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PELLEGRINO, GIULIA MICHELA. "LUNG FUNCTION AND DYSPNEA IN NEUROMUSCULAR DISEASES". Doctoral thesis, Università degli Studi di Milano, 2021. http://hdl.handle.net/2434/842435.
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Dyspnea is a common source of suffering for patients affected by cardiorespiratory or neuromuscular diseases. The symptom is complex and encompasses different sensory qualities with distinct intensities. The Multidimensional Dyspnea Profile (MDP) is an instrument specifically developed to assess the multidimensional dimensions of the symptom, and it is applicable in both the research and clinical setting. In order to allow its use for Italian speaking populations, we aimed to provide a linguistically validated, Italian translation of the MDP.
We conducted a structured translation and linguistic validation of the MDP questionnaire in accordance to the international guidelines and in cooperation with a specialized company (MAPI SAS, Language Services Unit, Lyon, France). Cognitive interviews on 8 patients were conducted in order to test clarity and understandability of the questionnaire. The multistep process was enriched by several quality checks which led to a translation conceptually equivalent to the original version (American English).
A final certified copy linguistically validated Italian translation of the MDP is now available. It measures the intensity of the breathing discomforts in five sensory qualities and assess its intensity and potential reactions.
W e here provide an Italian translation and linguistic validation of the MDP. This instrument, allows the assessment of dyspnea in both its sensory and emotional aspects, therefore representing a valuable method for research and therapy purposes.
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Kalmar, Jayne M. "The effects of caffeine on human neuromuscular function". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ33488.pdf.
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Weinberg, Jan. "Studies on ventilatory function in chronic neuromuscular disorders /". Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3936-5/.
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Auburn, Richard Peter. "Screening for genes involved in Drosophila neuromuscular function". Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621081.
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Penney, Jay. "Retrograde regulation of synaptic function at «Drosophila» neuromuscular junctions". Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=119497.
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Neuronal growth and synaptic function are key determinants of nervous system behaviour. Understanding the molecular mechanisms that regulate these processes is central to comprehending nervous system function, both in health and during disease states. My thesis has focused on trying to better understand the mechanisms controlling glutamatergic neuronal growth, synaptic function and synaptic plasticity using the Drosophila melanogaster larval neuromuscular junction (NMJ) as a model system. This work has concentrated on the role that protein synthesis regulators play in modulating NMJ function and plasticity, and has revealed important roles for multiple regulators of cap-dependent translation in these processes. Importantly, genetic manipulations predicted to enhance cap-dependent translation in postsynaptic muscle can induce retrograde enhancements in synaptic function. In each case, these manipulations are without effect on neuronal growth, the number of synaptic sites or glutamate receptor levels. Instead, enhanced postsynaptic cap-dependent translation leads to increased presynaptic release probability. This retrograde pathway plays a key role in the expression of homeostatic synaptic plasticity at NMJ synapses. Glutamate receptor subunit IIA (GluRIIA) mutants exhibit reduced postsynaptic receptor function which is compensated for by enhanced presynaptic release; cap-dependent translation, under control of the TOR (target of rapamycin) pathway, is essential for this retrograde homeostatic response. Furthermore, we find that Parkinson's disease related protein LRRK2 (leucine rich repeat kinase 2), and its Drosophila orthologue dLRRK, can regulate synaptic function at the NMJ via cap-dependent translation. Importantly, however, mutant forms of LRRK2 are defective in their ability to regulate synaptic strength. Together, these findings further our understanding of the molecular mechanisms regulating glutamatergic synaptic function and plasticity.La croissance neuronale et la fonction synaptique sont des constituants clés dans le comportement du système nerveux. Il est donc essentiel de comprendre les mécanismes moléculaires régulant ces processus à l'état normal ainsi qu'à l'état pathologique. Ma thèse a pour objectif une meilleure compréhension des mécanismes contrôlant la croissance neuronale, ainsi que la fonction et la plasticité synaptiques engendrés par la transmission glutamatergique, en utilisant comme modèle la jonction neuromusculaire (JNM) de la drosophile, Drosophila melanogaster. Cet ouvrage porte spécifiquement sur l'impact de régulateurs de la synthèse protéique sur la fonction et la plasticité synaptiques dans la JNM, et a identifié des rôles importants pour de multiples régulateurs de traduction coiffe-dépendante dans ces processus. Des manipulations génétiques menant à une augmentation de la traduction coiffe-dépendante dans le muscle post-synaptique induisent une augmentation rétrograde de la fonction synaptique. Dans chaque cas, ces manipulations n'affectent ni la croissance neuronale, ni le nombre de synapses, ni le niveau de récepteurs glutamatergiques. Plutôt, une traduction coiffe-dépendante post-synaptique conduit vers une augmentation de la probabilité de relâche pré-synaptique. Cette voie signalétique joue un rôle important dans l'expression de la plasticité homéostatique des synapses neuromusculaires. Des mutants du récepteur glutamatergique IIA (GluRIIA) montrent une réduction dans la fonction post-synaptique, qui est compensée par une augmentation de la probabilité de relâche pré-synaptique. La traduction coiffe-dépendante, sous le contrôle de la voie signalétique TOR (target of rapamycin), est essentielle pour cette réponse homéostatique rétrograde. De plus, la protéine reliée à la maladie de Parkinson, LRRK2 (leucine rich repeat kinase 2), ainsi que son orthologue chez la drosophile, dLRRK, peuvent réguler la fonction synaptique de la JNM via la traduction coiffe-dépendante. Cependant, les formes mutantes de LRRK2 sont défectueuses dans leur habileté à réguler la fonction synaptique. Globalement, ces trouvailles nous aident à comprendre les mécanismes moléculaires régulant la fonction et la plasticité synaptiques glutamatergiques.
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El-Kabir, Desiree Ruth. "An assessment of ventilatory function and sleep in neuromuscular disease". Thesis, King's College London (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.440537.
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Benatar, Michael G. "Presynaptic function in development and disease at the neuromuscular junction". Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388959.
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Dhesi, Jugdeep. "Vitamin D and neuromuscular function in older people who fall". Thesis, King's College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.416021.
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Voegtle, Tracy. "The effect of an acute ankle joint injury on neuromuscular function". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ58098.pdf.
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Blunk, Aline D. (Aline Dorret). "Regulation of synaptic structure and function at the Drosophila neuromuscular junction". Thesis, Massachusetts Institute of Technology, 2013. http://hdl.handle.net/1721.1/84874.
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Thesis (Ph. D. in Neuroscience)--Massachusetts Institute of Technology, Department of Brain and Cognitive Sciences, 2013.Cataloged from PDF version of thesis.
Includes bibliographical references.
Neuronal communication requires a spatially organized synaptic apparatus to coordinate neurotransmitter release from synaptic vesicles and activation of postsynaptic receptors. Structural remodeling of synaptic connections can strengthen neuronal communication and synaptic efficacy during development and behavioral plasticity. Here, I describe experimental approaches that have revealed how the actin cytoskeleton participates in transynaptic signaling to control synapse assembly. I also describe my studies on how regulation of endocytic trafficking controls synaptic growth during neuronal development. To identify regulators of synapse assembly, I carried out a large-scale EMS mutagenesis screen of the second chromosome. From this screen I identified a mutation in actin 57B that disrupts synaptic morphology and presynaptic active zone organization. Actin 57B is one of six actin genes in Drosophila and is expressed in body wall muscle during larval development. The isolated allele harbors a point mutation disrupting a highly conserved amino acid present throughout the actin family. Homozygous mutant larvae show impaired alignment and spacing of presynaptic active zones. Additionally, disruption of the organization of the postsynaptic density is observed, with mislocalization of the Spectrin cytoskeleton and the PSD-homolog Disc-Large. Phallodin staining reveals a severe disruption of postsynaptic actin surrounding presynaptic boutons, with the formation of aberrant large actin swirls. Based on these results, we hypothesize that the loss of a synaptic interaction mediated by actin 57B leads to disruption of postsynaptic cytoskeletal organization and dysregulation of signals required to organize presynaptic active zones. Additionally, I present data that provide new insights into the mechanisms controlling synaptic growth signaling during transit through the endocytic pathway. Nervous Wreck (Nwk) is a presynaptic F-BAR/SH3 protein that regulates synaptic growth signaling in Drosophila. Here, I show that Nwk acts through a physical interaction with Sorting Nexin 16 (SNX16). SNX16 promotes synaptic growth signaling by activated BMP receptors, and live imaging in neurons reveals that SNX16-positive early endosomes undergo transient interactions with Nwkcontaining recycling endosomes. We identify an alternative signal termination pathway in the absence of Snx16 that is controlled by ESCRT-mediated internalization of receptors into the endosomal lumen. Our results define a presynaptic trafficking pathway mediated by SNX116, NWK and the ESCRT complex that functions to control synaptic growth signaling at the interface between endosomal compartments. Together, these experiments have expanded our understanding of the molecular mechanisms that control synaptic growth and assembly, highlighting the role of the postsynaptic actin cytoskeleton and the presynaptic endosomal trafficking pathway as key regulators.
by Aline D. Blunk.
