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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.
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Muscle function after exercise-induced muscle damage has traditionally been evaluated by measures of isometric strength at a single joint angle or muscle length. The thesis investigates the effect of muscle damage on other muscle function parameters such as, isometric strength as a function of muscle length, concentric strength as a function of angular velocity, strength across muscle actions, the stretch-shortening cycle, power output, and fatigability. Study 1 The first part of this study aimed to determine how the muscle length at which strength is measured affects reductions in isometric strength following eccentric exercise-induced muscle damage. The damaging exercise protocol consisted of 100 maximal voluntary eccentric actions of the knee extensors, performed in the prone position through a range of motion from 40° to 140° (0° = full extension) at an angular velocity of 90 deg's-1. Isometric strength of the knee extensors was measured at short muscle length (10° knee flexion) and optimal length (80°). A significantly greater relative loss of strength was observed at short versus optimal muscle length (76.3 ± 2.5% vs. 82.1 ± 2.7% of pre-exercise values, P<0.05) over the seven day testing period following eccentric exercise. The second part of the study investigated isometric strength at optimal length and concentric strength at slow (30 deg's 1) and fast (180 deg's 1) angular velocities of movement. No differences were apparent in the magnitude and rate of recovery of strength across isometric (82.1 ± 2.7%) and slow (86.6 ± 2.0%) and fast (84.3 ± 1.5%) concentric muscle actions. Both the popping sarcomere hypothesis of 2 muscle damage and a failure in excitation-contraction coupling are possible explanations for the reduction in strength being affected by the muscle length at which it is measured. Both would be expected to affect strength to a greater extent at short versus optimal muscle lengths. Study 2 The second study investigated knee extensor muscle strength during isometric, concentric and eccentric muscle actions and vertical jump performance under conditions of squat jump (SJ), countermovement jump (CMJ) and drop jump (DJ). These measures were taken before, 1 hour after, and on days 1,2,3,4 and 7 following a damaging exercise protocol consisting of 100 barbell squats (10 sets x 10 reps @ 70% body mass load). Strength was significantly reduced for four days, however, no differences were observed in the magnitude or rate of recovery of isometric strength at 80° knee flexion and concentric and eccentric strength at 90 deg's'. Vertical jump performance was significantly reduced for three days and was dependent on the type of jump being performed. The relative decline in SJ performance was significantly greater than that in CMJ performance (91.6 ± 1.1% vs. 95.2 ± 1.3% of pre-exercise values, P<0.05) and the relative decline in SJ was significantly greater than that in DJ performance (91.6 ± 1.1% vs. 95.2 ± 1.4%, P<0.05). No differences were observed in the relative decline in CMJ and DJ performance (95.2 ± 1.3% vs. 95.2 ± 1.4%, P> 0.05). The stretch-shortening cycle (SSC) of muscle function is utilised in CMJ and DJ but not in SJ. The SSC has a clear purpose: to allow the final phase (concentric action) to take place with greater force or power output, as compared to the condition where the movement is initiated by a concentric action alone. 3 Utilisation of the SSC in performance seems to attenuate the detrimental performance effects of exercise-induced muscle damage. Study 3 The third and final study investigated the effects of exercise-induced muscle damage on maximal power output and knee extensor fatigability under isometric and dynamic conditions. Under isometric conditions, strength was assessed at 40° and 80° knee flexion and fatigability was assessed by a sustained 60s maximum voluntary contraction (MVC) at each joint angle. For dynamic conditions, maximum power output and fatigue were assessed during a maximal 30s cycle ergometer test. These measures were taken before, 1 hour after, and on days 1,2,3, and 7 following a damaging exercise protocol consisting of 100 eccentric squats (10 sets x 10 reps @ 80% concentric 1 RM). Isometric strength was significantly reduced (P < 0.05) for seven days but no significant differences were observed in the magnitude of strength loss and the pattern of recovery between the two joint angles. Fatigability was quantified as the slope (b) of a linear regression line fitted to the torque and power decay during the 60s MVC and the 30s cycle test, respectively. Prior to muscle damage, subjects were significantly less fatigable (P < 0.05) at 40° (b = -2.39 ± 0.26) versus 80° (b = -5.50 ± 0.72). After muscle damage, subjects became significantly less fatigable at both 40° and 80° with recovery taking three days at 401 and seven days at 80°. Before damaging exercise, a greater rate of fatigue was observed under dynamic (b = -12.75 ± 2.3) versus isometric (80°) conditions (b = -5.50 ± 0.72). Isometric and dynamic fatigue 4 followed a similar temporal pattern after damaging exercise. When the effects of muscle damage on strength at 801 and maximal power output were compared, differences in the extent of performance loss and the time course of recovery were observed. At 1 hour post-exercise, strength was affected to a greater extent (30% reduction) than power (13% reduction) and whereas strength followed a linear recovery pattern, power suffered further decrements at day 1 (18%) and day 2 (16%) before starting to recover. The results indicate that under conditions of voluntary activation muscle becomes weaker but less fatigable under isometric and dynamic conditions following exercise-induced muscle damage. The lower starting torque / power output and the slower rate of decline in torque / power output observed in post-damage fatigue curves may be a phenomenon of selective type II fibre damage. Evidence suggests that type II fibres are selectively damaged during eccentric exercise and therefore post-damage fatigue curves may be missing their contribution to performance. The different recovery patterns observed for isometric and dynamic performance may indicate an inability to maintain central motor drive during complex dynamic tasks when damage is present.
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Donnelly, A. E. "Delayed onset muscle soreness and damage." Thesis, University of Aberdeen, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234314.
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The aims of the studies undertaken were to investigate the physiological and serum biochemical changes associated with muscle damage, and to test possible treatments for this condition. Initial studies examined the effects of walking 37 km daily for 4 days and of running 21.1 km and 25.6 km road race events in different groups of subjects. Prolonged walking produced little soreness, but daily increases in serum creatine kinase (CK) activity were recorded. In the two running studies, delayed increases in the serum activity of the enzymes CK, lactate dehydrogenase (LD) and aspartate transaminase (AST) were observed, as were changes in the CK and LD isoenzyme pattern. In a further study, the CK-MM isoform response to a maximal eccentric arm exercise was studied in 8 subjects. Although total CK activity continued to increase for 5 days after exercise, the CK MM1:MM3 ratio peaked at 48 h after exercise, when muscle soreness also peaked. Two non-steroidal anti-inflammatory drugs were assessed for their effectiveness in the muscle soreness condition. Diclofenac and ibuprofen were tested in double-blind crossover studies in which drug or placebo were administered before and after two bouts of 45 minutes downhill running. Neither drug proved effective in reducing muscle soreness or serum enzyme changes after the eccentric exercise. The effect of prior vitamin C supplementation on the same parameters was assessed, but this treatment also proved ineffective. A final study examined the effect of exercise during the period of muscle soreness and damage. In this study, a light eccentric exercise bout was performed 24 h after a heavy eccentric bout, using the same arm muscles. Performance of the light bout did not alter the symptoms of muscle soreness, but did effect serum CK activity changes and resistance to muscle fatigue during later eccentric exercise.
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Penailillo, 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.
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Eccentric cycling, in which the knee extensor muscles perform eccentric contractions while trying to brake the backward rotational movements of the cranks of a cycle ergometer, has been shown to effectively increase muscle function and volume with a low metabolic cost. However, acute responses to repeated eccentric cycling bouts have not been well documented. Thus, the primary purposes of this PhD project were to investigate muscle damage and metabolic profiles of eccentric cycling in comparison to concentric cycling (Studies 1-3), and muscle-tendon behaviour (Study 4) during eccentric cycling in relation to muscle damage.
