at the muscle surface are called surface mechanomyograms (S-MMGs). In this study, S-MMGs were recorded over a 3 x 5 grid of skin mounted accelerometers on the biceps brachii muscle during submaximal voluntary isometric contractions with the arm in a pronated position for ten healthy and young male subjects with no overt sign of neuromuscular diseases. For a given pair of accelerometers, the spatial coherence of S-MMG is a measure of the similarity of the S-MMG signals propagating between those two sensors. Two common techniques to estimate the spatial coherence for narrowband S-MMG signals, namely the magnitude squared coherence function and the maximum of the time-domain cross-correlation function, were found to yield similar results. In particular, high spatial coherence values were measured for sensor pairs aligned along the proximal to distal ends of the biceps, i.e. the longitudinal direction. On the other hand, the spatial coherence values for sensor pairs oriented perpendicular to the muscle fiber, i.e. along the transverse direction, were found to be significantly lower. This finding indicates that coherent S-MMGs were mainly propagating along the muscle fibers direction (longitudinal) of the biceps brachii within a frequency band varying between 10Hz to 50Hz. Additionally, the spatial coherence of S-MMGs along the longitudinal direction was found to decrease with increasing frequency and increasing sensor separation distance and to increase with contraction level varying between 20% to 60% of the maximum contraction level.
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Crowther, Gregory John. "An analysis of metabolic fluxes in contracting human skeletal muscle /." Thesis, Connect to this title online; UW restricted, 2002. http://hdl.handle.net/1773/10538.
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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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Carriou, Vincent. "Multiscale, multiphysic modeling of the skeletal muscle during isometric contraction." Thesis, Compiègne, 2017. http://www.theses.fr/2017COMP2376/document.
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Les systèmes neuromusculaire et musculosquelettique sont des systèmes de systèmes complexes qui interagissent parfaitement entre eux afin de produire le mouvement. En y regardant de plus près, ce mouvement est la résultante d'une force musculaire créée à partir d'une activation du muscle par le système nerveux central. En parallèle de cette activité mécanique, le muscle produit aussi une activité électrique elle aussi contrôlée par la même activation. Cette activité électrique peut être mesurée à la surface de la peau à l'aide d'électrode, ce signal enregistré par l'électrode se nomme le signal Électromyogramme de surface (sEMG). Comprendre comment ces résultats de l'activation du muscle sont générés est primordial en biomécanique ou pour des applications cliniques. Évaluer et quantifier ces interactions intervenant durant la contraction musculaire est difficile et complexe à étudier dans des conditions expérimentales. Par conséquent, il est nécessaire de développer un moyen pour pouvoir décrire et estimer ces interactions. Dans la littérature de la bioingénierie, plusieurs modèles de génération de signaux sEMG et de force ont été publiés. Ces modèles sont principalement utilisés pour décrire une partie des résultats de la contraction musculaire. Ces modèles souffrent de plusieurs limites telles que le manque de réalisme physiologique, la personnalisation des paramètres, ou la représentativité lorsqu'un muscle complet est considéré. Dans ce travail de thèse, nous nous proposons de développer un modèle biofidèle, personnalisable et rapide décrivant l'activité électrique et mécanique du muscle en contraction isométrique. Pour se faire, nous proposons d'abord un modèle décrivant l'activité électrique du muscle à la surface de la peau. Cette activité électrique sera commandé par une commande volontaire venant du système nerveux périphérique, qui va activer les fibres musculaires qui vont alors dépolariser leur membrane. Cette dépolarisation sera alors filtrée par le volume conducteur afin d'obtenir l'activité électrique à la surface de la peau. Une fois cette activité obtenue, le système d'enregistrement décrivant une grille d'électrode à haute densité (HD-sEMG) est modélisée à la surface de la peau afin d'obtenir les signaux sEMG à partir d'une intégration surfacique sous le domaine de l'électrode. Dans ce modèle de génération de l'activité électrique, le membre est considéré cylindrique et multi couches avec la considération des tissus musculaire, adipeux et la peau. Par la suite, nous proposons un modèle mécanique du muscle décrit à l'échelle de l'Unité Motrice (UM). L'ensemble des résultats mécaniques de la contraction musculaire (force, raideur et déformation) sont déterminées à partir de la même commande excitatrice du système nerveux périphérique. Ce modèle est basé sur le modèle de coulissement des filaments d'actine-myosine proposé par Huxley que l'on modélise à l'échelle UM en utilisant la théorie des moments utilisée par Zahalak. Ce modèle mécanique est validé avec un profil de force enregistré sur un sujet paraplégique avec un implant de stimulation neurale. Finalement, nous proposons aussi trois applications des modèles