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Byrne, Christopher. "Muscle function after exercise-induced muscle damage". Thesis, Bangor University, 2001. https://research.bangor.ac.uk/portal/en/theses/muscle-function-after-exerciseinduced-muscle-damage(2bbf5fe1-f35b-4b7b-9790-ff3a04b86875).html.
Pełny tekst źródłaDonnelly, A. E. "Delayed onset muscle soreness and damage". Thesis, University of Aberdeen, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234314.
Pełny tekst źródłaPenailillo, Luis. "Muscle damage and metabolic profiles of eccentric cycling". Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2013. https://ro.ecu.edu.au/theses/706.
Pełny tekst źródłaAhmadi, Sirous. "Monitoring muscle oxygenation and myoelectric activity after damage-inducing exercise". Thesis, The University of Sydney, 2007. http://hdl.handle.net/2123/2240.
Pełny tekst źródłaAhmadi, Sirous. "Monitoring muscle oxygenation and myoelectric activity after damage-inducing exercise". University of Sydney, 2007. http://hdl.handle.net/2123/2240.
Pełny tekst źródłaIn this thesis, three experiments were conducted to monitor: (i) muscle oxygenation and electromyographic activity of the biceps brachii after exercise-induced muscle damage (ii) muscle oxygenation after downhill walking-induced muscle damage, and, (iii) muscle oxygenation following a bout of vigorous concentric exercise. Maximal eccentric exercise (EE) of biceps brachii resulted in significantly increased mean resting oxygen saturation and decreased deoxyhaemoglobin. During isometric contractions at 50% and 80% of subjects’ maximum voluntary torque (MVT), oxygen desaturation and resaturation kinetics and volume were significantly decreased after EE, and these declines were significantly prevalent over the following 6 days. Additionally, a significant shift in median frequency intercept (measured by electromyography; EMG) towards lower frequencies was observed during isometric contractions at both 50% and 80% MVT after EE in the exercised arm. After an exhaustive session of downhill walking, another form of EE, resting total haemoglobin and oxyhaemoglobin decreased. Furthermore, during isometric contractions at 30%, 50% and 80% of MVT, prolonged and significant increases were observed in oxygen desaturation and resaturation kinetics and volumes after ambulatory EE. In contrast to the two EE experiments, concentric contractions did not evoke any prolonged changes in muscle oxygenation. Collectively, the findings of this thesis revealed significant and prolonged changes in muscle oxygenation at rest and during exercise, following sessions of strenuous eccentric exercise. Although not clear, the possible mechanism responsible for the changes in muscle oxygenation after EE could be increased resting muscle oxygen utilization due to probable muscle damage and a subsequent requirement of energy demanding repair processes. Concentric exercise resulted in fatigue, but it did not affect muscle oxygenation. Although a prolonged reduction in EMG median frequency intercept was observed after EE, this was not closely time-associated with the biochemical, anthropometric or functional markers of muscle damage.
Saxton, John Michael. "Exercise-induced damage to human skeletal muscle". Thesis, University of Wolverhampton, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385185.
Pełny tekst źródłaEmslie-Smith, A. M. "The acute inflammatory response to muscle damage". Thesis, University of Newcastle Upon Tyne, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382877.
Pełny tekst źródłaSwanson, Scott Carl. "Muscle glycogen concentrations, GLUT4 and muscle damage in humans following eccentric exercise /". The Ohio State University, 1996. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487942476407478.
Pełny tekst źródłaFARR, Trevor. "EFFECTS OF HYPOXIA ON EXERCISE INDUCED MUSCLE DAMAGE". Edith Cowan University. Computing, Health And Science: School Of Exercise, Biomedical & Health Science, 2007. http://adt.ecu.edu.au/adt-public/adt-ECU2007.0017.html.
Pełny tekst źródłaByrne, Julie Alison. "Mechanisms of damage in isolated skeletal muscle cells". Thesis, University of Liverpool, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333620.
Pełny tekst źródłaFarr, Trevor M. "Effects of hypoxia on exercise induced muscle damage". Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2006. https://ro.ecu.edu.au/theses/30.
Pełny tekst źródłaIsaacs, Ashwin Wayne. "Muscle damage and adaptation in response to plyometric jumping". Thesis, Stellenbosch : Stellenbosch University, 2012. http://hdl.handle.net/10019.1/20384.