Ph.D.in Neuroscience
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Cummings, Sarah. "Investigating Oligodendrocyte Biology and Function: Insights from Neurological and Neuromuscular Diseases". Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/41489.
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Oligodendrocytes (OLs) are the cells responsible for myelin production in the central nervous system (CNS). Myelin serves to increase the efficiency of signal propagation down the axon and is essential for proper communication between the CNS and the periphery. As a result, pathologies affecting the OL, including multiple sclerosis (MS) and multiple system atrophy (MSA), present with a wide range of symptoms including impaired muscle control, loss of coordination, as well as cognitive deficits. While the biology of the OL continues to garner research interest, much remains to be understood about cell function in a healthy context, and also how the biology of these cells goes awry in disease. Our objective was to explore the effects of varying disease models on OL biology and use those findings to further our knowledge on the biology of OL development and regeneration. Here we explore OL function and dysfunction in the context of spinal muscular atrophy (SMA), MSA and MS. We have thoroughly characterized the OL response to SMN-depletion and have determined that SMN is not required for the development of OLs in the neonatal brain. Additionally, we have sought to characterize the endogenous role of MSA-disease relevant protein alpha-synuclein in OL development and have determined that this protein is not required for OL differentiation or CNS myelination. Lastly, we have explored the biology of the OL in the context of the inhibitory milieu it faces during remyelination in MS. We have investigated different pathways that may be involved in mediating signalling of one such inhibitory cue (chondroitin sulphate proteoglycans, CSPGs), and have extended this model to interrogate OL cytoskeletal dynamics in the context of CSPGs. Together, this work uses disease frameworks to investigate basic OL biology, as well as provides insights into how the OL and its interactions with the extracellular milieu should be considered in disease pathogenesis and therapeutic exploration.
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Hartigan, Erin. "Knee function after ACL rupture and reconstruction effects of neuromuscular training". Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 203 p, 2009. http://proquest.umi.com/pqdweb?did=1896910991&sid=7&Fmt=2&clientId=8331&RQT=309&VName=PQD.
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Opar, David A. "Neuromuscular hamstring function in response to intermittent running and previous injury". Thesis, Queensland University of Technology, 2013. https://eprints.qut.edu.au/64107/4/David_Opar_Thesis.pdf.
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This thesis examined the impact of previous hamstring injury and fatigue on the function of the hamstring muscles and their neural control. The work established the role of neuromuscular inhibition after hamstring injury and involved the development of a new field testing device for eccentric hamstring strength, which is now in high demand in elite sport worldwide. David has four peer-reviewed publications from this doctoral work.
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Côté, Patrice D. "Dystroglycan function in development and neuromuscular disease : a study by gene targeting". Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=36900.
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The dystrophin associated protein (DAP) complex has been implicated in such basic physiological processes as the maintenance of cellular homeostasis, the assembly of basement membranes (BM), and synaptogenesis. The dystroglycans, alpha and beta, constitute the functional core of the DAP complex since they establish the transmembrane link between dystrophin, whose mutations lead to Duchenne (DMD) or Becker (BMD) muscular dystrophy, and the extracellular matrix (ECM). The alpha and beta subunits of dystroglycan result from posttranslational processing of a single propeptide encoded by DAG1. No clinical cases or animal models have been identified with spontaneous mutations in that gene. Therefore, to gain insight to the function of dystroglycans I have used gene targeting to disrupt the coding sequence of Dag1 in murine embryonic stem (ES) cells. We find that dystroglycans are critical in the early stages of development and that a null mutation in Dag1 results in embryonic lethality at embryonic day (E) 6.5 because of a disruption in Reichert's BM. In culture however, the absence of dystroglycan in ES cells targeted for both Dag1 alleles does not obviously hinder their developmental potential. Consequently, I reasoned that it might be possible to circumvent the early lethality observed in 'classical' knockout mice, by injecting Dag1-null ES cells into wild-type blastocysts to generate chimeric mice only partially devoid of dystroglycan. Several chimeric mice developed to maturity and Dag1 -null ES cells were found to contribute extensively to the hindlimb musculature thus allowing the analysis of dystroglycan depleted muscles. These muscles are severely dystrophic, have low levels of dystrophin and a disrupted residual DAP complex, but have apparently normal BMs. Chimeric muscles also have disrupted neuromuscular junctions. In culture, myotubes derived from Dag1-null ES cells form clusters of acetylcholine receptors (AChRs) but these occupy a surface area three time
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Tsang, Ka Wai Karen. "A microRNA cluster negatively regulates synaptic function at «Drosophila» larval neuromuscular junction". Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86715.
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Proper synaptic growth and plasticity are critical for higher brain functions including memory and learning. We are interested in identifying and characterizing mechanisms that underlie the regulation of morphological and functional synaptic plasticity. To that end, we conducted a forward genetic gain-of-function screen aimed at identifying novel regulators of synaptic growth, using Drosophila larval neuromuscular junction (NMJ) as a model synapse. From this screen, we identified a well-conserved microRNA cluster, miR-310-313, whose expression affects synaptic plasticity at Drosophila NMJ. We generated a deletion of this miRNA cluster by imprecise excision of a P-element. Our results show that lack of miR-310-313 leads to a significant increase in evoked post-synaptic current and in quantal content, a measure of the efficiency of presynaptic neurotransmitter release. This phenotype can be rescued by overexpressing miR-310-313 during larval stage in nervous system, suggesting the temporal and tissue-specific requirement of this miR-310-313 cluster. miRNAs repress expression of their targets via base-pairing with the 3'UTR of their mRNAs. Computational algorithms predicted Khc-73, a member of Kinesin Superfamily proteins (KIFs), as one of the highest-scoring targets for miR-310-313. We hypothesize that miR-310-313 cluster regulates synaptic function by downregulating Khc-73. In support of our hypothesis, overexpressing Khc-73 in Drosophila motoneurons enhances synaptic function, a phenotype resembling miR-310-313 deletion. Further evidence shows that genetic removal of Khc-73, by using Khc-73 RNAi or by a deficiency uncovering Khc-73 genomic region, is sufficient to restore normal synaptic function in miR-310-313 deletion. Taken together, our data present a novel pathway by which synaptic plasticity is regulated.La croissance et la plasticité synaptiques sont des éléments critiques pour le bon fonctionnement du cerveau, et participent aux processus de la mémoire et l'apprentissage. Le but de nos recherches est d'identifier et de caractériser les mécanismes moléculaires qui sous-tendent le règlement de la plasticité synaptique morphologique ainsi que fonctionnelle. À cette fin, nous avons élaboré un crible d'augmentation-de-fonction génétique dont le but était d'identifier de nouveaux régulateurs de croissance synaptique, en utilisant la jonction neuromusculaire (JNM) larvaire de la mouche drosophile (Drosophila melanogaster) comme synapse modèle. Grâce à ce crible, nous avons identifié un groupe de microARN (miARN) bien conservé au niveau évolutionnaire, miR-310-313, dont l'expression affecte la plasticité synaptique à la JNM de la drosophile. Nous avons produit une délétion de ce groupe de miARN par l'excision imprecise d'un élément génétique mobile (P-element). Nos résultats démontrent que la perte de miR-310-313 entraîne une augmentation significative du courant post-synaptique évoqué et du contenu quantique, une mesure de l'efficacité de la libération de neurotransmetteur présynaptique. Ce phénotype peut être rescapé en surexprimant miR-310-313 pendant le stade larvaire du système nerveux, suggérant une exigence d'expression génétique temporelle et spatiale spécifique pour ce groupe de miARN. Les miARN répriment l'expression de leurs cibles par appariement de bases avec le 3'UTR de leur mARN. Des algorithmes quantificatifs ont prédit Khc-73, un membre de la superfamille des protéines Kinesin (KIFs), comme une des cibles les plus plausibles pour miR-310-313. Nous émettons l'hypothèse que le groupe miR-310-313 régule la fonction synaptique en réprimant l'expression de Khc-73. Dans le soutien de notre hypothèse, nous démontrons que la surexpression de Khc-73 dans les neurones moteurs de la drosophile améliore la fo
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Whitney, Garrett Lynn. "The Effects of Electromyographic Biofeedback and Therapeutic Exercise on Quadriceps Neuromuscular Function". University of Toledo / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1396484469.