proposés afin d'illustrer leurs fiabilités ainsi que leurs utilité. Tout d'abord une analyse de sensibilité globale des paramètres de la grille HDsEMG est présentée. Puis, nous présenterons un travail fait en collaboration avec une autre doctorante une nouvelle étude plus précise sur la modélisation de la relation HDsEMG/force en personnalisant les paramètres afin de mimer au mieux le comportement du Biceps Brachii. Pour conclure, nous proposons un dernier modèle quasi dynamique décrivant l'activité électro-mécanique du muscle en contraction isométrique. Ce modèle déformable va actualiser l'anatomie cylindrique du membre sous une hypothèse isovolumique du muscleThe neuromuscular and musculoskeletal systems are complex System of Systems (SoS) that perfectly interact to provide motion. From this interaction, muscular force is generated from the muscle activation commanded by the Central Nervous System (CNS) that pilots joint motion. In parallel an electrical activity of the muscle is generated driven by the same command of the CNS. This electrical activity can be measured at the skin surface using electrodes, namely the surface electromyogram (sEMG). The knowledge of how these muscle out comes are generated is highly important in biomechanical and clinical applications. Evaluating and quantifying the interactions arising during the muscle activation are hard and complex to investigate in experimental conditions. Therefore, it is necessary to develop a way to describe and estimate it. In the bioengineering literature, several models of the sEMG and the force generation are provided. They are principally used to describe subparts of themuscular outcomes. These models suffer from several important limitations such lacks of physiological realism, personalization, and representability when a complete muscle is considered. In this work, we propose to construct bioreliable, personalized and fast models describing electrical and mechanical activities of the muscle during contraction. For this purpose, we first propose a model describing the electrical activity at the skin surface of the muscle where this electrical activity is determined from a voluntary command of the Peripheral Nervous System (PNS), activating the muscle fibers that generate a depolarization of their membrane that is filtered by the limbvolume. Once this electrical activity is computed, the recording system, i.e. the High Density sEMG (HD-sEMG) grid is define over the skin where the sEMG signal is determined as a numerical integration of the electrical activity under the electrode area. In this model, the limb is considered as a multilayered cylinder where muscle, adipose and skin tissues are described. Therefore, we propose a mechanical model described at the Motor Unit (MU) scale. The mechanical outcomes (muscle force, stiffness and deformation) are determined from the same voluntary command of the PNS, and is based on the Huxley sliding filaments model upscale at the MU scale using the distribution-moment theory proposed by Zahalak. This model is validated with force profile recorded from a subject implanted with an electrical stimulation device. Finally, we proposed three applications of the proposed models to illustrate their reliability and usefulness. A global sensitivity analysis of the statistics computed over the sEMG signals according to variation of the HD-sEMG electrode grid is performed. Then, we proposed in collaboration a new HDsEMG/force relationship, using personalized simulated data of the Biceps Brachii from the electrical model and a Twitch based model to estimate a specific force profile corresponding to a specific sEMG sensor network and muscle configuration. To conclude, a deformableelectro-mechanicalmodelcouplingthetwoproposedmodelsisproposed. This deformable model updates the limb cylinder anatomy considering isovolumic assumption and respecting incompressible property of the muscle
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Glund, Stephan. "Molecular mechanisms governing contraction-induced metabolic responses and skeletal muscle reprogramming /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-436-5/.
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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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Lou, Fang. "A study of the contractile properties of vertebrate skeletal muscle with special reference to the force-velocity relationship and the cellular mechanisms of muscle fatigue /." Lund : Dept. of Pharmacology, University of Lund, 1994. http://books.google.com/books?id=zO9qAAAAMAAJ.
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Ning, Jie. "Estrogen receptor [alpha] and [beta] knock-out effects on skeletal muscle in mature female and male mice, and aromatase knock-out effects on skeletal muscle in mature male mice." Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/6273.
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Thesis (M.S.)--University of Missouri-Columbia, 2007."August 2007" The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. Includes bibliographical references.
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Hoskins, Brooke Kiera. "Skeletal muscle contraction : time-resolved x-ray diffraction and mechanical studies." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298654.
