Dissertations / Theses: 'Muscular science'

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Björkman, Pontus. "A Muscular Rig for Smooth Skinning in Autodesk Maya." Thesis, University of Gävle, Department of Mathematics, Natural and Computer Sciences, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:hig:diva-147.

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The limitations of the default skinning methods in Autodesk Maya can be compensated for when seeking realistic skin deformations of a human being. The main focus is put on the construction of an example muscular rig in Autodesk Maya, and an explanation of what criteria the rig is supposed to fulfill. From a merged three dimensional and artistic view, the components of the rig is discussed and evaluated to establish an understanding of how the system needs to work in order to produce realistic skin deformations. The research is performed via design and creation experiments on the various parts of the system, and even though the initial theory has met its demands, some of the practical performance yet abandons a lot to wish.

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Paulsson, Agne. "Entities of muscular type : hur kroppen ger mening åt abstrakta begrepp." Thesis, Högskolan Kristianstad, Sektionen för lärande och miljö, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:hkr:diva-12159.

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Kognitivismen med rötter i analytisk filosofi och logik beskriver tänkande som symbolmanipulation efter logiska regler. Begrepp har sin mening genom att de refererar till objekt och händelser i världen. Embodied cognition (EC) eller kroppsbasserad kognition, med rötter i biologi, fenomenologi och pragmatism ser istället tänkande som ett emergent fenomen som uppstår ur erfarandet av kroppens aktivitet i världen. Begrepps mening har istället sin grund i det sensomotoriska systemet. Abstrakta begrepp får sin mening via metaforer och metonymer. Likt konstruktivism ser EC lärande som modifiering av tidigare kunskap. Den skiljer sig dock från konstruktivism i avseende på dualism, hur kunskap finns organiserad och var begreppens mening finns. EC:s inflytande på didaktisk forskning inom naturvetenskap och matematik undersöktes genom sökning av artiklar där orden EC eller enactivism finns med. Resultatet visade ett klart större genomslag för EC inom matematikdidaktik med fler artiklar där teorin beskrivs utförligare. Inom naturvetenskapens didaktik har EC uppmärksammats i mycket mindre grad. Orsakerna till detta diskuteras.

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Forbes, Hollie Samantha. "Isokinetic muscular strength and performance in youth football : relationships with age, seasonal variation and injury." Thesis, University of Hull, 2012. http://hydra.hull.ac.uk/resources/hull:6863.

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The primary aim of the current project was to investigate the isokinetic muscular strength and performance of elite male youth footballers, and the relationships with age, seasonal variation and injury. A secondary aim was to use the information gathered to target muscle strain injury prevention strategies to particular age groups and times, and evaluate the effect. The primary aim was achieved by establishing normative patterns for muscular strength and performance of elite male youth footballers (grouped according to chronological and biological age) across a competitive season of youth football in Chapters Four and Five. Isokinetic muscular strength (characterised by peak torque (PT) and peak torque relative to body weight (PTBW)) of the hamstrings (H) and quadriceps (Q) using both concentric (CQ, CH) and eccentric muscle actions (EH) was evaluated. Muscular performance of the same muscle groups (characterised by H:Q ratios (conventional (CHQ) functional (FHQ)), asymmetry (dominant (dom):non dominant (ndom) leg ratios (e.g. CQ:CQ)), and angle of peak torque (AoPT)) was also investigated which necessitated an isokinetic speed of 60 °/s. Isokinetic evaluation was completed three times over the course of a regular playing season (start of season (SS) mid season (MS) and end of season (ES)). Participants were grouped according to chronological age (n=152, under 12 (U12) - under 18 (U18)) and biological maturation (according to Pubertal Development Scale (PDS 1 - 5) n=134). Forty seven participants completed SS, MS and ES isokinetic evaluation. Bilateral isokinetic evaluation consisted of five maximal repetitions of CQ and CH, followed by five repetitions of EH, leg dominance was counter-balanced. Repetitions two-four were used to calculate PT, PTBW, dom:ndom and AoPT for CQ, CH and EH, CHQ and FHQ; these measures were compared across chronological and biological age groups using a mixed model ANOVA. Dom:ndom CQ, CH and EH were compared across chronological and biological age groups using a one way ANOVA, while the relationship between AoPT and PT/PTBW was considered using a Pearson’s correlation. Additionally, the relationship between chronological and biological age, and PT/PTBW was investigated using a mixed model ANOVA within PDS group three. For analysis of seasonal variation a mixed model ANOVA was applied for all isokinetic measurements which considered time (SS, MS, ES), leg dominance (dom, ndom) and age group (U12 -U15) with a further mixed model ANOVA performed on CQ:CQ, CH:CH and EH:EH. Where appropriate SIDAK corrections were applied and the level of significance was accepted at p≤0.05. The main findings were that youth footballers did not increase their PT and PTBW EH in-line with CQ and CH as chronological and biological ageing progressed, this lead to a significant FHQ imbalance at U18. Dom:ndom CH comparisons identified that the chronologically younger and biologically less developed groups displayed a significantly stronger dom leg which may be explained through the concepts of skill acquisition and trainability. Biological age was not found to exert any additional effect over and above that of chronological ageing as significant differences in muscle strength still existed according to chronological age group within PDS group three. Additionally, AoPT EH and PT EH were found to be significantly negatively correlated on both legs which supported a potential mechanism for non contact hamstring muscle strain injury during running. Analysis of seasonal variation revealed that all PTBW measures showed a MS decrease. This may be related to breaks in normal training activity and links appropriately to times of peak injury incidence highlighted in youth football. In order to achieve the secondary aim of the current project Chapters Four, Five and Six investigated the relationship between isokinetic muscular strength and performance, muscle strain injury of the thigh, and injury risk attenuation. A retrospective and prospective injury audit was undertaken for the elite male youth football participants. For the retrospective approach participants were grouped according to chronological age (n=147) or biological age (n=128) and indicated using a self-report injury form their history (ever, (Hx)) or recent history (12 months, (Hx12)) of hamstring, quadriceps and adductor injuries. Approximately each player had an Hx of muscle strain injury and 0.56-0.59 of players had an Hx12. The hamstrings were the most commonly injured muscle group and the prevalence of muscle strain injury Hx and Hx12 increased with chronological and biological age. The prospective audit (n=50) identified that 0.16 of players sustained a muscle strain injury during the season, 0.08 of these being to the hamstrings. Between group comparisons (one way ANOVA with SIDAK correction) were also performed to investigate the difference in isokinetic measures between those participants who had an Hx12 of muscle strain injury and those who did not. It was discovered that for Hx12 of an injury to the dom hamstrings the injured group had less PTBW CH and EH on the dom leg. The injured group also had more inner range AoPT CH. These findings linked appropriately to the reported mechanisms and risk factors for hamstring injury but the exact direction of cause and effect could not be established. To this end a logistic regression analysis was undertaken in an attempt to predict which group (injured vs. non injured the 50 participants would belong to, using evidenced based risk factors in the experimental model. No predictive relationship between risk factors (including altered isokinetic muscular strength and performance) could be established. The information regarding the relationship between injury and muscular strength and performance may highlight a role for isokinetic screening to ensure adequate rehabilitation from injury. Injury risk attenuation strategies were investigated through an exercise intervention using the U18 age group following a break from football activity. The participants were split based on their FHQ at initial isokinetic evaluation (via odd and even placing) to form control (n=8) and intervention groups (n=8). Isokinetic evaluation was conducted as previously outlined and the exercise intervention targeted the hamstrings. Only six of the control group and seven of the intervention group completed the study and were compared using a mixed model ANOVA. Results showed that the intervention group were not significantly different to the control group post intervention for any of the isokinetic muscular strength and performance measures, though both groups significantly improved over time for the ndom leg CHQ and PTBW EH, and FHQ improved for both legs. Contamination of the control group may explain the lack of significant difference between groups. However, the exercise intervention was not targeted to individuals who displayed prior alterations to isokinetic muscular strength and performance, and this approach was discussed using the results of one member of the intervention group. In summary, the current project achieved the stated aims by discovering normative patterns of isokinetic muscular strength and performance according to age and seasonal variation. Injury risk attenuation strategies were targeted appropriately to the U18 age group following a break from football activity. However, the applied evidence based exercise may have been more effective if targeted to ‘risk’ after isokinetic screening.

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Boyer, William Robert II. "The Associations Between HOMA-IR and Muscular Strengthening Activity in Euglycemic U.S. Adults." UNF Digital Commons, 2014. http://digitalcommons.unf.edu/etd/512.

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Background: Muscular strengthening activity (MSA) has been shown to be inversely associated with insulin resistance (IR). The associations between quartiles of the homeostatic model assessment of insulin resistance (HOMA-IR) and self-reported MSA in a nationally representative sample of euglycemic U.S. adults were examined. Methods: Sample included adult participants (≥20 years of age [n=2,543]) from the 1999-2004 National Health and Nutrition Examination Survey (NHANES). HOMA-IR was categorized into quartiles based on every 25th percentile. No MSA was the dependent variable. Results: Following adjustment for covariates, those with HOMA-IR values in third (p Conclusions: Having a higher HOMA-IR value is associated with greater odds of reporting no MSA in euglycemic U.S. adults.

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Riding, Teri. "Contributions of Muscle Fatigue to a Neuromuscular Neck Injury in Female Standard Ballroom Dancers." BYU ScholarsArchive, 2006. https://scholarsarchive.byu.edu/etd/755.

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Objective: To investigate the potential etiology of a loss of neck control injury in female standard ballroom dancers. The median frequency (MF) as measured by electromyography (EMG) of the left upper trapezius (UT), left splenius capitius (SPL), and right sternocleidomastoid (SCM) of injured dancers was compared to non-injured dancers. This comparison was performed to identify whether dancers with a history of loss of neck control have a greater amount of fatigue than those with no history of this particular injury. Design and Setting: A 2 x 6 factorial design was used for this investigation. The independent variables were group (injured vs. non-injured) and time (before and after the three rounds of dancing). The dependent variables were MF as measured by EMG, range of motion, and neck length. All testing was performed at the university biomechanics laboratory and ballroom dance studio. Subjects: Twenty female subjects (10 injured group {mean height 167.40 ± 4.12 cm and weight 59.30 ± 5.41 kg}, 10 non-injured group {mean height 166.76 ± 4.62 cm and weight 58.93 ± 5.30 kg}), with at least one year experience in competitive ballroom dancing, in the standard division participated in this study. All subjects competed at a Dancesport competition either in the novice, pre-championship, and/or amateur standard classifications. Inclusion criteria for the injured group included female ballroom dancers who had a loss of neck control episode. Measurements: Surface EMG activity was recorded from the left UT, left SPL, and right SCM muscles before and after dancing the five standard dances. Results: The decrease in EMG MF was not significant between groups. There was no difference in neck lengths from the external occipital protuberance to inferior angle of the scapula between groups. There were also no significant differences in range of motion of left and right lateral flexion and extension in either group from pre to post dancing. Conclusions: Based on the results of this study, subjects with a history of neuromuscular neck injury did not appear to have acute fatigue of the three muscles studied here following the routine used in this study.

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Woodland, Scott T. "The Effect of Anterior Knee Pain on Serum Cartilage Oligomeric Matrix Protein and Muscular Cocontraction During Running." BYU ScholarsArchive, 2013. https://scholarsarchive.byu.edu/etd/4042.