Study 1 compared muscle damage and metabolic profiles between a bout of concentric cycling (CONC) and two bouts of eccentric cycling (ECC1, ECC2) performed by 10 healthy men (28 ± 8 y), with a 2-wk interval between bouts. All cycling bouts were performed for 30 min at 60% of CONC maximal power output (POmax). Heart rate (HR), oxygen consumption, blood lactate (BLa) and rate of perceived exertion were 19-65% lower during ECC1 than CONC, and HR and BLa were 12-35% lower during ECC2 than ECC1. Exercise-induced decreases in knee extensor maximal voluntary contraction (MVC) torque and vertical jump height as well as increases in muscle soreness were significantly greater after ECC1 than CONC and ECC2, and no significant changes in these variables were found one day after CONC and ECC2. It was concluded that eccentric cycling was less metabolically demanding than CONC, and muscle damage was minimal after the second eccentric cycling bout.
Study 2 examined fat and carbohydrate utilisation during and immediately after cycling, and resting energy expenditure before and both 2 and 4 days post-cycling using indirect calorimetry. An oral glucose tolerance test was performed before, and 1 and 3 days post-cycling. Fat utilisation was greater during ECC1 (72%) and ECC2 (85%) than CONC, and was 48% greater during ECC2 than ECC1. Post-exercise energy expenditure and fat utilisation were less after ECC1 than CONC (30% and 52%, respectively), but similar between CONC and ECC2. Glucose uptake increased 3 days post-ECC1. These results suggest greater fat utilisation during and after eccentric than concentric cycling without glucose uptake impairment.
Study 3 tested the hypothesis that rate of force development (RFD) would be a more sensitive marker of muscle damage than MVC torque by comparing the changes in MVC torque and RFD after CONC, ECC1 and ECC2. Decreases in MVC torque were significantly greater immediately and 1-2 days after ECC1 than CONC and ECC2. RFD decreased immediately after all cycling bouts, but RFD measured in the interval 100-200 ms (RFD100-200) decreased at all time points after ECC1 (24-32%) as well as immediately after ECC2 (23%), but did not change after CONC. The magnitude of decrease in RFD100-200 after ECC1 was 7-19% greater than MVC torque. These suggest that RFD100-200 is a more specific and sensitive marker of eccentric exercise-induced muscle damage than MVC torque.
To investigate the mechanisms underpinning the repeated bout effect in eccentric cycling, Study 4 examined the hypothesis that vastus lateralis muscle-tendon behaviour would be different between two (i.e. repeated) eccentric cycling bouts. Eleven healthy men (27.1 ± 7.0 y) performed 10 min of eccentric cycling at 65% of CONC POmax twice (ECC1, ECC2) separated by 2 weeks. Greater muscle soreness was developed 1-2 days after ECC1 than ECC2. Electromyogram and crank torque were similar between bouts, but the magnitude of fascicle elongation during ECC2 was 16% smaller than ECC1. These results suggest that smaller elongation of fascicles was associated with less muscle soreness after ECC2, and possibly the repeated bout effect.
These studies revealed the muscle damage profile of eccentric cycling, one of the potential mechanisms of the repeated bout effect, and metabolic characteristics of repeated eccentric cycling bouts. Since muscle damage is minimal and can be abolished by proper prescription, eccentric cycling may be an ideal exercise for elderly and frail individuals with impaired muscle oxidative function (e.g. diabetes and chronic obstructive pulmonary disease). Further studies are warranted in these populations.
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Ahmadi, Sirous. "Monitoring muscle oxygenation and myoelectric activity after damage-inducing exercise." Thesis, The University of Sydney, 2007. http://hdl.handle.net/2123/2240.
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In 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.
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Ahmadi, Sirous. "Monitoring muscle oxygenation and myoelectric activity after damage-inducing exercise." University of Sydney, 2007. http://hdl.handle.net/2123/2240.
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Doctor of PhilosophyIn 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.
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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.
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Emslie-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.
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Swanson, 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.
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FARR, 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.
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The present study investigated the hypothesis that maximal voluntary contractions (MVC) peak torque, VJ, muscle tenderness, and plasma creatine activity would be significantly less for the condition that subjects were exposed to hypoxic (H) condition for 4 hours after eccentric exercise compared with the normoxic (N) condition.
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Byrne, 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.
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Farr, 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.
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The present study investigated the hypothesis that maximal voluntary contractions (MVC) peak torque, VJ, muscle tenderness, and plasma creatine activity would be significantly less for the condition that subjects were exposed to hypoxic (H) condition for 4 hours after eccentric exercise compared with the normoxic (N) condition.
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Isaacs, Ashwin Wayne. "Muscle damage and adaptation in response to plyometric jumping." Thesis, Stellenbosch : Stellenbosch University, 2012. http://hdl.handle.net/10019.1/20384.
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Thesis (MSc)--Stellenbosch University, 2012.ENGLISH 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.
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The aim of this thesis was to examine proprioceptive and activation changes that occur in triceps surae in response to exercise induced muscle damage (EIMD). While proprioceptive changes have previously been demonstrated in association with EIMD, the present investigation examined the role of a number of potential contributing factors to these changes, following both single and repeated bouts of eccentric exercise.
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Kendall, 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.
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Oestrogen is believed to be a potent antioxidant, with potential membrane stabilising and gene regulatory effects. Oestrogen has been shown to be an effective cardioprotectant, with for example a lower incidence of atherosclerosis in pre menopausal females compared to age-matched males and in post menopausal females on hormone replacement therapy compared to age-matched males. What has yet to be determined is the extent to which oestrogen can protect skeletal muscle. It has been shown that certain markers of exercise-induced muscle damage (EIMD) are lower in females in both animal and human studies, but as yet no conclusive evidence from human studies has shown that oestrogen provides a protective mechanism against ERvID or whether susceptibility to EIKID varies across the normal menstrual cycle, where oestrogen fluctuations are high. Furthermore, if oestrogen provides a protective mechanism against EIlVID, it is unknown at which phase during the muscle damage and repair cycle this occurs. It is also debatable if the potential inhibitory effects that oestrogen has on the inflammatory response, with regard to repair and regeneration of the skeletal muscle are positive or negative. The thesis is comprised of a critical review of the nature of EIMD and the potential effects that oestrogen has on the muscle damage and repair cycle. This is followed by three empirical studies which were designed to explore this question. These are outlined below: Study 1 Study one was in two parts. The first part of this study aimed at determining if the phase of the menstrual cycle, could in anyway affect eumennorheic (normally 2 menstruating) females in their susceptibility to exercise-induced muscle damage. An eccentric exercise procedure (elbow flexor muscle group) was performed on a randomly assigned arm during either the menses or ovulatory phase of the menstrual cycle. The contra-lateral limb underwent the same procedure during the alternate phase (random assignment determined in which phase the participant was first damaged). Simple markers of EDM were assessed at baseline and every 24 h up to three days post exercise, during both phases. No significant differences were seen in any markers of BIMD across phases of the menstrual cycle. The second part of this study investigated whether prolonged ingestion of exogenous oestrogen, in the form of the combined oral contraceptive pill attenuated any of the symptoms associated with EIMD. The only symptom to show a significant interaction between groups was perceived soreness, with the pill users reporting significantly (P<0.01) less soreness than the eumennorheic females in the days following the exercise protocol. This suggested that oestrogen may modulate the pain associated with EIMD. Study 2 The second study focussed on gender differences in exercise-induced muscle damage, with particular focus on the secondary symptoms and events which occur following ERVID. Male and female participants performed a bout of eccentrically biased exercise. Markers of both EIMD and inflammation were taken prior to the eccentric exercise and across a 7-day follow up period. Gender differences in the response to EIMD were seen in creatine kinase activity and mid-thigh circumference, with males showing a larger response on both variables. In addition to this, males reported significantly less soreness than females following the exercise protocol. 3 Interestingly, with the exception of neutrophil elastase release, there were no differences in other markers of inflammation between men and women. Total elastase concentration, a marker of neutrophil activation, did not differ between genders. However, elastase release per neutrophil was significantly lower in females, which may be indicative of gender differences in the inflammatory response associated with EDvID. Study 3 With the recognition that oestrogen could potentially reduce or inhibit the inflammatory response the third and final study investigated whether female skeletal muscle was more susceptible to exercise-induced muscle damage after a second bout of eccentric exercise, due to poor regeneration and repair following the initial bout. Males and females performed a bout of eccentrically biased exercise. Markers of EEVM included creatine kinase, soreness, isometric strength and isokinetic strength assessment. The procedure was then repeated two weeks later to determine if gender differences existed in terms of the repeated bout effect associated with EIlvID. Only one variable showed a gender x time x bout interaction (P<0.05), that was the fatigue index. It was shown that following the initial bout of damage, males and females responded very differently, with female muscle being less fatiguable in the 48 h following damage compared to the males, but with both groups responding very similarly in the repeated bout. This may be due to differences in gender and their response to EIlVID, or due to differences in fibre type between genders.
