Relevant bibliographies by topics / Muscle damage

Academic literature on the topic 'Muscle damage'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Muscle damage.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Muscle damage"

1

Chen, Ting, Timothy M. Moore, Mark T. W. Ebbert, Natalie L. McVey, Steven R. Madsen, David M. Hallowell, Alexander M. Harris, et al. "Liver kinase B1 inhibits the expression of inflammation-related genes postcontraction in skeletal muscle." Journal of Applied Physiology 120, no. 8 (April 15, 2016): 876–88. http://dx.doi.org/10.1152/japplphysiol.00727.2015.

Full text
Abstract:
Skeletal muscle-specific liver kinase B1 (LKB1) knockout mice (skmLKB1-KO) exhibit elevated mitogen-activated protein kinase (MAPK) signaling after treadmill running. MAPK activation is also associated with inflammation-related signaling in skeletal muscle. Since exercise can induce muscle damage, and inflammation is a response triggered by damaged tissue, we therefore hypothesized that LKB1 plays an important role in dampening the inflammatory response to muscle contraction, and that this may be due in part to increased susceptibility to muscle damage with contractions in LKB1-deficient muscle. Here we studied the inflammatory response and muscle damage with in situ muscle contraction or downhill running. After in situ muscle contractions, the phosphorylation of both NF-κB and STAT3 was increased more in skmLKB1-KO vs. wild-type (WT) muscles. Analysis of gene expression via microarray and RT-PCR shows that expression of many inflammation-related genes increased after contraction only in skmLKB1-KO muscles. This was associated with mild skeletal muscle fiber membrane damage in skmLKB1-KO muscles. Gene markers of oxidative stress were also elevated in skmLKB1-KO muscles after contraction. Using the downhill running model, we observed significantly more muscle damage after running in skmLKB1-KO mice, and this was associated with greater phosphorylation of both Jnk and STAT3 and increased expression of SOCS3 and Fos. In conclusion, we have shown that the lack of LKB1 in skeletal muscle leads to an increased inflammatory state in skeletal muscle that is exacerbated by muscle contraction. Increased susceptibility of the muscle to damage may underlie part of this response.
APA, Harvard, Vancouver, ISO, and other styles
2

Asp, S., S. Kristiansen, and E. A. Richter. "Eccentric muscle damage transiently decreases rat skeletal muscle GLUT-4 protein." Journal of Applied Physiology 79, no. 4 (October 1, 1995): 1338–45. http://dx.doi.org/10.1152/jappl.1995.79.4.1338.

Full text
Abstract:
The effects of concentric and muscle-damaging eccentric contractions on muscle glucose transporter GLUT-4 content were studied in rat muscles. Rats were anesthetized, the calf muscles on one side were stimulated electrically for concentric or eccentric contractions, and bilateral calf muscles were obtained in the postexercise period. Inflammatory and phagocytic cells accumulated in the eccentric white and red gastrocnemius muscles, whereas there were only discrete changes in the eccentric soleus. Glycogen was depleted to the same extent in the white and red gastrocnemius muscles after both types of stimulation, and it remained decreased > 2 days in eccentric muscles. The total GLUT-4 protein content was decreased in the eccentric white and red gastrocnemius muscles 1 and 2 days after the eccentric stimulation, whereas the maximal activity of glycogen synthase was unaffected at these time points. In conclusion, our one-legged stimulation model caused eccentric muscle damage in the white and red gastrocnemius, whereas only minor damage was observed in the soleus muscle. In damaged muscle, muscle glycogen and GLUT-4 protein content were decreased for > 2 days. These findings may suggest (but do not prove) that decreased muscle GLUT-4 protein is involved in the delayed glycogen resynthesis after eccentric exercise.
APA, Harvard, Vancouver, ISO, and other styles
3

Clarkson, Priscilla M. "Muscle Damage." Medicine &amp Science in Sports &amp Exercise 30, no. 3 (March 1998): 473,474. http://dx.doi.org/10.1097/00005768-199803000-00022.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Thacker, Neepa M., Federico G. Velez, Joseph L. Demer, Marilene B. Wang, and Arthur L. Rosenbaum. "Extraocular Muscle Damage Associated with Endoscopic Sinus Surgery: An Ophthalmology Perspective." American Journal of Rhinology 19, no. 4 (July 2005): 400–405. http://dx.doi.org/10.1177/194589240501900414.