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Knee pain can alter lower-extremity neuromechanics and often results in functional disability. The relationship between lower-extremity neuromechanical alterations, due to anterior knee pain, and articular cartilage condition is unclear. The purpose of this study was to determine the independent effect of anterior knee pain during running on articular cartilage condition, as reflected by serum cartilage oligomeric matrix protein concentrations and muscle cocontraction duration. Seven men and five women completed a 30-min run in three different sessions: control (no infusion), sham (isotonic saline infusion), and pain (hypertonic saline infusion). Saline was infused into the right infrapatellar fat pad for the duration of the run. Subject-perceived pain was recorded every 3 min on a 100-mm visual analog scale. During the run, bilateral electromyography was recorded for five leg muscles, and heel and toe markers were used to track foot position. During the 30-min run of the pain session average subject-perceived pain was 27.8 (SD = 2.3 mm) and 19.7 (SD = 1.9) mm greater than during the control (0.0 mm) and sham (8.1 mm) session, respectively (p < 0.01). Knee pain while running did not result in changes in muscular cocontraction duration (p = 0.13). Blood samples were drawn prior to the run, immediately following the run, and 60 min following the run. Samples were analyzed using enzyme-linked immunosortbent assay to determine serum cartilage oligomeric matrix protein concentration. Average serum cartilage oligomeric matrix protein concentration was 14% greater at immediate post run (132.19 ± 158.61 ng/ml; Range = 22.61-290.81 ng/ml) relative to pre run (116.02 ± 118.87 ng/ml; Range = 19.81-234.89 ng/ml) (p < 0.01), and 18% less at 60 min post run (108.45 ± 171.78 ng/ml; Range = 20.84-280.23 ng/ml) relative to immediate post run (Figure 4; p < 0.01). Serum cartilage oligomeric matrix protein did not significantly differ between baseline and 60 min post-exercise (p = 0.29). There was not a difference in cartilage oligomeric matrix protein concentration between sessions. Knee pain while running does not cause an increase in serum cartilage oligomeric matrix protein concentration (p = 0.29). There are two important findings from this study. First, anterior knee pain during a 30 min running session does not appear to independently affect cartilage oligomeric matrix protein concentrations. This implies other factors, aside from anterior knee pain alone, influence articular cartilage degradation during movement that occurs while individuals are experiencing anterior knee pain. Second, the present experimental anterior knee pain model can be used to evaluate the independent effects of anterior knee pain over an extended duration while subjects perform a dynamic activity like running.

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Stevenson, Deja Lee. "Whole-Body Vibration and Its Effects on Electromechanical Delay and Vertical Jump Performance." Diss., CLICK HERE for online access, 2005. http://contentdm.lib.byu.edu/ETD/image/etd867.pdf.

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Berbert, Monalise Costa Batista. "Avaliação quantitativa de força de bochechas em humanos." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2013. http://hdl.handle.net/10183/86436.

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Atualmente, a avaliação da tonicidade de bochechas é realizada de forma perceptual e dependente da experiência do avaliador. Por esse motivo, este trabalho propôs uma alternativa para diminuir a subjetividade da forma de avaliação atual da força das bochechas, a qual pode complementar o diagnóstico fonoaudiológico. Desenvolveu-se um protótipo constituído de uma célula de carga acoplada a uma haste, sistema de conversão, amplificação e transmissão do sinal elétrico. Um estudo inicial buscou avaliar a repetitividade e reprodutibilidade de medições realizadas em sujeitos normais e alterados quanto à força das bochechas. Num segundo estudo visou-se quantificar e analisar a performance de indivíduos com força adequada. Os valores de força no sexo masculino, tanto para força média quanto para força máxima, foram estatisticamente maiores do que os valores entre o sexo feminino. Cinco tipos de curva caracterizam o comportamento da bochecha durante o ensaio. O método de avaliação quantitativa da força das bochechas desenvolvido colaborou para a diminuição da subjetividade da avaliação e foi capaz de registrar a força exercida pelas bochechas.
Currently clinical evaluation of cheeks tone is performed at a perceptual level and depends on the evaluator's experience. Therefore, this study aimed to propose an alternative way of reducing the subjectivity in cheeks strength assessments, which can complement the speech therapist diagnosis. We developed a prototype consists of a load cell coupled to a handle, the conversion system, amplification, and the electrical signal transmission. An initial study was toanalyze of repeatability and reproducibility of measurements performed in normal and abnormal individuals regarding cheek strength. In a second study sought to quantify and analyze the performance of subjects with adequate strength. The force values in males, both for strength and for average maximum force were statistically higher than the values among females. Five types of curve characterize the behaviour of the cheek during the test. The method of quantitative assessment of the cheeks strength developed helped to reduce the subjectivity of the evaluation and it was able to record the force exerted by the cheeks.

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Zalcman, Amy. "The Use of Magnetic Resonance Imaging and Proton Spectroscopy to Identify Critical Tissues in Dogs with Duchenne Muscular Dystrophy for Future Assessment of Therapeutic Intervention| A Pilot Study." Thesis, University of Missouri - Columbia, 2019. http://pqdtopen.proquest.com/#viewpdf?dispub=13850759.

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Duchenne’s Muscular Dystrophy is a debilitating disease that affects skeletal and cardiac muscle of 1 in 5000 male births. In the last thirty years, the gene responsible for the encoding of Dystrophin has been identified, sequenced and the variations of mutations described. There remains a void in the successful treatment of the disease although corticosteroid use has proven useful in delaying progression. Novel therapies are produced in the categories of virus-mediated gene delivery and stem cells, but evaluating their efficacy is hindered by an inability to contemporaneously assess the changes in muscle. The purpose of this pilot study was to characterize the changes in skeletal and cardiac muscle in a clinically advanced population of dogs affected with Duchenne Muscular Dystrophy. Using traditional sequences, delayed gadolinium enhancement, novel sequences and spectroscopy, changes in the investigated muscle were characterized. By establishing the differences between affected and unaffected dogs, the long-term goal of this body of work is to characterize these changes longitudinally and design a non-invasive method for tissue assessment as novel treatments are trialed.

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Worcester, Katherine Sara. "EFFECTS OF INERTIAL LOAD ON SAGITTAL PLANE KINEMATICS DURING FLYWHEEL-BASED RESISTANCE TRAINING SQUATS." UKnowledge, 2018. https://uknowledge.uky.edu/khp_etds/57.

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Background: Training to increase muscular power is essential for improving athletic performance in most sports. Weight training (WT) is a common means for training muscular power. Another modality, flywheel resistance training (FRT), may be superior for improving muscular power. However, few studies have examined if FRT is kinematically similar to WT, or if FRT kinematics change with increasing inertial load. The purposes of this study were to determine how sagittal plane joint kinematics are affected by increasing inertial load during FRT squats, and to determine how FRT squat joint kinematics compare to WT squat joint kinematics. Methods: Subjects (n=9) completed three visits for this study. On the first visit subjects completed squat 1 repetition maximum (1RM) testing. The second visit served as a full FRT familiarization session in which subjects performed one set of 5 maximal effort FRT squats at each inertial load (0.050, 0.075, and 0.100 kgm2). On the third visit, subjects were videoed in the sagittal plane while performing the FRT squat protocol. Subjects then completed 5 maximal velocity repetitions of WT squats with the barbell loaded according to the Kansas Squat Test (KST) protocol. Kinematic differences between inertial loads were determined via 1-way repeated measures ANOVAS while differences between FRT and WT were determined with paired T-tests. Results: There were no differences in peak sagittal plane knee, trunk-hip, trunk (absolute) or ankle angles between inertial loads. Peak and mean joint angular velocities decreased with increasing inertial loads at the knee and trunk-hip. Mean joint angular velocities decreased at the ankle with increasing inertial loads, while peak and mean trunk (absolute) angular velocities were unaffected. No statistical analyses were conducted for FRT and WT comparison as not enough subjects met the criteria (n=3). Conclusions: Sagittal plane joint kinematics are largely maintained despite increasing inertial load during FRT squats. Lower extremity joint angular velocities decreased with increasing inertial load. If training for muscular power and knee extensor velocity is the goal, then the inertia of 0.050 kgm2 is most suitable.

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Debraux, Pierre. "Etude des déterminants de la performance en cyclisme: puissance musculaire et aérodynamisme. Application en BMX." Reims, 2010. http://theses.univ-reims.fr/sciences/2010REIMS013.pdf.

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Les compétitions de BMX se déroulent sur une piste spécifique de 300-400 m parsemée de bosses et de virages avec un départ sur plan incliné. Les vitesses atteintes par les pilotes peuvent être supérieures à 70 kmh-1 quelques secondes après le départ. Peu d’études scientifiques ont été consacrées aux paramètres liés à la performance en BMX. Néanmoins une étude a montré que la phase de départ était primordiale et que la puissance maximale musculaire était un des principaux facteurs de la performance lors de cette phase. L’objectif de cette thèse est d’étudier les déterminants de la performance dans cette discipline à partir de deux paramètres essentiels : la production de puissance musculaire des membres inféieurs et une variable de l’aérodynamisme, l’aire frontale projetée. Dans un premier temps, l’étude de la production de puissance musculaire des membres inférieurs au cours de tests de sprints sur cyclo-wattmètre et d’exercices de ½ Squat chez des cyclistes sur route et des pilotes de BMX a montré que l’aire de section musculaire et la force maximale étaient des indicateurs de la performance pour des sprints courts (~ 6-30s). La comparaison des profils musculaires inertiels à des athlètes de force a montré que les pilotes de BMX produisaient une puissance maximale à des charges relatives faibles et qu’il était nécessaire d’augmenter la puissance produite à des charges élevées. Dans un deuxième temps, une nouvelle méthode de terrain pour la mesure de l’aire frontale projetée en cyclisme a été testée, elle est reproductible et valide en comparaison aux méthodes de pesage des photographies et de digitalisation. Cette méthode a permis de mesurer l’aire frontale projetée de pilotes de BMX lors de sprints de 80 m. Ces sprints ont permis de mettre en évidence l’importance de la puissance maximale, de l’aire frontale projetée et de la cadence moyenne de pédalage sur la performance chronométrique, et la nécessité de trouver un braquet optimal pour diminuer la différence entre la cadence moyenne et la cadence optimale. Pour optimiser la performance en compétition chez les pilotes de BMX, il apparait nécessaire : i) de suivre un entraînement en musculation pour augmenter la masse musculaire et la force maximale des membres inférieurs ; ii) d’adapter le braquet selon le niveau des pilotes ; et iii) d’optimiser l’aire frontale projetée selon les phases de course. Des solutions sont proposées dans cette thèse
The BMX competitions take place on a specific track of 300-400 m with bumps and turns, and with a downhill start. The displacement velocity reached by the riders may be greater than 70 kmh-1 a few seconds after the start. Few scientific studies focused to the parameters related to the performance in BMX. Nevertheless, a study showed that the starting phase was capital and that the maximum muscle power was a major contributor to performance during this phase. The aim of this thesis is to study the determinants of performance in this sport in focusing on two main parameters: the muscular power output of the lower limbs and a variable of aerodynamics, the projected frontal area. Firstly, the study of the muscular power output in lower body during sprints on a cycle ergometer and a ½ Squat among road cyclists and BMX riders showed that the muscle cross-sectional area and maximal muscle strength were indicators of performance for all-out sprints (~ 6-30s). A comparison of muscular inertial profiles has shown that BMX riders produced a maximal power output with relative light loads and it was necessary to increase muscular power output at heavy loads. Secondly, a new field method for measuring the projetcted frontal area in cycling has been tested. This method is reproducible and valid in comparison to the methods of weighing photographs and digitization. This method was used to measure the projected frontal area of BMX riders during 80 m sprints. These sprints allowed to highlight the importance of the maximal power, the projected frontal area and the average pedaling rate on the chronometric performance and the need to find an optimal gear to decrease the difference between the average pedaling rate and the optimal pedaling rate. To optimize the performance in competition among the BMX riders, it seems necessary: i) to follow a resistance training to increase muscle mass and muscle maximal strength of the lower limbs; ii) to adjust the gear ratio depending on the riders; and iii) to optimize the projected frontal area for some phases of the race. Solutions are proposed in this thesis

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Cormack, Stuart J., and n/a. "The changes in strength, power and associated functional physiological measures in elite women soccer players during a 12 month preparation for a major event." University of Canberra. Health and Biomedical Science, 2003. http://erl.canberra.edu.au./public/adt-AUC20050411.134745.

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The assessment of strength and power and the relationship of these measures to functional variables such as speed and vertical jump ability are understood poorly. This is particularly the case when dealing with a long-term preparation for a major event in a sport such as women's soccer. The results of this research suggest that a number of isoinertial speed strength measures may be sensitive to aspects of a training program and therefore be useful tools for determining the level of development of various underlying neuromuscular capacities. Further results provide a question mark about the role of maximum strength in the development of high velocity functional movements, as increases in maximum strength did not correlate to changes in measures of functional performance. An important finding from this research is the potential role of specific isoinertial speed strength parameters in the detection of neuromuscular fatigue. Time course analysis of the results in this study suggests that the use of these measures to detect fatigue warrants further investigation.

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Brais, Bernard. "Oculopharyngeal muscular dystrophy : from phenotype to genotype." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0002/NQ44369.pdf.