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Vaughan, Jeremiah A. "Neuromuscular Function and Fatigue and Metabolic Responses while Cycling in the Heat". Kent State University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=kent1542212848069694.
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Tang, Teresa. "Effects of plasmas from seronegative myasthenia gravis patients on the function of skeletal muscle nicotinic acetylcholine receptor". Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365322.
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Bouhana, Antoine. "Análise cinemática do teste de Thomas modificado e sua influência na função neuromuscular". Bachelor's thesis, [s.n.], 2017. http://hdl.handle.net/10284/5884.
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Projeto de Graduação apresentado à Universidade Fernando Pessoa como parte dos requisitos para obtenção do grau de Licenciado em FisioterapiaIntrodução: A ação preventiva da Fisioterapia é fundamental para reduzir o risco de lesão. A maior parte de lesões resultam de um número enorme de fatores, entre eles a flexibilidade, força muscular entre outros. Existem vários testes em Fisioterapia que podem ser utilizados no sentido de avaliar a flexibilidade, entre eles temos o teste Thomas modificado. Objetivo: perceber as repercussões biomecânicas (cinemáticas e musculares) da execução do teste de Thomas modificada e sua relação com na função neuromuscular. Metodologia: Análise da cinemática tridimensional do teste de Thomas Modificado através do sistema de captura e análise de movimento 3D, Qualisys Oqus Camera Series. Resultados: Após a análise dos dados obtidos, os resultados parecem que o modo de execução do teste permite uma estabilização razoável dos mesmos, ainda que a posição final do membro em teste não tem relação com a função neuromuscular em extensão. Por outro lado, um potencial encurtamento a nível do reto femoral, não parece influenciar a força produzida nos extensores do joelho. Conclusão: A força executada pelo paciente não influenciou o lado contralateral (em teste), e que o teste de Thomas Modificado parece ser um teste fiável, uma vez que não se verificaram compensações segmentares significativas na execução do mesmo.
Introducton: The preventive action of Physiotherapy plays an essential part in reducing injury risk, especially in sports. Most of those injuries occur due to flexibility, muscular strength issues, among other factors. There are several tests used in Physiotherapy to evaluate the patients’ flexibility, and the Modified Thomas Test is one of them. Objective: Understand the biomechanical repercussions (kinematic and muscular) of the Modified Thomas test and its influence in neuromuscular function. Methodology: Tridimensional kinematic analysis of the Modified Test of Thomas with Qualisys Oqus Camera Series, 3D movement capture and analysis program. Results: After data analysis results seem that the test procedure allows a reasonable stabilization, although the final position of the limb under test has no relation with the isokinetic neuromuscular function in extension. On the other hand, a potential shortening in the rectus femoris does not seem to influence the force produced in the knee extensors. Conclusion: The force exerted by the patient did not influence the contralateral side (under test), and that the modified Thomas test seems to be a reliable test, since there were no significant segmental compensations in the execution of the test.
N/A
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Grönlund, Christer. "Spatio-temporal processing of surface electromyographic signals : information on neuromuscular function and control". Doctoral thesis, Umeå universitet, Institutionen för strålningsvetenskaper, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-958.
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During muscle contraction, electrical signals are generated by the muscle cells. The analysis of those signals is called electromyography (EMG). The EMG signal is mainly determined by physiological factors including so called central factors (central nervous system origin) and peripheral factors (muscle tissue origin). In addition, during the acquisition of EMG signals, technical factors are introduced (measurement equipment origin). The aim of this dissertation was to develop and evaluate methods to estimate physiological properties of the muscles using multichannel surface EMG (MCsEMG) signals. In order to obtain accurate physiological estimates, a method for automatic signal quality estimation was developed. The method’s performance was evaluated using visually classified signals, and the results demonstrated high classification accuracy. A method for estimation of the muscle fibre conduction velocity (MFCV) and the muscle fibre orientation (MFO) was developed. The method was evaluated with synthetic signals and demonstrated high estimation precision at low contraction levels. In order to discriminate between the estimates of MFCV and MFO belonging to single or populations of motor units (MUs), density regions of so called spatial distributions were examined. This method was applied in a study of the trapezius muscle and demonstrated spatial separation of MFCV (as well as MFO) even at high contraction levels. In addition, a method for quantification of MU synchronisation was developed. The performance on synthetic sEMG signals showed high sensitivity on MU synchronisation and robustness to changes in MFCV. The method was applied in a study of the biceps brachii muscle and the relation to force tremor during fatigue. The results showed that MU synchronisation accounted for about 40 % of the force tremor. In conclusion, new sEMG methods were developed to study muscle function and motor control in terms of muscle architecture, muscle fibre characteristics, and processes within the central nervous system.
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Patrón, Lilian Adilene, i Lilian Adilene Patrón. "DCAF12 Is Required For Synaptic Function and Plasticity at the Drosophila Neuromuscular Junction". Diss., The University of Arizona, 2017. http://hdl.handle.net/10150/624292.
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We employed imaging, electrophysiological, and molecular techniques with the genetically tractable model organism Drosophila melanogaster to unravel fundamental biological and genetic underpinnings regulating synaptic function and plasticity.
Using a forward genetic screen, we identified mutations in the Drosophila ortholog of a human WD40 repeat-containing protein termed DDB1 and CUL4 associated factor 12 (DCAF12). We show that DCAF12 likely serves as an adaptor protein for the DDB1-Cul4 E3 ubiquitin ligase complex by recruiting specific target proteins for ubiquitination.
DCAF12 is expressed in neurons, muscles, and glia. In mitotically active cells such as muscles, DCAF12 is localized to nuclei and co-localizes in distinct foci with CUL4, suggesting that DCAF12 mediates a nuclear role for the CUL4 E3 ubiquitin ligase complex. In neurons, DCAF12 is localized to both cytoplasmic and nuclear compartments of motor neuron cell bodies, where it colocalizes with Cul4 in nuclei. DCAF12 is also expressed at the periactive zone of presynaptic terminals, but does not distinctly associate with DDB1 or Cul4 at this region.
Evoked neurotransmitter release at larval NMJs is significantly reduced in DCAF12 mutants. These defects are rescued by presynaptic expression of wild-type DCAF12, demonstrating that DCAF12 is required presynaptically and serves as an important component of the machinery that facilitates evoked release.
In addition, our studies show that DCAF12 is required for the differential expression of glutamate receptor subunits at the larval NMJ through transcriptional and post-translational mechanisms. GluRIID subunit mRNA levels and GluRIIA/C/D subunit protein levels are increased at DCAF12 mutant NMJs. Normal GluRIIA subunit levels can be restored by postsynaptic expression of wild-type DCAF12, but not with a truncated DCAF12 protein lacking a nuclear localization signal (∆NLS-DCAF12). Furthermore, DCAF12 overexpression in muscle nuclei reduces synaptic GluRIIA levels, an effect that can be suppressed by removing a copy of Cul4. These data strongly indicate that DCAF12 in muscle nuclei is required for GluRIIA expression and/or function in a Cul4-dependent manner. Moreover, homozygous DCAF12-GluRIIA double mutants show a strong synthetic lethality phenotype, providing further support for the hypothesis that GluRIIA directly or indirectly requires DCAF12.
Mutations in glutamate receptors at larval NMJs trigger a retrograde trans-synaptic signal that leads to a compensatory increase in presynaptic release, which precisely restores the normal efficacy of synaptic transmission and muscle excitation. Reducing the gene dosage of DCAF12 by one gene copy suppresses the initiation and maintenance of GluRIIA-mediated synaptic homeostatic potentiation. This block of synaptic homeostatic potentiation can be rescued by presynaptic expression of DCAF12.
In our studies, we determined that DCAF12 is critical for 3 distinct synaptic mechanisms: evoked neurotransmitter release, neurotransmitter reception by regulation of GluR subunit composition, and retrograde synaptic homeostatic signaling. Future research will strive to identify presynaptic and postsynaptic protein targets of DCAF12 and the Cul4 E3 ubiquitin ligase complex and the role of ubiquitination in regulating these synaptic processes.
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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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Scheurer, Sarah Ann. "The Relationship between Corticomotor Excitability and Quadriceps Neuromuscular Function in ACL Reconstructed Patients". University of Toledo / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1525287124424035.