Pełny tekst źródłaENGLISH ABSTRACT: The aim of the study was to investigate skeletal muscle changes induced by an acute bout of plyometric exercise before and after plyometric training. The study consisted of an acute study and training intervention study. The acute study, investigated whether direct evidence of ultrastructural damage and identification of indirect factors were more evident in subjects presenting with rhabdomyolysis. Moreover the training intervention study investigated whether plyometric training would protect the muscle from ultrastructural damage and rhabdomyolysis. During the acute intervention, twenty six healthy untrained individuals completed an acute bout of plyometric exercise (10 x 10 squat-jumps, 1 min rest). After, thirteen subjects continued with the training intervention. Eight of these subjects completed 8 weeks of plyometric jump training, while five subjects were instructed to rest from physical activity for 8 weeks. Seven days after the final training session the training and rest group repeated a second acute bout of plyometric exercise. Acute Study: Creatine kinase (CK) activity increased significantly following the single bout of plyometric exercise in all subjects (baseline: 129 to day 4: 5348 U/l). This was accompanied by an increase in perceived pain, C-reactive protein (CRP) a marker of inflammation as well as white blood cells (WBCs). Electron micrographs of muscle biopsies taken 3 days post exercise showed evidence of ultrasructural damage and membrane damage was apparent by immunofluorescence by the loss of dystrophin staining. A stretch of the c-terminus of titin was observed by immunogold, and western blot analysis indicated an increase in calpain-3 autolysis. Based on individual CK responses (CK range: 153-71,024 U/L at 4days after exercise) the twenty six subjects were divided into two groups, namely the high (n=10) and low responders (n=16). Training intervention: Following training the trained group did not experience: a rise of CK activity (110.0 U/l), perceived pain, CRP, WBCs, Z-line streaming, a stretch of titin or calpain-3 activation; while in the control group only two subjects presented with Z-line streaming. The results indicate that high responders have a more pronounced inflammatory response compared to low responders after eccentric exercise, therefore more WBCs and more specifically neutrophils are recruited to damaged areas resulting in greater membrane damage by respiratory burst in high responders. This damage can be limited with training by remodelling sarcomeric proteins via calpain activation resulting in the stable assembly of proteins in the sarcomere preventing the release of proteins.
AFRIKAANSE OPSOMMING: Die doel van die studie was om skeletspier veranderinge wat teweeggebring is deur voor en na afloop van akute pleometriese oefening, te ondersoek. Die studie bestaan uit ‘n akute intervensie en ‘n oefeningsintervensie gedeelte. Die akute intervensie het ondersoek ingestel na die direkte bewyse van ultrastrukturele skade en identifikasie van indirekte faktore meer sigbaar is in proefpersone wat met rhabdomiolose presenteer. Meerso het die oefningsintervensie die moontlikheid dat pleometriese oefening die spier van ultrastrukturele skade en rhabdomiolose beskerm, ondersoek. Tydens die akute intervensie is 26 gesonde ongeoefende individue die akute pleometriese oefeningsessie (10 x 10 hurkspronge, 1 min rus) voltooi. Hierna het 13 proefpersone voortgegaan met die oefeningsintervensie. Agt van hierdie proefpersone het agt weke pleometriese sprongsessie oefeninge voltooi, terwyl vyf proefpersone gevra is om vir 8 weke geen oefeninge te doen nie. Sewe dae na afloop van die finale oefeningssessie het die oefening en kontrole groep in ‘n tweede herhaalde akute pleometriese oefeningsessie deelgeneem. Akute intervensie: kreatienkinase (KK) aktiwiteit het betekenisvol verhoog na die enkel pleometriese oefeningsessie in all proefpersone (basislyn: 129 tot op dag vier: 5348 U/l). Hierdie is vergesel met ‘n toename in die persepsie van pyn, c-reaktiewe proteïen (CRP) ‘n merker van inflammasie sowel as witbloedselle (WBS). Elektronmikrograwe van spierbiopsies wat geneem is drie dae na afloop van die oefeninge, het tekens van ultrastrukturele skade en membraanskade getoon wat ook deur immunofluoresensie duidelik warneembaar was deur die verlies van distrofienverkleuring. ‘n Verrekking van die c-terminus van titin is ook waargeneem deur middel van immunogold. Westernblot analyse het ‘n toename in calpain-3 outolise getoon. Gegrond op individuele KK response (KK grense: 153-71,024 U/L na vier dae post oefening) is 26 proefpersone verdeel in twee groepe naamlik ‘n hoë (n=10) en lae responders (n=16). Oefeningintervensie:: Na oefening het die geoefende groep nie ‘n toename in KK aktiwiteit getoon nie (KK aktiwiteit (110.0 U/l)), pynervaring, CRP, WBS, Z-lynstroming, ‘n strekking van titin of calpain-3 aktivering; terwyl in die kontrole groep daar slegs twee proefpersone met Z-lynstroming geïdentifiseer is. Die resultate wyse daarop dat hoë responders ‘n meer uitgesproke inflammatoriese reaksie toon vergeleke met die lae responders na afloop van essentriese oefening. Daar word dus meer WBS en spesifiek meer neutrofiele na beskadigde areas gelokaliseer wat in grootter membraanskade deur respiratoriese inspanning in die hoë responders. Hierdie skade kan beperk word deur oefening waardeur hermodulering van sarkomeriese proteïene via calpain aktivering tot stabiele rangskiking van proteïene in die sarcomere lei en daardeur proteïen vrystelling verhinder.