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Woodcock, Alan. "Electrical stimulation of chronically denervated muscle." Thesis, University of Surrey, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301288.
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Meulen, 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.
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Sanders, 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.
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Brown, Stephen James. "Exercise induced damage to skeletal muscle and connective tissue." Thesis, University of Wolverhampton, 1997. http://hdl.handle.net/2436/88296.
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McLoughlin, 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.
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Wilkinson, 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.
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McCall, 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.
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Chapman, 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.
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Lengthening contraction velocity appears to be one of the factors affecting the magnitude of muscle damage, however limited human studies have investigated this issue. The purpose of this thesis was to clarify the effect of lengthening contraction velocity on changes in indirect markers of muscle damage after maximal voluntary lengthening exercise of the elbow flexors. This thesis incorporates five individual studies that have been published or submitted for publication in peer review journals.
The first study investigated the hypothesis that the variability of changes in indirect markers of muscle damage would be explained by work performed and/or torque generated during lengthening contraction exercise. Fifty-three subjects performed 60 maximal lengthening contractions of the elbow flexors through a range of movement from 60° to 180° of elbow flexion at a constant angular velocity of 90°·s -1 • Pearson's correlation coefficient was used to examine relationships between exercise parameters (total work, change in total work, torque produced during exercise, change in peak torque) and markers of muscle damage (maximal voluntary isometric contraction torque, range of motion, plasma creatine kinase activity and muscle soreness) were measured before, immediately after, and 24 - 96 hours after exercise. The analysis revealed that a large inter-subject variability was evident for both work and torque during exercise, and for changes in all markers of muscle damage. Contrary to the hypothesis, total work (normalised for individual pre-exercise MVC) absorbed during the exercise did not correlate significantly with any markers of muscle damage, with the exception of MVC (r = 0.3). Total work absorbed and changes in total work showed higher correlations with some markers, but nor-values exceeded 0.4. Normalised exercise torque and the changes in peak torque during exercise were not correlated with changes in MVC, nor other markers. The findings from this investigation suggested that the large inter-subject variability in responses to maximal voluntary lengthening exercise is not associated with work performed or torque generated during lengthening exercise.
The aim of the second study was to verify the lengthening torque-velocity relationship of human elbow flexors by considering whether muscle damage induced in maximal lengthening torque measurements influences the relationship. Twenty subjects were tested twice, separated by seven days, for maximal isometric strength at 90° of elbow flexion and maximal dynamic strength during lengthening contractions at velocities of 30°·s-1 followed by 90°, 150°, 210°·s-1 , and a repeated 30°·s-1 using a range of movement from 60° to 140°, where 180° was considered full extension. Assessment of maximal isometric strength preceded each lengthening contraction to assess the effects of muscle damage and/or fatigue on the measures. The difference in lengthening contraction strength at 30°·s-1 between the first and second attempts was used to adjust the torque values. The reliability of the measurements was supported by high intra-class correlation coefficients (0.96 - 0.99) and low coefficient of variation (6.3 - 9.1 %). Peak lengthening contraction strength across all velocities was significantly greater than maximal isometric strength (14 - 16%), but no significant differences were evident within velocities. The second lengthening contraction performed at 30°·s-1 was significantly lower (-10%) than the first, and maximal isometric strength decreased significantly over the measurements (-10%). Following adjustment, no significant differences in maximal dynamic lengthening torque among velocities were evident. It was concluded that lengthening contraction torque is approximately 15% higher than isometric torque without an influence of angular velocity for the elbow flexors in an untrained population.
The purpose of the third study was to investigate the effect of lengthening contraction velocity on muscle damage. Sixteen men were placed into two groups performing either 30 (n = 8) or 210 (n = 8) maximal lengthening contractions of the elbow flexors on an isokinetic dynamometer. Dominant and non-dominant arms were randomly assigned for a slow (S: 30°·s-1 ) or a fast (F: 210°·s-1 ) velocity exercise separated by 14 days. Maximal voluntary strength of isometric contractions (iMVC) and isokinetic concentric contractions ( cMVC), range of motion (ROM), upper arm circumference, muscle soreness and serum creatine kinase (CK) activity were measured before, immediately after, and 1 - 120 hours following exercise. Changes in these measures over time were compared by a two-way repeated measures ANOV A to examine the effect of velocity in the same number of contractions (S30 vs F30; S210 vs F210) or the effect of contraction number at the same velocity (S30 vs S21 O; F30 vs F210). A significant interaction effect was evident only for iMVC (90° P = 0.020 and 150° P = 0.033) between S30 and F30, but for iMVC (90° P = 0.040 and 150° P= 0.000), cMVC (150°·s-1 P= 0.042), ROM (P= 0.001) and CK (P = 0.000) between S210 and F210. Changes in most of the measures were significantly smaller after 30 (S30 and F30) than 210 contractions (S210 and F210). These results suggest that the effect of contraction velocity on the magnitude of muscle damage following 30 contractions is minor; however, when 210 lengthening contractions were performed, the effect of contraction velocity became conspicuous. It is concluded that fast velocity lengthening contractions are likely to induce greater muscle damage than slow velocity contractions; however, muscle fatigue appears to be a confounding factor for the velocity effect.
The fourth study tested the hypothesis that the first bout of exercise consisting of slow velocity (30°·s- 1 ) maximal lengthening contractions would not confer protection against a subsequent bout of exercise consisting of fast velocity (210°·s- 1 ) lengthening contractions. Eighteen men (26.3 ± 4.2 yrs) were randomly placed into two groups; repeated bout group (n = 10) and control group (n = 8). The repeated bout group performed two bouts of exercise consisting of 210 (3 5 sets of 6) maximal lengthening contractions of the elbow flexors separated by 14 days using their nondominant arm at a velocity of 30°·s-1 for the first bout and 210°·s-1 for the second bout. The control group performed the fast velocity bout only. Changes in maximal isometric strength, range of motion, upper arm circumference, muscle thickness, muscle soreness, serum creatine kinase and lactate dehydrogenase activities were measured before, immediately after, and 24 - 96 hours after exercise. Changes in the measures over time after the fast velocity exercise were compared between groups by a two-way repeated measure ANOV A. For the repeated bout group, changes in the measures were compared between bouts by a two-way repeated measure ANOV A. The repeated bout group showed significantly smaller changes or faster recovery of all criterion measures except for muscle soreness after the fast velocity exercise compared with the control group. A significant difference in the changes in the criterion measures between the slow and fast velocity bouts of the repeated bout group was evident only for range of motion. These results suggest that a bout of slow velocity lengthening contractions confers protection against muscle damage induced by fast velocity lengthening contractions, although the magnitude of protective effect conferred by the slow velocity exercise is not strong.