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Suchomel, Timothy J., Sophia Nimphius, Christopher R. Bellon, and Michael H. Stone. "The Importance of Muscular Strength: Training Considerations." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/etsu-works/4659.

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This review covers underlying physiological characteristics and training considerations that may affect muscular strength including improving maximal force expression and time-limited force expression. Strength is underpinned by a combination of morphological and neural factors including muscle cross-sectional area and architecture, musculotendinous stiffness, motor unit recruitment, rate coding, motor unit synchronization, and neuromuscular inhibition. Although single- and multi-targeted block periodization models may produce the greatest strength-power benefits, concepts within each model must be considered within the limitations of the sport, athletes, and schedules. Bilateral training, eccentric training and accentuated eccentric loading, and variable resistance training may produce the greatest comprehensive strength adaptations. Bodyweight exercise, isolation exercises, plyometric exercise, unilateral exercise, and kettlebell training may be limited in their potential to improve maximal strength but are still relevant to strength development by challenging time-limited force expression and differentially challenging motor demands. Training to failure may not be necessary to improve maximum muscular strength and is likely not necessary for maximum gains in strength. Indeed, programming that combines heavy and light loads may improve strength and underpin other strength-power characteristics. Multiple sets appear to produce superior training benefits compared to single sets; however, an athlete’s training status and the dose–response relationship must be considered. While 2- to 5-min interset rest intervals may produce the greatest strength-power benefits, rest interval length may vary based an athlete’s training age, fiber type, and genetics. Weaker athletes should focus on developing strength before emphasizing power-type training. Stronger athletes may begin to emphasize power-type training while maintaining/improving their strength. Future research should investigate how best to implement accentuated eccentric loading and variable resistance training and examine how initial strength affects an athlete’s ability to improve their performance following various training methods.

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Roberts, Thomas C. "Duchenne muscular dystrophy : RNA-based therapeutics and microRNA biology." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:f53ea1f3-92db-4f90-ba95-01f2a56eae8f.

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Duchenne muscular dystrophy (DMD) is a progressive muscle wasting disorder caused by absence of functional dystrophin protein. This thesis describes investigations into the role of small non-coding RNAs in both DMD pathology, and as potential therapeutic molecules. MicroRNAs (miRNAs) are a class of small RNAs that regulate gene expression and are implicated in wide-ranging cellular processes and pathological conditions. This study has compared differential miRNA expression in proximal and distal limb muscles, diaphragm, heart and serum in the mdx dystrophic mouse model relative to wild-type controls. Global transcriptome analysis revealed muscle-specific patterns of differential miRNA expression as well as commonalities between tissues, including previously identified dystromirs. miR-1, miR-133a and miR-206 were found to be highly abundant in mdx serum, suggesting that these miRNAs are promising disease biomarkers. Indeed, the relative serum levels of these miRNAs were normalised in response to peptide-PMO mediated dystrophin restoration therapy. This study has revealed further complexity in the miRNA transcriptome of the mdx mouse, an understanding of which will be valuable for the development of novel DMD therapeutics and for monitoring their efficacy. Myostatin is a secreted growth factor that negatively regulates muscle mass and is therefore a potential pharmacological target for the treatment of muscle wasting disorders such as DMD. This study describes a novel myostatin inhibition approach in which small interfering RNAs (siRNAs) complementary to a promoter-associated transcript induce transcriptional gene silencing (TGS) in cultured myotubes. Silencing was sensitive to treatment with the histone deacetylase inhibitor Trichostatin A, and the silent state chromatin mark H3K9me2 was enriched at the myostatin promoter following siRNA transfection, suggesting epigenetic remodelling underlies the silencing effect. These observations suggest that long-term epigenetic silencing may be feasible for myostatin and that TGS is a promising novel therapeutic strategy for the treatment of muscle wasting disorders. The work in this thesis therefore demonstrates the potential of small RNAs as therapeutic agents and as disease biomarkers in the context of DMD.

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Geisemeyer, Sarah. "Duchenne muscular dystrophy : a genetic, cognitive and psychosocial approach." Thesis, Kingston University, 2017. http://eprints.kingston.ac.uk/40678/.

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Duchenne muscular dystrophy (DMD) is a severe, progressive muscle wasting disorder that affects 1 in 3600 male births. It is caused by genetic mutations in the dystrophin gene. This study investigated several aspects of the neuromuscular disorder within a population of Brazilian DMD boys and their families. This study's framework was laid out within the prism of an interacting cycle of genetic factors, cognitive functioning, and psychosocial aspects that underlie the neuromuscular disorder. It focuses on DMD's aetiology, history and previous research on genetic, cognitive and psychosocial aspects. Mixed methods were adopted to allow for a more encompassing view of the neuromuscular disorder: cognitive tests, an emotion recognition battery, genetic analyses, well-being questionnaires, and interviews were applied. Correspondent, quantitative and qualitative data analysis was carried out. The findings of 32 DMD patients (mean age 10.4 years, SD= 2 years) and 31 control subjects (mean age 9.4 years, SD= 3 years) revealed severe cognitive dysfunctioning in all assessed cognitive domains in the DMD population, as well as in the ability of emotion recognition. In the DMD group, it could be shown that poor executive functioning stood in a positive correlation with a poor ability of emotion recognition. The DMD patients' cognitive phenotypes were correlated with the genetic mutations in their dystrophin gene, but no relationship between the patients' genotype and cognitive phenotype could be confirmed. These results were contrary to previous research, which suggested that specific mutations in the dystrophin gene cause cognitive impairment. The DMD group scored poorly on the emotion recognition task, which is also a characteristic of autism spectrum disorder. However, when diagnosing for autistic characteristics through means of an interview, only a few similarities between the two disorders could be found. In order to assess the psychosocial components that come along with the disorder, well-being questionnaires were supplied. Interestingly, DMD boys scored higher on well-being than the boys in the control group. Moreover, 30 of the DMD caregivers (mean age app. 31 years) also revealed high levels of well-being, which correlated positively with the well-being of their sons, suggesting high levels of resilience. Given the participants' socio-economic hardship and the lack of governmental help, it was concluded that participants showed an incredible level of resilience that most likely resided within their faith, which nearly all of them stated to be the reason for their strength to strive. The relevant and new information about cognitive, genetic and social aspects of DMD uncovered in this study will pave the way for further (and much needed) studies into psychosocial aspects of the disorder.

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17

Wallace, Brian Joseph. "MUSCULAR AND NEURAL CONTRIBUTIONS TO POSTACTIVATION POTENTIATION." UKnowledge, 2015. http://uknowledge.uky.edu/khp_etds/21.

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Muscle performance is partially a consequence of its recent contractile history. Postactivation potentiation (PAP) can occur after muscle contractions and leads to enhanced neuromuscular performance. The purpose of this dissertation was to explain the relationship between muscle factors (twitch potentiation, TP) and neural factors (reflex potentiation, RP) contributing to overall PAP following a non-fatiguing volitional muscle contraction. The tibial nerves of fifteen resistance trained volunteers (eleven men, four women) were stimulated intermittently at supramaximal (Mmax) and submaximal (Hmax) intensities for 20 minutes on separate days under three conditions: rest (Control); after a after a 10 second maximum voluntary isometric contraction (MVIC) of the plantarflexors; and after a low frequency fatigue protocol prior to the MVIC. Plantarflexion isometric torque and rate of force development (RFD), and soleus and gastrocnemius EMG Hmax/Mmax ratios, were analyzed. Both experimental conditions resulted in TP at 10 seconds post-MVIC compared to the control condition. The two experimental conditions were not different for any measure. Torque and RFD at Hmax (overall PAP) were highest at 3 and 4.5 minutes post MVIC, respectively, but were not significantly different from the control condition. EMG values generally were insignificantly increased in the experimental conditions versus the control condition. Mmax torque and RFD significantly contributed to Hmax torque and RFD at 20 seconds, Hmax peak, and 20 minute post-MVIC time points. The soleus significantly contributed to Hmax torque at 20 seconds and 20 minutes post-MVIC, and Hmax RFD at 20 seconds, 4.5 minutes, and 20 minutes post-MVIC. The results of this study suggest that both muscle and neural factors play a significant role in overall PAP, and that neural factors may play a more meaningful role in RFD potentiation than torque potentiation.

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Risco, Quiroz Milagros. "Development of a Novel Strategy to Treat Spinal Muscular Atrophy." Thesis, University of Ottawa (Canada), 2010. http://hdl.handle.net/10393/28595.

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Spinal muscular atrophy (SMA) is an autosomal recessive disorder caused by reduced levels of the survival motor neuron (SMN) protein, which results in degeneration of motor neurons, leading to muscle weakness, and, ultimately, death. To provide an effective therapy for SMA, SMN expression must be restored in motor neurons. The goal of our research is to develop protein-based therapeutics for SMA. Protein transduction domain (PTD), from the human immunodeficiency virus-transactivator of transcription (HIV-TAT), mediates the transduction of any polypeptide to which they are fused. We produced bacterial expression cassettes of PTD-SMN. The PTD-SMN is able to transduce cells in vitro, reaching the nucleus and forming punctate structures similar to that of endogenous SMN. Internalization of PTD-SMN results in an increased nuclear-staining foci (gems) number. Importantly, this PTD-SMN co-localizes with coiled bodies, indicating PTD-SMN is able to localize to the correct region of the nucleus. However, we were unable to detect interaction of PTD-SMN with SMN known binding partners, suggesting that majority of PTD-SMN has low activity. Our results suggest that PTD-SMN produced from a prokaryotic source may be useful for SMA therapy, but optimization of protein production is required before this therapy can reach its full potential.

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Travis, Spencer K. "Peaking for Maximal Strength: Muscular Adaptations and Performance Outcomes." Digital Commons @ East Tennessee State University, 2021. https://dc.etsu.edu/etd/3935.

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The purposes of this dissertation were to 1) determine what tapering and peaking practices appear to be most effective via systematic review, 2) to identify the tapering and peaking practices used by North American powerlifters, 3) to experimentally compare muscular adaptations and performance changes following two different training cessation periods, and 4) to experimentally compare the two most common taper models following a training program aimed at peaking maximal strength. Based on the scientific literature, a step and exponential taper appeared to be the most effective tapering models used when volume-load is reduced by half over 2±1 week. Interestingly, North American powerlifters reported that the step taper was most often used while reducing volume-load by 41-50% over 7-10 days. Furthermore experimentally, there were no changes in lower body maximal strength following 3 or 5 days of training cessation. However, upper body maximal strength decreased following 5 days of training cessation. Thus, at the end of a taper, a training cessation period of 3 days appears to be effective for maintaining upper and lower body maximal strength. Furthermore, a work-matched step taper and exponential taper produced similar outcomes for 1RM back squat, bench press, and deadlift, powerlifting total and Wilks Score in strength athletes, yet deadlift 1RM changes favored the exponential taper. However, there were clear physiological differences observed at the whole muscle and muscle fiber levels that appeared to contribute to performance outcomes. This was one of the first investigations demonstrating whole muscle and muscle fiber hypertrophy following a peaking program in strength athletes. Immunohistochemical and immunoblotting analyses demonstrated an increase in myosin-heavy chain IIA content with concomitant decreases in myosin-heavy chain I and IIX content, particularly following the step-taper. These myosin isoform shifts towards a faster, higher quality phenotype were related to changes in underlying myocellular signaling (i.e. Sox6 upregulation, micro RNA-499a downregulation) responsible for fiber-type transitions. These findings indicate a shorter taper may produce favorable muscular adaptations followed by a period of short-term training cessation to prevent the loss of taper-induced performance adaptations. Overall, the findings from these investigations support the use of tapering to enhance maximal strength.

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20

Mulhim, Ramson Albert. "Muscular control of vocal complexity in the túngara frog (Engystomops pustulosus)." Scholarly Commons, 2015. https://scholarlycommons.pacific.edu/uop_etds/175.