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Melillo, Julie Ann. "Influence of Muscle Motor Point Identification on Quadriceps Function Following Neuromuscular Electrical Stimulation". University of Toledo / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1556547710451478.
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McKay, Marnee. "1000 NORMS PROJECT: MEASURES OF PHYSICAL FUNCTION ACROSS THE LIFESPAN". Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/16588.
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Meaningful, reliable, and sensitive outcome measures are required to track the progression of neuromuscular disorders and evaluate the significance of changes attributed to therapies. Determining whether changes are statistically significant as well as clinically meaningful, relies on comparison with normative reference data. Knowledge of what is normal is essential to accurately identify and evaluate pathology that is abnormal. The aim of this thesis was to generate normative reference data for clinimetrically sound performance-related outcome measures, assessing muscle strength, joint range of motion, spatiotemporal and plantar pressure gait and functional capabilities and to investigate the influence of demographic and physical characteristics. Chapter 2 describes the recruitment process and development of the standardised and reliable protocol used to assess 1000 healthy people aged from 3-101 years in the 1000 Norms Project. Chapter 3 presents age- and gender-stratified normative reference data for 13 active joint movements assessed using goniometry and the isometric strength of 12 muscle groups assessed using hand held and fixed dynamometry. Chapter 4 presents reference data for 15 spatiotemporal gait parameters assessed using an instrumented walkway system and 16 measures of plantar pressure for four regions of the foot captured by a capacitance pressure distribution platform. Chapter 5 presents reference data for 12 functional capability measures classified as gross motor function (6-minute walk test, stair climb test, sit to stand test, reaction time, vertical and long jump), fine motor function (9-hole peg test, Functional Dexterity test) and balance (dynamic: star excursion balance test and static: single leg and tandem stance). Chapter 6 summarises the findings of Chapters 2-5 and discusses the influence of demographic and physical characteristics on performance-related outcome measures across the lifespan and implications for future research. The normative reference data presented in this thesis provide a framework to determine the presence and extent of impairments in children and adults with neuromuscular disorders as well as other neurological and musculoskeletal conditions.
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Clark, David Rodney. "Neuromuscular assessment of trunk muscle function in loaded, free barbell back squat : implications for development of trunk stability in dynamic athletic activity". Thesis, University of Stirling, 2018. http://hdl.handle.net/1893/28080.
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Traditional core stability training was developed as a method of treating and preventing back pain. It was however, seamlessly applied to healthy and athletic populations without scientific evidence supporting its efficacy. Traditional core stability focussed on isolating and training the anatomical region between the pelvis and diaphragm, using isometric or low load exercises to enhance spinal stability. Scientific research challenged this approach for healthy function and athletic performance, resulting in a more functional anatomical definition, which included pelvic and shoulder girdles. Hence, a revised definition of dynamic trunk stability; the efficient coordination, transfer and resistance by the trunk, of force and power generated by upper and lower appendicular skeletal extremities during all human movement. This led to an integrated exercise training approach to dynamic trunk stability. Although early evidence suggested loaded compound exercises preformed upright, in particular back squat, were effective in activating and developing trunk muscles, evidence was inconclusive. Accordingly, the aims of this PhD were to investigate neuromuscular trunk function in loaded, free barbell back squat to understand training implications for trunk stability in dynamic athletic activity. Five research studies were conducted; 4 are published and 1 is being prepared for re-submission. The literature review revealed evidence that back squat was an effective method of activating trunk stabilzers and showed that these muscles were load sensitive (study 1). A survey of practitioners reported an understanding and appreciation of the challenge against core stability training for athletic populations. Furthermore, perceptions were aligned with growing evidence for dynamic and functional trunk stability training (study 2). A test-retest neuromuscular study established interday reliability and sensitivity of electromyographical measurement of trunk muscle activity in squats (study 3). Trunk muscle activation in back squat was higher than hack squat at the same relative, but lower absolute loads (study 4). Trunk muscle activation was lower in squats and bodyweight jumps in the strong compared to weak group (study 5). Furthermore, activation of the trunk muscles increased in each 30o segment of squat descent and was highest in first 30o segment of ascent for all loads (study 5). In conclusion, this series of studies confirmed acute effect of squats on trunk stabilizers and demonstrated that external load increases activation in these muscles. Parallel squat depth is important in optimizing trunk muscle activation. Finally, high levels of squat strength result in lower trunk muscle activation in loaded squats and explosive jumps.
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Sundman, Eva. "Pharyngeal function, airway protection and anesthetic agents /". Stockholm : [Karolinska institutets bibl.], 2002. http://diss.kib.ki.se/2002/91-7349-161-6.
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Cerantola, Silvia. "Toll-like receptor 4, enteric nervous system and gut neuromuscular function in models of functional and inflammatory bowel disorders". Doctoral thesis, Università degli studi di Padova, 2019. http://hdl.handle.net/11577/3423310.
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The interaction between the constituents of the intestinal wall and commensal microflora is essential for the maintenance of mucosal barrier, the promotion of digestive system development and the modulation of gastrointestinal (GI) activities, such as motility, secretion, mucosal immunity and visceral sensitivity. Alterations in the gut microflora composition have been associated to several GI disorders (e.g. inflammatory bowel disease, IBD, and irritable bowel syndrome, IBS) while changes in intestinal microbiome during childhood and adolescence, caused by infections or antibiotics, predispose at the onset of these diseases. Furthermore, dysfunctions of the enteric nervous system (ENS) such as structural abnormalities and/or changes in the content of neurotransmitters have been associated with the onset of IBD and/or IBS. In this context, a sophisticated system of proteins, so-called Toll-like receptors (TLRs), plays a key role in mediating the inflammatory response against pathogens and activates beneficial signals to ensure tissue integrity in physiological and pathological conditions. Polymorphisms in the genes encoding TLRs, including TLR2 and TLR4, have been associated with different disease phenotypes in patients with GI disorders. Therefore, in this study, we evaluated the structural and functional alterations of murine ENS in the absence of the signal mediated by TLR4, a receptor of innate immunity, in mouse models of: i) ex vivo inhibition of enteric glial cells activities; ii) obesity induced by a high fat diet (HFD); iii) experimental colitis by in vivo administration of sodium dextran sulfate (DSS).
Firstly, the role of the TLR4 receptor in maintaining intestinal function was investigated by performing in vitro contractility experiments, using ileal preparations from C57BL/6J WT mice exposed to a cocktail of antibiotics to induce microbiota depletion to be compared to mice deficient for TLR4 signaling. The effects provoked by the antibiotic-induced microbiota depletion are similar to those evidenced by the absence of TLR4 signaling on GI function, in particular, a significant reduction of the cholinergic excitatory contractile response accompanied by an altered ratio of neurons positive for the neuronal nitric oxide synthase (nNOS), associated to alterations in the distribution and expression of the glial S100β protein. These observations suggest that the lack of the intestinal microbiota, and, especially, the lack of TLR4 signaling may influence the integrity of the enteric neuronal and glial network. Given the importance of a correct commensal microbiota signal in maintaining the neuroglial network and the ENS neurochemical code, intestinal function was evaluated by in vitro contractility experiments using the isolated organ bath technique on ileal segments from WT and TLR4-/- mice. Thanks to functional and immunofluorescence studies with confocal microscopy, it was possible to demonstrate that the absence of the TLR4 signaling not only determines a significant decrease in the excitatory response but induces a marked increase in inhibitory neurotransmission mediated by both nitric oxide (produced both by nNOS than from the inducible NOS (iNOS)) and ATP, which mediated its actions through the P2Y1 purinergic receptor. In order to characterize the origin of the altered inhibitory tone in intestinal preparations of TLR4-/- mice, ex vivo experiments with the gliotoxin fluoroacetate were performed revealing the primary role of P2Y1 purinergic receptors, expressed in the enteric glia, in support of inhibitory transmission. Therefore, the evaluation of TLR4-/- mice highlighted the primary role of this receptor in modulating the interaction of both neuronal and glial signals of the ENS to ensure correct intestinal neuromuscular activity.
In order to investigate the role of TLR4 in mild inflammatory conditions, the effects of obesity induced by high-fat diet (HFD; 60% kcal of lipids) on the functional and morphological integrity of the ENS were evaluated in WT and TLR4-/- mice. The HFD determines reduced cholinergic excitatory activity and increased inhibitory tone with consequent slower intestinal transit, associated with reactive gliosis. The absence of TLR4 protects mice from weight gain and the relative functional and structural neuromuscular anomalies induced by HFD, to highlight the primary role of this receptor in modulating the harmful effects of obesity in the GI tract, such as constipation. In TLR4-/- mice the serotonergic neurotransmission, mediated by 5-HT3 receptors, is increased and insensitive to ketanserin, an antagonist of 5-HT2A receptors, and was not subjected to changes following HFD to underline the influence of the signal mediated by the TLR4 in the modulation of the neuromuscular serotonergic response. These alterations were associated to significantly increased tissue levels of serotonin and its metabolites, tryptophan and kynurenine, induced by the absence of the TLR4 signaling and further enhanced by the HFD.
