Dissertations / Theses on the topic 'Physiological hypertrophy'
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Crampton, Matthew S., and n/a. "Differential Gene Expression in Pathological and Physiological Cardiac Hypertrophy." Griffith University. School of Biomolecular and Biomedical Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20070104.165826.
Full textCrampton, Matthew S. "Differential Gene Expression in Pathological and Physiological Cardiac Hypertrophy." Thesis, Griffith University, 2006. http://hdl.handle.net/10072/366605.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
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Ferreira, Linda. "A Molecular Analysis of Cardiac Hypertrophy." Thesis, Griffith University, 2007. http://hdl.handle.net/10072/367757.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Griffith University. School of Medical Science.
Griffith Health
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McMahon, Gerard. "The physiological and biomechanical bases of muscular hypertrophy/atrophy." Thesis, Manchester Metropolitan University, 2013. http://e-space.mmu.ac.uk/314030/.
Full textSculthorpe, Nicholas. "Left ventricular long axis dynamics in pathological and physiological left ventricular hypertrophy." Thesis, University of South Wales, 2002. https://pure.southwales.ac.uk/en/studentthesis/left-ventricular-long-axis-dynamics-in-pathological-and-physiological-left-ventricular-hypertrophy(eeeb9f18-b0d5-433b-b261-2907df223717).html.
Full textKim, Jeong-Su. "The relationship of growth factor and muscle soreness to muscle hypertrophy." Virtual Press, 1998. http://liblink.bsu.edu/uhtbin/catkey/1101585.
Full textSchool of Physical Education
Arthur, Gavin Donald. "Calcium activated neutral protease : defining a physiological role in the development of cardiac hypertrophy." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0027/NQ48598.pdf.
Full textPugh, Jamie K. "Physiological responses to concurrent resistance exercise and high-intensity interval training : implications for muscle hypertrophy." Thesis, Loughborough University, 2016. https://dspace.lboro.ac.uk/2134/25092.
Full textWansapura, Arshani N. "The role of alpha Na,K-ATPase isoforms in mediating cardiac hypertrophy in response to endogenous cardiotonic steroids." University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1282577884.
Full textKirby, Tyler. "GLOBAL-SCALE ANALYSIS OF THE DYNAMIC TRANSCRIPTIONAL ADAPTATIONS WITHIN SKELETAL MUSCLE DURING HYPERTROPHIC GROWTH." UKnowledge, 2015. http://uknowledge.uky.edu/physiology_etds/22.
Full textBull, Mathew Michael. "Experimentally Altering the Compliance of Titin's Spring Region." Diss., The University of Arizona, 2016. http://hdl.handle.net/10150/613257.
Full textEssandoh, Kobina. "The Role of Tsg101 in the Development of Physiological Cardiac Hypertrophy and Cardio-Protection from Endotoxin-Induced Cardiac Dysfunction." University of Cincinnati / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1563526987921154.
Full textLopez, Johanna. "The MAKAPbeta Signalosome Is Involved In Cardiac Myocyte Hypertrophy Through The Recruitment Of Calcineurin Abeta: A Study On How Multimolecular Complexes Are Important For The Integration And Fidelity Of Signal Transduction Behind Cellular And Physiological Responses." Scholarly Repository, 2009. http://scholarlyrepository.miami.edu/oa_theses/226.
Full textNoorkoiv, Marika. "Neuromuscular adaptations of joint angle-specific force change after isometric training." Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2013. https://ro.ecu.edu.au/theses/531.
Full textSilva, Vitor Loureiro da. "Participação do trânsito de cálcio e suas proteínas reguladoras na melhoria da função cardíaca de ratos com estenose aórtica supravalvar e disfunção ventricular submetidos a treinamento físico." Botucatu, 2019. http://hdl.handle.net/11449/181555.