The final study investigated the hypothesis that muscle damage induced by fast velocity lengthening contractions would be greater for old than young men. Ten old ( 64 ± 4 yrs) and 10 young (25 ± 6 yrs) men performed 5 sets of 6 maximal voluntary lengthening contractions, through a range of movement from 60° to 180° at the angular velocity of 210°·s-1 • Changes in maximal isometric strength, optimum angle, elbow joint range of motion (ROM), upper arm circumference, muscle thickness and echo intensity assessed by B-mode ultrasonography, muscle soreness, and serum CK and LDH activities before, 1, 24 - 96 hrs post exercise were compared between the young and old groups by a two-way repeated measure ANOV A. Prior to exercise no significant differences were observed between groups for criterion measures, and for the work performed during exercise. A significant group x time interaction effect was found for isometric strength and muscle soreness, with the old group showing significantly slower recovery of strength and less development of soreness compared with the young group. Changes in other measures were not significantly different between groups. The results of this study refuted the hypothesis that old men are more susceptible to muscle damage, but confirmed the previous studies reporting that recovery of muscle strength is slower for old than young individuals. The mechanical factors, work absorbed and torque developed during lengthening contractions were not related to the magnitude of muscle damage. In addition it was determined that the torque developed during voluntary lengthening contractions with increasing velocities did not differ significantly. These works were used to justify the major findings from these studies indicating that lengthening contraction velocity has a significant effect on the magnitude of muscle damage with fast velocity lengthening contractions resulting in significantly greater damage than slow velocity lengthening contractions. It was proposed that the results are indicative of a stress susceptible group of muscle fibres that may not be fibre type specific but consists of a greater proportion of type II muscle fibres.
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Howatson, Glyn. "Eccentric exercise and muscle damage : treatment, prevention and cross-education." Thesis, Kingston University, 2005. http://eprints.kingston.ac.uk/20368/.
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Eccentric biased muscular contractions, when compared to concentric and isometric muscle actions have a number of benefits, which include greater hypertrophy, increased strength and a reduced metabolic cost at any given intensity. The literature has reported the benefits of eccentric contractions in a variety of populations, which include exercisers, athletes, geriatric and chronically diseased communities. However, eccentric contractions can result in temporary exercise-induced muscle damage (EIMD) that reduces function and causes soreness. Consequently, a number of interventions, such as post-exercise therapies and prior exercise have been used in an attempt to attenuate the negative effects of this muscle action. Therefore, the purpose of this thesis is to provide novel data to expand the existing body of knowledge and investigate a cryotherapeutic intervention that may attenuate the symptoms of exercise-induced muscle damage. Furthermore, this work examines the adaptation to prior exercise (the repeated bout effect) in the ipsilateral and contralateral limbs to provide additional novel data to elucidate the possible mechanisms responsible for adaptation. Study 1: The aims of the first study were to investigate the effects of repeated applications of ice massage on the markers of muscle damage using a within-subject, cross-over design and to examine the effects on muscle function during static and dynamic contractions. The results suggest that ice massage does not reduce any of the signs or symptoms of EIMD after high intensity eccentric exercise, nor does it return the function of static or dynamic muscle actions following a damaging bout of exercise. Study 2: The aims of this investigation were firstly, to determine the reliability of functional testing and the associated surface EMG signal on five consecutive days, and secondly to elucidate the reliability and precision of other dependent measures commonly used in the assessment of muscle damage following a bout of eccentric contractions. All variables displayed good reliability and therefore may be appropriate to examine longitudinal changes as a result of a damaging protocol. Study 3: The purpose of this investigation was to examine the magnitude of the repeated bout effect (RBE) from high and low volume maximal eccentric exercise followed by a high volume bout of maximal eccentric exercise after full recovery from the initial bout (two weeks later). There were no differences in dependent variables between groups in the repeated bout, indicating that the magnitude of the RBE is similar following initial low and high volume bouts of maximal eccentric exercise, which was attributable, at least in part, to changes in electromyographic frequency content. The initial high volume bout did however result in greater EIMD than the initial low volume bout; in addition, the magnitude of change from the initial bout was more profound after high volume exercise. Study 4: The aims of this investigation were to elucidate the existence of a contralateral RBE in the upper limb and to compare the magnitude of change to an ipsilateral model, which had been previously been established in Study 3. Significant differences in some variables provide evidence that a repeated bout effect is evident in the contralateral limb after a single bout of eccentric exercise. This adaptation appears to be mediated by neural mechanisms, as there is no direct stimulus for change from the initial bout to the contralateral homologous muscle group. The magnitude of change between contralateral and ipsilateral models was different for some variables suggesting that the RBE is not as profound in contralateral homologous muscle as in the ipsilateral model. These investigations provide additional novel data on interventions used to combat the negative effects of eccentric contractions and temporary EIMD. In particular, Study 4 has shown that adaptation occurs in the contralateral homologous muscle group, which has implications for a variety of populations and also for future research study design. Further investigations are warranted to elucidate the exact mechanisms responsible for the repeated bout effect.
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Child, R. B. "Exercise and free radical induced damage to human skeletal muscle." Thesis, University of Wolverhampton, 1997. http://hdl.handle.net/2436/96616.
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Burniston, 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.
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Phoenix, 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.
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McArdle, 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.
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Bushell, 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.
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Van, 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.
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Thesis (PhD)--Stellenbosch University, 2013.ENGLISH 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.
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Burt, Dean. "The effects of exercise-induced muscle damage on endurance performance." Thesis, University of Chester, 2013. http://hdl.handle.net/10034/314972.
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It is well documented that engaging in resistance exercise can lead to further improvements in endurance performance. Whilst, not fully understood, it is speculated that increased motor unit recruitment, improved muscle coordination and enhanced utilisation of stored elastic energy after resistance-based exercise improves exercise economy. Nevertheless, while prolonged exposure to resistance training improves endurance performance in the long-term, a consequence of such training when unaccustomed is the appearance of exercise-induced muscle damage (EIMD). Exercise-induced muscle damage is well known to affect athletic performance requiring muscular strength and power; however, its effects on markers of endurance exercise are unclear. Therefore, the aim of this thesis was to investigate the effects of EIMD on endurance performance, with an emphasis on the physiological (oxygen uptake; , minute ventilation; ), metabolic (blood lactate; [La]), perceptual (rating of perceived exertion; RPE) and kinematic (stride length; SL, stride frequency; SF) responses during sub-maximal endurance exercise.
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Bosio, 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.
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Locomotor muscle fatigue develops during endurance events and it is traditionally thought to limit performance despite no direct experimental evidence in favour of this hypothesis. Similarly, muscle damage is known to limiting strength and power performance, but there was no evidence that it can reduce endurance exercise performance. The aims of this thesis are to investigate the effects of locomotor muscle fatigue and damage on endurance performance and the physiological and perceptual response to exercise. In the first study, we tested the hypothesis that exercise-induced muscle damage can decrease performance during a 30 min running time trial. A significant relative 4%decrease in running performance was showed in subjects with exercise-induced muscle damage. In the second study locomotor muscle fatigue was induced with an eccentric exercise protocol to test its detrimental effect on time to exhaustion during high-intensity constant-power cycling independently of metabolic stress. A significant 15% drop in lower limb strength (compared to baseline) determined a shortening of the time to exhaustion from 750 ± 281 s to 636 ± 278 s. The third study provides a more in depth analysis of the effects of reduced locomotor muscle force per se on the physiological and perceptual response to high intensity endurance exercise. Locomotor muscle fatigue entailed an increase in heart rate, breathing frequency, and perceived exertion despite no change in the metabolic requirements. The same exercise protocol was used in the fourth study to investigate effects of locomotor muscle fatigue on incremental exercise performance and physiological/perceptual responses during cycling at di fferent intensities. Although no changes occurred in the physiological responses to incremental exercise, the 13% decrease in locomotor muscle force determined a 2% decrease in the peak power output (an overall difference of 21 W ) and a significant increase in the perceived leg effort. Overall, our findings show that both locomotor muscle fatigue and damage significantly and reliably impair endurance exercise performance between 10 and 30 minutes. However, the effects of increased central motor command to weaker locomotor muscles on cardiorespiratory responses seem to be dependent upon the degree of strength loss and the intensity of exercise. Finally, perception of effort is augmented by locomotor muscle fatigue and damage, and provides the most plausible explanation for the curtailment of endurance performance.