Full text
Abstract:
Background Orbital complications associated with endoscopic sinus surgery are well documented. Damage to the medial rectus muscle results in complicated strabismus and disturbing diplopia. The aim of this study was to characterize the types of extraocular muscle injury and the number of muscles involved that may complicate endoscopic sinus surgery and correlate its occurrence to factors in the surgical procedure itself. Methods A retrospective chart review was performed of 14 patients with strabismus after endoscopic sinus surgery. Operative notes of the surgical procedure, pathology reports of the intraoperative specimens, postoperative pattern of strabismus, the extraocular muscle involved, and the type of muscle injury characterized by orbital imaging were reviewed in each patient. Results In our series, not only the medial rectus muscle but also the inferior rectus and the superior oblique muscles were damaged with multiple muscles being involved in one patient. Extraocular muscle injury varied from hematoma, entrapment of muscle in the fractured orbital wall, damage to the oculomotor nerve entry zone, muscle transection, and partial or complete muscle destruction with entrapment in scar tissue. Use of the microdebrider causes extensive irreparable muscle damage. Conclusion Extraocular muscle damage complicating endoscopic sinus surgery can produce therapeutically challenging complicated strabismus.
APA, Harvard, Vancouver, ISO, and other styles
5

Lieber, R. L., and J. Friden. "Muscle damage is not a function of muscle force but active muscle strain." Journal of Applied Physiology 74, no. 2 (February 1, 1993): 520–26. http://dx.doi.org/10.1152/jappl.1993.74.2.520.

Full text
Abstract:
Contractile properties of rabbit tibialis anterior muscles were measured after eccentric contraction to investigate the mechanism of muscle injury. In the first experiment, two groups of muscles were strained 25% of the muscle fiber length at identical rates. However, because the timing of the imposed length change relative to muscle activation was different, the groups experienced dramatically different muscle forces. Because muscle maximum tetanic tension and other contractile parameters measured after 30 min of cyclic activity with either strain timing pattern were identical (P > 0.4), we concluded that muscle damage was equivalent despite very different imposed forces. This result was supported by a second experiment in which the same protocol was performed at one-half the strain (12.5% muscle fiber length). Again, there was no difference in maximum tetanic tension after cyclic 12.5% strain with either strain timing. Data from both experiments were analyzed by two-way analysis of variance, which revealed a highly significant effect of strain magnitude (P < 0.001) but no significant effect of stretch timing (P > 0.7). We interpret these data to signify that it is not high force per se that causes muscle damage after eccentric contraction but the magnitude of the active strain (i.e., strain during active lengthening). This conclusion was supported by morphometric analysis showing equivalent area fractions of damaged muscle fibers that were observed throughout the muscle cross section. The active strain hypothesis is described in terms of the interaction between the myofibrillar cytoskeleton, the sarcomere, and the sarcolemma.
APA, Harvard, Vancouver, ISO, and other styles
6

Donnelly, Alan E., Priscilla M. Clarkson, and Ronald J. Maughan. "Exercise-induced muscle damage: effects of light exercise on damaged muscle." European Journal of Applied Physiology and Occupational Physiology 64, no. 4 (1992): 350–53. http://dx.doi.org/10.1007/bf00636223.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Clarkson, Priscilla M., and Stephen P. Sayers. "Etiology of Exercise-Induced Muscle Damage." Canadian Journal of Applied Physiology 24, no. 3 (June 1, 1999): 234–48. http://dx.doi.org/10.1139/h99-020.

Full text
Abstract:
Muscle damage is caused by strenuous and unaccustomed exercise, especially exercise involving eccentric muscle contractions, where muscles lengthen as they exert force. Damage can be observed both directly at the cellular level and indirectly from changes in various indices of muscle function. Several mechanisms have been offered to explain the etiology of the damage/repair process, including mechanical factors such as tension and strain, disturbances in calcium homeostasis. the inflammatory response, and the synthesis of stress proteins (heat shock proteins). Changes in muscle function following eccentric exercise have been observed at the cellular level as an impairment in the amount and action of transport proteins for glucose and lactate/H+, and at the systems level as an increase in muscle stiffness and a prolonged loss in the muscle's ability to generate force. This paper will briefly review factors involved in the damage/repair process and alterations in muscle function following eccentric exercise. Key words: eccentric exercise, inflammation, stress proteins, muscle function
APA, Harvard, Vancouver, ISO, and other styles
8

Thabet, M., T. Miki, S. Seino, and J. M. Renaud. "Treadmill running causes significant fiber damage in skeletal muscle of KATP channel-deficient mice." Physiological Genomics 22, no. 2 (July 14, 2005): 204–12. http://dx.doi.org/10.1152/physiolgenomics.00064.2005.