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Luo, Ye. "Regulation of the kinetics of contraction and relaxation in skeletal muscle /." The Ohio State University, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486398528556222.
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Martin, Rex E. (Rex Edward). "Neuroregulation and Myosin Light Chain Phosphorylation in Ascaris Suum Obliquely Striated Skeletal Muscle." Thesis, North Texas State University, 1985. https://digital.library.unt.edu/ark:/67531/metadc504635/.
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Extraction and quantitation of myosin light chain two coupled with myograph recordings from Ascaris muscle perfused with calmodulin inhibitors and neurotransmitters in conjunction with their respective agonists and antagonists have been used to establish the regulation of contraction in this muscle. Densitometric tracings of isolectric focusing gels separating the regulatory light chain were used to quantitate phosphorylation in resting, contracted and flaccid muscle. These studies indicated that inhibitory neurostimulation is mediated by a true GABA receptor. Myosin-mediated contraction is responsible for maintaining the level of tension observed in resting actin-mediated muscle. Actin-mediated contraction is responsible for the rapid rise in tension following excitatory stimuli. Both systems function simultaneously and are independant.
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Stefanova, Helena Ivanova. "Calcium and phosphate transport in sarcoplasmic reticulum." Thesis, University of Southampton, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303376.
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Deshmukh, Atul S. "Nutrient and energy sensing in skeletal muscle." Stockholm : Department of Molecular Medicine and Surgery, Karolinska Institutet, 2009. http://diss.kib.ki.se/2009/978-91-7409-674-3/.
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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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Sivathanu, Vivek. "Disrupting dynamic f-actin enhances skeletal muscle contraction due to mechanical softening." Thesis, Massachusetts Institute of Technology, 2018. http://hdl.handle.net/1721.1/115667.
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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Mechanical Engineering, 2018.Cataloged from PDF version of thesis.
Includes bibliographical references (pages 128-135).
Skeletal muscle wasting disorders such as sarcopenia affect the daily mobility of millions of aging people globally due to decreased muscle mass and decreased muscle efficiency. In this study we discover a novel target to improve the efficiency of skeletal muscle by targeting the dynamic f-actin cytoskeleton. Using two model systems, an ex-vivo mouse muscle model and a novel in vitro optogenetic skeletal muscle micro-tissue model, we show that disruption of the dynamic f-actin cytoskeleton using small molecule actin dynamics inhibitors leads to a persistent 2-fold improvement in muscle active contractility. We explored possible drawbacks of f-actin disruption, including loss of mechanical integrity, cell death, and intracellular organelle damage. None of these downsides actually present themselves with f-actin disruption. Muscle fatigue resistance however does seem to be slightly affected. We performed a detailed characterization of the cytoskeletal modifications that occur during f-actin disruption using dose-response-recovery studies, live f-actin imaging, fluorescence recovery after photobleaching and more targeted f-actin disruption. Using these studies we conclude that treatments which shorten f-actin filaments seem to improve contraction. We also uncovered previously unidentified roles of branched and tropomyosin stabilized f-actin in force transmission. Biomechanical testing at the cell level using AFM and at the tissue level using a micro-tensile test shows a drop in mechanical stiffness that correlates well with a corresponding improvement in muscle force. We ruled out a range of alternate hypotheses involving changes to sarcomeric proteins and energetic activity, that could explain the force improvement, concluding that the force improvement due to f-actin disruption is due to mechanical softening of the cells which pose to a lower resistance to their own contraction. As a potential application, we show that a weak 3D printed muscle powered biological robot starts walking with f-actin disruption. This target has significant therapeutic potential in muscle disorders due to its disease non-specificity. We conclude by discussing possible future experiments that could reveal the best therapeutic applications. Key words: Muscle strength, f-actin, cytoskeleton, Skeletal Muscle Tissue Engineering, Muscle Disorders.
by Vivek Sivathanu.
Ph. D.
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Bertocchini, Federica. "Expression and functional analysis of murine ryanodine receptor type 3." Thesis, Open University, 1998. http://oro.open.ac.uk/57732/.