Finally, we evaluated the importance of the TLR-ENS axis in maintaining ENS integrity in inflammatory conditions, obtained by inducing experimental colitis in WT and TLR4-/- mice. This model of experimental colitis, recognized for its simplicity, reproducibility, and versatility, offers the opportunity to mimic the inflammatory processes involved in the development of ulcerative colitis in humans and to study the involvement of immunity. DSS-induced colitis led to marked structural alterations in the neurochemical code of the ENS, which resulted in an increased excitatory neuromuscular response more marked in WT mice than in those deficient for TLR4. In TLR4-/- mice treated with DSS, the increased response to serotonin is markedly reduced and is mediated by 5-HT3 receptors but not by 5-HT2A receptors. These changes were associated to a marked reduction of serotonin and kynurenine tissue levels. These results further highlight the role of the TLR4 receptor in the modulation of neuroimmuno-mediated processes, involving both the serotonergic system and the enteric microbiota.
In conclusion, our findings underline the key role of TLR4 signaling in ensuring gut homeostasis by finely tuning enteric glioplasticity, inhibitory neuromuscular response, mediated by iNOS-produced NO, and gut motility during pathological conditions, such as in case of low-grade systemic inflammation (e.g. obesity) or high-grade acute inflammation (i.e. IBD).
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Heraghty, Jane Lesley. "Investigations of respiratory muscle function in children with neuromuscular disease using a novel device". Thesis, University of Bristol, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.702155.
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In progressive neuromuscular diseases such as Duchenne muscular dystrophy (DMD), loss of respiratory muscle strength and endurance leads initially to nocturnal hypercapnia and then daytime respiratory failure. Non-invasive ventilation has improved quality of life and survival but requires overnight sleep assessments and there remains uncertainty about the optimal time to initiate non-invasive ventilation. The aim of this project was to develop a method to identify patients at high risk of nocturnal hypoventilation in a clinic-based setting. The main work was modifying and testing measurements made with a novel device, the respiratory muscle analyser (MicroRMA) that was developed to measure respiratory muscle endurance. The MicroRMA allowed incremental loading of the respiratory muscles after a pre determined number of breaths. The device calculated energy as a product of time, pressure and flow. Protocols were developed in healthy adults, then healthy children to produce a brief and tolerable 6-minute test of respiratory muscle endurance. Several protocols were tested and the outputs of the device compared. The main hypothesis was that children at high risk of nocturnal hypoventilation would be more likely to fail to complete a standardised test protocol or would adapt their respiration to use less cumulative energy to accomplish test completion. Children with neuromuscular weakness had a lower completion rate on some protocols but test failure was not associated with other markers of disease severity, including lower forced vital capacity or nocturnal hypercapnia. Similarly, in children completing the test protocol, no relationship between MicroRMA outputs and disease severity was detected. In addition, handgrip strength was also evaluated in DMD but lower strength was not related to worse nocturnal gas exchange. Finally, overnight oximetry was compared with oxicapnography but, using recommended threshold criteria, only identified half of the children with nocturnal hypercapnia. In conclusion, none of the tests evaluated were able to predict which children with neuromuscular weakness had nocturnal hypercapnia.
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Panchumarthi, Sarvari. "The Drosophila Serrate is Required for Synaptic Structure and Function at Larval Neuromuscular Junctions". Diss., The University of Arizona, 2010. http://hdl.handle.net/10150/194269.
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Drosophila melanogaster is an excellent model system to identify genes involved in synaptic growth and function. In Drosophila, the Serrate (Ser) gene encodes a transmembrane protein that is a ligand for Notch receptor. Several previous studies implicated a role for Serrate in normal wing development and patterning. In this study, I demonstrate that Serrate is required for normal synaptic growth and function. I characterized the phenotype of a Serrate mutation (serB936) that was identified by an EMS-induced genetic screen aimed at identifying novel genes that play a role in synaptic growth and function. Co-localization studies show that Serrate protein is expressed at both the pre- and postsynaptic side of larval neuromuscular junctions (NMJs). Mutations in ser impair synaptic transmission at larval NMJs. This defect is entirely presynaptic, as nerve-evoked excitatory junction potentials (EJP) and quantal content (QC) of neurotransmitter release are significantly reduced when compared to wild-type control. Further, mutations in ser also alter the growth of the NMJ and the underlying muscle. Mutations in ser significantly reduce the size of larval body wall muscles (length and surface area) as well as the number and size of synaptic boutons, and the number of secondary axonal branches. Ubiquitous or muscle-specific expression of normal Serrate in serB936 mutants restores a normal muscle size but not a normal size and structure of the innervating NMJ. However, expression of normal Serrate in the motor axon restores a normal number of synaptic boutons and secondary branches at serB936 mutant NMJs. In addition, it restores normal neurotransmitter release. These data suggest that Serrate protein is required presynaptically for normal synaptic growth and function. Interestingly, overexpression of Serrate in a wild type background resulted in similar phenotypes than to those of loss-of-function mutants. In conclusion, these data suggest a new functional role for Serrate in synaptic growth and function.
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Uzel, Sébastien G. M. "Microfluidic and optogenetic technologies to model spinal cord development and neuromuscular junction formation and function". Thesis, Massachusetts Institute of Technology, 2015. http://hdl.handle.net/1721.1/103850.
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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Mechanical Engineering, 2015."June 2015." Cataloged from PDF version of thesis.
Includes bibliographical references (pages 106-118).
Motor neurons located in the spinal cord and innervating muscle cells throughout the body are responsible for virtually all motor functions, from locomotion to respiration or speech. They arise from differentiation of progenitor cells within the neural tube under spatiotemporally well-defined morphogen concentration profiles, and extend axons into the peripheral nervous system following a precisely orchestrated sequence of events involving secreted chemo-attractants and repellents and dynamic expression of the corresponding ligand receptors. Finally, they form neuromuscular junctions, the synapses that transmit electrical signals to the muscle effectors. Failure for these motor neurons to develop or function properly, caused by developmental or neurodegenerative genetic disorders, or as a result of traumatic injuries, lead to highly incapacitating or even lethal malformation and conditions. Microfabricated platforms and optogenetic technologies have proven to be valuable tools to control the microenvironment, biochemical cues and the stimulation applied to neuronal tissues. Precise control of the geometry of microfluidic devices together with their ability to host 3D cell culture has enhanced the physiological relevance of such neuronal tissues relative to traditional 2D culture assays. And the ability to selectively excite neuronal cells with light has opened tremendous opportunities in the field of neuroscience. In this thesis, we combine these two technologies to stimulate and subject cells to chemical and physical microenvironments that emulate their in vivo counterpart. First, we present a microfluidic platform that generates orthogonal concentration gradients and emulates the confined appearance of motor neurons within the developing spinal cord. Then, we introduce a new device capable of forming a 3D compartmentalized neuron-muscle coculture and demonstrate remote stimulation of the myofibers by the motor neurons resulting in muscle contraction. By targeting the stem cells from which the motor neurons are derived with the light sensitive ion channel Channelrhodopsin, we form, in this microfluidic device, the first in vitro light-activatable neuromuscular junction. Keywords: microfluidics, optogenetics, morphogenesis, cell migration, neuromuscular junctions.
by Sébastien G. M. Uzel.
Ph. D.
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Walker, John W. "Use of Nordic Hamstring Exercise to Improve Hamstrings Function in Patients after ACL Reconstruction". University of Toledo / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1556811041471286.
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Sujkowski, Alyson L. "GABAA Receptor Homeostasis at the C. elegans Neuromuscular Junction". University of Toledo / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1278964838.
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Mork, Mikie Tanya Michelle. "The effects of a specific exercise intervention on Delayed Onset Muscle Soreness, DOMS, and neuromuscular function". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ62802.pdf.
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Clark, Brian C. "Adaptations in human neuromuscular function following prolonged unweighting Neurological and skeletal muscle properties and countermeasure efficacy /". Related electronic resource: Current Research at SU : database of SU dissertations, recent titles available full text, 2006. http://proquest.umi.com/login?COPT=REJTPTU0NWQmSU5UPTAmVkVSPTI=&clientId=3739.