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Many animals use communication to increase their chance of successful reproduction. Advertisement signals vary in complexity and their diversity can be best understood through the study of the simplest case, in which a species with a single-note mating call evolves a second note. Túngara frogs ( Engystomops pustulosus ) provide the best-known example of complex calling among frogs. The initial part of the mating call, called "whine", is always present and mediates species recognition. The frog can facultatively add one to seven additional notes called "chucks" to the mating call. Frogs initiate phonation by compressing pulmonary air to pass it through the larynx, inducing vibration of vocal cords. In male túngara frogs, a pair of fibrous masses is attached to the vocal cords and vibrates to produce the chuck. The mechanism that controls the optional production of the chucks was previously unknown. This study examined the muscles of the larynx thought most likely to be involved in controlling the production of the chuck. Four pairs of laryngeal muscles were previously known in amphibians. The laryngeal dilator muscle is the largest of them and has the role of opening the larynx. In the túngara frog, the laryngeal dilator muscle is divided into two bundles of fibers with distinct attachments. The superficial bundle of the dilator muscle originates at the posteromedial process of the hyoid cartilage and inserts medially into the arytenoid cartilages. The deep bundle attaches to the medial aspect of the arytenoid cartilages and to the base of the fibrous mass, extending through a fissure between the cricoid and arytenoid cartilages. This attachment to the fibrous mass may allow the deep bundle of the laryngeal dilator muscle to control the vibration of the fibrous mass and the production of the chuck. This possibility was evaluated by examination of the muscle innervations and by electrical stimulation. The long laryngeal nerve innervates all laryngeal muscles except the deep portion of the laryngeal dilator muscle, which is innervated by the short laryngeal nerve. Electrical stimulation confirmed that the long laryngeal nerve stimulates all laryngeal muscles, except the deep portion of the laryngeal dilator muscle. Stimulation of the short laryngeal nerve only resulted in contraction of the deep portion of the laryngeal dilator muscle, which leads to the fibrous mass. These results indicate that the short laryngeal nerve controls the deep portion of the laryngeal dilator muscle, which may position the fibrous masses in a way that allows them to vibrate with airflow adding chucks to the mating call. The deep portion of the laryngeal dilator should be recognized as a separate muscle in the amphibian larynx, for having distinct attachments, innervation and role. The recognition of this muscle resolves the issue of multiple innervation of the laryngeal dilator muscle in amphibians. Based on innervation, the new muscle is likely homologous to the mammalian cricothyroid muscle.

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21

Martínez, Hernàndez Rebeca. "Desarrollo neuromuscular en la atrofia muscular espinal." Doctoral thesis, Universitat de Barcelona, 2012. http://hdl.handle.net/10803/97097.

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BACKGROUND: Spinal muscular atrophy (SMA) is a neuromuscular disease characterized by degeneration and loss of spinal cord motor neurons leading to denervation and muscular atrophy. It is caused by defects in the Survival Motor Neuron 1 gene (SMN1) and it is classified by age of onset and motor milestones into three main types which strongly correlate with the copy number of its homologous gene, SMN2. SMN2 expresses markedly less full‐length protein than SMN1, provoking disease manifestations. The essential neuropathological feature in SMA is motor neuron death. Previous studies in SMA foetal samples showed early pathological changes in spinal cord suggesting that the disease is a developmental disorder. Studies in mouse SMA models support that neuromuscular junctions (NMJs) may play a significant role in the disease, although this implication has not yet been addressed in humans. AIMS AND METHODOLOGIES: To better understand the mechanisms of SMA disease, a comprehensive histologic, immunohistochemical and ultrastructural analysis of the muscle and neuromuscular junctions in prenatal and postnatal SMA samples was carried out. To further correlate neuropathological findings with early developmental manifestations of the disease, foetal motility between 11‐14 gestational weeks was recorded and analyzed by 2D ultrasound in pregnancies predicted to develop SMA. RESULTS: At 12 weeks, most SMA myotubes were smaller than controls, indicating a delay in muscle maturation. At this stage, the presence of early acetylcholine receptor (AChR) clusters in developing SMA muscles suggested that pre‐patterned and nerve‐independent AChR clustering would not be affected by the disease. However, as development proceeded in the following weeks, early degeneration of nerve terminals was present associated with a dispersion of AChRs and abnormal preterminal accumulation of vesicles. These findings pointed towards a defect in maintenance of the initial innervation in developmental SMA muscle. Furthermore, postnatal muscle of type I SMA patients showed persistence of the foetal subunit of acetylcholine receptors, suggesting a continuous delay in maturation of neuromuscular junctions. Therefore, if nerve terminals are unable to efficiently maintain functional NMJs, a dying‐back process leading to motor neuron degeneration and loss may appear, with the consequent increase in programmed cell death. Despite all these early neuropathological findings, we did not observe qualitative differences in foetal movements between unaffected and SMA prenatal cases. The synaptic defects in SMA at this stage of development, therefore, might be compensated by several mechanisms. During perinatal and postnatal periods compensation would no longer be present, resulting in the drastic SMA pathology and clinical manifestations. CONCLUSIONS: These developmental studies open new possibilities to improve our knowledge of presymptomatic SMA stages. Early therapeutic strategies should be investigated to reverse the process of denervation, maintain activity of the NMJ, and improve maturity of the motor endplates.
INTRODUCCIÓN: La atrofia muscular espinal (AME) es una enfermedad neuromuscular infantil caracterizada por la muerte de las neuronas motoras del asta anterior de la médula espinal. Como consecuencia de ello hay una degeneración y atrofia muscular, por lo que los pacientes mueren a menudo de insuficiencias respiratorias graves. La AME se clasifica en tres tipos principales según el grado de gravedad, la edad de aparición y las pautas motoras. Se trata de una enfermedad con patrón de herencia autosómico recesivo causada por ausencia o mutaciones en el gen Survival Motor Neuron 1 (SMN1). Existe un gen homólogo, SMN2, que está presente en todos los pacientes aunque a diferencia del SMN1, produce mucha menor proteína SMN completa y, por lo tanto, no evita la aparición de la enfermedad. Sin embargo se ha demostrado una importante correlación con el tipo de AME y el número de copias de SMN2. El rasgo patológico esencial de la AME es la muerte de las neuronas motoras. Estudios hechos en muestras fetales indican que ya existen hallazgos patológicos en el estadio prenatal lo que sugiere que la AME sería un trastorno del desarrollo. Además en modelos de ratón AME se ha determinado que la unión neuromuscular tendría un papel importante en la patogenia de la enfermedad aunque en humanos todavía no existen investigaciones al respecto. OBJETIVOS Y METODOLOGÍA: Con el fin de profundizar en los conocimientos de la patogenia de la AME, en esta tesis se ha realizado un análisis histológico, inmunohistoquímico y utraestructural del músculo y la unión neuromuscular en muestras prenatales y postnatales de controles y AME. Paralelamente, se han correlacionado los resultados neuropatológicos obtenidos con el estudio de la motilidad fetal por ecografía 2D entre las 11 y 14 semanas de gestación en embarazos diagnosticados genéticamente como AME. RESULTADOS: A partir de las 12 semanas, los miotubos AME son más pequeños que los controles lo que es compatible con un retraso en la maduración muscular. En esta etapa, la presencia de receptores de acetilcolina agrupados en músculo AME sugiere que éste es capaz de formar la placa neuromuscular. Sin embargo en semanas posteriores se observa una degeneración temprana de los terminales nerviosos asociados a una dispersión de los receptores de acetilcolina y acumulación anormal de vesículas presinápticas. Esto indica que en este período uno de los principales defectos sería la falta de mantenimiento de la unión neuromuscular. El músculo postnatal AME muestra persistencia de la expresión del receptor fetal de acetilcolina que refuerza la idea de una maduración retardada de la unión neuromuscular que persiste durante todo el desarrollo. La falta de mantenimiento de las uniones neuromusculares justificaría el inicio de un proceso de muerte retrograda (“dying back process”) dando lugar a una excesiva pérdida de neuronas motoras en la médula espinal. El estudio de los movimientos fetales, sin embargo, no demostró diferencias cualitativas entre los fetos normales y los AME. La falta de correlación entre la neuropatología descubierta en los fetos con AME tipo I y la presencia de movimientos fetales normales en ese mismo grupo indica que deben existir mecanismos compensatorios en el feto AME que enmascaran las posibles consecuencias funcionales de los defectos sinápticos hallados. Estos mecanismos compensatorios desaparecerían más tarde dando lugar a las graves manifestaciones de la enfermedad en las etapas perinatal y neonatal. CONCLUSIONES: Los resultados obtenidos contribuyen al mejor conocimiento de esta enfermedad en etapas presintomáticas, y abre nuevas perspectivas para investigar estrategias terapéuticas a fin de revertir los procesos de denervación, mantener la actividad de las uniones neuromusculares y mejorar la maduración de las placas motoras.

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Suchomel, Timothy J., Sophia Nimphius, and Michael H. Stone. "The Importance of Muscular Strength in Athletic Performance." Digital Commons @ East Tennessee State University, 2016. https://dc.etsu.edu/etsu-works/4641.

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This review discusses previous literature that has examined the influence of muscular strength on various factors associated with athletic performance and the benefits of achieving greater muscular strength. Greater muscular strength is strongly associated with improved force-time characteristics that contribute to an athlete’s overall performance. Much research supports the notion that greater muscular strength can enhance the ability to perform general sport skills such as jumping, sprinting, and change of direction tasks. Further research indicates that stronger athletes produce superior performances during sport specific tasks. Greater muscular strength allows an individual to potentiate earlier and to a greater extent, but also decreases the risk of injury. Sport scientists and practitioners may monitor an individual’s strength characteristics using isometric, dynamic, and reactive strength tests and variables. Relative strength may be classified into strength deficit, strength association, or strength reserve phases. The phase an individual falls into may directly affect their level of performance or training emphasis. Based on the extant literature, it appears that there may be no substitute for greater muscular strength when it comes to improving an individual’s performance across a wide range of both general and sport specific skills while simultaneously reducing their risk of injury when performing these skills. Therefore, sport scientists and practitioners should implement long-term training strategies that promote the greatest muscular strength within the required context of each sport/event. Future research should examine how force-time characteristics, general and specific sport skills, potentiation ability, and injury rates change as individuals transition from certain standards or the suggested phases of strength to another.

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Olson, Theodore. "Transcriptional Regulation of Neurogenic Atrophy-Induced Gene Expression by Muscle Ring Finger-1 and Myogenic Regulatory Factors." UNF Digital Commons, 2014. http://digitalcommons.unf.edu/etd/495.

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Skeletal muscle wasting is a consequence of numerous physiological conditions, including denervation, corticosteroid treatment, immobilization, and aging. The E3 ubiquitin ligases, MuRF1 and MAFbx, are induced under nearly all atrophy conditions and are believed to play a key role in protein degradation in atrophying muscle. However, the preliminary data described in this study provides new evidence that MuRF1 may also act as a transcriptional modulator of atrophy-induced gene activity, including the regulation of MAFbx and MuRF1 expression. To characterize the transcriptional regulation of MuRF1 and MAFbx, reporter gene constructs containing fragments of the proximal promoter regions of these genes were developed, transfected into C2C12 cells with or without a MuRF1 expression plasmid and monitored for differences in reporter gene activity. The MuRF1 and MAFbx reporters each showed repressed activity in cells ectopically expressing MuRF1 compared to cells that did not overexpress MuRF1. Furthermore, ectopic expression of the myogenic regulatory factors (MRFs), MyoD1 and myogenin, caused significant activation of the MuRF1 and MAFbx reporter constructs. However, co-overexpression of MuRF1 with MyoD1 or myogenin resulted in reversal of MRF induction of reporter gene activity, and synergistic repression of a constructed E-box reporter system. To further characterize the role of the MuRF1 gene product in repression of MuRF1 expression, a MuRF1 RING domain mutant and a MuRF1 c-terminal mutant were created. The mutant constructs were then co-transfected along with MRF expression plasmids and the MuRF1 reporter construct into C2C12 cells and reporter gene activity was assessed. The MuRF1 RING mutant failed to reverse MRF activation of the reporter gene, while the c-terminal mutant successfully reversed activation of the reporter gene. These findings suggest that ubiquitin ligase activity is required for MuRF1 transcriptional regulatory effects. These data offer exciting evidence of a potential new function for MuRF1 as a transcriptional modulator of atrophy-induced changes in gene expression.

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24

Ifrén, Anette. "The influences of social facilitation on a muscular endurance bench press-test." Thesis, Mittuniversitetet, Avdelningen för hälsovetenskap, 2018. http://urn.kb.se/resolve?urn=urn:nbn:se:miun:diva-34187.

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Bruce, Lindsay, and Allan Forsman. "Effects of Spaceflight on the Muscular Layers of Mouse Uterine Tissue." Digital Commons @ East Tennessee State University, 2021. https://dc.etsu.edu/asrf/2021/presentations/2.