Full text
Abstract:
Although it has been suggested that the ATP-sensitive K+ (KATP) channel protects muscle against function impairment, most studies have so far given little evidence for significant perturbation in the integrity and function of skeletal muscle fibers from inactive mice that lack KATP channel activity in their cell membrane. The objective was, therefore, to test the hypothesis that KATP channel-deficient skeletal muscle fibers become damaged when mice are subjected to stress. Wild-type and KATP channel-deficient mice (Kir6.2−/− mice) were subjected to 4–5 wk of treadmill running at either 20 m/min with 0° inclination or at 24 m/min with 20° uphill inclination. Muscles of all wild-type mice and of nonexercised Kir6.2−/− mice had very few fibers with internal nuclei. After 4–5 wk of treadmill running, there was little evidence for connective tissues and mononucleated cells in Kir6.2−/− hindlimb muscles, whereas the number of fibers with internal nuclei, which appear when damaged fibers are regenerated by satellite cells, was significantly higher in Kir6.2−/− than wild-type mice. Between 5% and 25% of the total number of fibers in Kir6.2−/− extensor digitum longus, plantaris, and tibialis muscles had internal nuclei, and most of such fibers were type IIB fibers. Contrary to hindlimb muscles, diaphragms of Kir6.2−/− mice that had run at 24 m/min had few fibers with internal nuclei, but mild to severe fiber damage was observed. In conclusion, the study provides for the first time evidence 1) that the KATP channels of skeletal muscle are essential to prevent fiber damage, and thus muscle dysfunction; and 2) that the extent of fiber damage is greater and the capacity of fiber regeneration is less in Kir6.2−/− diaphragm muscles compared with hindlimb muscles.
APA, Harvard, Vancouver, ISO, and other styles
9

Sloboda, Darcée D., and Susan V. Brooks. "Reactive oxygen species generation is not different during isometric and lengthening contractions of mouse muscle." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 305, no. 7 (October 1, 2013): R832—R839. http://dx.doi.org/10.1152/ajpregu.00299.2013.

Full text
Abstract:
Skeletal muscles can be injured by lengthening contractions, when the muscles are stretched while activated. Lengthening contractions produce structural damage that leads to the degeneration and regeneration of damaged muscle fibers by mechanisms that have not been fully elucidated. Reactive oxygen species (ROS) generated at the time of injury may initiate degenerative or regenerative processes. In the present study we hypothesized that lengthening contractions that damage the muscle would generate more ROS than isometric contractions that do not cause damage. To test our hypothesis, we subjected muscles of mice to lengthening contractions or isometric contractions and simultaneously monitored intracellular ROS generation with the fluorescent indicator 5-(and-6)-chloromethyl-2′,7′-dichlorodihydrofluorescein (CM-DCFH), which is oxidized by ROS to form the fluorescent product CM-DCF. We found that CM-DCF fluorescence was not different during or shortly after lengthening contractions compared with isometric controls, regardless of the amount of stretch and damage that occurred during the lengthening contractions. The only exception was that after severe stretches, the increase in CM-DCF fluorescence was impaired. We conclude that lengthening contractions that damage the muscle do not generate more ROS than isometric contractions that do not cause damage. The implication is that ROS generated at the time of injury are not the initiating signals for subsequent degenerative or regenerative processes.
APA, Harvard, Vancouver, ISO, and other styles
10

Cevik, Hilal, Isabelle Gangadin, Justin G. Boyer, Douglas Millay, and Stephen N. Waggoner. "Key contribution of NK cells to inflammation after muscle injury." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 165.14. http://dx.doi.org/10.4049/jimmunol.208.supp.165.14.