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Ryanodine receptors (RyRs) are intracellular homotetrameric Ca2+-release channels constituting a family of three different isoforms, named RyRl, RyR2 and RyR3. RyRl and RyR2 are highly expressed in skeletal and cardiac muscles respectively, where they localize in the terminal cisternae of the sarcoplasmic reticulum (SR). Although RyRl and RyR2 have been found to be expressed in several other tissues at much lower level than in striated muscles, their major functional role is related to Ca2+-release from the SR following electrical depolarization of the plasma membrane, a process referred to as excitation-contraction (e-c) coupling and known to regulate striated muscle contraction. The third isoform, RyR3, is characterized by a wide pattern of expression, without any specific association to a tissue or a cell-type. The finding that RyR3 is also expressed in mammalian skeletal muscles parallels the presence of two distinct isoforms, o- and P-RyR, in non-mammalian vertebrate skeletal muscles, and suggests that two functionally distinct RyRs may be involved in the regulation of skeletal muscle contraction. The expression of RyR3 was analyzed in murine skeletal muscle from late foetal stages to adult, throughout neonatal phases of development. RyR3 was expressed widely during skeletal muscle post-natal development, disappearing in all muscles analyzed except diaphragm and soleus. RyR3 knockout mice were generated, and contractile properties of skeletal muscles were analyzed. Skeletal muscle contraction in RyR3-/- mice was impaired during the neonatal phase of development. In skeletal muscles isolated from RyR3-1- mice, the twitch elicited by electrical stimulation was strongly depressed. A significant reduction of the contractile activity was also elicited after stimulation with caffeine, an activator of Ca2+-release through RyRs. In the adults, no differences were detected between wild-type and mutant mice. These results are the first demonstrations of a physiological role of RyR3 in excitation-contraction coupling mechanisms of skeletal muscle, and support the model of a two-channel system regulating skeletal muscle contraction. In order to further characterize the RyR3-1- mouse, [3H]ryanodine binding experiments were performed on diaphragm and total hindlimb skeletal muscles from RyR3+/+ and RyR3-1- mice. Preliminary results will be presented and discussed.
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Reed, Michael John. "Skeletal muscle glucose transporters in lean and obese SHHF/Mcc- cp rats : effects of muscle contraction /." The Ohio State University, 1991. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487688973685112.
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McKnight, David. "Fatigue-induced change in the rates of human skeletal muscle contraction and activation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq22865.pdf.
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Boppart, Marni D. "Regulation of stress-activated protein kinases by exercise and contraction in skeletal muscle." Thesis, Boston University, 2000. https://hdl.handle.net/2144/36769.
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Thesis (Sc.D.)--Boston UniversityPLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
The c-Jun NH2-terminal kinase (JNK) and p38 intracellular signaling cascades are mitogen-activated protein kinase (MAPK) signaling pathways that are activated in mammalian cells by a variety of stressors, including proinflammatory cytokines, osmotic shock, and shear stress. The purpose of this dissertation research was to examine the effect of injury-producing exercise on JNK and p38 activities in human skeletal muscle and to determine whether mechanical stress is a primary stimulator of JNK and p38 activities with contraction. Twelve healthy subjects (7M/5F) completed maximal concentric or eccentric knee extensions on an isokinetic dynamometer (10 sets, 10 reps). Needle biopsies were obtained from the vastus lateralis muscle 24 h before exercise, immediately post-exercise, and 6 h post-exercise. While both forms of exercise increased JNK activity immediately post-exercise, eccentric contractions resulted in a much higher activation (15-fold vs. 4-fold increase above basal for eccentric and concentric, respectively). By 6 h post-exercise, JNK activity decreased back to baseline values. In a separate study, 14 male subjects completed a 42.2 km marathon. Biopsies were obtained from the vastus lateralis muscle 10 days prior to the marathon, immediately following the race, and 1, 3, and 5 days after the race. JNK activity increased 7-fold over basal immediately postexercise, but decreased back to basal 1, 3, and 5 days after the exercise. The activity of p38y also was increased and decreased in a similar pattern. However, no regulation was observed for p38α. In a third study, the effects of contraction and static stretch on JNK activity and p38 phosphorylation were determined in the rat soleus muscle in vitro. Static stretch dramatically increased JNK activity and p38 phosphorylation, whereas isometric contraction resulted in much smaller increases in JNK activity and p38 phosphorylation. The regulation of focal adhesion proteins also was examined following both exercise and contraction. The work presented in this thesis demonstrates that injury-producing exercise results in the marked activation of the JNK and p38 stress-activated protein kinases and provides evidence that mechanical stress may be a major contributor to increases in JNK and p38 activities observed following contraction in rat and human skeletal muscle.