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Jonsson, Malin. "Nicotinic transmission and drugs in anesthesia : neuromuscular blocking agents and propofol : consequences for carotid body function /". Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-660-3/.
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Talubmook, Chusri. "The influence of elevated glucose levels and the diabetic state on neuromuscular function in the gut". Thesis, University of Hertfordshire, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247307.
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Tavoian, Dallin. "Tools and Technologies for Assessing, and Exercise Strategies for Promoting, Neuromuscular Function and Mobility in Aging". Ohio University / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1615816378173099.
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Takeno, Katsumi. "Neuromuscular Function of the Shoulder Girdle and Upper Extremity Muscles in Individuals with Glenohumeral Labral Repair". University of Toledo / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1596111099423871.
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Copley, LaRae Meschelle. "Investigation of the function of myotubularin through the examination of protein-protein interactions and exclusion of MTMR1 as a frequent cause of X-linked myotubular myopathy". Connect to this title online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1080146560.
Pełny tekst źródłaStreszczenie:
Thesis (Ph. D.)--Ohio State University, 2004.Title from first page of PDF file. Document formatted into pages; contains xix, 156 p.; also includes graphics (some col.). Includes bibliographical references (p. 144-153).
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Overton, Amanda Julie. "Neuromuscular Fatigue and Biomechanical Alterations during High-Intensity, Constant-Load Cycling". Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2013. https://ro.ecu.edu.au/theses/612.
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Neuromuscular fatigue is an inevitable process at play during prolonged exercise, and may be caused by multiple alterations within the central nervous system and peripheral musculature. As fatigue develops, the neuromuscular system must adapt to these changes by making compensatory movement pattern adjustments so as to use motor pathways that are less fatigued in an effort to maintain task performance; motor variability is thus increased. The primary purpose of the four studies contained within this doctoral thesis was to detail the progression of exercise-induced neuromuscular fatigue, and to improve our understanding of the muscle activation and joint kinematic alterations that occur as fatigue accumulates. Within this context, cycling was used as the exercise model, and the relationship between physiological and biomechanical aspects of high-intensity, moderate duration (<10 >min) cycling were specifically examined. The first two studies of this thesis were aimed at understanding the progression of neuromuscular fatigue as well as the associated motor control and biomechanical (i.e. muscle activation and kinematic) changes that occur during exhaustive cycling. Specifically, the time course and relative contributions of central and peripheral fatigue mechanisms, and the associated changes in muscle activation and both lower (i.e. hip, knee and ankle joint) and upper (i.e. trunk) limb kinematics were examined during a high-intensity cycling time to exhaustion (TTE) test. This was performed at 90% maximal aerobic power (Pmax) with nine well-trained cyclists. Temporal relationships between joint kinematics and changes in markers of central and peripheral fatigue were also examined. Peripheral fatigue (i.e. impaired contractile function: reduced peak twitch torque, −39.9%; twitch contraction time, −10.7%; and the average rates of twitch torque development −34.7% and relaxation −36.7% at task failure i.e., T100) developed early in the exercise bout from 60% of the time to task failure (p < 0.05). However, a central facilitation, measured as an increase in peak vastus medialis (38.9%) and gluteus maximus electromyogram (87.2%) amplitudes at T100, rather than central fatigue, occurred towards the end of the exercise task (p < 0.05). Thus, neuromuscular fatigue development was associated with an increase in the magnitude of lower limb muscle activity, which may have represented an attempt to increase muscle force to maintain the required power output of the cycling task. Increases in trunk flexion were observed from 60% of the time to task failure (p < 0.05), and were therefore notable at or after the point of significant peripheral fatigue. Conversely, increases in trunk medio-lateral sway (lateral flexion), hip abduction/adduction and knee valgus/varus were observed only from 80% of the time to task failure (p < 0.05), which paralleled the increase in central motor drive. The results of this study therefore indicate that significant trunk kinematic changes in the sagittal plane occurred at or after the point of significant peripheral fatigue development, whereas, significant changes at the trunk, hip and knee joints in the coronal plane occurred later in the exercise task and paralleled the facilitation of central motor drive during the cycling task. In the third study, the effects of real-time, kinematic feedback provision for trunk flexion (TTETflex), trunk medio-lateral sway (TTETsway) and hip abduction/adduction (TTEHabd/add) during a high-intensity TTE cycling test (90% Pmax) in nine well-trained cyclists were examined. The times taken to reach task failure were compared to a TTE test completed with no feedback. The times taken to reach task failure were not significantly different when provided with trunk flexion (TTETflex) and hip abduction/adduction (TTEHabd/add) feedback compared to the non-feedback condition (p > 0.05). There was, however, a significant decrease in the time to task failure during the TTETsway test (p < 0.05). Not all participants could maintain trunk and/or hip movement within a set movement pattern criteria; and three participants were therefore excluded from the kinematic analyses for both the TTETflex and TTETsway tests (n = 6) as were two participants from the TTEHabd/add test (n = 7). For participants who correctly used the kinematic feedback, no differences in the times taken to reach failure were observed in between the feedback (TTETflex, TTETsway and TTEHabd/add) and nonfeedback test conditions (p > 0.05). Despite being given feedback, changes in joint kinematics were similar across all test conditions; significant alterations were observed at the trunk and knee joints in the sagittal plane and at the hip and knee joints in the coronal plane (p < 0.05). Given trunk flexion feedback (TTETflex), significant increases in left hip flexion and trunk medio-lateral sway ROM were observed (p < 0.05), whereas given trunk medio-lateral sway feedback (TTETsway), increases in right hip flexion ROM also occurred (p < 0.05). These results indicate that, regardless of whether or not well-trained cyclists are able to control the level of kinematic variability when fatigued, acute exposure to real-time kinematic feedback to limit trunk or hip movement during high-intensity cycling may influence cycling kinematics (i.e. technique) and, in some cases (e.g. trunk medio-lateral sway), may reduce performance. The final study examined the relationship between joint kinematics, measured in non-fatigued and fatigued high-intensity cycling, and the cyclists’ physiological profiles (i.e., physiological attributes indicative of successful cycling ability, including both maximal oxygen consumption and peak power output relative to body mass, maximal heart rate, both power output and heart rate at the first and second ventilatory thresholds and cycling economy at 100 W) and the time taken to reach task failure. Submaximal physiological attributes were correlated with hip (abduction/adduction angle and ROM), knee (flexion angle) and ankle (flexion ROM) kinematics measured in a non-fatigued state at the start of the trial (r > 0.40; p < 0.05). However, both physiological attributes associated with maximal exercise capacity and cycling economy were correlated with trunk (flexion angle) and ankle (flexion angle and ROM) kinematics measured in a fatigued state at the end of the test (r > 0.40; p < 0.05). Trunk flexion and medio-lateral sway ROM in a non-fatigued state, and trunk flexion angle in a fatigued state, were associated with the time to task failure (r > 0.50; p < 0.05). Thus, the degree of trunk flexion and medio-lateral sway may be important kinematic variables that are indicative of cycling performance. These findings reveal an interdependence between cycling kinematics and both the physiological attributes indicative of successful cycling performance and the time taken to reach task failure during high-intensity, constant-load cycling. In conclusion, the findings presented in this thesis indicate that the temporal patterns of central and peripheral neuromuscular fatigue differ (Study 1; Chapter 3). Task failure during high intensity cycling appears to be associated with the development of peripheral fatigue despite the presence of an increase in central motor drive. Subsequent to the development of neuromuscular fatigue, muscle activation and joint kinematic alterations can be observed, which may represent compensatory mechanisms employed by the neuromuscular system to continue task performance (Studies 1 and 2; Chapters 3 and 4). Joint kinematic alterations in the sagittal plane were associated with the development of peripheral fatigue whereas coronal plane adjustments occurred in parallel with central facilitation, and/or when a more substantial level of peripheral fatigue accumulated. Such compensatory kinematic strategies are also associated with an athlete’s physiological attributes and their cycling performance (i.e., time to task failure) (Study 4; Chapter 6). Importantly, imposing specific joint kinematic restrictions (trunk flexion, trunk medio-lateral sway and hip abduction/adduction) during exhaustive cycling, influenced cycling kinematics (i.e. technique) and, in some cases (e.g. trunk medio-lateral sway), reduced the time taken to reach task failure for well-trained cyclists (Study 3; Chapter 5). Such findings enhance our understanding of how the neuromuscular system copes with fatigue development, and should assist coaches and/or occupational health practitioners to better understand the fatigue process and neuromuscular strategies utilised during exercise tasks with similar characteristics to that used in the current studies.