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Nottle, Carmel. "Proprioceptive and muscle activation changes in triceps surae associated with exercise induced muscle damage". Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2004. https://ro.ecu.edu.au/theses/779.
Pełny tekst źródłaKendall, Becky. "The role of oestrogen in exercise-induced muscle damage". Thesis, Bangor University, 2003. https://research.bangor.ac.uk/portal/en/theses/the-role-of-oestrogen-in-exerciseinduced-muscle-damage(8158fa02-da06-4dc9-a701-f89d23a72657).html.
Pełny tekst źródłaWoodcock, Alan. "Electrical stimulation of chronically denervated muscle". Thesis, University of Surrey, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301288.
Pełny tekst źródłaMeulen, Jacob Hendrikus van der. "Exercise-induced muscle damage: morphological, biochemical and functional aspects". [Maastricht : Maastricht : Rijksuniversiteit Limburg] ; University Library, Maastricht University [Host], 1991. http://arno.unimaas.nl/show.cgi?fid=5654.
Pełny tekst źródłaSanders, LesLee F. "Attenuation of exertional muscle damage with a nutritional supplement /". Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/6609.
Pełny tekst źródłaBrown, Stephen James. "Exercise induced damage to skeletal muscle and connective tissue". Thesis, University of Wolverhampton, 1997. http://hdl.handle.net/2436/88296.
Pełny tekst źródłaMcLoughlin, Cormac Coburn. "Clinical and experimental aspects of suxamethonium induced muscle damage". Thesis, Queen's University Belfast, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334537.
Pełny tekst źródłaWilkinson, Ann Elizabeth. "Skeletal muscle damage in patients with multiple organ failure". Thesis, University of Liverpool, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283453.
Pełny tekst źródłaMcCall, Karin Elizabeth. "Mechanisms of cellular damage in isolated mouse soleus muscle". Thesis, University of Liverpool, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317007.
Pełny tekst źródłaChapman, Dale W. "Lengthening contraction velocity and exercise-induced muscle damage of the elbow flexors in humans". Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2008. https://ro.ecu.edu.au/theses/211.
Pełny tekst źródłaHowatson, Glyn. "Eccentric exercise and muscle damage : treatment, prevention and cross-education". Thesis, Kingston University, 2005. http://eprints.kingston.ac.uk/20368/.
Pełny tekst źródłaChild, R. B. "Exercise and free radical induced damage to human skeletal muscle". Thesis, University of Wolverhampton, 1997. http://hdl.handle.net/2436/96616.
Pełny tekst źródłaBurniston, Jatin George. "Clenbuterol-induced growth and damage of cardiac and skeletal muscle". Thesis, Liverpool John Moores University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.400532.
Pełny tekst źródłaPhoenix, Joanne. "The protective role of vitamin E in skeletal muscle damage". Thesis, University of Liverpool, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333696.
Pełny tekst źródłaMcArdle, Anne. "Mechanisms skeletal muscle damage in the dystrophin-deficient MDX mouse". Thesis, University of Liverpool, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385144.
Pełny tekst źródłaBushell, Alison Jayne. "Protection of skeletal muscle against ischaemia and reperfusion induced damage". Thesis, University of Liverpool, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365914.
Pełny tekst źródłaVan, de Vyver Mari. "The contribution of inflammatory mediators to delayed secondary muscle damage". Thesis, Stellenbosch : Stellenbosch University, 2013. http://hdl.handle.net/10019.1/79787.