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As NASA and other space programs around the world prepare to send astronauts into space for longer missions, it is becoming imperative to understand the biological effects of spaceflight on the human body. In order to better understand how the long-term spaceflight environment affects humans biologically, researchers often utilize other model organisms, like mice, whose biological systems are comparable to human body systems. Our study was performed to determine if spaceflight had any effect on the thickness of the muscular layers of the uterine tissue of female mice. In other words, how does the thickness of the muscular layers in the uterus of spaceflight mice compare to that of control mice that were not subjected to spaceflight. For this study mice were divided into 4 groups (flight animals, baseline animals, vivarium controls, and ground controls) and the flight mice subjected to 37 days of spaceflight. Upon tissue retrieval and histological preparation, five random measurements of the outer longitudinal muscular layer and five random measurements from the inner circular muscular layer of each tissue sample were made. The average thickness for each layer was then calculated and statistical analysis used to determine differences between the four groups of mice. At the time of this presentation final measurements and statistics had not been completed.

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Desguerre, Isabelle. "Subphénotypes de la maladie de Duchenne et caractérisation de la myofibrose dystrophique humaine et expérimentale." Phd thesis, Université Paris-Est, 2008. http://tel.archives-ouvertes.fr/tel-00462105.

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La dystrophie musculaire de Duchenne (DMD) est la maladie neuromusculaire la plus fréquente de l'enfant. Son évolution progressive inexorable conduit habituellement au décès dans la troisième décade. La DMD constitue cependant une affection hétérogène pour la sévérité de l'atteinte musculaire, cognitive et cardiaque, et cette hétérogénéité n'est pas totalement expliquée par la localisation des mutations dans le gène de la dystrophine. Ma thèse comporte trois volets: (1) une analyse clinique multivariée d'une cohorte de DMD suivie à long terme qui nous a permis de définir 4 phénotypes distincts de DMD; (2) une étude de corrélation clinico-pathologique qui a identifié la fibrose endomysiale précoce comme seul facteur histologique prédictif de sévérité motrice; (3) la mise au point d'un modèle murin original de myofibrose dystrophique chez la souris mdx déficiente en dystrophine. 1- Étude multiparamétrique clinique. La saisie par la même équipe des données fonctionnelles musculaires, cardiaques, respiratoires et cognitives de 75 patients atteints de DMD (tous génotypés et présentant une absence complète de dystrophine musculaire), suivis pendant >10 ans, a permis d'établir un modèle multiparamétrique satisfaisant à deux dimensions principales, cognitive et motrice, et de définir 4 clusters phénotypiques : (i) DMD cognitive et motrice congénitale (20%), (ii) DMD classique (28%), (iii) DMD motrice pure modérée (22%), (iv) DMD motrice pure sévère (30%). La corrélation génotypephénotype était restreinte à la seule atteinte cognitive. Des indicateurs pronostics précoce ont été identifiés et validés sur une 2ème série de 34 patients. 2- Étude histopathologique. Les variations de sévérité de l'atteinte musculaire n'étant pas expliquées par la génétique moléculaire, nous avons cherché à corréler les paramètres moteurs et la biopsie musculaire prélevée dans le quadriceps à un stade précoce (3-7 ans) chez 25 patients (analyse stéréologique des images numérisées pour les paramètres élémentaires: nécrose/régénération, fibres hypercontractées, adipocytes, fibrose endomysiale et périmysiale). Seule la fibrose endomysiale était associée à un pronostic moteur défavorable (p<0.002) attesté par l'âge de perte de marche, la force du quadriceps et le testing musculaire global à 10 ans. Cette fibrose endomysiale dissociait les capillaires des myofibres (écartement x 2.5), et s'accompagnait d'une augmentation sélective des macrophages CD206+ activés dans la voie alterne (M2) et d'une diminution relative des cellules satellites musculaires (p<0.0001). Ces données suggèrent un rôle clé de la fibrose endomysiale (et des macrophages M2 profibrosant) et dans la sévérité clinique de la DMD. 3- Étude expérimentale. Ces éléments rendent nécessaire la mise au point d'un modèle expérimental de myofibrose dystrophique, la souris mdx présentant peu de fibrose et un déficit moteur modéré et tardif. Nous avons mis au point une nouvelle méthode de lésion musculaire focale profibrosante du tibialis antérieur chez la souris mdx (piqûres multiples quotidiennes pendant 15 jours). Une fibrose endomysiale attestée par un fort immunomarquage du collagène I (à 8, 30, 60 et 90 jours) a été quantifiée et corrélée à la perte de la force musculaire dans la patte lésée (comparée au muscle contralatéral). Ces résultats légitiment et préparent les futures stratégies thérapeutiques "anti-fibrosantes" dans la DMD

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Mailman, Matthew David. "Molecular analysis of patients with recessive 5q-spinal muscular atrophy : increased diagnostic and prognostic sensitivity /." The Ohio State University, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486572165277248.

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Sinadinos, Anthony. "P2X7 receptor knockout alleviates the pathology in the mdx mouse model of Duchenne muscular dystrophy." Thesis, University of Portsmouth, 2014. https://researchportal.port.ac.uk/portal/en/theses/p2x7-receptor-knockout-alleviates-the-pathology-in-the-mdx-mouse-model-of-duchenne-muscular-dystrophy(bda70872-da60-443d-a5c7-5763d6e9c94d).html.

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Duchenne muscular dystrophy (DMD) is a hereditary, X-linked, muscle wasting disease with no known cure. It is caused by altered mechanical stability of muscle cell membranes combined with altered cell signalling and inflammatory infiltrations due the absence of the cytoskeletal protein dystrophin, the product of the DMD gene. Progressive muscle fibre degeneration combined with chronic inflammation leads to a severe functional impairment, progressive disability, and ultimately to premature death. DMD presents predominantly in skeletal muscles but brain and bone are also affected. Analyses in the mdx mouse, the most commonly used model of DMD, has led to the identification of an increased expression and function of the P2X7 purinoceptor in dystrophic muscle cells and muscles in situ. This ATP-gated receptor has been implicated in a number of human diseases that, combined with its well-known role in inflammatory cells, suggested that P2X7 upregulation might also be important for the pathogenesis of DMD. To test the role of the P2X7 purinoceptor in DMD pathogenesis and its potential as a target for treatment, two mdx/P2X7-/- double mutant mouse strains were generated and compared to the mdx mouse with respect to several critical disease parameters during an acute degenerative stage of disease. Histological, molecular, biochemical, and functional analyses revealed reductions in both muscle and non-muscle pathology in mdx/P2X7-/- mice, with significant improvements in key molecular and structural parameters. These included lower serum creatine kinase levels and decreased sarcolemma permeability to blood-born molecules, indicative of less sarcolemma damage. P2X7 ablation also resulted in increased minimum Feret’s diameter, a morphological indicator of muscle regeneration. While the fraction of muscle fibres with centralised nuclei was not significantly different, levels of myogenin, a protein indicator of muscle differentiation, were also higher in mdx/P2X7-/- mice. These changes were concomitant with an overall decreased inflammatory signature in mdx/P2X7-/- mice compared to mdx and an increase in muscle strength, in vitro. Examination of diaphragms (undergoing continuous degeneration/regeneration in the mdx mouse) from 20 month old mice also showed the increase in minimum Feret’s diameter and continued reduced inflammation in the mdx/P2X7-/- group. Aged heart tissue from these mdx/P2X7-/- also presented less inflammatory infiltrate and reduced fibrosis compared to mdx. Moreover, micro-CT analyses showed greatly reduced osteopenia in mdx/P2X7-/- bones when compared to 6 month mdx mice. Amelioration of all symptoms was proportional to the extent of receptor depletion, where single P2X7 isoform loss was less effective than the complete knockout. These observations support involvement of the P2X7 purinoceptor in the dystrophic pathology in this model of DMD and are consistent with the well-known role of this receptor in other disorders. P2X7 purinoceptors are likely to act via several different molecular pathways, for example increased Ca2+ influx that affects dystrophic cells directly as well as through reduced inflammation. Indeed, this study represents the first known analysis of an effect of P2X7 ablation on a chronic inflammatory phenotype localised to skeletal muscle. These data from the most widely used model of DMD suggest that the P2X7 receptor can be also involved in human pathology and specific receptor antagonists could be considered for targeted pharmacological intervention to delay progression of this lethal disease.

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De, Larichaudy Joffrey. "Implication des céramides dans l'atrophie musculaire." Phd thesis, INSA de Lyon, 2012. http://tel.archives-ouvertes.fr/tel-00743546.

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Le muscle squelettique fait preuve d'une remarquable plasticité en réponse aux changements physiologiques, comme l'activité physique, et aux situations pathologiques. Il subit notamment une atrophie sévère lors de la cachexie qui accompagne diverses pathologies chroniques comme le cancer, le SIDA, etc. L'atrophie musculaire est aussi une composante de la sarcopénie qui survient lors du vieillissement normal, et se caractérise par un déclin de la force et de la masse musculaire. L'atrophie musculaire, qui entraîne une augmentation de la mortalité et diminue l'efficacité des traitements, constitue donc un problème de santé majeur.La fonte musculaire se caractérise par une altération de l'équilibre entre synthèse et dégradation protéiques dans les fibres adultes. Des taux particulièrement élevés de cytokines circulantes, dont le TNFα, qui affectent l'homéostasie du muscle via différentes voies de signalisation, semblent être à l'origine de l'atrophie. Les mécanismes de la réponse atrophique musculaire à ces taux circulants élevés sont cependant mal définis. Le TNFα a des effets complexes. Il peut activer de multiples voies de signalisation, parmi lesquelles l'induction de la synthèse de sphingolipides, et plus particulièrement de céramides, par la voie de novo et par l'activation des sphingomyélinases. Au niveau musculaire, les céramides sont connus pour leurs effets sur la signalisation de l'insuline, sur l'apoptose et sur la différenciation myogénique. Par contre, leur implication dans le cadre de l'atrophie n'avait jamais été prise en compte. L'objectif de ce travail a été dans un premier temps de démontrer le rôle des céramides dans l'atrophie. Dans un deuxième temps, nous avons caractérisé la voie de signalisation par laquelle l'augmentation intramusculaire de céramide induite par le TNFα aboutit à une chute de la synthèse protéique, couplée à une augmentation de la protéolyse. Dans ce but, nous avons mis au point des modèles in vitro d'atrophie, impliquant des myotubes traités par des concentrations physiologiques de TNF. Nous avons en parallèle étudié un modèle in vivo de cachexie induite chez la souris par l'implantation d'un adénocarcinome C26. L'analyse des sphingolipides nous a permis de montrer l'augmentation des taux de céramides concomitante à l'atrophie générée in vitro et in vivo. Le rôle des céramides dans l'atrophie a été démontré par l'effet protecteur des inhibiteurs de leur synthèse, dans les modèles in vitro et in vivo. Nous montrons de plus dans un modèle in vitro que les effets atrophiques des céramides sont dus à l'inhibition de la voie de signalisation Phospholipase D/mTOR/Akt. Nos résultats nous ont permis de prouver le rôle des sphingolipides dans le contrôle de l'homéostasie protéique du muscle. La modulation du métabolisme des sphingolipides apparaît donc comme une nouvelle cible thérapeutique prometteuse dans le traitement de la perte musculaire associée à diverses pathologies.

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30

Amir, Al Timimi. "Elektroneurografi - analys av distala latenstider vid registrering över musculus lumbricalis II och musculus interosseus dorsalis II." Thesis, Örebro universitet, Institutionen för hälsovetenskaper, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-51315.

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31

Sirieix, Chrystelle. "Rôle du noyau paragigantocellulaire latéral dans le réseau du sommeil paradoxal chez le rat." Phd thesis, Université Claude Bernard - Lyon I, 2011. http://tel.archives-ouvertes.fr/tel-00857424.