Full text
Abstract:
Abstract Immune activation after tissue injury is required for removal of dead cells and debris to permit subsequent regenerative healing. Natural killer (NK) cells are innate lymphocytes that are essential for immune defense and for regulation of inflammation. NK cells limit fibrosis after cardiac muscle damage, yet the role of these cells during skeletal muscle inflammation is less clear. We hypothesize that NK cells promote acute inflammation after muscle damage but that NK cell responses must be resolved to permit regenerative healing. Following bilateral injection of cardiotoxin into tibialis anterior and gastrocnemius muscles of C57BL/6 mice, NK cell accumulation in injured muscle was detectable within 18 hours and peaked four days post-injury. Selective depletion of NK cells using a titrated dose of anti-NK1.1 antibody prior to cardiotoxin injection resulted in a substantial reduction in the overall infiltration of numerous immune cell types, including T and B cells, into the injured muscle. Thus, NK cells are an important mediator of cellular inflammation following muscle damage. Future studies will determine the mechanism by which NK cells contribute to this inflammatory response and how ablation of NK-cell mediated inflammation impacts healing of damaged muscles. Supported by National Institute of Heath (NIH) (R01-AI148080)
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Muscle damage"

1

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
2

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
3

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
4

Ahmadi, Sirous. "Monitoring muscle oxygenation and myoelectric activity after damage-inducing exercise." Thesis, The University of Sydney, 2007. http://hdl.handle.net/2123/2240.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
5

Ahmadi, Sirous. "Monitoring muscle oxygenation and myoelectric activity after damage-inducing exercise." University of Sydney, 2007. http://hdl.handle.net/2123/2240.

Full text
Abstract:
Doctor of Philosophy
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.
APA, Harvard, Vancouver, ISO, and other styles
6

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
10

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Muscle damage"

1

Stanley, Salmons, ed. Muscle damage. Oxford: Oxford University Press, 1997.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

1955-, Tiidus Peter M., ed. Skeletal muscle damage and repair. Champaign, IL: Human Kinetics, 2008.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Brown, Stephen James. Exercise induced damage to skeletal muscle and connective tissue. Wolverhampton: University of Wolverhampton, 1997.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Child, R. B. Exercise and free radical induced damage to human skeletal muscle. Wolverhampton: University of Wolverhampton, 1997.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

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.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Harrison, Rosemarie C. The effect of elevated muscle fluid volume on indices of muscle damage following an acute bout of eccentric exercise. St. Catharines, Ont: Brock University, Faculty of Applied Health Sciences, 2008.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Lin, Chen. Development of human muscle protein measurement with MRI: Final report for NASA cooperative agreement (NCC 9-36), round 1 subcontract. [Washington, DC: National Aeronautics and Space Administration, 1997.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Saxton, John Michael. Exercise-induced damage to human skeletal muscle: A thesis presented for the degree of Ph.D. at the University of Wolverhampton. Wolverhampton: University of Wolverhampton, 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Kathy, Kuipers, ed. Management of upper limb hypertonicity. San Antonio, Tex: Therapy Skill Builders, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Heap, Sarah Heap. Microcirculation and performance in damaged skeletal and cardiac muscle. Birmingham: University of Birmingham, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Muscle damage"

1

Hubal, Monica J. "Muscle Damage." In Encyclopedia of Exercise Medicine in Health and Disease, 604–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_140.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Proske, Uwe, David L. Morgan, Tamara Hew-Butler, Kevin G. Keenan, Roger M. Enoka, Sebastian Sixt, Josef Niebauer, et al. "Eccentric Muscle Damage." In Encyclopedia of Exercise Medicine in Health and Disease, 269–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_60.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Proske, Uwe, David L. Morgan, Tamara Hew-Butler, Kevin G. Keenan, Roger M. Enoka, Sebastian Sixt, Josef Niebauer, et al. "Exercise-Induced Muscle Damage." In Encyclopedia of Exercise Medicine in Health and Disease, 327. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_4215.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Bedford, Steve. "Exercise-Induced Muscle Damage." In Recovery from Strenuous Exercise, 28–31. New York: Routledge, 2022. http://dx.doi.org/10.4324/9781003156994-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Brazeau, G. A. "Drug-induced muscle damage." In Oxidative Stress in Skeletal Muscle, 295–315. Basel: Birkhäuser Basel, 1998. http://dx.doi.org/10.1007/978-3-0348-8958-2_19.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Jackson, Malcolm J. "Molecular mechanisms of muscle damage." In Molecular and Cell Biology of Muscular Dystrophy, 257–82. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1528-5_10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Hochman, A. "Oxidative damage after ischemia/reperfusion in skeletal muscle." In Oxidative Stress in Skeletal Muscle, 239–56. Basel: Birkhäuser Basel, 1998. http://dx.doi.org/10.1007/978-3-0348-8958-2_15.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Jackson, M. J. "Free radical mechanisms in exercise-related muscle damage." In Oxidative Stress in Skeletal Muscle, 75–86. Basel: Birkhäuser Basel, 1998. http://dx.doi.org/10.1007/978-3-0348-8958-2_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Năstase, Leonard, Dragos Cretoiu, and Silvia Maria Stoicescu. "Skeletal Muscle Damage in Intrauterine Growth Restriction." In Advances in Experimental Medicine and Biology, 93–106. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-1435-3_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Jackson, M. J., and R. H. T. Edwards. "Free Radicals, Muscle Damage and Muscular Dystrophy." In Reactive Oxygen Species in Chemistry, Biology, and Medicine, 197–210. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-0417-4_14.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Muscle damage"