Pełny tekst źródłaENGLISH ABSTRACT: Background: Understanding the contribution of divergent individual response patterns remains a key objective in identifying mechanisms of inflammation and potential factors limiting the resolution of inflammation. The purpose of this research project was to investigate downstream effects of inflammation following exercise-induced muscle damage in human subjects. Methods: For three different studies, a total of 53 untrained healthy male participants were recruited and divided into a non-exercising control (n=13) and exercise-induced muscle damage groups (n=40). The study design for the three studies was the same (with few exceptions): Downhill running (DHR) (12 x 5min bouts, 10% decline, 15 km.h-1) with blood samples taken pre, post, after 2 and 4 hours post-exercise (2h, 4h) and on days 1, 2, 3, 4 and 7 (d1-d7). Serum was analysed for creatine kinase activity (CK), myoglobin (Mb), cortisol, cytokine (TNFα, IL-1ra, IL-1β, IL-4, IL-6, IL-8, IL-10, sIL-6R), chemokine (G-CSF, MIP-1β) and adhesion factor (sICAM-1, sP-selectin) concentrations. Tissue degradation was assessed by serum matrix metalloprotease (MMP-9) and myeloperoxidase (MPO) content. White blood cell differential count was determined and the surface expression of various cluster of differentiation factors (CD11b, CD163, CD68, CD88, CD34) as well as intracellular MPO were assessed in whole bood using flow cytometry. Nuclear localization of the inflammatory mediator NFĸB in isolated perhipheral blood mononuclear cells (PBMCs) was determined using immunofluorescence microscopy. Muscle biopsies (vastus lateralis) taken at baseline, 4h, d1 and d2 were analysed for fibre type, inflammatory and stress-induced pathways (STAT3, IĸBα, p38MAPK), myogenic factors (MyoD, myogenin), neutrophil activity (MPO) and satellite cell number (Pax7). Results: Participants in the DHR group were subdivided into those with a normal recovery (DHR1) and those who developed secondary damage (DHR2). CK peaked on d1 in both subgroups (DHR1: 1512 ± 413 u.L-1, DHR2: 1434 ± 202 u.L-1) and again on d4 only in the DHR2 group (1110 ± 184 u.L-1). A similar IL-6 and IL-10 response was evident immediately post DHR in all individuals. Additional IL-6 was released in the DHR2 subgroup peaking at 4h (10.3 ± 4.2 pg.mL-1) whereas IL-10 had returned to baseline. IL-1ra (23.6 ± 8.8 pg.mL-1), CD68+ (5%) and CD163+ (3%) monocytes were significantly higher in the DHR2 subgroup. Neutrophil count at 2h (DHR1: 8.6 ± 0.8 x109 cells.L-1, DHR2: 11.4 ± 1.8 x109 cells.L-1) was significantly (p<0.02) correlated to CK activity on d4. PBMC NFĸB p65 nuclear localization was slightly less at 2h in the DHR2 compared to the DHR1 and control groups. Intramuscular STAT3 signalling and MPO were significantly higher in the DHR2 compared to the DHR1 subgroup at 4h and d2 respectively. The progenitor cell response was similar for all DHR individuals with an increase in Pax7+ SC observed at 4h (0.06 ± 0.01 Pax+ SCs/fibre) and d1 (0.07 ± 0.02 Pax+ SCs/fibre). Conclusion: Healthy young men can be divided into those with a adequate and those with a less efficient capacity to control the post damage inflammatory response. The early cytokine response, especially IL-6, seems to be a key role player in the cascade of events leading to late secondary skeletal muscle damage.