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Criss, Cody R. "Central Nervous System Contributions to Subjective and Objective Measures of Function after Anterior Cruciate Ligament Reconstruction". Ohio University / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1617279837916864.
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Fathi, Behrooz H. "The effect of snake venom phospholipase A2 on cloned voltage-gated potassium channels and on neuromuscular function". Thesis, University of Strathclyde, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248762.
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Buhl, Lauren Kaye. "Synaptic structure and function at the Drosophila larval neuromuscular junction : a molecular analysis of complexin and radish". Thesis, Massachusetts Institute of Technology, 2011. http://hdl.handle.net/1721.1/65285.
Pełny tekst źródłaStreszczenie:
Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Brain and Cognitive Sciences, 2011.Cataloged from PDF version of thesis.
Includes bibliographical references.
From yeast to humans, the fusion of vesicles with target membranes is driven by the formation of a parallel four-helix bundle of SNARE proteins that are present on both the vesicular (v-SNAREs) and target plasma membranes (t-SNAREs). The full zippering of this bundle is thought to provide the driving force for membrane fusion. At synapses, vesicle fusion is exquisitely regulated by Ca2+ such that neurotransmitter release can occur within 1 ms of an action potential reaching the presynaptic terminal. This feat implies the presence of both a Ca2+ sensor and a fusion clamp that prevents vesicles from fusing in the absence of Ca2+. The presynaptic Ca2+ sensor for synchronous vesicle release is widely accepted to be Synaptotagmin-1 (Syt1), and there is growing evidence that Complexin (Cpx), which binds to the SNARE complex with high affinity and 1:1 stoichiometry, can act as a vesicle fusion clamp. As suggested by its name, however, Cpx appears to play a more complex role in vesicle release, carrying out different functions in spontaneous vs. evoked fusion events. Here we show the Drosophila express at least two Cpx isoforms that differ in the C-terminus (Cpx7A and Cpx7B) and can be further regulated by RNA editing and phosphorylation. These isoforms show different effects on spontaneous vs. evoked neurotransmitter release, with Cpx7A being a better fusion clamp and Cpx7B being a better fusion promoter. In addition, these isoforms have different effects on synaptic growth, which may be linked to their effects on synaptic physiology.
by Lauren Kaye Buhl.
Ph.D.
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Breuer, Marlen [Verfasser], i Annette [Akademischer Betreuer] Brochers. "The analysis of Cav1α function in Xenopus motoneuron outgrowth and neuromuscular integrity / Marlen Breuer ; Betreuer: Annette Brochers". Marburg : Philipps-Universität Marburg, 2021. http://d-nb.info/1227580274/34.
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Hannah, Ricci. "The influence of sex-differences and exercise on knee joint neuromuscular function: implications for dynamic joint stabilisation". Thesis, Nottingham Trent University, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.657623.
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Henaghan, Sharon M. "The effects of moderate sleep loss on sleepiness levels and neuromuscular function in healthy males a thesis submitted to Auckland University of Technology in partial fulfillment of the degree of Master of Health Science, April 2004". Full thesis. Abstract, 2004. http://puka2.aut.ac.nz/ait/theses/HenaghanS.pdf.
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Rohadhia, Wafina. "Cardio-metabolic and neuromuscular adaptations following whole-body eccentric resistance training in older adults". Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2019. https://ro.ecu.edu.au/theses/2203.
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Regular exercise is key to minimise the negative effects of aging on health; however, it is reported that 65% of older Australians are categorised as physically inactive. Recent studies reported that eccentric resistance training (ECC-RT) is an effective modality to produce cardio-metabolic and neuromuscular benefits for older adults. The present study tested the hypothesis that ECC-RT of several major muscle groups would produce positive changes in cardio-metabolic and neuromuscular parameters in older adults with metabolic syndrome.
Six men and 11 women aged between 60 and 80 (70.0 ± 5.0) years old with dyslipidaemia and BMI >25 kg/m2 participated in this study. It is important to note that no control group nor control period applied before the participants commenced their training. All participants performed a whole-body ECC-RT program consisting of eight exercises (i.e. chest press, lateral pulldown, leg extension, leg curl, biceps curl, triceps extension, calf raises and abdominal crunch). The training sessions were performed twice a week for 8-weeks (16 sessions in total), with progressively increasing intensity from 10-100% of the individual’s one repetition maximum (1RM) for each exercise. Physical function (400-m walk, 30-s repeated chair rise, timed up-and-go), 1RM strength for all exercises, blood lipid profiles (total cholesterol, LDL, HDL, triglyceride), and glycaemic control parameters (fasting glucose, insulin, fructosamine, HOMA-IR index) were measured at baseline, mid-point (after 8 training sessions), and post-training (1-2 days after the last training session). Sensory organisation (SOT), body composition and isometric (MVIC) and isokinetic concentric (MVCC) maximal voluntary contraction (MVC) strength of the knee and elbow extensors and flexors were measured at baseline and post-training.
1RM strength increased significantly (p<0.05) for all exercises with 34–115% improvements from baseline. Physical function variables such as 400-m walk (12 ± 7%), 30-s repeated chair rise (18 ± 15%), timed up-and-go (13 ± 6%), and sensory organisation test (6 ± 8%) also showed significant improvements from baseline to post-training. However, no significant increases in isometric and isokinetic concentric MVC strength of the knee and elbow extensors and flexors were found. Although some participants showed some changes in body composition variables, no significant changes in percentage of body fat, fat mass and lean body mass were evident as a group. Total cholesterol (TC) (-5 ± 11%) and LDL-cholesterol (-8 ± 13%) decreased significantly after 4-weeks of training, and HDL-cholesterol showed a significant increase after 8-weeks (4 ± 9%), but the magnitude of changes in these variables were not large. Triglyceride (TG), fasting glucose, insulin, HOMA-IR and fructosamine did not show any significant changes over time. These results did not necessarily support the hypothesis, but were in agreement with previous studies that showed improvements in muscle strength and physical functions following ECC-RT. Interestingly, the magnitude of the changes in 1RM strength (leg extension, leg curl, triceps extension, biceps curl) did not necessarily correlate with those of MVIC and MVCC assessed by the isokinetic dynamometer for the same muscle groups (i.e. the increases in 1RM strength were much greater than that of MVIC and MVCC). Although the TC, LDL and HDL-cholesterol showed some improvements, the magnitude of the changes was not large. TG and other glycaemic control parameters did not show significant changes, although previous studies reported greater changes after ECC-RT of the knee extensors or descending stair walking training. It is interesting that the amount of muscles trained in the present study appear to be much greater than that of previous studies, but the training effects found in the present study were less. It may be that 16 sessions of whole-body ECC-RT over 8-weeks were not enough to induce large changes in some of the parameters. Thus, future studies need to examine whether ECC-RT with varying frequency, volume, intensity and duration could produce more positive changes in body composition and blood markers in older adults.
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Dwyer, Daniel, i na. "Serotonin as a Mediator of Fatigue During Exercise and Training". Griffith University. School of Health Science, 2004. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20040521.130535.