1

Loerakker, Sandra, Emmy Manders, Gustav J. Strijkers, Frank P. T. Baaijens, Dan L. Bader, Klaas Nicolay, and Cees W. J. Oomens. "Effect of Ischemia and Reperfusion on Skeletal Muscle Damage." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19341.

Full text
Abstract:
Sustained mechanical loading of soft tissues covering bony prominences, as experienced by bedridden and wheelchair-bound individuals, may cause skeletal muscle damage. This can result in a condition termed pressure-related deep tissue injury (DTI), a severe kind of pressure ulcer that initiates in deep tissue layers, and progresses towards the skin. Damage pathways leading to DTI can involve ischemia, ischemia/reperfusion injury, impaired lymphatic drainage, and sustained tissue deformation. Recently, we have provided evidence that in a controlled animal model, deformation is the main trigger for damage within a 2h loading period [1,2]. However, ischemia and reperfusion may play a more important role in the damage process during prolonged loading periods.
APA, Harvard, Vancouver, ISO, and other styles
2

Linder-Ganz, Eran, Nogah Shabshin, and Amit Gefen. "Biomechanical Analysis of a Serious Pressure Ulcer Case in a Real-World Scenario." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-205038.

Full text
Abstract:
Deep tissue injury (DTI) is a serious pressure ulcer, characterized by necrotic tissue mass under intact skin. There is evidence that elevated tissue strains/stresses over prolonged times cause DTI, via paths of physical damage to cells, ischemia and impaired diffusion. Skeletal muscle is considered less tolerable to mechanical loads, likely because of higher metabolic demand and denser vascularization. When damaged in compression, muscle tissue stiffens up to ∼3-fold, depending on the magnitude and duration of loading [1]. Cell-death thresholds for loaded muscle, that are a Boltzmann-type downward-step sigmoid function of the magnitude of compression strain/stress and time, were developed based on meta-analysis of animal experiments [2]. These cell-death thresholds allow extrapolation of biological damage trends from computational stress analyses of muscle in load bearing postures.
APA, Harvard, Vancouver, ISO, and other styles
3

Higginson, J., T. Kesar, R. Perumal, and S. Binder-Macleod. "Simulation-Guided Stimulation for Paretic Ankle Muscles During Stroke Gait." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176365.

Full text
Abstract:
Stroke is the leading cause of long-term adult disability in the U.S. Neuronal damage in the brain results in impaired muscle coordination which induces asymmetric and abnormal walking patterns. Muscle-actuated forward dynamic simulation of walking patterns of healthy young adults has elucidated unique and synergistic roles of the uniarticular and biarticular plantarflexors. Neptune and colleagues (2001) reported that soleus delivers energy to the trunk, gastrocnemius accelerates the leg forward, and both contribute significantly to vertical support of the center of mass [1]. In a simulation of post-stroke hemiparetic gait, Higginson et al. (2006) observed that non-paretic muscles mimicked the function of healthy muscles, while paretic ankle plantarflexor function was limited and required supplemental effort by hip and knee extensors [2].
APA, Harvard, Vancouver, ISO, and other styles
4