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Le LPGi est la région bulbaire qui contient le plus grand nombre de neurones exprimant Fos pendant l'hypersomnie de SP. 10% de ces neurones Fos dans le LPGi projettent au locus coereleus, une région SP-Off. Récemment, Sapin et al. ont montré que 70% des neurones exprimant Fos pendant l'hypersomnie de SP sont de nature GABAergique. Notre hypothèse est que le LPGi contient des neurones de nature SP-On dont une partie participerait à l'inhibition des noyaux SP-Off. Nous cherchons à vérifier cette hypothèse, d'autre part à identifier les régions afférentes au LPGi actives au cours du SP et enfin, à identifier les projections du LPGi. Nous avons utilisé l'enregistrement extracellulaire des neurones du LPGi chez le rat vigile en contention stéréotaxique. Nous avons couplé cette technique avec le protocole de privation/ rebond de SP par la technique de la piscine. L'analyse du taux de décharge des neurones enregistrés au sein du LPGi montre que celui-ci contient trois types neuronaux différents (SP-On, SP-Off et indifférents). L'analyse des données neuroanatomiques montre que l'afférence majeure du LPGi, active au cours du SP, réside dans le SLD. Le LPGi est donc bien impliqué dans le réseau du SP car il contient des neurones faisant varier leur taux de décharge avec les différents états de vigilance. Le SLD, considéré comme la structure exécutive du SP, de nature glutamatergique, exciterait le LPGi au cours du SP. Ce dernier, de nature GABAergique, inhiberait le noyau moteur facial. Ce travail met pour la première fois en évidence l'activité de la voie SLD-bulbe rachidien ventrolatéral et suggère que le LPGi participe en partie à l'atonie musculaire caractéristique du SP

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32

Thompson, Cynthia. "Effects of tendon and plantar cutaneo-muscular vibration on postural control during quiet and perturbed standing." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66753.

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Modulation of lower limb somatosensory information can have a profound effect on postural orientation and balance control during both quiet and perturbed stance. Vibration is a powerful stimulus known to activate the muscle spindle Ia afferents as well as the cutaneous receptors and causes directionally specific, vibration-induced falling reactions. These reactions have been well-documented during quiet stance. However, little is known of the effects of manipulating, either separately or concurrently, somatosensory inputs arising from the muscle and plantar cutaneous receptors on the postural strategies triggered to maintain balance during quiet and especially perturbed stance. The aim of this thesis was to study the whole-body postural responses developed to maintain balance during quiet and perturbed stance, in conditions where somatosensory inputs from the lower limb muscles and plantar cutaneous receptors are altered by vibration. The first study showed that applying bilateral Achilles tendon vibration during quiet stance produces backwards leaning, characterized by changes in angular positions in the trunk, pelvis, hips, knees and ankles. Those changes are associated with modifications in the activation of muscles located away from the vibrated site. Moreover, the effects of vibration persisted after the end of vibration. The second study demonstrated that the amplitude of the balance reactions following support surface tilts can be increased or decreased depending on the magnitude of backward leaning caused by bilateral Achilles tendon vibration prior to the onset of the perturbation. The equilibrium reactions for tilts given during vibration involved changes in the peak angular excursions and muscle activity of the trunk, hips, knees and ankles. The last study showed that bilateral vibration of the plantar soles rearfoot regions produced a forward whole-body tilt with increased flexion in trunk, h
La modulation des informations somatosensorielles provenant des membres inférieurs affectent la posture et l'équilibre en position debout stationnaire ainsi qu'en présence de perturbations du sol. La vibration est un stimulus qui active les afférences Ia provenant des fuseaux neuromusculaires et les récepteurs cutanés. Elle provoque ainsi des réactions de chute qui sont orientées de façon spécifique et dépendent de la région vibrée. Ces réactions sont bien documentées en position stationnaire debout, mais peu d'informations sont disponibles sur les effets de la vibration tendineuse et / ou cutanée sur les réactions posturales déclenchées par des perturbations externes. Le but de cette thèse était d'étudier les réactions posturales développées pour maintenir l'équilibre en position stationnaire debout et en présence de perturbations externes lorsque les informations somatosensorielles des membres inférieurs sont altérées par l'application de vibration. La première étude a montré que la vibration bilatérale des tendons d'Achille en position stationnaire debout produit une inclinaison du corps vers l'arrière, qui est caractérisée par des changements d'orientation du tronc, du bassin, des hanches, des genoux et des chevilles. Ces changements d'orientation sont aussi associés à des modifications du niveau d'activité de plusieurs muscles localisés à distance de la région vibrée. De plus, ces effets posturaux persistent après l'arrêt de la vibration. La seconde étude a démontré que l'amplitude des réactions posturales déclenchées par des perturbations externes est augmentée ou diminuée en présence de vibration des tendons d'Achille. L'augmentation ou la diminution des réactions posturales dépend de l'amplitude de l'inclinaison vers l'arrière causée par cette vibration avant le début de la perturbation. La modification de ces réactions posturales impli

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Dmitriev, Petr. "Le rôle de l'élément répété D4Z4 et du facteur de transcription KLF15 dans la dystrophie musculaire facioscapulohumérale (FSHD)." Phd thesis, Université Paris Sud - Paris XI, 2011. http://tel.archives-ouvertes.fr/tel-00679863.

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La dystrophie musculaire facioscapulohumérale (FSHD) est la troisième myopathie la plus fréquente en Europe. La maladie atteint progressivement les muscles du visage, des bras et des jambes. Les symptômes apparaissent dans la majorité des cas avant 20 ans et la maladie, souvent douloureuse, provoque fréquemment un handicap majeur qui nécessite de se déplacer en fauteuil roulant. J'ai démontré que la protéine KLF15 est surexprimée dans les tissus des patients FSHD et dans les myoblastes cultivés in vitro et prélevés sur des patients FSHD. Des résultats préliminaires indiquent que la surexpression du facteur KLF15 pourrait être expliquée par le stress oxydant induit par DUX4 et la surexpression de certains facteurs de myogenèse induits par DUX4c. J'ai démontré que KLF15 interagit directement avec les répétitions D4Z4 et contrôle leur fonction d'activation de transcription. Ainsi KLF15 sert de médiateur entre les répétitions D4Z4 et deux gènes dans la région 4q35: FRG2 et DUX4c ce que explique la surexpression de ces deux gènes dans la FSHD. La surexpression du gène DUX4c, homologue du DUX4, perturbe le programme de différentiation musculaire en activant certains facteurs de myogenèse (myomiRs ou microRNAs myogéniques). En somme, la découverte du rôle du facteur KLF15 dans la FSHD met en évidence une boucle de rétrocontrôle positif qui relie la surexpression du facteur KLF15 avec la surexpression des gènes codés dans la région 4q35. Le rôle central du facteur KLF15 dans ce nouveau modèle de la maladie permet d'envisager une nouvelle piste thérapeutique pour la dystrophie FSHD basé sur l'inhibition du facteur KLF15.

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Kitagawa, Aya Christine. "Core muscular endurance differences in recreational runners with a previous history of running-related musculoskeletal injuries and healthy runners." University of Toledo / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1396447742.

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35

Lecomte, Virginie. "Rôle des facteurs de transcription SREBP-1 dans la fonction musculaire : implication des répresseurs transcriptionnels BHLHB2 et BHLHB3." Phd thesis, Université Claude Bernard - Lyon I, 2009. http://tel.archives-ouvertes.fr/tel-00583077.

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Les protéines SREBP-1, Sterol Response Element Binding Proteins, sont des régulateurs clés du métabolisme des lipides et du cholestérol. A ce titre, ils ont été largement étudiés dans le foie et le tissu adipeux. Les facteurs SREBP-1 sont également exprimés dans le muscle squelettique au sein duquel ils sont les principaux médiateurs des effets géniques de l'insuline.Les travaux de thèse présentés dans ce manuscrit ont eu pour but de définir le rôle spécifique de SREBP-1 dans le muscle squelettique. L'étude transcriptomique de cellules musculaires humaines révèle plus de1500 gènes régulés par SREBP-1 dans le muscle squelettique humain, dont la moitié est réprimée. L'analyse fonctionnelle de ces gènes révèle l'implication de SREBP-1 dans des fonctions musculaires dépassant la cadre du métabolisme glucido-lipidique. Ainsi, SREBP-1 inhibe l'expression de plusieurs gènes impliqués dans la différenciation et le maintien du phénotype musculaire. En conséquence, la sur expression de SREBP-1 bloque la différenciation myogénique in vitro et induit une atrophie marquée in vitro, sur des myotubes différenciés et in Vivo, dans le muscle squelettique de souris.En parallèle, deux répresseurs transcriptionnels : BHLHB2 et BHLHB3 apparaissent, après étude de leur promoteur, comme deux nouvelles cibles directes de SREBP-1. Ainsi, 20% des gènes inhibés par SREBP-1sont des cibles de BHLHB2 et BHLHB3, de nombreux gènes muscle-spécifiques y compris. De plus, BHLHB2 apparaît, de la même façon que SREBP-1, comme un acteur essentiel dans l'action de l'insuline sur le muscle squelettique, et dans le développement de l'insulino-résistance musculaire chez les patients diabétiques de type2.Le blocage de la différenciation myogénique et l'atrophie induite par SREBP-1 in vitro étant reversées par l'inhibition de l'expression de BHLHB2 et BHLHB3, nous concluons que BHLHB2 et BHLHB3 sont responsables de l'effet répressif de SREBP-1 sur le phénotype musculaire.Ces résultats mettent donc en évidence un nouveau rôle pour les facteurs SREBP-1 dans la régulation de la myogenèse et le maintien de la masse musculaire. SREBP-1 intègrent ainsi la régulation métabolique au contrôle du phénotype musculaire

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36

Hagberg, Catharina. "Electromyography and bite force studies of muscular function and dysfunction in masticatory muscles." Doctoral thesis, Umeå : Umeå universitet, 1986. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-141308.

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Electromyographic (EMG) activity versus bite force was studied during a gradually increased isometric contraction up to maximal effort for patients with painful masseter muscles and referents. The masseter muscle, the anterior temporal muscle and the descending part of the trapezius muscle were chosen for the recordings. Bite force was registered with a bite force sensor placed between the first molars. The effects of double blind intramuscular injections of lidocaine and saline in the patients' masseter muscle were evaluated by EMG versus bite force and by assessments of discomfort. EMG activity during unilateral chewing was compared in terms of relative masticatory force between referents and patients by amplitude probability distribution analysis. Regression analyses showed intra-individually steeper slopes for high force levels than for low force levels for the masseter muscle. This was not observed for the anterior temporal muscle. These differences in slopes of the EMG versus force regressions for the masseter muscle and the anterior temporal muscle could be due to differences in recruitment pattern. The same intra-individual relationship between low and high force levels was found for referents and patients. An increased activity, especially among the patients, was found for the descending part of the trapezius muscle during stronger activity of the mandibular elevators. The EMG versus force relationship for low force levels of the masseter muscle was less steep after an intramuscular injection of lidocaine but not after saline. Both solutions for injection had a positive effect on the patients' assessments of discomfort one week after the injection. Three days after injection the patients who received lidocaine experienced a reduction in muscular discomfort. This reduction was not found among patients receiving saline. The amplitude probability distribution analysis revealed that the patients used greater relative masticatory forces than the referents during the chewing of an almond for all probability levels analysed below the peak load of the masseter muscles. Rough estimates of the peak masticatory forces in Newton (N) were for chewing an almond 364 N (referents); 373 N (patients) and for gum-chewing 239 N (referents); 238 N (patients) as regards the masseter muscle. The values were similar for the anterior temporal muscle.
digitalisering@umu

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37

Young, Christopher Nicholas James. "Abnormalities in P2X7 receptor expression and function in muscle of the mdx mouse model of Duchenne muscular dystrophy." Thesis, University of Portsmouth, 2011. https://researchportal.port.ac.uk/portal/en/theses/abnormalities-in-p2x7-receptor-expression-and-function-in-muscle-of-the-mdx-mouse-model-of-duchenne-muscular-dystrophy(d78dc008-6621-4cc8-bcd0-0c78c3561540).html.