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Thiriot, Kathleen Nichole. "The Effect of Photobiomodulation Therapy on Exercise-Induced Muscle Damage." BYU ScholarsArchive, 2018. https://scholarsarchive.byu.edu/etd/6743.
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Purpose: To explore the difference between continuous and pulsed photobiomodulation (PBMT) versus a placebo treatment when using a red-blue light combination over multiple treatment sessions to decrease the symptoms of muscle damage in the quadriceps muscle after a bout of muscle damaging exercise. Methods: Thirty-six healthy, nonactive male and female participants were randomly assigned to one of three groups: continuous PBMT, pulsed PBMT, and placebo treatment. Participants were assessed for muscle damage with knee extension maximal isometric and isokinetic contractions, as well as Visual Analog Scale (VAS) and Lower Extremity Functional Scale (LEFS) scores. Blood creatine kinase (CK) was also analyzed. Participants were given treatment immediately prior to undergoing a bout of damaging eccentric exercise. Participants were treated with PBMT for the next 4 consecutive days for a total of 5 treatments. Results: The continuous treatment group lost significantly less isokinetic average peak torque than the placebo treatment when averaged across all time points postexercise. However, for isometric testing, the continuous group had more reduction in force compared to the placebo group. Between the treatment groups, the continuous treatment group had significantly more muscle soreness measured by the VAS and had significantly less function in daily tasks reported on the LEFS patient-oriented outcome scale. There was no significant difference in level of creatine kinase between the treatment groups. Conclusion: Pulsed photobiomodulation treatments had no significant effect when compared to the placebo group. Continuous photobiomodulation helped to reduce isokinetic force loss, yet exacerbated all other muscle damage markers following exercise relative to the placebo condition.
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Deyhle, Michael Roger. "The Role of T Cells in Muscle Damage Protective Adaptation." BYU ScholarsArchive, 2018. https://scholarsarchive.byu.edu/etd/7455.
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Skeletal muscle is prone to damage from a range of stimuli. The muscle repair process that ensues is complex, involving several phases and requiring the participation of many different cell types. Among the cells involved are various immune cells including neutrophils, macrophages, monocytes, and eosinophils. More recently, T cells were added to this list of immune cells known to participate in effective muscle repair from traumatic injuries in mice. We recently published data showing that T cells also accumulate in human muscle following contraction-induced damage. These data suggested that T cells might be involved an adaptation known as the repeated bout effect that renders muscle protected from future damage after an initial exposure. This document contains research on the role of the immune system, particularly T cells, in the "repeated bout effect."
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Sorensen, 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.
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The age-related loss of skeletal muscle mass and function is accompanied by a decline in regenerative capacity. The processes that facilitate healthy muscle repair are complex, involving several phases of degradation and rebuilding of muscle tissue and the surrounding microenvironment. Specifically, myogenic progenitor cells known as satellite cells are the most influential in repairing damaged muscle tissue. Following injury, satellite cells become activated and migrate, proliferate and fuse with mature skeletal muscle fibers to restore homeostasis to the tissue. However, satellite cells do not act in isolation, a robust inflammatory response is necessary to facilitate successful and rapid healing. Macrophages are one of the first and most abundant immune cells to infiltrate damaged skeletal muscle tissue. Primarily, macrophages adapt to a proinflammatory state to clear the area of cellular debris, promote degradation of the extracellular matrix and stimulate satellite cell activation and proliferation. Afterwards, a timely transition to an anti-inflammatory state directs rebuilding of the extracellular matrix and terminal differentiation of satellite cells. Indeed, the inhibition of macrophage activity leads to impaired healing and loss of skeletal muscle function. Little is known regarding the behavior of macrophages in aged skeletal muscle following injury in humans. Thus, the objective of this dissertation is to investigate the age-related response of macrophages in human skeletal muscle, and their role in muscle repair.
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Magoffin, 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.
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Current scientific evidence suggests that when whole body vibration (WBV) is used as a warm-up prior to performing eccentric exercise, delayed-onset muscle soreness (DOMS) is mitigated and strength loss recovers faster. These benefits were observed primarily in nonresistance-trained individuals. The aim of this study was to determine if WBV could mitigate soreness and expedite strength recovery for resistance-trained individuals when used as a warm-up prior to eccentric exercise. Thirty resistance-trained males completed 300 maximal eccentric contractions of the quadriceps after warming up with (WBV) or without (CON) WBV. Both CON and WBV experienced significant isometric (27.8% and 30.5%, respectively) and dynamic (52.2% and 47.1%, respectively) strength loss immediately postexercise. Isometric strength was significantly depressed after 24 hours in the CON group (9.36% p < 0.01), but not in the WBV group (5.8% p = 0.1). Isometric strength was significantly depressed after 48 hours in the CON group (7.18% p < 0.05), but not in the WBV group (4.02% p = 0.25). Dynamic strength was significantly decreased in both the CON and WBV groups both at 24 hours (19.1% p < 0.001, and 16.1% p < 0.001, respectively), 48 hours (18.5% p < 0.01, and 14.5% p < 0.03), and 1 week postexercise (9.3% p = 0.03, and 3.5%, respectively). Pain as measured by visual analog scale (VAS) was significant in both CON and WBV groups at 24 and 48 hours postexercise, but the WBV experienced significantly less soreness than the CON group after 24 hours (28 mm vs. 46 mm p < 0.01 respectively), and 48 hours (38 mm vs. 50 mm p < 0.01). Pain as measured by pain pressure threshold (PPT) increased significantly in both groups after 24 and 48 hours, but there was no difference in severity of perceived soreness. The use of WBV as a warm-up may mitigate DOMS but does not appear to expedite the recovery of strength in the days following eccentric exercise in resistance-trained individuals.
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Widen, Cecilia, and 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.
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The overall aim of this Thesis was to characterise the energetic properties of the mouse papillary muscle as this preparation could become a useful model to study alterations of energetic aspects of cardiac pathologies and heart-focussed genetic changes. Measurements of resting and active metabolism of the papillary muscles were made in vitro using the myothermic technique. In the first study the mechanism underlying impaired contractility of post-ischaemic rat papillary muscle was investigated. The rat preparation is well established and was used to develop protocols and approaches that could later be used as the basis for studies with mouse papillary muscle. The muscles were exposed to simulated ischaemia for 60 min and change in energetics was studied 30 min into the reperfusion phase. The work output was reduced to 66 ± 3% of the pre-ischaemia value and the enthalpy output decreased to 71 ± 3% of pre-ischaemia value. However, there was no change in either initial, 19 ± 3%, or net mechanical efficiency, 9.0 ± 0.9%. These data, in combination with studies of Ca2+ handling, suggests that the reduced work output was caused by attachment of fewer cross-bridges in each twitch, but with no change in work generated by each cross-bridge. The following two studies involved characterisation of the energetics of the mouse papillary muscle and included measurements of resting and active metabolism. The resting metabolic rate varied with muscle size but the mean initial value was tilda 25 mW g-1 and the estimated steady value tilda 5 mW g-1 . The resting metabolic rate declined exponentially with time towards a steady value, with a time constant of 18 ± 2 min. There was no alteration in isometric force output during this time. The magnitude of resting metabolism depended inversely on muscle mass, more than doubled following a change in substrate from glucose to pyruvate and was increased 2.5-fold when the osmolarity of the bathing solution was increased by addition of 300 mM sucrose. Addition of 30 mM BDM affected neither the time course of the decline in metabolic rate nor the eventual steady value. The energy requirements associated with contractile activity were tilda7 mJ g-1 twitch-1 at a contraction frequency of 1 Hz. The enthalpy output was not affected by changing substrate from glucose to pyruvate but did decrease with an increase in temperature. The enthalpy output was partitioned into force-dependent and force-independent components using BDM to selectively inhibit cross-bridge cycling. The force-independent enthalpy output was 18.6 ± 1.9% of the initial enthalpy output. Muscle initial efficiency was &tilda32% and net efficiency tilda 17% when shortening at a realistic velocity. The enthalpy output decreased with increased contraction frequency but was independent of shortening velocity. On the basis of these values, it was calculated that the twitch energetics were consistent with ATP splitting by half the cross-bridges and the pumping of one Ca 2+ into the SR for every three cross-bridge cycles. The lack of influence of shortening velocity on energy cost supports the idea that the amount of energy to be used is determined early in a twitch and is not greatly influenced by events that occur during the contraction. The suitability of the mouse papillary muscle as a model to study ischaemia and reperfusion damage was also assessed. This preparation is excellent for studying muscle specific changes in work and enthalpy output; however, due to the long-term instability and variability amongst preparations, the suitability of this preparation in prolonged experiments remains uncertain.