Full textResumo: Introdução: Diversos modelos experimentais têm avaliado o processo de remodelação cardíaca (RC); dentre eles, destaca-se a indução à estenose aórtica supravalvar (EAo). Os mecanismos fisiopatológicos responsáveis pela depressão da função cardíaca incluem alterações no trânsito de cálcio (Ca2+) e em suas proteínas regulatórias. O treinamento físico (TF) tem sido utilizado na terapêutica das cardiopatias. Na patologia cardíaca por sobrecarga pressórica, o TF restaura, total ou parcialmente, a atividade e/ou expressão das proteínas regulatórias do trânsito de Ca2+, otimizando o fluxo de Ca2+ intracelular e atenuando o prejuízo funcional cardíaco. Objetivo: Analisar a participação do trânsito de Ca2+ e suas proteínas reguladoras na melhoria da função cardíaca de ratos com EAo e disfunção ventricular pelo TF. Material e Métodos: Ratos Wistar machos (70-90 g), submetidos à cirurgia de EAo, foram divididos em dois grupos: controle operado (Sham) e EAo. Após 18 semanas da cirurgia, foi analisada função cardíaca para redistribuição dos grupos: não expostos ao TF (Sham, n= 36 e EAo, n= 29) e treinados (ShamTF, n= 33 e EAoTF, n= 32) durante 10 semanas. O treinamento físico aeróbio (TFa) em esteira foi realizado com velocidade equivalente ao limiar de lactato, obtida durante os testes de esforço (inicial, 4a e 7a semanas e final). A RC foi avaliada por ecocardiografia, músculo papilar e cardiomiócito isolados e macroscopia post mortem. O trânsito de cálcio miocárdico foi analisado pela e... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Introduction: Several experimental models have been proposed for the study of cardiac remodeling (CR); among them, the induction of supravalvular aortic stenosis (AoS). The pathophysiological mechanisms responsible for the cardiac function depression include changes in calcium (Ca2+) and its regulatory proteins. Exercise training (ET) has been used in the management of cardiopathies. In cardiac pathology due to pressure overload, ET completely or partially restores the activity and/or expression of regulatory proteins of Ca2+ handling, optimizing intracellular Ca 2+ flow and attenuating cardiac functional impairment. Objective: To analyze the participation of Ca2+ handling and its regulatory proteins in the improvement of the cardiac function of rats with aortic stenosis and ventricular dysfunction by ET. Material and Methods: Male Wistar rats (70-90 g) submitted to supravalvular aortic stenosis (AoS) were divided into two groups: operated control (Sham) and aortic stenosis (AoS). After 18 weeks of the surgical procedure, cardiac function analysis was performed for redistribution of the groups: non-exposed to exercise training (Sham, n = 36 and AoS, n = 29) and trained (ShamET, n = 33 and AoSET, n = 32) for 10 weeks. The treadmill exercise training was performed with a velocity equivalent to the lactate threshold, obtained during effort tests (initial, 4th and 7th weeks, and final). CR was evaluated by echocardiography, papillary muscle and cardiomyocyte isolated and postmort... (Complete abstract click electronic access below)
Doutor
Whyte, Gregory P. "Cardiac structure, and exercise gas exchange kinetics in elite multi-disciplinary athletes and hypertrophic cardiomyopathy patients." Thesis, University of Wolverhampton, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263329.
Full textWen, Yuhui. "The Physiological Consequences of Hypertrophic Cardiomyopathy (HCM) and Restrictive Cardiomyopathy (RCM) Related Mutations in Human Cardiac Troponin I." Scholarly Repository, 2008. http://scholarlyrepository.miami.edu/oa_dissertations/131.
Full textRocha, Eduardo Augusto Victor. "Avaliação da apoptose e neoangiogênese miocárdica no treinamento ventricular de cabritos jovens submetidos à sobrecarga de pressão contínua versus intermitente." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/5/5156/tde-06022017-155911/.