AFRIKAANSE OPSOMMING: Agtergrond: Die begrip van uiteenlopende individuele reaksie patrone, is belangrik in die identifisering van faktore asook meganismes betrokke in die ontwikkeling en resolusie van inflammasie. Die doel van hierdie navorsingsprojek was om die gevolge van oefening-geïnduseerde spierskade en inflammasie te ondersoek in menslike proefpersone. Metodiek: ‘n Totaal van 53 gesonde mans is tydens drie verskillende studies, gegroepeer in ’n kontrole (geen oefening) (n=13) en oefening geinduseerde spier skade (DHR) groep (n=40). Die uitleg van de studies was eenders (met min uitsonderings): Afdraende hardloop (12 x 5min hardloop sessies, 10% afdraende, 15km.h-1) met bloed monsters geneem voor, na, 2 ure, 4 ure (pre, post, 2h, 4h) en op dag 1, 2, 3, 4 en 7 (d1-7). Serum is ontleed vir die volgende: kreatien kinase aktiwiteit (CK), kortisol, sitokiene (TNFα, IL-1ra, IL-1β, IL-4, IL-6, IL-8, IL-10, sIL-6R), chemokien (G-CSF, MIP-1β) en adhesie molekuul (sICAM-1, sP-selectin) konsentrasies. Weefsel degradasie is vasgestel deur die teenwoordigheid van matriks metalo-protease-9 (MMP-9) en miëloperoksidase (MPO) in serum te meet. Differensiële witbloed sel (WBC) telling asook die teenwoordigheid van sekere differensiasie faktore (CD11b, CD163, CD68, CD88, CD34) op die sel oppervlak asook intrasellulêre MPO vlakke is bepaal deur gebruik te maak van vloeisitometrie. Die lokalisering van NFĸB in die selkerne van geïsoleerde bloed mononukleêre selle (PBMC) is bepaal deur fluoriserende mikroskopie. Spierbiopsies (vastus lateralis) geneem tydens rus (basislyn), na 4h, en op d1 en d2 is ontleed vir veseltipe, inflammatoriese en stresverwante faktore (STAT3, IĸBα, p38 MAPK), miogeniese faktore (myoD, myogenin), neutrofiel aktiwiteit (MPO) en aantal satelliet selle (Pax7). Resultate: Deelnemers in die DHR-groep is onderverdeel in twee groepe. Persone wat normaalweg herstel het is saam gegroepeer (DHR1) en diegene wat sekondêre skade ontwikkel het is saam gegroepeer (DHR2). CK aktiwiteit in serum het hoogtepunte bereik op d1 in beide subgroepe (DHR1: 1512 ± 413 u.L-1, DHR2: 1434 ± 202 u.L-1) en weer op d4 in die DHR2 groep (1110 ± 184 u.L-1). 'n Soortgelyke IL-6 en IL-10 reaksie is onmiddellik na oefening (in al die proefpersone) waargeneem. Addisionele IL-6 is vrygestel in die DHR2 subgroep en het ’n hoogtepunt bereik na 4h (10.3 ± 4.2 pg.mL-1), terwyl IL-10 reeds teruggekeer het na rustende waardes. IL-1ra (23.6 ± 8.8 pg.mL-1), CD68+ (5%) en CD163+ (3%) monosiete was aansienlik hoër in die DHR2 subgroep. Neutrofieltelling na 2h (DHR1: 8.6 ± 0.8 x109cells.L-1, DHR2: 11.4 ± 1.8 x109cells.L-1) het verband (p <0,02) gehou met CK-aktiwiteit op d4. In vergelyking met die DHR1 en kontrole groep was die lokalisering van NFĸB p65 in PBMC selkerne na 2h effens minder in die DHR2 subgroep. STAT3- en MPO-vlakke in die spiere was aansienlik hoër in die DHR2 subgroep as in die DHR1 subgroep na 4h en op d2 onderskeidelik. Die spierherstel proses was eenders vir alle individue wat aan die oefening deelgeneem het; 'n toename in Pax7+ Satelietselle (SC) is waargeneem na 4h (0.06 ± 0.01 Pax+ SC/spiervesel) en op d1 (0.07 ± 0.02 Pax+ SC/spiervesel). Gevolgtrekking: Gesonde jong mans kan verdeel word in diegene met 'n bevoegde en diegene met 'n minder doeltreffende vermoë om oefenings-geïnduseerde spierskade en die inflammatoriese reaksie te beheer. Die sitokien-reaksie, veral IL-6, blyk om 'n belangrike rolspeler in die ontwikkeling van sekondêre skeletspierskade te wees.
Burt, Dean. "The effects of exercise-induced muscle damage on endurance performance". Thesis, University of Chester, 2013. http://hdl.handle.net/10034/314972.
Pełny tekst źródłaBosio, Andrea. "The effect of muscle fatigue and damage on endurance performance". Thesis, Bangor University, 2010. https://research.bangor.ac.uk/portal/en/theses/the-effect-of-muscle-fatigue-and-damage-on-endurance-performance(bdf9fd6a-4486-42f5-b2cb-7729986aa111).html.