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Widen, Cecilia. "Energetics of Mouse Papillary Muscle." Thesis, Griffith University, 2006. http://hdl.handle.net/10072/367649.
Full textAbstract:
The overall aim of this Thesis was to characterise the energetic properties of the mouse papillary muscle as this preparation could become a useful model to study alterations of energetic aspects of cardiac pathologies and heart-focussed genetic changes. Measurements of resting and active metabolism of the papillary muscles were made in vitro using the myothermic technique. In the first study the mechanism underlying impaired contractility of post-ischaemic rat papillary muscle was investigated. The rat preparation is well established and was used to develop protocols and approaches that could later be used as the basis for studies with mouse papillary muscle. The muscles were exposed to simulated ischaemia for 60 min and change in energetics was studied 30 min into the reperfusion phase. The work output was reduced to 66 ± 3% of the pre-ischaemia value and the enthalpy output decreased to 71 ± 3% of pre-ischaemia value. However, there was no change in either initial, 19 ± 3%, or net mechanical efficiency, 9.0 ± 0.9%. These data, in combination with studies of Ca2+ handling, suggests that the reduced work output was caused by attachment of fewer cross-bridges in each twitch, but with no change in work generated by each cross-bridge. The following two studies involved characterisation of the energetics of the mouse papillary muscle and included measurements of resting and active metabolism. The resting metabolic rate varied with muscle size but the mean initial value was tilda 25 mW g-1 and the estimated steady value tilda 5 mW g-1 . The resting metabolic rate declined exponentially with time towards a steady value, with a time constant of 18 ± 2 min. There was no alteration in isometric force output during this time. The magnitude of resting metabolism depended inversely on muscle mass, more than doubled following a change in substrate from glucose to pyruvate and was increased 2.5-fold when the osmolarity of the bathing solution was increased by addition of 300 mM sucrose. Addition of 30 mM BDM affected neither the time course of the decline in metabolic rate nor the eventual steady value. The energy requirements associated with contractile activity were tilda7 mJ g-1 twitch-1 at a contraction frequency of 1 Hz. The enthalpy output was not affected by changing substrate from glucose to pyruvate but did decrease with an increase in temperature. The enthalpy output was partitioned into force-dependent and force-independent components using BDM to selectively inhibit cross-bridge cycling. The force-independent enthalpy output was 18.6 ± 1.9% of the initial enthalpy output. Muscle initial efficiency was &tilda;32% and net efficiency tilda 17% when shortening at a realistic velocity. The enthalpy output decreased with increased contraction frequency but was independent of shortening velocity. On the basis of these values, it was calculated that the twitch energetics were consistent with ATP splitting by half the cross-bridges and the pumping of one Ca 2+ into the SR for every three cross-bridge cycles. The lack of influence of shortening velocity on energy cost supports the idea that the amount of energy to be used is determined early in a twitch and is not greatly influenced by events that occur during the contraction. The suitability of the mouse papillary muscle as a model to study ischaemia and reperfusion damage was also assessed. This preparation is excellent for studying muscle specific changes in work and enthalpy output; however, due to the long-term instability and variability amongst preparations, the suitability of this preparation in prolonged experiments remains uncertain.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Physiotherapy and Exercise Science
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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.
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This study investigated muscle damage of bodybuilders who performed an unaccustomed intense resistive exercise bout. Ten male bodybuilders (age: 23 ± 2 y, height: 177.6 ± 6.3 cm, body mass: 85.7 ± 8.1 kg) with a minimum of 4-years resistance training experience performed 17 exercises targeting the pectoral muscles. Eight of the 10 bodybuilders repeated the same exercises two weeks later. Muscle function (bench press throw, maximal isokinetic elbow extension and flexion concentric torque: MVC torque), muscle soreness using a visual analogue scale (VAS: 100-mm), and plasma creatine kinase (CK) activity were assessed before, immediately after and 24, 48 and 72 hours after exercise. Bench press throw peak force decreased immediately (23 ± 20%) and 24 hours after the first exercise bout (9 ± 15%), but, returned to baseline (930 ± 129 N) by 48 hours post-exercise (P<0.05). MVC torque also decreased but, returned to baseline by 48 hours post-exercise. Muscle soreness peaked 24 hours post-exercise (57 ± 22 mm). No significant changes in plasma CK activity were evident after the exercise at any corresponding time point. When compared between the first and second bouts, changes in bench press throw parameters and MVC torque were similar, but muscle soreness was less (P<0.05) after the second (47 ± 26 mm) than the first bout (68 ± 27 mm). Similarly, the magnitude of volume performed was significantly greater in the second bout (11,433 ± 674 kg) as opposed to the first (10,384 ± 670 kg) due to the repetitions to volition failure (P<0.001). It is concluded that bodybuilders still experience minor loss of muscle function lasting for 2 days after unaccustomed exercise targeting the chest muscles, but muscle soreness was relatively severe, and no repeated bout effect was evident for muscle function measures, but minor repeated bout effect was evident for muscle soreness. This may be a due to potential limitations of continual adaptations.
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Jones, Garrett Collier. "Skeletal Muscle Recovery and Vibration." BYU ScholarsArchive, 2019. https://scholarsarchive.byu.edu/etd/8285.
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In the past decade there has been a significant increase in focus on the effect upper body vibration (UBV) has on the recovery of skeletal muscle after exercise-induced muscle damage. Recovery can be defined and investigated using a wide variety of methods. This study used three different measurements to track muscle recovery over 7 days following an exercise muscle damage protocol and applied vibration to a mathematical model. A visual analog scale (VAS) was used to measure muscle pain, a strain gauge was used to obtain maximum voluntary isometric contraction (MVIC) strength measurements, and shear wave elastography (SWE) represented muscle stiffness over the 7-day experiment. Thirty-three participants were divided into three groups. The first was a control group (C) that experienced no exercise and no therapy. The no vibration group (NV) performed the damage an exercise protocol but received no therapy. The vibration group (V) performed the same exercise protocol but also received vibration therapy. The exercise protocol consisted of 100 dumbbell curls at starting at 50% of their MVIC with one minute of rest after each set of ten. The data provided convincing evidence (27.2%, p < 0.0001) that group NV was not back to its normal stiffness after 7 days unlike group V, which was shown not to be any different from its baseline at the end of the week (9.15%, p = 0.137). Three vibration factors (����1, ����2, ����3) were added to a skeletal muscle regeneration model (SK) to simulate how vibration affects muscle regeneration. The three factors were determined by analyzing previous research to understand how vibration affects cells in the regeneration process. Adding these into SK decreased the time to recovery from about 13 days to about 7 days. Recovery was defined by reaching 10% of the original number of myofibers within the damaged muscle.