Rahayu, Setya, Mohammad Ali, Natsuangkorn Kongchulagul, Ebenezer Silaban, Didit Nugroho, Muchamad Sadhali, Sugiarto Sugiarto, and Gustiana Anggita. "Physical Exercises cause Muscle Damage and Potential Treatments to Increase Range of Motion." In Proceedings of the 5th International Seminar of Public Health and Education, ISPHE 2020, 22 July 2020, Universitas Negeri Semarang, Semarang, Indonesia. EAI, 2020. http://dx.doi.org/10.4108/eai.22-7-2020.2300310.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Rodrigues, Eliane C., and Leonardo A. Elias. "A computer simulation study on the influences of loss and damage of primary muscle spindle afferents on soleus muscle stretch reflex." In 2019 41st Annual International Conference of the IEEE Engineering in Medicine & Biology Society (EMBC). IEEE, 2019. http://dx.doi.org/10.1109/embc.2019.8857466.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Loerakker, Sandra, Anke Stekelenburg, Gustav J. Strijkers, Klaas Nicolay, Dan L. Bader, Frank P. T. Baaijens, and Cees W. J. Oomens. "Effect of Continuous and Intermittent Mechanical Loading on the Development of Skeletal Muscle Damage - A Combined Experimental/Numerical Approach." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206354.

Full text
Abstract:
Prolonged mechanical loading of soft tissues, as present when individuals are bedridden or wheelchair-bound, can lead to degeneration of skeletal muscle tissue. This can result in a condition termed pressure-related deep tissue injury (DTI), a severe kind of pressure ulcer that initiates in deep tissue layers, e.g. skeletal muscle, near bony prominences and progresses towards the skin. Complications associated with DTI include sepsis, renal failure, and myocardial infarction. Damage pathways leading to DTI involve ischemia, ischemia-reperfusion injury, impaired lymphatic drainage, and sustained tissue deformation. Recently, the role of tissue deformation in the onset of skeletal muscle damage was established by combining animal experiments with finite element (FE) modeling [1]. After 2 hours of continuous loading, a clear correlation between maximum shear strain and damage was found.
APA, Harvard, Vancouver, ISO, and other styles
7

Makhsous, Mohsen, Atek Pandya, Mauli Modi, Briana Reprogle, Christopher C. Chadwick, and Fang Lin. "Serum and Urine Biomarker Elevation Indicating the Onset of Deep Tissue Injury as Examined on a Rat Model." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19313.

Full text
Abstract:
Deep tissue injury (DTI) is a serious pressure ulcer (PU) which initiates in deep tissue, mainly muscle, and progresses rapidly to a full-thickness wound [1, 2]. Therefore, an early indication should help in increasing awareness and providing prompt intervention to prevent it from progressing to an open wound, which is susceptible to infection and typically needs prolonged and aggressive care. However, the diagnosis of DTI is currently still vague at best[2] with only subjective tools. This situation calls for tools for objectively sensing the tissue changes while the skin is still intact, to allow development of evidence-based protocols for early diagnosis and treatment. Since DTI initiates from deep muscle layer around a bony prominence, a tool that sensitive to muscle damage may have the potential to objectively sense the onset of a DTI in clinical application. A number of molecular biomarkers have been reported in the literature as suitable for indicating muscle damage. Some of the most promising biomarkers are myoglobin and heart-type fatty acid binding protein (H-FABP). Myoglobin and H-FABP are two relatively small muscle proteins that show a very fast release time after skeletal muscle damage/necrosis when no myocardial infarction or damage is present; therefore, they may be used to identify skeletal muscle injury in DTI formation. The objective of this study was to initially test whether myoglobin and H-FABP in serum and urine respond quickly to pressure induced deep tissue injury on a rat model. It is expected that knowledge gained from this study may lead to a promising new methodology to sense the visually invisible DTI.
APA, Harvard, Vancouver, ISO, and other styles
8

Loerakker, Sandra, Gustav J. Strijkers, Klaas Nicolay, Frank P. T. Baaijens, Dan L. Bader, and Cees W. J. Oomens. "The Relative Contributions of Muscle Deformation and Ischemia to Pressure Ulcer Development." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80239.