2031-01-01
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Jiang, Yandong. "Effects of modulating calcium transients on the contraction- relaxation cycle of skeletal muscle /." The Ohio State University, 1996. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487935958847887.
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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.
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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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Martin, Brit Leigh Martin. "Toward the use of whole, live developing zebrafish as models for skeletal and cardiac muscle contraction." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1500611447591388.
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Hughes, William Edward. "Dynamics of skeletal muscle blood flow and vasodilation with age." Diss., University of Iowa, 2018. https://ir.uiowa.edu/etd/6142.
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Aging is associated with attenuated blood flow and vasodilator responses during rhythmic exercise. Older adults also demonstrate attenuated blood flow and vasodilator responses following single skeletal muscle contractions (contraction-induced rapid onset vasodilation, ROV) within the forearm. These age-associated attenuations within the forearm have been demonstrated to be a result of endothelial and neural mechanisms. The objective of this research was to examine: 1) whether age-associated attenuations within the forearm are from mechanical factors; 2) whether age-associated attentions in ROV are present within the leg, as well as explore potential mechanisms for these age-associated attenuations in ROV; 3) examine whether aging is associated with a slower rate of adjustment in vasodilation (vasodilator kinetics) during rhythmic exercise preceding steady-state exercise; and 4) examine approaches to ameliorate age-related attenuations in blood flow and vasodilation within the leg across the entire exercise transient (onset to steady-state).
The novel findings of this research are that 1) age-associated attenuations in ROV within the forearm are independent of mechanical factors; 2) older adults demonstrate attenuated ROV responses within the leg; 3) age-related attenuations in ROV within the leg are not explained by enhanced sympathetic adrenergic vasoconstriction; 4) older adults exhibit prolonged vasodilator kinetics preceding steady-state exercise; and 5) when examined in a cross-sectional design chronic exercise training improves ROV, vasodilator kinetics, as well as steady-state blood flow and vasodilator responses in older adults; 6) acute supplementation with dietary nitrate fails to exert any effect on blood flow and vasodilator responses during any domain of exercise. Collectively, this work establishes that aging is associated with reductions in blood flow and vasodilation across the entire exercise transient (onset to steady-state) within the leg, which is offset by chronic exercise training. Mechanistically, the current data suggests that mechanical and sympathetic factors do not explain age-related reductions in ROV in the arm and leg, respectively. Furthermore, acute supplementation of dietary nitrate does not impact leg blood flow and vasodilator responses in older adults during any domain of the exercise transient.
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Jaramillo, Cienfuegos Paola. "Closed Loop Control of Muscle Contraction using Functional Electrical Stimulation." Diss., Virginia Tech, 2016. http://hdl.handle.net/10919/78471.
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A promising approach to treat patients with vocal fold paralysis using electrical stimulation is investigated throughout this research work. Functional Electrical Stimulation works by stimulating the atrophied muscle or group of muscles directly by current when the transmission lines between the central nervous system are disrupted. This technique helps maintain muscle mass and promote blood flow in the absence of a functioning nervous system. The goal of this work is two-fold: develop control techniques for muscle contraction to optimize muscle stimulation and develop a small-scale electromagnetic system to provide stimulation to the laryngeal muscles for patients with vocal fold paralysis. These studies; therefore, focus on assessing a linear Proportional-Integral (PI) controller and two nonlinear controllers: Model Reference Adaptive Controller (MRAC) and an Adaptive Augmented PI (ADP-PI) system to identify the most appropriate controller providing effective stimulation of the muscle. Direct stimulation is applied to mouse skeletal muscle in vitro to test the controllers along with numerical simulations for validation of these experimental tests. The experiments included muscle contractions following four distinct trajectories: a step, sine, ramp, and square wave. Overall, the closed-loop controllers followed the stimulation trajectories set for all the simulated and tested muscles. When comparing the experimental outcomes of each controller, we concluded that the ADP-PI algorithm provided the best closed-loop performance for speed of convergence and disturbance rejection. Next, the focus of the research work was on the implementation of an electromagnetic system to generate appropriate currents of stimulation using the aforementioned controllers. For this study, Nickel-Titanium shape memory alloys were used to assess activation (contraction) through a two-coil system guided by the controllers. The application of the two-coil system demonstrated the effectiveness of the approach and a main effect was observed between the PI, MRAC, and ADP-PI controllers when following the trajectories. Lastly, a small scale two-coil system is developed for animal testing in the muscle-mass-spring setup. Experiments were successful in generating the appropriate stimulation controlled by the output-based algorithms for muscle contraction. Trials conducted for this study were compared to the muscle contractions observed in the first study. The controllers were able to provide appropriate stimulation to the muscle system to follow the set trajectories: a step, ramp, and sinusoidal input. More trials are required to draw statistical conclusions about the performance of each controller. Regardless, the small-scale two-coil system along with the applied controllers can be reconfigured to be an implantable system and tested for appropriate stimulation of the laryngeal muscles.Ph. D.