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Jakeman, John Robert. "The efficacy of contemporary recovery strategies following exercise-induced muscle damage." Thesis, University of Exeter, 2010. http://hdl.handle.net/10036/106718.
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Following exercise, a rapid return to optimal performance is desirable for athletes. Some types of physical activity can result in exercise-induced muscle damage (EIMD), an occurrence which is well documented in adult populations. Symptoms of EIMD include increases in perceived muscle soreness, decrements in muscle strength and power, alterations in limb proprioception, increased myoprotein release, increased perceived exertion during exercise, and reduced endurance performance. Many strategies are currently employed in attempts to manage the symptoms of EIMD, though the majority are based on anecdotal or equivocal evidence. The aim of this thesis was to investigate a range of contemporary recovery strategies to determine their effectiveness and appropriateness for use with athletic populations. This thesis comprises eight chapters: • Chapter 1: Introduction • Chapter 2: Review of Literature • Chapter 3: Study 1 – Cold water immersion therapy as a recovery strategy following exercise-induced muscle damage • Chapter 4: Study 2 – Manual massage as a recovery strategy following exercise-induced muscle damage • Chapter 5: Study 3 – The use of compressive clothing as a recovery strategy following exercise-induced muscle damage • Chapter 6: Study 4 – Does the use of manual massage therapy have an added beneficial effect on symptoms of exercise-induced muscle damage when used in conjunction with compressive clothing? • Chapter 7: Study 5 – Muscle strength loss characteristics at optimal and short muscle lengths following exercise-induced muscle damage • Chapter 8: General discussion • Chapter 9: Conclusion and recommendation for further study Chapter 3 considers the efficacy of a single bout of cold water immersion therapy following strenuous exercise as a recovery strategy. The results indicate that this treatment protocol has no significant effect on moderating increases in soreness or creatine kinase activity, or reducing decrements in muscle function (p > 0.05). Although this type of recovery strategy is popular in elite sporting fields, this study is consistent with a number of others, indicating that a single bout of cold water immersion therapy is an ineffective recovery strategy following EIMD. Chapter 4 focuses on manual massage a post-exercise recovery strategy. Similar to cold water immersion therapies, the use of massage as a treatment is widespread within the athletic field, though few studies have considered its efficacy following EIMD. This study indicates that although no effect of massage was apparent on perceived soreness or creatine kinase activity, individuals receiving a thirty minute treatment immediately following damaging exercise demonstrated reduced decrements in muscle strength as assessed by isokinetic dynamometry (p < 0.05). This chapter concludes that immediate manual massage may be an effective treatment strategy to manage some of the symptoms of EIMD. Chapter 5 examines the use of clothing with specific compressive qualities as an increasingly popular method of managing symptoms of muscle damage, which is largely unsupported by scientific evidence. Following damaging exercise, the use of lower limb compression reduced decrements in isokinetic muscle function and jump performance, while moderating increases in perceived soreness. This chapter concludes that the use of lower limb compression clothing is an effective, non-invasive method of managing symptoms of EIMD. Data collected from chapters 4 and 5 indicated that manual massage and lower limb compression may manage some of the symptoms of EIMD. Chapter 6 investigates whether these two recovery strategies used in combination have an additive beneficial effect on symptoms of muscle damage. Data from study 3 (chapter 5) were used to compare the combined treatment with the compressive treatment as an independent recovery modality. A significant beneficial effect was observed on perceived soreness as a result of combining the massage and compression treatments, in comparison with compression alone. No consistent benefits on muscle function, above those offered by compression independently were derived as a result of the combined treatment. This chapter concludes that although some benefits are afforded by the addition of massage to the compressive treatment with regard to perceived soreness, logistically, this combination of treatments is unlikely to provide a substantial enough benefit to warrant use with groups of athletes. Exercise-induced muscle damage leads to losses of strength and alterations in the muscle length-tension relationship. Data collated from chapters 5 and 6 were used to investigate muscle strength loss characteristics following damaging exercise. Consistent with previous research, a disproportionate loss of muscle strength was observed at shorter muscle lengths, attributable to mechanical changes within the affected muscle. The use of isokinetic dynamometry was able to detect a shift in length-tension relationship in favour of a longer optimal muscle length for tension generation. The shift in length-tension relationship has been observed in previous studies, although no study has observed this shift in the knee extensor muscle group, and those considering the knee extensor group have inferred the shift as a result of the disproportionate nature of muscle strength loss. The final chapter of this thesis uses data collected from chapters 3-6 to determine the variations in response to different types of eccentrically biased exercise. Typically, plyometric drop jumps elicited greater decrements in isokinetic muscle function and higher perceptions of soreness following exercise in comparison with either downhill running or vertical plyometric jumps. Downhill running resulted in greater cellular permeability as indicated by creatine kinase activity.
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Hurley, 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.
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Childers, 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.
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Benson, Brenda. "Downhill Treadmill Running Does Not Induce Muscle Damage in FVB Mice." BYU ScholarsArchive, 2014. https://scholarsarchive.byu.edu/etd/4259.
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Downhill treadmill running is a commonly used method to cause exercise-induced muscle damage, especially in rodents. Previous studies have evaluated which muscles in rats are more prone to damage. However research using downhill run mice (DHR) has shown some inconsistencies in which muscle is best analyzed for damage. Purpose: The purpose of this study was to quantify the damage in various muscles in a mouse after a single bout of DHR. Methods: Male FVB mice (5 months) were injected with Evans Blue dye (EBD) and then either used as control (CON) or run downhill (-16°) at 20 meters per minute (m/min) for 30 minutes. Twenty-four hours after exercise, the gastrocnemius, soleus, plantaris, tibialis anterior (TA), quadriceps, and triceps brachii muscles were harvested (n = 6 per group per muscle). Cross-sectional slices were obtained, fixed, and mounted to analyze EBD infiltration, dystrophin (Dys), and centralized nuclei. The samples were then imaged using a fluorescent microscope. The entire sample was captured using 20x magnification, and the total number of cells, EBD+, Dys-, and centralized nuclei, were counted. A blood sample was collected to measure plasma creatine kinase (CK) activity. Results: Total number of cells was not different between groups (p > 0.05). No significant difference in any of the markers of muscle damage was found in any muscle between CON and DHR (p > 0.05). Conclusion: These data suggest that DHR does not induce muscle damage in adult (5 months) male FVB mice.
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Banyard, 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.
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Unaccustomed exercise consisting of eccentric contractions induces muscle damage that is characterised by muscle weakness, soreness, swelling and increased muscle stiffness. These symptoms affect daily activities and athletic performance; therefore, interventions to attenuate the symptoms and enhance recovery from muscle damage are necessary. Pulsed electromagnetic field therapy (PEMFT) is anecdotally reported to increase muscle blood flow and oxygenation to enhance tissue healing. One previous study showed that PEMFT was effective for alleviating muscle soreness and losses in range of motion after exercise. However, studies investigating the effect of PEMFT on recovery of muscle strength following eccentric exercise are lacking. The purposes of this study were to investigate the effects of PEMFT treatment on muscle temperature, blood flow and oxygenation (Study 1), and on the symptoms associated with eccentric exerciseinduced muscle damage (Study 2).