Full textIntroduction: Surgical correction of transposition of the great arteries beyond the neonatal period needs a previous pulmonary artery band to promote left ventricular hypertrophy thereby preparing the ventricle. Experimental studies have demonstrated that intermittent systolic overload causes a more efficient ventricular hypertrophy, as compared to traditional pulmonary artery banding. The adaptive mechanisms involved in the subpulmonary ventricle retraining are not completely established. Nevertheless, besides the hypertrophy and/or hyperplasia of the contractile cardiomyocytes, noncontractile cells (vascular and interstitial) from the stimulated ventricle also present structural phenotype changes. It remains unclear the ideal increasing rate of the myocardial interstitium as well as capillary vessel proliferation in the process of ventricular retraining before undertaking the arterial switch. Objective: This study sought to assess adaptive changes of the subpulmonary ventricle in regards to vascular endothelial growth factor (VEGF) expression and apoptosis in young goats submitted to continuous versus intermittent systolic overload by means of an adjustable pulmonary artery band. Methods: 21 young goats were separated into 3 groups: Control (no systolic overload), Continuous (96-hour continuous systolic overload), and Intermittent (four 12-hour periods of systolic overload paired with a 12-hour resting period). Systolic overload was adjusted to achieve a 0.7 RV / aortic pressure ratio. Hemodynamic evaluations were performed before and after systolic overload every day postoperatively. Echocardiograms were obtained preoperatively and at the end of protocol. After the study period, the animals were humanely killed for morphologic assessment, apoptosis and vascular endothelial growth factor (VEGF) expression. Results: Echocardiography revealed a marked increase in RV wall thickness in the Intermittent group (+129.2%), compared with the Continuous group (+58.2%; p<0.001), as well as both trained groups compared to Control group (p < 0.001). Regardless of the shorter systolic overload exposure of Intermittent group, both study groups had a similar increase in RV mass (Intermittent: + 115.8%; Continuous: +90.8%; p < 0.001), and septal mass (Intermittent: + 55.8%; Continuous: + 45.4%; p < 0.047), compared with the Control group. No significant changes in the left ventricle mass were seen. There was a negligible but significant increase in water content of RV (Continuous: +3.5%, Intermittent: +4.6%) and septal masses (both study groups: +3.5%) compared with that in the Control group (p < 0.002). RV VEGF expression was greater in the Intermittent group (2.89% ± 0.41%) than in the Continuous (1.80% ± 0.19%) and Control (1.43% ± 0.18%) groups (p < 0.023). VEGF expression in the myocardium of the right ventricle in the Intermittent group was also greater than that in the left ventricle and septum within the same group (p < 0.050). There was no significant difference in VEGF expression between the other cardiac sections or within the Control and Continuous groups. Regarding apoptosis, there were no significant changes in the RV myocardium of the three groups (Caspase: p=0,784; TUNEL: p=0,374). Conclusions: Both study groups have developed RV hypertrophy with no apoptosis or relevant myocardial edema. Nevertheless, intermittent systolic overload causes upregulation of VEGF expression in the subpulmonary ventricle, an adaptation that provides a mechanism for increased myocardial perfusion during the rapid myocardial hypertrophy of young goats. The association of the marked increase in RV mass and increased angiogenesis signaling has an important implication on the subpulmonary ventricle retraining protocol by promoting a compensatory growth of the coronary vasculature, allowing for a more efficient hypertrophy
Chieng, Hock-Ling, and 錢學霖. "Cav3.2 T-type Calcium Channel Participates in Swimming-induced Physiological Cardiac Hypertrophy." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/89729817816596845811.