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Lindqvist, Johan. "Cellular and Molecular Mechanisms Underlying Congenital Myopathy-related Weakness." Doctoral thesis, Uppsala universitet, Klinisk neurofysiologi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-219460.
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Congenital myopathies are a rare and heterogeneous group of diseases. They are primarily characterised by skeletal muscle weakness and disease-specific pathological features. They harshly limit ordinary life and in severe cases, these myopathies are associated with early death of the affected individuals. The congenital myopathies investigated in this thesis are nemaline myopathy and myofibrillar myopathy. These diseases are usually caused by missense mutations in genes encoding myofibrillar proteins, but the exact mechanisms by which the point mutations in these proteins cause the overall weakness remain mysterious. Hence, in this thesis two different nemaline myopathy-causing actin mutations and one myofibrillar myopathy-causing myosin-mutation found in both human patients and mouse models were used to investigate the cascades of molecular and cellular events leading to weakness. I performed a broad range of functional and structural experiments including skinned muscle fibre mechanics, small-angle X-ray scattering as well as immunoblotting and histochemical techniques. Interestingly, according to my results, point mutations in myosin and actin differently modify myosin binding to actin, cross-bridge formation and muscle fibre force production revealing divergent mechanisms, that is, gain versus loss of function (papers I, II and IV). In addition, one point mutation in actin appears to have muscle-specific effects. The presence of that mutant protein in respiratory muscles, i.e. diaphragm, has indeed more damaging consequences on myofibrillar structure than in limb muscles complexifying the pathophysiological mechanisms (paper II). As numerous atrophic muscle fibres can be seen in congenital myopathies, I also considered this phenomenon as a contributing factor to weakness and characterised the underlying causes in presence of one actin mutation. My results highlighted a direct muscle-specific up-regulation of the ubiquitin-proteasome system (paper III). All together, my research work demonstrates that mutation- and muscle-specific mechanisms trigger the muscle weakness in congenital myopathies. This gives important insights into the pathophysiology of congenital myopathies and will undoubtedly help in designing future therapies.
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Li, Mingxin. "Celluar and Molecular Mechanisms Underlying Regulation of Skeletal Muscle Contraction in Health and Disease." Doctoral thesis, Uppsala universitet, Klinisk neurofysiologi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-123005.
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Morphological changes, genetic modifications, and cell functional alterations are not always parallel. Therefore, assessment of skeletal muscle function is an integral part of the etiological approach. The general objective of this thesis was to look into the cellular and molecular events occurring in skeletal muscle contraction in healthy and diseased condition, using a single fiber preparation and a single fiber in vitro motility assay, in an attempt to approach the underlying mechanisms from different physiological angles. In a body size related muscle contractility study, scaling of actin filament sliding speed and its temperature sensitivity has been investigated in mammals covering a 5,500-fold difference in body mass. A profound temperature dependence of actin filament sliding speed over myosin head was demonstrated irrespective of MyHC isoform expression and species. However, the expected body size related scaling within orthologus myosin isoforms between species failed to be maintained at any temperature over 5,500-fold range in body mass, with the larger species frequently having faster in vitro motility speeds than the smaller species. This suggest that apart from the MyHC iso-form expression, other factors such as thin filament proteins and myofilament lattice spacing, may contribute to the scaling related regulation of skeletal muscle contractility. A study of a novel R133W β-tropomyosin mutation on regulation of skeletal muscle contraction in the skinned single fiber prepration and single fiber in vitro motility assay suggested that the mutation induced alteration in myosin-actin kinetics causing a reduced number of myosin molecules in the strong actin binding state, resulting in overall muscle weakness in the absence of muscle wasting. A study on a type IIa MyHC isoform missense mutation at the motor protein level demonstrated a significant negative effect on the function of the IIa MyHC isoform while other myosin isoforms had normal function. This provides evidence that the pathogenesis of the MyHC IIa E706K myopathy involves defective function of the mutated myosin as well as alterations in the structural integrity of all muscle irrespective of MyHC isoform expression.