In Study 1, the effects of 30 min PEMFT on muscle temperature, blood flow and oxygenation were examined using nine healthy men (23.6 ± 3.7 years). A device called e-cell™was used for PEMFT in this study, which is the size and shape of a computer mouse weighing approximately 140 g, and sham treatment used a visually identical device without pulsed electromagnetic field production. PEMFT was applied over the bicep brachii of one arm for 30 min, and the other arm received sham treatment, while each subject was lying supine on a massage table. The device was marked A or B; thus, both the investigator and subjects were blinded as to which device was active e-cell™ or sham, and the use of dominant or non-dominant arm for device A or B was randomised and counterbalanced among subjects. Pre-treatment muscle temperature was measured by a thermistor needle (22 gauge, 70 mm) inserted to a depth of 20 mm at 10 mm laterally adjacent to a near infrared spectroscopy (NIRS) probe unit that was attached to the skin at the mid-belly of the biceps brachii, and the post-treatment measurement was taken at 5 mm proximal to the first site. The NIRS was used to measure tissue oxygenation index (TOI), a measure of muscle oxygenation, and total haemoglobin content (tHb), an indirect measure of blood flow, which were recorded throughout the treatment period. Changes in muscle temperature from before to immediately posttreatment were compared between e-cell™ and sham conditions using a paired t-test, and changes in TOI and tHb from baseline to 30 min of treatment (0, 10, 20 and 30 min) were compared between conditions by a two-way repeated measures analysis of variance (ANOVA). Muscle temperature significantly (p
In Study 2, eight men and eight women (24.8 ± 6.2 years) performed two bouts of 60 maximal isokinetic (30°⋅s-1) eccentric contractions of the elbow flexors on each arm separated by 4 weeks. In each eccentric contraction, the elbow joint was forcibly extended from a flexed (90°) to a fully extended position (0°). At immediately after, and 1-4 days following the exercise, the exercised arm received 30 min of either e-cell™ or sham treatment described above. The arm dominance and the order of treatment conditions were randomised and counterbalanced among the subjects, and the study was conducted in a double-blinded manner. Dependant variables included maximal voluntary contraction (MVC) strength, range of motion (ROM), upper arm circumference (CIR), muscle soreness by a visual analogue scale, muscle tenderness measured by pressure pain threshold (PPT) and plasma CK activity. Changes in these variables for 7 days following the exercise were compared between e-cell™ and sham treatment conditions, men and women, and the first and second bouts of exercise by a two-way repeated measures ANOVA. The changes in the variables from pre- to post-treatment were also analysed by a two-way repeated measures ANOVA. All variables changed significantly (p
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Ekstrand, 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.
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Introduction: The effect of electrical stimulation on muscle degeneration and regeneration is largely unknown and it has not been studied in conjunction with telomeres. The consumption of non-steroidal anti-inflammatory drugs (NSAIDs) is widespread in athletes and the general population when faced with muscle soreness or injury. Furthermore, the effect of NSAIDs on muscle regeneration is controversial and its effect on telomere lengths is also unknown. Methods: Young adult males performed 200 electrically stimulated maximal isokinetic contractions with one leg (ES) and the other worked as a control (CON). They received either 1200mg ibuprofen (IBU) per day or placebo (PLA) from 21 days pre- to 30 days post-exercise. Muscle biopsies were obtained from the vastus lateralis of the CON leg at baseline (H0) and ES leg at 2.5h (H2.5) and both legs at 2, 7 and 30 days post-exercise. Blood samples were obtained at the same time points and at day 4 post-exercise. Afterwards the muscle and blood specimen were analysed for skeletal muscle and peripheral blood telomere lengths by Southern blot and signs of muscle degeneration and regeneration were quantified histologically. Results: Histological changes occurred in the ES leg, including; increased proportion of damaged myofibres (2.1±2.8%) and infiltrated myofibres (5.0±6.0%) at day 7, small myofibres (3.0±4.4%) and internally located myonuclei (2.9±3.1%) at day 30. The IBU group had significantly less internally located myonuclei at day 30 compared to PLA (1.7±2.4% vs. 4.1±3.8%). No significant differences were observed in skeletal muscle mean and minimum telomere lengths between ES and CON leg, between IBU and PLA group or between time points. Peripheral blood mean telomere lengths were not significantly different between IBU and PLA group, but between time points; H0 (9.6±1.2kb) and H2.5 (9.1±1.1kb) were significantly shorter than day 4 (10.3±1.6kb) and day 7 (10.1±1.5kb) (P<0.05). Conclusion: Electrically stimulated contractions caused significant muscle degeneration and regeneration in the 30 days post-exercise. Electrical stimulation also appeared to cause fluctuations in peripheral blood telomere lengths, but not skeletal muscle telomeres. The intake of ibuprofen appeared to interfere with muscle regeneration, but did not seem to affect the peripheral blood or skeletal muscle telomeres. However, due to marked individual variations and the small participant group it is difficult to conclude on the effects of electrical stimulation and ibuprofen on proliferative potential. Further studies are warranted to elucidate the effects of electrical stimulation and ibuprofen on blood and skeletal muscle telomeres.
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Glasgow, 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.
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Komulainen, 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.
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Grose, 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.
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The senses of position and movement are known collectively as kinaesthesia. Muscle spindles are length sensitive receptors, considered pivotal to these senses. Mechanical muscle vibration artificially stimulates muscle spindles and this can lead to illusory limb postures and movements, thereby disrupting kinaesthesia. Exercise induced fatigue also impairs kinaesthesia and this impairment persists if the exercise involves lengthening contractions that create eccentric muscle damage. It is not entirely clear why these lasting impairments occur. Using a targeted movement sequence with the unseen arm (a task that relies heavily on muscle spindles), this study utilized a novel paradigm to investigate task performance both before and after an eccentric based exercise protocol. By investigating the influence of vibration applied to the involved musculature, the results provide insight into how exercise acutely disrupts kinaesthesia. It was found that mechanical muscle vibration created a robust effect on task accuracy at all points during the study, causing participants to undershoot the targets (as previously described in the literature). The effects of exercise also caused a consistent error in task performance, but did not appear to influence the effect of vibration. This suggests that the nervous system continues to rely heavily on muscle spindles, even when they reside in a muscle exposed to damaging eccentric contractions.Education, Faculty of
Kinesiology, School of
Graduate
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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.
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Achieving adequate and appropriate recovery from exercise is essential in ensuring optimal performance during repeated bouts of exercise. The use of various recovery interventions has become popular in an attempt to enhance subsequent performance and accelerate post-exercise recovery. The application of various post-exercise hydrotherapy interventions has become increasingly popular, however, the majority of current recovery practices appear to be based largely on anecdotal evidence as opposed to rigorous scientific research or evidence based findings. Physiologically, various hydrotherapy protocols have been shown to affect the body via fluid shifts (interstitial to intravascular space), changes in blood flow and cardiovascular function, and reductions in oedema. The possible psychological effects of water immersion must also be considered, with athletes commonly reporting reduced sensations of fatigue and soreness following immersion. Current literature suggests both hydrostatic pressure and water temperature to be important factors influencing the success of hydrotherapy. The overall aim of the present thesis was to enhance current knowledge and understanding with regards to the physiological and performance effects of various forms of hydrotherapy, used as a post-exercise recovery intervention. Initially, four cold water immersion interventions were compared to active recovery, performed between two bouts of high intensity cycling in hot environmental conditions. Effectiveness of recovery was determined via performance in a subsequent exercise bout; in addition, core body temperature, lactate, and heart rate were recorded. The remaining studies were designed to investigate the effects of cold water immersion, hot water immersion, contrast water therapy, and passive recovery 4 (control) following exercise-induced fatigue and exercise-induced muscle damage. Rate of recovery was assessed through changes in performance, core body temperature, thigh girths, blood markers, and perceived exertion/soreness. The results of the combined studies indicate cold water immersion to be more effective than active recovery when performed immediately post-exercise between two bouts of high intensity cycling in hot environmental conditions. Additionally, both cold water immersion and contrast water therapy were effective in aiding recovery from exercise-induced fatigue and exercise-induced muscle damage. Performance variables indicated an improved maintenance or return of performance following these recovery protocols. The present studies have provided additional information to the limited knowledge base regarding the effect of post-exercise hydrotherapy interventions, specifically, the effect of such interventions on subsequent athletic performance. In conclusion, cold water immersion and contrast water therapy appear to be superior to hot water immersion, active recovery, and passive recovery following fatiguing and muscle damaging exercise. Functional and physiological recovery was enhanced following the use of these two recovery protocols.
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Rochester, 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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