Pełny tekst źródłaThiriot, Kathleen Nichole. "The Effect of Photobiomodulation Therapy on Exercise-Induced Muscle Damage". BYU ScholarsArchive, 2018. https://scholarsarchive.byu.edu/etd/6743.
Pełny tekst źródłaDeyhle, Michael Roger. "The Role of T Cells in Muscle Damage Protective Adaptation". BYU ScholarsArchive, 2018. https://scholarsarchive.byu.edu/etd/7455.
Pełny tekst źródłaSorensen, Jacob R. "Repair and Adaptation of Aged Skeletal Muscle to Nonpathological Muscle Damage: The Influence of Macrophage Polarization". BYU ScholarsArchive, 2018. https://scholarsarchive.byu.edu/etd/7691.
Pełny tekst źródłaMagoffin, Ryan Darin. "The Effect of Whole Body Vibration on Exercise-Induced Muscle Damage and Delayed-Onset Muscle Soreness". BYU ScholarsArchive, 2016. https://scholarsarchive.byu.edu/etd/6217.
Pełny tekst źródłaWiden, Cecilia, i n/a. "Energetics of Mouse Papillary Muscle". Griffith University. School of Physiotherapy and Exercise Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20070228.121312.
Pełny tekst źródłaWiden, Cecilia. "Energetics of Mouse Papillary Muscle". Thesis, Griffith University, 2006. http://hdl.handle.net/10072/367649.
Pełny tekst źródłaThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Physiotherapy and Exercise Science
Full Text
Blowfield, Kennedy. "Muscle damage and the repeated bout effect in male bodybuilders following unaccustomed resistance exercise". Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2016. https://ro.ecu.edu.au/theses/1935.
Pełny tekst źródłaJones, Garrett Collier. "Skeletal Muscle Recovery and Vibration". BYU ScholarsArchive, 2019. https://scholarsarchive.byu.edu/etd/8285.
Pełny tekst źródłaJakeman, John Robert. "The efficacy of contemporary recovery strategies following exercise-induced muscle damage". Thesis, University of Exeter, 2010. http://hdl.handle.net/10036/106718.
Pełny tekst źródłaHurley, Michael V. "Muscle function, inhibition and rehabilitation following traumatic and degenerative joint damage". Thesis, King's College London (University of London), 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321690.
Pełny tekst źródłaChilders, Martin K. "Contraction-induced muscle damage in dogs with golden retriever muscular dystrophy". free to MU campus, others may purchase free online, 2002. http://wwwlib.umi.com/cr/mo/preview?3074385.
Pełny tekst źródłaBenson, Brenda. "Downhill Treadmill Running Does Not Induce Muscle Damage in FVB Mice". BYU ScholarsArchive, 2014. https://scholarsarchive.byu.edu/etd/4259.
Pełny tekst źródłaBanyard, Henry. "Effects of pulsed electromagnetic field therapy on symptoms associated with eccentric exercise-induced muscle damage". Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2013. https://ro.ecu.edu.au/theses/705.
Pełny tekst źródłaEkstrand, Mathias. "The effects of muscle damaging electrically stimulated contractions and ibuprofen on muscle regeneration and telomere lengths in healthy sedentary males". Thesis, Örebro universitet, Institutionen för hälsovetenskap och medicin, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-27906.
Pełny tekst źródłaGlasgow, Philip D. "Delayed Onset Muscle Soreness (DOMS) : relevance of induction parameters and management by electrotherapeutic modalities". Thesis, University of Ulster, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365921.
Pełny tekst źródłaKomulainen, Jyrki. "Muscle water content and serum creatine kinase activity in exercise-induced damage". Jyväskylä, Finland : LIKES--Research Center for Physical Culture and Health, 1994. http://catalog.hathitrust.org/api/volumes/oclc/34903296.html.
Pełny tekst źródłaGrose, George Sebastian. "The effect of exercise-induced fatigue and eccentric muscle damage on kinaesthesia". Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/61726.
Pełny tekst źródłaEducation, Faculty of
Kinesiology, School of
Graduate
Vaile, Joanna. "Effect of hydrotherapy on recovery of muscle-damage and exercise-induced fatigue". University of Western Australia. School of Sport Science, Exercise and Health, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0221.
Pełny tekst źródłaRochester, John Robert. "Investigation of reperfusion injury in chronically ischaemic skeletal muscle using in-vitro microscopy". Thesis, University of Sheffield, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319434.
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