Pełny tekst źródłaStreszczenie:
Exercise has been shown to cause an increase in the concentration of brain serotonin (5-hydroxytryptamine, 5-HT) in humans and experimental animals. The increase in brain serotonin coincides with the onset of fatigue and is referred to as "central fatigue". Experiments in humans and animals involving serotonin receptor agonists have demonstrated reductions in exercise performance by simulating the exercise-induced increase in endogenous serotonin. Conversely, the administration of serotonin receptor antagonists has been shown to extend exercise performance in experimental animals, but not in humans. Although the relationship between the concentration of brain serotonin and exercise performance is well described in the literature, the precise effect of central fatigue on muscle function per se is unclear. Furthermore, there appear to be differences in serotonergic function between trained and untrained cohorts. However, it is not clear whether the differences are due to a training adaptation or if the differences are inherent in the individual. In addition, the time course of these adaptations and the mechanisms of adaptation are not known. The initial purpose of this thesis was to determine whether six weeks of endurance exercise training had any effect on central serotonin receptor sensitivity in Wistar rats. The rats ran on a treadmill 4 times per week with 2 exercise tests of endurance performance per week. Receptor sensitivity was determined indirectly, at the end of each training week, by the reduction in endurance performance, under the influence of a 5-HT1a agonist, (m-Chlorophenylpiperazine, m-CPP). Improved tolerance to the fatiguing effects of the serotonin agonist would suggest desensitisation of central serotonin receptors, probably 5-HT1a receptors. Two groups of controls were used to examine, i) the effect of the injection per se on exercise performance and ii) changes in serotonin receptor sensitivity associated with maturation, in the absence of any exercise training. In the training group, undrugged exercise performance significantly improved by 47% after 6 weeks of training (mean ± SEM, 4518 ± 729 s vs. 6640 ± 903 s, p=0.01). Drugged exercise performance also increased significantly from week 1 to week 6 (306 ± 69 s to 712 ± 192 s, p=0.004). Control group results indicated that the dose of m-CPP alone caused fatigue during exercise tests and that maturation was not responsible for any decrease in receptor sensitivity. Endurance training appears to stimulate an adaptive response to the fatiguing effects of increased brain serotonin, which may enhance endurance exercise performance. The purpose of the second set of experiments described in this thesis was to investigate changes in serotonin receptor sensitivity in response to exercise training in human subjects. Twelve male volunteers completed 30 minutes of stationary cycling at 70% of VO2peak, on 3 days per week, for 9 weeks. Serotonin receptor sensitivity was assessed indirectly by measuring the prolactin response to a serotonin receptor agonist (buspirone hydrochloride), using a placebo controlled, blind cross-over design. A sedentary group of control subjects were also recruited to control for possible seasonal variations in serotonin receptor sensitivity. Endurance capacity was also assessed as time to exhaustion while cycling at 60% of VO2peak. The exercise training caused a significant increase in aerobic power (VO2peak, 3.1±0.16 to 3.6±0.15 L.m-1, p< 0.05) and endurance capacity (93±8 to 168±11 min, p<0.05), but there was no change (p>0.05) in the prolactin response to a serotonin agonist. However, 25% of the subjects in the training group demonstrated a decrease in receptor sensitivity, as indicated by a decrease in prolactin response. These results suggest that while the exercise training caused an increase in aerobic power and endurance capacity, there was no measurable change in 5-HT receptor sensitivity. In addition, it is possible that changes in receptor sensitivity may take longer to occur, the training stimulus used in the present investigation was inadequate or that changes occurred in other 5-HT receptor subtypes that were not assessed by the present methodology. The third set of experiments described here, investigated the changes in neuromuscular function under the influence of a serotonin receptor agonist (buspirone hydrochloride). Subjects were administered the agonist or a placebo in a blind cross over design. Measures of neuromuscular function included reaction time (RT), hand eye coordination (HEC), isometric neuromuscular control (INC), maximal voluntary isometric contractile force (MVIC-F), isometric muscular endurance capacity (IMEC) and various electromyographic (EMG) indices of fatigue in biceps brachii. A preliminary experiment was conducted to determine a drug dose that did not cause sedation of the research subjects. The agonist caused a significant (p<0.05) decrease in MVIC-F, INC and IMEC. There was a non significant (p = 0.08) decrease in EMG amplitude during the MVIC-F trial with the agonist, compared to the effect of the placebo. The median EMG frequency during the IMEC test was also significantly less with the agonist, when compared to the placebo effect. There was a decline in RT and HEC, although this was not significant. These findings indicate that a serotonin receptor agonist causes a decrease in neuromuscular function during isometric muscle contractions. The decrements in muscle function reported in this study may help to explain previous reports of an association between increased brain serotonin concentration and a reduction in endurance performance. Although the present study does not exclude the possibility that an increase in brain serotonin does cause fatigue by affecting organs peripheral to the brain, it provides evidence of fatigue within the central nervous system. Further examination of the effect of a serotonin agonist on muscle function during non-isometric muscle contractions is warranted.
50
Dwyer, Dan. "Serotonin as a Mediator of Fatigue During Exercise and Training". Thesis, Griffith University, 2004. http://hdl.handle.net/10072/366705.
Pełny tekst źródłaStreszczenie:
Exercise has been shown to cause an increase in the concentration of brain serotonin (5-hydroxytryptamine, 5-HT) in humans and experimental animals. The increase in brain serotonin coincides with the onset of fatigue and is referred to as "central fatigue". Experiments in humans and animals involving serotonin receptor agonists have demonstrated reductions in exercise performance by simulating the exercise-induced increase in endogenous serotonin. Conversely, the administration of serotonin receptor antagonists has been shown to extend exercise performance in experimental animals, but not in humans. Although the relationship between the concentration of brain serotonin and exercise performance is well described in the literature, the precise effect of central fatigue on muscle function per se is unclear. Furthermore, there appear to be differences in serotonergic function between trained and untrained cohorts. However, it is not clear whether the differences are due to a training adaptation or if the differences are inherent in the individual. In addition, the time course of these adaptations and the mechanisms of adaptation are not known. The initial purpose of this thesis was to determine whether six weeks of endurance exercise training had any effect on central serotonin receptor sensitivity in Wistar rats. The rats ran on a treadmill 4 times per week with 2 exercise tests of endurance performance per week. Receptor sensitivity was determined indirectly, at the end of each training week, by the reduction in endurance performance, under the influence of a 5-HT1a agonist, (m-Chlorophenylpiperazine, m-CPP). Improved tolerance to the fatiguing effects of the serotonin agonist would suggest desensitisation of central serotonin receptors, probably 5-HT1a receptors. Two groups of controls were used to examine, i) the effect of the injection per se on exercise performance and ii) changes in serotonin receptor sensitivity associated with maturation, in the absence of any exercise training. In the training group, undrugged exercise performance significantly improved by 47% after 6 weeks of training (mean ± SEM, 4518 ± 729 s vs. 6640 ± 903 s, p=0.01). Drugged exercise performance also increased significantly from week 1 to week 6 (306 ± 69 s to 712 ± 192 s, p=0.004). Control group results indicated that the dose of m-CPP alone caused fatigue during exercise tests and that maturation was not responsible for any decrease in receptor sensitivity. Endurance training appears to stimulate an adaptive response to the fatiguing effects of increased brain serotonin, which may enhance endurance exercise performance. The purpose of the second set of experiments described in this thesis was to investigate changes in serotonin receptor sensitivity in response to exercise training in human subjects. Twelve male volunteers completed 30 minutes of stationary cycling at 70% of VO2peak, on 3 days per week, for 9 weeks. Serotonin receptor sensitivity was assessed indirectly by measuring the prolactin response to a serotonin receptor agonist (buspirone hydrochloride), using a placebo controlled, blind cross-over design. A sedentary group of control subjects were also recruited to control for possible seasonal variations in serotonin receptor sensitivity. Endurance capacity was also assessed as time to exhaustion while cycling at 60% of VO2peak. The exercise training caused a significant increase in aerobic power (VO2peak, 3.1±0.16 to 3.6±0.15 L.m-1, p< 0.05) and endurance capacity (93±8 to 168±11 min, p<0.05), but there was no change (p>0.05) in the prolactin response to a serotonin agonist. However, 25% of the subjects in the training group demonstrated a decrease in receptor sensitivity, as indicated by a decrease in prolactin response. These results suggest that while the exercise training caused an increase in aerobic power and endurance capacity, there was no measurable change in 5-HT receptor sensitivity. In addition, it is possible that changes in receptor sensitivity may take longer to occur, the training stimulus used in the present investigation was inadequate or that changes occurred in other 5-HT receptor subtypes that were not assessed by the present methodology. The third set of experiments described here, investigated the changes in neuromuscular function under the influence of a serotonin receptor agonist (buspirone hydrochloride). Subjects were administered the agonist or a placebo in a blind cross over design. Measures of neuromuscular function included reaction time (RT), hand eye coordination (HEC), isometric neuromuscular control (INC), maximal voluntary isometric contractile force (MVIC-F), isometric muscular endurance capacity (IMEC) and various electromyographic (EMG) indices of fatigue in biceps brachii. A preliminary experiment was conducted to determine a drug dose that did not cause sedation of the research subjects. The agonist caused a significant (p<0.05) decrease in MVIC-F, INC and IMEC. There was a non significant (p = 0.08) decrease in EMG amplitude during the MVIC-F trial with the agonist, compared to the effect of the placebo. The median EMG frequency during the IMEC test was also significantly less with the agonist, when compared to the placebo effect. There was a decline in RT and HEC, although this was not significant. These findings indicate that a serotonin receptor agonist causes a decrease in neuromuscular function during isometric muscle contractions. The decrements in muscle function reported in this study may help to explain previous reports of an association between increased brain serotonin concentration and a reduction in endurance performance. Although the present study does not exclude the possibility that an increase in brain serotonin does cause fatigue by affecting organs peripheral to the brain, it provides evidence of fatigue within the central nervous system. Further examination of the effect of a serotonin agonist on muscle function during non-isometric muscle contractions is warranted.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Health Sciences
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