Full text國立臺灣大學
動物學研究所
96
Voltage-gated T-type Ca2+ current (T-current) is temporarily recorded in cardiac myocytes during embryonic and postnatal period in some rodents (Leuranguer et al., 2000; Niwa et al., 2004) and was found linearly correlated with growth rate in rat of both sexes (Xu and Best, 1992). The growth of body weight and heart size has been well studied to be affected by chronically elevated growth hormone (GH) through the action of Insulin-like growth factor-1 (IGF-1) (Boguszewski et al., 1997; Ong et al., 2002; Xu and Best, 1991). Moreover, through the approach of patch-clamp, IGF-1 was found to be able to increase the current density of T-channels (Piedras-Renteria et al., 1997). Collectively, physiological cardiac hypertrophy in athletes is associated with increased cardiac IGF-1 formation, implying that T-channel might play a role in the physiological cardiac hypertrophy formation. To test the hypothesis that T-channels are involved in that cardiac remodeling during physiological cardiac hypertrophy, CaV3.2 T-type calcium channel deficient mice (CaV3.2-/-) were subjected to swimming training for 3 weeks and the development of cardiac hypertrophy was examined with echocardiography. At the basal level, there is no significant difference between wild type (WT) and CaV3.2-/- left ventricular mass (LVM) but after 3 weeks of swimming, WT showed a significant increase of LVM (0.11 ±0.0028 g (WT non-swim, n=7) and 0.13 ± 0.0029 g (WT swim, n=7, p<0.001). In contrast, swimming-induced physiological cardiac hypertrophy was blunted in CaV3.2-/-, the LVM were 0.1099 ± 0.005 (CaV3.2-/- non-swim, n=5) and 0.1036 ± 0.0028 (CaV3.2-/- swim 21ds, n=5, p=0.3). These findings suggest that CaV3.2 is necessary for triggering swimming-induced physiological cardiac hypertrophy.
Chieng, Hock-Ling. "Cav3.2 T-type Calcium Channel Participates in Swimming-induced Physiological Cardiac Hypertrophy." 2008. http://www.cetd.com.tw/ec/thesisdetail.aspx?etdun=U0001-2507200802074600.
Full textMiklas, Jason. "In Vitro Human Engineered Myocardium: A Study into both Pathological and Physiological Hypertrophy." Thesis, 2013. http://hdl.handle.net/1807/43241.
Full textBrower, Brooke E. "Influence of COX-inhibitors on myofiber hypertrophy and capillarization in response to resistance exercise in older individuals." 2013. http://liblink.bsu.edu/uhtbin/catkey/1721291.
Full textClimstein, Mike. "Myocardial structure and function differences between steroid using and non-steroid using elite powerlifters and endurance athletes." Thesis, 1989. http://hdl.handle.net/1957/38133.
Full textGraduation date: 1990
Lee, Jonah D. "Acute metabolic and chronic hypertrophic responses of skeletal muscle to low-volume high-intensity resistance exercise in humans." 2010. http://liblink.bsu.edu/uhtbin/catkey/1597249.
Full textAccess to thesis permanently restricted to Ball State community only
School of Physical Education, Sport, and Exercise Science
Yeh, Tzu-Shao, and 葉姿劭. "Studies on the Astragalus membranaceus Enhanced Myotube Hypertrophy in Skeletal Muscle and Improved Physiological Recovery after Exercise Injury in Human." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/fprubj.
Full text臺北醫學大學
保健營養學研究所
102
Herbal supplements and food factors are important resources to investigate about muscle hypertrophy or protein synthesis. We investigated Astragalus membranaceus (AM) whether those herbal supplements induce hypertrophy in myotubes through the phosphatidylinositol 3-kinase (PI3K)/Akt (also termed PKB)/mammalian target of the rapamycin (mTOR) pathway. Then, we study the safety assessment and exercise ability of AM supplements which can promote skeletal muscle hypertrophy. The results revealed that AM can promote hypertrophy in myotubes through the PI3K/Akt/mTOR pathway. Biochemical parameters and histopathological examination revealed no toxic effect of 6-week AM (0.615 and 3.075 g / kg B.W. / day) administration in training ICR mice. Furthermore, AM supplement (2.8 g / day, contain total astragalosides 1.455 mg / g ) can enhance serum insulin-like growth factor-1 (IGF-1) concentrations and increase the oxygen content of muscle tissue in human. According to our study, we suggest that AM may be used as a candidate nutritional supplement to promote athletic performance.
Nelson, Matthew Jay. "Impact of N-2-mercaptopropionylglycine (MPG) and simvastatin on exercise-induced cardiac adaptations." 2008. http://hdl.handle.net/2152/17945.
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