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Roberts, Paul Andrew. "The functional role of the pyruvate dehydrogenase complex during ischaemic canine skeletal muscle contraction." Thesis, University of Nottingham, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394870.
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Modak, Ghabiba. "Characterisation of dynamics associated with skeletal muscle contraction initiated by Acetylcholine injection Ghabiba Modak." Master's thesis, University of Cape Town, 2011. http://hdl.handle.net/11427/11994.
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Includes abstract.Includes bibliographical references.
Lower motor neuron damage often results in flaccid paralysis in which the affected muscles are unable to be stimulated artificially via the supplying nerve. Such damage is common in patients who suffer from spinal cord injury and Multiple Sclerosis. Current practice for artificial recovery of muscle function involves stimulating the muscles directly by means of Functional Electrical Stimulation (FES), which requires 100-1000 times more current than that required for nerve stimulation, thus presenting the risk of pain receptor activation. A potential alternative exists in chemical stimulation by means of administration of the neurotransmitter, Acetylcholine (ACh). This study investigates the potential of this possibility by examining the response of two muscle types to extracellular administration of ACh.
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Hancock, Chad R. "Metabolic and functional consequences of adenylate kinase deficiency in skeletal muscle." Diss., Columbia, Mo. : University of Missouri-Columbia, 2005. http://hdl.handle.net/10355/5824.
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Thesis (Ph. D.)--University of Missouri-Columbia, 2005."May 2005" The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. Includes bibliographical references.
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Aaker, Aaron Paul. "Vasomotor responses of rat skeletal muscle arterioles to norepinephrine and adenosine." free to MU campus, to others for purchase, 2001. http://wwwlib.umi.com/cr/mo/fullcit?p3012943.
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Kosterina, Natalia. "Modelling of muscular force induced by non-isometric contraction." Doctoral thesis, KTH, Strukturmekanik, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-95418.
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The main objective of the study was to investigate and simulate skeletal muscleforce production during and after isometric contractions, active muscle lengtheningand active muscle shortening. The motivation behind this work was to improve thedominant model of muscle force generation based on the theories of Hill from 1938. Effects of residual force enhancement and force depression were observed after concentric and eccentric contractions, and also during stretch-shortening cycles. It wasshown that this force modification is not related to lengthening/shortening velocity, butinstead the steady-state force after non-isometric contractions can be well describedby an initial isometric force to which a modification is added. The modification isevaluated from the mechanical work performed by and on the muscle during lengthvariations. The time constants calculated for isometric force redevelopment appearedto be in certain relations with those for initial isometric force development, an observation which extended our basis for muscle modelling. A macroscopic muscular model consisting of a contractile element, and paralleland series elastic elements was supplemented with a history component and adoptedfor mouse soleus muscle experiments. The parameters from the experiment analysis, particularly the force modification after non-isometric contractions and the timeconstants, were reproduced by the simulations. In a step towards a general implementation, the history modification was introduced in the muscluloskeletal model ofOpenSim software, which was then used for simulations of full body movements.QC 20120525
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Wretman, Charlott. "Changes in mitogen-activated protein kinase phosphorylation and inorganic phosphate induced by skeletal muscle contraction /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-320-1/.
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Iwanaka, Nobumasa. "Leucine modulates contraction- and insulin-stimulated glucose transport and upstream signaling events in skeletal muscle." Kyoto University, 2010. http://hdl.handle.net/2433/120438.
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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15472号
人博第502号
新制||人||123(附属図書館)
21||人博||502(吉田南総合図書館)
27950
京都大学大学院人間・環境学研究科共生人間学専攻
(主査)准教授 林 達也, 教授 森谷 敏夫, 教授 石原 昭彦
学位規則第4条第1項該当
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Larsson, Barbro. "Evaluation of surface electromyography and aspects of muscle strength in persons without motor impairment and in children with hemiplegic cerebral palsy /." Linköping : Univ, 2005. http://www.bibl.liu.se/liupubl/disp/disp2005/med882s.pdf.
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Macgregor, Lewis James. "Neuromuscular markers of high performance sport preparation : muscle contractile mechanics." Thesis, University of Stirling, 2016. http://hdl.handle.net/1893/24445.