Full text
Abstract:
Sustained mechanical loading of soft tissues covering bony prominences may lead to degeneration of skeletal muscle tissue. This can result in a condition termed deep tissue injury (DTI), a severe kind of pressure ulcer that initiates in deep tissue layers, and progresses towards the skin. Previously, we have provided evidence that in a controlled animal model, deformation is the main trigger for damage within a 2 h loading period [1,2]. Recently, we also showed that ischemia and reperfusion may contribute to the damage process during prolonged loading [3]. In the present study, we investigated the relative effects of deformation, ischemia, and reperfusion on the temporal and spatial damage process of skeletal muscle tissue during a 6 h period using magnetic resonance imaging (MRI) techniques.
APA, Harvard, Vancouver, ISO, and other styles
9

Chen, Dongsheng, Nan Zeng, Celong Liu, and Hui Ma. "Characterization of muscle stretching and damage using polarization-sensitive optical coherence tomography (PS-OCT)." In Photonics Asia, edited by Qingming Luo, Ying Gu, and Xingde D. Li. SPIE, 2012. http://dx.doi.org/10.1117/12.999951.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Avdelidis, N. P., V. Kappatos, G. Georgoulas, P. Karvelis, C. K. Deli, P. Theodorakeas, G. Giakas, A. Tsiokanos, M. Koui, and A. Z. Jamurtas. "Detection and characterization of exercise induced muscle damage (EIMD) via thermography and image processing." In SPIE Smart Structures and Materials + Nondestructive Evaluation and Health Monitoring, edited by Norbert G. Meyendorf. SPIE, 2017. http://dx.doi.org/10.1117/12.2261278.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Muscle damage"

1

Hoffman, Eric P. Molecular Aspects of Muscle Damage and Denervation with Public Access Tools. Fort Belvoir, VA: Defense Technical Information Center, December 2004. http://dx.doi.org/10.21236/ada455552.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Halevy, Orna, Sandra Velleman, and Shlomo Yahav. Early post-hatch thermal stress effects on broiler muscle development and performance. United States Department of Agriculture, January 2013. http://dx.doi.org/10.32747/2013.7597933.bard.

Full text
Abstract:
In broilers, the immediate post-hatch handling period exposes chicks to cold or hot thermal stress, with potentially harmful consequences to product quantity and quality that could threaten poultry meat marketability as a healthy, low-fat food. This lower performance includes adverse effects on muscle growth and damage to muscle structure (e.g., less protein and more fat deposition). A leading candidate for mediating the effects of thermal stress on muscle growth and development is a unique group of skeletal muscle cells known as adult myoblasts (satellite cells). Satellite cells are multipotential stem cells that can be stimulated to follow other developmental pathways, especially adipogenesis in lieu of muscle formation. They are most active during the first week of age in broilers and have been shown to be sensitive to environmental conditions and nutritional status. The hypothesis of the present study was that immediate post-hatch thermal stress would harm broiler growth and performance. In particular, growth characteristics and gene expression of muscle progenitor cells (i.e., satellite cells) will be affected, leading to increased fat deposition, resulting in long-term changes in muscle structure and a reduction in meat yield. The in vitro studies on cultured satellite cells derived from different muscle, have demonstrated that, anaerobic pectoralis major satellite cells are more predisposed to adipogenic conversion and more sensitive during myogenic proliferation and differentiation than aerobic biceps femoris cells when challenged to both hot and cold thermal stress. These results corroborated the in vivo studies, establishing that chronic heat exposure of broiler chicks at their first two week of life leads to impaired myogenicity of the satellite cells, and increased fat deposition in the muscle. Moreover, chronic exposure of chicks to inaccurate temperature, in particular to heat vs. cold, during their early posthatch periods has long-term effects of BW, absolute muscle growth and muscle morphology and meat quality. The latter is manifested by higher lipid and collagen deposition and may lead to the white striping occurrence. The results of this study emphasize the high sensitivity of muscle progenitor cells in the early posthatch period at a time when they are highly active and therefore the importance of rearing broiler chicks under accurate ambient temperatures. From an agricultural point of view, this research clearly demonstrates the immediate and long-term adverse effects on broiler muscling and fat formation due to chronic exposure to hot stress vs. cold temperatures at early age posthatch. These findings will aid in developing management strategies to improve broiler performance in Israel and the USA. BARD Report - Project4592 Page 2 of 29
APA, Harvard, Vancouver, ISO, and other styles
3

Cahaner, Avigdor, Sacit F. Bilgili, Orna Halevy, Roger J. Lien, and Kellye S. Joiner. effects of enhanced hypertrophy, reduced oxygen supply and heat load on breast meat yield and quality in broilers. United States Department of Agriculture, November 2014. http://dx.doi.org/10.32747/2014.7699855.bard.