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Duchenne muscular dystrophy (DMD) is the second most commonly inherited disorder in man, the phenotype of which displays pathological characteristics of altered skeletal muscle function including, amongst others, abnormal Ca2+ homeostasis and cell signaling. This study used the mdx mouse model of DMD to analyse purinergic responses in dystrophic muscle cells in vitro and skeletal muscles in situ. Initial investigations excluded reduction in ATPe hydrolysing potential from explaining previous observations of heightened nucleotide sensitivities in dystrophic myoblasts. Instead, this study demonstrates for the first time that significant P2X7 receptor abnormalities exist in dystrophic myoblasts and skeletal muscles of the adult mdx mouse; significantly elevated levels of P2X7 receptor mRNA and protein expression were found in primary myoblast cultures, myoblast lines and muscles in situ at 4 months of age and this was extended to analysis of changes in individual P2X7 splice variants. These abnormalities were shown to extend to functional responses in cultured myoblast lines, where heightened P2X7 receptor-specific sensitivity was shown to be associated with significantly higher basal and induced levels of, and altered time course of, extracellular-signal regulated kinase (ERK1/2)phosphorylation in dystrophic myoblasts. ERK activation responses were shown to be inducible by ATP and BzATP stimulation, inhibited by P2X7 antagonists, and unresponsive to ivermectin, thus confirming P2X7 receptor involvement. Similar up-regulation of P2X7 receptor expression coinciding with ERK phosphorylation was demonstrated in mdx muscles in vivo. Additionally, NAD was identified as a mediator of P2X7 responses in dystrophic myoblasts. This study has also employed a mass spectrometry based approach to investigate the immediate downstream effects of P2X7 activation in cultured myoblasts; allowing identification of multiple potential signaling relays for future study that are discussed. The potential for a link between P2X7 receptor and dystrophin expression has been suggested here through the demonstration that abnormalities in P2X7 receptor expression and function are corrected by micro-dystrophin expression in dystrophic myoblasts. In vivo pharmacological P2X7 receptor inhibition using CBBG significantly reduced the number of revertant fibres in dystrophic muscle, indicating a reduction in degenerative/regenerative activity. The data presented in this thesis highlight a novel role for P2X7 receptor signaling in dystrophic myoblasts and muscles in situ; proposing the potential for beneficial therapeutic strategies aimed at manipulating P2X7 signaling responses in vivo, with a view to slowing the progression of what is at present an incurable and invariably fatal disease.

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Wechsler, Daniel Steven Gary. "Immune mechanisms of cure in Trypanosoma musculi infection." Thesis, McGill University, 1987. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=75348.

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Trypanosoma musculi is a protozoan parasite which produces a characteristic, self-limiting murine infection of approximately three weeks duration; the infection comprises a growth phase, a plateau phase and an elimination phase. Following clearance of parasitaemia, a mouse is cured and immune to reinfection. The present studies examine the immune mechanisms which operate during the elimination phase.
Passive transfer of plasma from an immune mouse to an infected recipient brings about rapid and complete clearance of parasitaemia in C57BL/6 mice. This curative activity is labile to heat treatment for 30 minutes at 56$ sp circ$C. A protein A- derived immunoglobulin fraction of immune plasma (IP) shares these properties. Further purification shows that the curative activity resides primarily in the IgG2a subclass, and that this antibody is intrinsically heat-labile. Complement component C3 (but not the lytic C5-C9 sequence) is necessary for antibody-mediated cure of infection. Cellular elements (macrophages) are also essential for elimination of parasitaemia to occur. The ultimate T. musculi effector mechanism thus requires the interaction of both humoral and cellular components.

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39

Avraam, More. "MR-fluid brake design and its application to a portable muscular device." Doctoral thesis, Universite Libre de Bruxelles, 2009. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210235.

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Many devices are available on the market for the evaluation and rehabilitation of patients suffering from muscular disorders. Most of them are small, low-cost, passive devices based on the use of springs and resistive elements and exhibit very limited (or even not any) evaluation capabilities; extended muscular force evaluation is only possible on stationary, expensive, multi-purpose devices, available only in hospitals, which offer many exercise modes (e.g. isokinetic mode) that are not available on other devices.

The objective of this thesis is to make the functionalities currently only implemented on bulky multi-purpose devices available at a lower cost and in a portable fashion, enabling their use by a large number of independent practitioners and patients, even at home (tele-medecine applications).

In order to achieve this goal, a portable rehabilitation device, using a magneto-rheological fluid brake as actuator, has been designed. This particular technology was selected for its high level of compactness, simple mechanical design, high controllability, smooth and safe operation. The first part of this thesis is devoted to the design of MR-fluid brakes and their experimental validation. The second part is dedicated to the design of the rehabilitation device and the comparison of its performances with a commercial multi-purpose device (CYBEX).
Doctorat en Sciences de l'ingénieur
info:eu-repo/semantics/nonPublished

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40

Botha, Sune St Clair. "The effects of hot-deboning on the physical quality characteristics of ostrich (Struthio camelus) Muscularis gastrocnemius, pars interna and Muscularis iliofibularis." Thesis, Stellenbosch : University of Stellenbosch, 2005. http://hdl.handle.net/10019.1/1513.

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Thesis (Msc Food Sc (Food Science))--University of Stellenbosch, 2005.
The aim of this study was to investigate the effects of hot-deboning (1 h post-mortem) on the shelf-life and the physical meat quality characteristics, including tenderness, pH, purge (%), cooking loss (%), and raw meat colour of vacuum packed ostrich (Struthio camelus var. domesticus) meat cuts from the M. gastrocnemius, pars interna and the M. iliofibularis during post-mortem refrigerated aging for respectively 21 d at 4ºC and 42 d at -3º to 0ºC.

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41

Larochelle, Nancy. "Gene therapy for muscular dystrophy : evaluation of a muscle-specific promoter for adenovirus-mediated gene transfer." Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=20231.

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Replication-defective (E1+E3 deleted) human adenovirus vectors are promising means of therapeutic gene delivery to skeletal muscle cells. Since the tropism of adenovirus is non-selective, muscle-specific expression of systemically administered vectors can only be achieved by the use of a tissue-specific promoter/enhancer that is small enough to fit the insert capacity of the vector. We have generated a replication-defective adenovirus recombinant (AV) in which the reporter gene (firefly luciferase) was driven by a truncated (1.35 kb) muscle creatine kinase (MCK) promoter/enhancer. Highly efficient and muscle-specific transgene expression was demonstrated in immunodeficient mice after local injection of AV into muscles at early age. Luciferase levels produced by AVMCKlux compared favourably to those in parallel experiments from injection of AVRSVlux in which lux expression is driven by the ubiquitously active LTR sequences of RSV. In nonmuscle tissues (brain, liver, kidney, lung), the transgene expression was extremely low even though in these tissues in situ polymerase chain reaction showed as high an infectivity of the cells by the AV as in muscle, and high levels of expression were obtained with AVRSVlux. The relatively small size, the good efficiency and the muscle specificity of the MCK promoter/enhancer would make it ideal to drive the 6.3 kb (truncated) dystrophin cDNA in first generation AV (with a limited (8 kb) insert capacity) designed for gene therapy of Duchenne muscular dystrophy.

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Betts, Corinne A. "Exon skipping peptide-pmos for correction of dystrophin in mouse models of duchenne muscular dystrophy." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:545d586a-ad7b-4089-8537-b2677957b874.

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Duchenne muscular dystrophy (DMD) is a fatal, muscle-wasting disorder due to mutations/deletions in the dystrophin gene. Whilst improvements in palliative care have increased the life expectancy of patients, cardiomyopathy and respiratory complications are still the leading causes of death. A potential therapy for the treatment of DMD is antisense oligonucleotides (AOs), which modulate dystrophin pre-mRNA splicing to restore the dystrophin reading frame and generate a truncated functional protein. Conjugation of AOs to cell penetrating peptides (CPP), such as Pip5e-, significantly improves delivery to skeletal muscles and to the heart, which is imperative given the impact of cardiomyopathy to mortality. However, it should be noted that the contribution of skeletal muscles, such as the core respiratory muscle, the diaphragm, in dystrophic cardiopulmonary function is poorly understood. The specific aims of the work in this thesis were to (i) understand the effect of the diaphragm on cardiac function using magnetic resonance imaging (MRI), (ii) screen a number of derivatives of Pip5e (Pip6) in an effort to discover further promising peptides and define the properties integral to heart penetrating capacity, and (iii) assess whether Pip6-PMOs restore cardiac function (MRI) following a repeat, low dose regimen. In short, the specific restoration of dystrophin in the diaphragm of the dystrophic mouse model, the mdx mouse, did not improve cardiac function, highlighting the importance of a body-wide therapy. The screening of multiple Pip5e-PMO derivatives revealed 3 promising peptides with improved cardiac splicing capacity; however, serial deletions of amino acids from the central core resulted in the diminution of dystrophin restoration, possibly due to a reduction in hydrophobicity. Finally, the Pip6-PMO treatment regimen substantially restored dystrophin protein (28% in heart) and stabilised cardiac function, even with an increased work load. In conclusion, this study illustrates the importance of a body-wide treatment, such as the CPP strategy (Pip-PMO). These Pip-PMO conjugates demonstrate high dystrophin restoration in a number of muscles, including cardiac muscle, and have a beneficial effect on cardiac function.

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Divljak, Gordan. "Muscular strength and power development to high and low resistance loads in trained individuals. : 8-week intervention." Thesis, Gymnastik- och idrottshögskolan, GIH, Institutionen för idrotts- och hälsovetenskap, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:gih:diva-4911.

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Aim The purpose of this study was to examine high versus low resistance training loads performed to muscular failure and its effect on muscular strength, power and strength endurance. Method 11 men and 3 women (age 26,4 ±4,4 years, weight 79,9 ±10,7 kg, height 179,4 ±76 cm) were recruited to train for 2 days/week for 8-weeks in the leg press and leg extension. One leg was randomly allocated to a high load (HL) program performing 3-5 reps and the other leg was allocated to the low load (LL) program, performing 20-25 reps. All sets were executed to muscular fatigue. The participants were measured for 1RM strength, strength endurance and muscular power before and after the study. Results HL and LL leg significantly improved strength gains in the LP exercise by 20,3%, respectively 21%, P< 0,001, but no difference was noted between legs P= 0,876. HL displayed significant increases in the LE exercise by 10,3%, P< 0,05, while no significant improvement occurred for the LL leg, -2,7%, P> 0,05. Strength remained insignificantly similar between protocols P> 0,05. The mean power results indicated no significant improvements within protocols, HL P= 0,309, LL P= 0,112. There was also no significant difference between the two protocols after the intervention P= 0,646. As for muscular strength endurance, the LL performed more repetitions which was significantly greater than for the HL leg 26,5 reps, respectively 23,9 reps, P= 0,045. Conclusion This study concludes that similar strength gains can be accomplished when training with heavier or lighter loads as long as all resistance training is performed to muscular failure. It was also determined that performing lower loads to failure is superior for local strength endurance. Finally, traditional resistance training has no benefit for augmenting muscular power whether training with higher or lighter loads to exhaustion

Kursen Projektarbete

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Silva, Vinícius da Eira. "Avaliação da espectroscopia de ressonância magnética para quantificação de carnosina muscular em humanos." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/5/5164/tde-27102017-090103/.