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Assessments of skeletal muscle functional capacity or bilateral muscular asymmetry often necessitate maximal contractile effort, which exacerbates muscle fatigue or injury. Tensiomyography (TMG) has been investigated in laboratory settings, as a means to assess muscle contractile function following fatigue; however observations have not been contextualised by concurrent physiological measures. TMG has more sparingly been applied in the field, with elite athletes. The aim of this thesis was to examine acute alterations and underlying variations in muscle contractile mechanics, through the application of TMG, contextualised with established physiological measures; and to apply TMG within high performance sports programmes. TMG successfully detected fatigue, evident from reduced strength, by displaying impaired muscle displacement, accompanied by elevated resting muscle tension. Greater asymmetry was detected in individuals with asymmetric strength; however, symmetry was masked during more complex tasks. Increased day-to-day variability was detected among highly trained athletes compared to recreationally active individuals. Acute training adaptations were detected, in contractile mechanics, in individual muscles. TMG could be useful in establishing fatigue status of skeletal muscle without exacerbating the functional decrements of the muscle, whilst also providing useful screening information for detecting asymmetry which may not be apparent during functional actions.
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Nordlund, Maria M. "On spinal mechanisms for reflex control in man : modulation of Ia-afferent excitation with changes in muscle length, activation level and fatigue /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-821-1/.
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Zhou, Hehe. "A novel method to measure finite strain fields in human skeletal muscles with cine phase contrast MRI in vivo, non-invasively and dynamically." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 207 p, 2006. http://proquest.umi.com/pqdweb?did=1172112541&sid=3&Fmt=2&clientId=8331&RQT=309&VName=PQD.
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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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Brousal, Jeffrey P. "Role of phosphorylation of the alpha one subunit in cyclic adenosine monophosphate dependent modulation of skeletal muscle calcium channels /." Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/6305.
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Cai, Weisong, and 蔡蔚松. "Cystic fibrosis transmembrane conductance regulator is involved in therelease of ATP from contracting skeletal muscle." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B49618088.
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Contracting skeletal muscle releases ATP into the interstitial space where it is subsequently broken down to adenosine by the action of ecto-5’-nucleotidase. Both ATP and adenosine are vasodilators that contribute to the exercise hyperaemia. However, the mechanism for the release of ATP from muscle during exercise remains unknown. Cystic fibrosis transmembrane conductance regulator (CFTR) is involved in ATP release from muscle at low intracellular pH: this study was performed to investigate whether CFTR was involved in the ATP release from skeletal muscle during contractions.
Experiments were performed in rats anaesthetised with sodium pentobarbitone and breathing spontaneously. A microdialysis probe was placed in one gastrocnemius muscle: ATP was determined in interstitial microdialysate samples using a bioluminescence assay. The sciatic nerve was stimulated to induce two bouts of muscle contractions, separated by a recovery period of 40 mins; one of the inhibitors was administered prior to the second bout of contractions.
Muscle contractions elevated the interstitial ATP by 1500 to 3000%. In the control experiments, no drug was given: both the contractile force and the increase in interstitial ATP were reproducible in repeated contraction bouts. Infusion of a specific inhibitor of CFTR, CFTRinh-172, did not alter the contractile force, but significantly lowered the interstitial ATP during muscle contractions, suggesting that CFTR was involved in the contraction-induced ATP release. Similarly, infusion of the Protein Kinase A inhibitor, KT5720, significantly reduced interstitial ATP during muscle contractions without altering contractile force, suggesting that CFTR in skeletal muscle is activated through the cAMP/PKA pathway. The increase in interstitial ATP during muscle contraction was also inhibited by the Na/H exchanger inhibitor, amiloride, or the Na/Ca exchanger inhibitor, SN6. It has been also shown that two gap junction hemichannel inhibitors, gadolinium and carbenoxolone, could attenuate the increase of ATP during muscle contraction.
These data suggest that CFTR, activated through the cAMP/protein kinase A pathway, is involved in the ATP release during muscle contraction, and that activation of the Na/H exchanger and Na/Ca exchanger was also required, indicating that the signal transduction mechanism for CFTR activation during muscle contractions may be similar to that which is reported to occur at low pH. The preliminary data showed that the gap junction hemichannels might mediate the ATP release from skeletal muscle cells during muscle contraction.published_or_final_version
Physiology
Master
Master of Philosophy