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Introdução: A carnosina (beta-Alanil-L-Histidina) é um dipeptídeo encontrado em altas concentrações em diversos tecidos excitáveis, tais como o coração, cérebro e músculo. Embora o número de evidencias sobre os efeitos benéficos da carnosina esteja aumentando, muitos desses estudos apresentam uma importante limitação: a falta de mensuração da carnosina intramuscular. O principal motivo é a necessidade de realização de biópsias musculares. Nesse sentido, um novo método não invasivo baseado na ressonância magnética de hidrogênio (1H RNM) foi apresentado como alternativa. Objetivos: Determinar a reprodutibilidade, acurácia e sensibilidade do 1H MRN na determinação do conteúdo de carnosina muscular em seres humanos contra a referência \"padrão-ouro\" de quantificação de carnosina, cromatografia líquida de alta eficiência (HPLC) em extratos musculares obtidas por biópsia muscular. Métodos: O estudo foi dividido em duas sub-investigações, sendo a primeira delas uma investigação in vitro que testou a linearidade do sinal da carnosina na 1H RMN. Para a segunda investigação dezesseis homens fisicamente ativos (18 - 35 anos) sem doença crônico-degenerativa ou qualquer disfunção no aparelho locomotor se voluntariaram. Os participantes foram submetidos a duas sessões no total. Na sessão inicial, características antropométricas e de composição corporal foram mensuradas, cada indivíduo teve sua concentração de carnosina muscular do gastrocnêmio avaliada através da análise 1H MRN (um teste-reteste foi realizado com uma sub amostra para verificar a reprodutibilidade do método), em seguida uma biópsia muscular do gastrocnêmio foi realizada. Os voluntários então se submeteram a um período de quatro semanas de suplementação de 6,4 g. de beta-alanina por dia, estimulo que comprovadamente aumenta a carnosina muscular, durante esse período também foi realizada uma avaliação nutricional para determinar a quantidade carnosina ingerida em suas dietas. Na segunda sessão os indivíduos mais uma vez tiveram suas composições corporais avaliadas e realizaram o teste de 1H RMN e biópsia muscular para acessar suas concentrações de carnosina muscular. Resultados: In vitro: A linearidade de sinal de 1H RMN para as concentrações de carnosina testadas apresentou valores de R2 de 0,9771. In vivo: O teste-reteste da 1H RMN apresentou coeficiente de variação médio de 9,9 ± 10,34% e coeficiente de correlação interclasse de = 0,775 (95% C.I.: 0,324-0,939). Comparando-se os dois métodos: As concentrações de carnosina (em mmol/kg musculo seco) não foram estatisticamente diferentes tanto no pré (1H RMN -20,8±6,2; HPLC -23,3±10,5; p=0,45; 95% CI= -4,5 -9,6) quanto no pós-suplementação (1H RMN - 35,2±13,2; HPLC-27,8±11,7; p=0,15; 95% CI= -3,5 - 17,8) (n=13). Os valores de delta da concentração de carnosina muscular (em %) também não foram estatisticamente diferentes (1H RMN - 69,7±66,7; HPLC -38,2±58,2 p=0,16; 95% CI= -14,5 -77,5; ES=0,90). Ao observar os dados individuais, nota-se também baixa correlação dos dados individuais entre os métodos (R2 = 0,0448; r =0,212; p= 0,229). Conclusão: A 1H RMN apresentou baixa reprodutibilidade e acurácia quando comparada ao padrão ouro (HPLC), não sendo possível sua utilização para mensuração de carnosina muscular
Introduction: Carnosine (beta-Alanyl-L-Histidine) is a dipeptide found in high-concentrations in human tissue, such as heart, brain and muscle tissue. Although the body of evidence relating beneficial effects of carnosine is increasing, most of these studies have an important limitation: the lack of intramuscular carnosine measurement. The main reason for the absence of this measurement is the method of analysis; a muscle sample must be obtained via a muscle biopsy. In this regard, a new method non-invasive based on hydrogen magnetic resonance (1H NMR) has been used as an alternative. Objectives: The present study aims to determine the reproducibility, accuracy, and sensitivity of H-MRS in the determination of muscle carnosine content in humans; comparative data analysis will be performed against the \"standard\" reference of HPLC carnosine quantification in muscle extracts obtained by muscle biopsy. Methods: The study was divided into two sub-investigations. The first of which was an in vitro investigation that tested the linearity of the carnosine signal at 1 H NMR. For the second investigation, sixteen physically active men (18-35 years) without chronic-degenerative disease or any dysfunction in the locomotor apparatus volunteered. The participants were submitted to 2 sessions in total; Upon arrival to the initial session, anthropometric and body composition characteristics were collected before each individual underwent a muscle carnosine measurement of the gastrocnemius via H-MRS analysis (a test-retest was performed with a sub-sample to verify the reproducibility of the method) followed by a gastrocnemius muscle biopsy. Thereafter volunteers were submitted to a 4-week supplementation period of 6.4 g. of beta-alanine per day, a stimulus proven to increase muscle carnosine, during this period, volunteers had their carnosine dietary ingestion evaluated as well. Following the supplementation period, individuals were subjected to another body composition evaluation, 1H RMN and muscle biopsy. Results: In vitro: The linearity of 1 H NMR signal for carnosine concentrations tested showed R2 values of 0.9771. In vivo: 1 H NMR test-retest showed a mean coefficient of variation of 9.9 ± 10.34% and ICC= 0.775 (95% C.I.: 0.324-0.939).Comparing the methods: Carnosine concentrations (in mmol / kg dry muscle) were not significant difference either the in pre (1 H NMR -20.8 ± 6.2, HPLC -23.3 ± 10, 5, p = 0.45, 95% CI = -4.5 -9.6) and post-supplementation (1 H NMR - 35.2 ± 13.2, HPLC-27.8 ± 11.7, p = 0.15, 95% CI = -3.5-17.8) . The delta values of muscle carnosine concentration (in %) were not statistically different (1 H NMR - 69.7 ± 66.7; HPLC -38.2 ± 58.2 p = 0.16; 95 % CI = -14.5 -77.5; ES = 0.90). Comparing the individual data, there was a low correlation between the methods (R2 = 0.0448, r = 0.212, p = 0.229). Conclusion: 1H NMR showed low reproducibility and accuracy when compared to the gold standard (HPLC), not being possible its use for carnosine quantification

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Drinkwater, Eric J. "Muscular Strength, Fitness and Anthropometry in Elite Junior Basketball Players." 2006. http://eprints.vu.edu.au/535/1/535contents.pdf.

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Basketball is a sport with many complex demands that require a combination of fitness, skills, team tactics and strategies, and motivational aspects. However key areas that are likely to play an important role in a basketball player's success are muscular strength, fitness and body size. Methods of evaluating and developing these characteristics have been extensively tested in controlled research settings, but there is a dearth of research exploring the value of, and methods of improving, muscular strength, fitness and body size of basketball players within the demanding schedule of an elite junior development program. These were therefore explored in this thesis.

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Teuschler-Stewart, Sarah Marie. "Equine muscular adaptations to effective use of dietary fat during exercise." 2009. http://digital.library.okstate.edu/etd/TeuschlerStewart_okstate_0664M_10258.pdf.

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Carrasco, Alexander Jason. "Effects of exercise-induced dehydration on cognitive ability, muscular endurance and surfing performance : a thesis presented in partial fulfilment of the requirements for the degree of Master of Science in Sport and Exercise Science, Massey University, Auckland, New Zealand." 2008. http://hdl.handle.net/10179/759.

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The aim of this study was to measure the degree of dehydration experienced during surf practice and examine the effect this might have on surfing performance, cognitive function and muscular endurance of elite surfers. Twelve male national and international level surfers volunteered to take part in the study. Their mean (± SD) age, body mass, height and surfing experience were 27.0 ± 3.3 years, 73.2 ± 7.1 kg, 1.7 ± 0.05 m and 21.0 ± 3.1 years, respectively. The participants were randomly assigned to one of two trials: no fluid ingestion (NF) or fluid ingestion (FI) during 100 min of surf practice in a steamer wetsuit. The experiment was designed to emulate not only the physical and cognitive demands of surfing but also the ambient environment in which it takes place. Before and immediately after surf practice, the participants had their hydration status measured, completed a cognitive test battery and upper and lower-body muscular endurance tests. Surfing performance was assessed during the first and last 20 min of practice. At the conclusion of the NF trial, participants showed a 3.9 ± 0.7% body mass (BM) loss, this was significantly greater (P < 0.05) than the 1.6 ± 0.7% BM loss seen at the end of the FI trial. In the NF trial, surfing performance decreased by 20.3 ± 7.1%, but showed a slight improvement in the FI trial (1.9 ± 10.2%). Of the six cognitive domains assessed (short-term memory, information processing speed, working memory, attention, visuomotor skill and visual acuity) all were significantly impaired when at a 3.9 ± 0.7% BM loss (P < 0.05) yet were unaffected at a 1.6 ± 0.7% BM loss. Information processing speed and working memory were the most strongly correlated to surfing performance (r = 0.74; P < 0.05). At the conclusion of the NF trial upper and lower-body muscular endurance were diminished by 21.2 ± 5.5% and 4.4 ± 5.8%, respectively. At the conclusion of the FI trial upper-body muscular endurance was reduced by 17.0 ± 4.1% while lower-body muscular endurance was marginally better (1 ± 3%). There was a significant difference in muscular endurance capacity between trials yet no significant correlation was observed between muscular endurance and surfing performance. The findings of this study suggest that surf practice for 100 min in a steamer wetsuit results in BM loss severe enough to significantly impair surfing performance, cognitive function and muscular endurance. Yet, when water is consumed during surf practice, surfing performance, cognitive function and lower body (but not upper-body) muscular endurance is maintained. Keywords: fluid ingestion, surf training, steamer wetsuit, hypohydration.

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Kucherenko, Mariya. "Determination of Genetic Interactions Required for Dystrophin-Dystroglycan Function and Regulation in a Drosophila Model of Muscular Dystrophy." Doctoral thesis, 2009. http://hdl.handle.net/11858/00-1735-0000-0006-AD8B-3.

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Guetchom, Boniface. "Rôle d'un ajout de vitamine E alimentaire dans la prévention de la myopathie du poulet de chair." Thèse, 2011. http://hdl.handle.net/1866/5106.

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Des études précédentes ont montré qu’une carence en vitamine E prédispose à la myopathie du poulet de chair. L’effet d’un ajout de vitamine E dans la diète commerciale sur la dégénérescence des fibres musculaires de la poitrine et de la cuisse a été étudié chez les poulets de chair. Des poulets mâles ROSS 308 (n = 1100) ont été assignés de façon aléatoire à deux traitements alimentaires (aliment commercial + 25 à 50 mg de vitamine E surajouté par kg vs aliment commercial + 0 mg de vitamine E supplémentaire). Les poulets ont été répartis sur 10 parquets (cinq répétitions par traitement). Le poids corporel et la consommation d’aliment ont été mesurés hebdomadairement. Aux jours j28, j35, j42 et j49, du sang a été prélevé pour mesurer le niveau de vitamine E et l’activité de la créatine kinase (CK). Les muscles Pectoralis superficialis et Adductor magnus ont été prélevés pour des analyses histologiques aux jours j28, j42 et j49; les fibres dégénérées ont été dénombrées sur chaque muscle prélevé. La concentration plasmatique de vitamine E était plus élevée dans le groupe supplémenté (P = 0.001). L’activité de la CK n’était pas différente dans les deux groupes (P = 0.20) mais très élevée, et n’était pas toujours en relation avec les dommages musculaires, à cause de grandes fluctuations de la CK entre les individus du même groupe. Le nombre de fibres endommagées était plus élevé dans le muscle Pectoralis superficialis (poitrine) que dans le muscle Adductor magnus (cuisse) dans les deux groupes; il y avait aussi moins de fibres dégénérées à j28 dans la poitrine des poulets qui ont reçus la diète supplémentée. Ces résultats suggèrent que l’ajout de vitamine E à la diète conventionnelle augmente le niveau de vitamine E dans le plasma et dans les tissus, diminue le nombre de fibres dégénérées dans la poitrine des jeunes poulets sans pour autant modifier la conversion alimentaire. La mesure de l’activité plasmatique de la CK ne saurait suffire à elle seule pour détecter précocement la myopathie nutritionnelle dans les élevages de poulets de chair.
Previous studies have shown that vitamin E deficiency could lead to nutritional myopathy in broiler chickens. Vitamin E was added to a conventional commercial diet to evaluate its effect on breast and thigh muscle fibers degeneration in broiler chickens. Male chickens ROSS 308 (n = 1100) were randomly assigned to two dietary treatments (a commercial diet with 25 to 50 mg of extra vitamin E per kg of commercial diet and a commercial diet without extra vitamin E). Chickens were randomly divided into 10 pens (five replicates per treatment). Body weight and feed intake were monitored weekly. At d28, d35, d42 and d49 blood from chickens were sampled and assayed for level of vitamin E and creatine kinase (CK) activity. Both Pectoralis superficialis and Adductor magnus muscles from chickens were sampled for histological examination at d28, d42 and d49, and degenerated fibers were numbered. Plasma levels of vitamin E were higher in the supplemented group (P = 0.001), whereas activity of CK was high in both groups, but not significantly different (P = 0.20) due to strong fluctuations in CK activities within groups of these fast growing chickens. Pectoralis superficialis muscle had more damaged fibers than adductor’s in both groups. There were less degenerated fibers in pectoral muscle from d28 chickens receiving the supplemented diet. These results suggested that adding vitamin E into conventional diet increases plasma vitamin E and decreases the number of degenerated muscle fibers within pectoral muscle of young chickens. Measuring the CK activity in plasma is not sufficient for early detection of nutritional myopathy in broiler chicken’s farms.

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Rodrigues, Jéssica Filipa Esteves. "Estratégias nutricionais para hipertrofia muscular." Bachelor's thesis, 2017. https://repositorio-aberto.up.pt/handle/10216/106944.

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Dissertations / Theses on the topic 'Muscular science'

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