Full text
Abstract:
Original objectivesThe objectives of this project were to evaluate the growth performance, meat yield and quality attributes of broiler strains widely differing in their genetic potential under normal temperature vs. warm temperature (short and long-term) conditions. Strain differences in breast muscle accretion rate, metabolic responses under heat load and, gross and histopathological changes in breast muscle under thermal load was also to be characterized. BackgroundTremendous genetic progress has been made in broiler chicken growth rate and meat yield since the 1950s. Higher growth rate is driven by higher rates of feed intake and metabolism, resulting in elevated internal heat production. Hot rearing conditions negatively affect broiler growth by hindering dissipation of heat and may lead to a lethal elevation in body temperature. To avoid heat-induced mortality, broilers reduce feed intake, leading to depressed growth rate, lower weight gain, reduce breast meat yield and quality. Thus, the genetic potential of contemporary commercial broilers (CCB) is not fully expressed under hot conditions. Major conclusions, solutions, and achievementsResearch conducted in Israel focused on three broiler strains – CCB, Featherless, Feathered sibs (i.e., sharing similar genetic background). Complimentary research trials conducted at Auburn utilized CCB (Cobb 500, Cobb 700, Ross 308, Ross 708), contrasting their performance to slow growing strains. Warm rearing conditions consistently reduced feed intake, growth rate, feed efficiency, body weight uniformity and breast muscle yield, especially pronounced with CCB and magnified with age. Breast meat quality was also negatively affected, as measured by higher drip loss and paler meat color. Exposure to continuous or short-term heat stress induced respiratory alkalosis. Breast muscle histomorphometrics confirmed enhanced myofiber hypertrophy in CCB. Featherless broilers exhibited a significant increase in blood-vessel density under warm conditions. Rapid growth and muscle accretion rate was correlated to various myopathies (white striping, woody and necrotic) as well as to increases in plasma creatinekinase levels. Whether the trigger(s) of muscle damage is loss of cellular membrane integrity due to oxidative damage or tissue lactate accumulation, or to loss of inter-compartmental cation homeostasis is yet to be determined. Based on genome-wide single-nucleotide polymorphism array genotyping, identification of the gene with the recessive mutation Scaleless (sc) facilitated the development a dCAPS assay to discriminate between sc carrier (sc/+) and non-carrier (+/+) individuals. ImplicationsThis project confirmed that featherless broiler strains grow efficiently with high yield and quality of breast meat, even under warm rearing conditions that significantly depress the overall performance of CCB. Therefore, broiler meat production in hot regions and climates can be substantially improved by introducing the featherless gene into contemporary commercial broiler stocks. This approach has become more feasible with the development of dCAPS assay. A novel modification of the PCR protocol (using whole blood samples instead of extracted DNA) may contribute to the efficient development of commercial featherless broiler strains. Such strains will allow expansion of the broiler meat production in developing countries in warm climates, where energy intensive environmental control of rearing facilities are not economical and easily achievable.
APA, Harvard, Vancouver, ISO, and other styles
4

Kanner, Joseph, Mark Richards, Ron Kohen, and Reed Jess. Improvement of quality and nutritional value of muscle foods. United States Department of Agriculture, December 2008. http://dx.doi.org/10.32747/2008.7591735.bard.

Full text
Abstract:
Food is an essential to our existence but under certain conditions it could become the origin to the accumulative health damages. Technological processes as heating, chopping, mincing, grounding, promote the lipid oxidation process in muscle tissues and meat foodstuffs. Lipid oxidation occurred rapidly in turkey muscle, intermediate in duck, and slowest in chicken during frozen storage. Depletion of tocopherol during frozen storage was more rapid in turkey and duck compared to chicken. These processes developed from lipid peroxides produce many cytotoxic compounds including malondialdehyde (MDA). The muscle tissue is further oxidized in stomach conditions producing additional cytotoxic compounds. Oxidized lipids that are formed during digestion of a meal possess the potential to promote reactions that incur vascular diseases. A grape seed extract (1% of the meat weight) and butylated hydroxytoluene (0.2% of the lipid weight) were each effective at preventing formation of lipid oxidation products for 3 hours during co-incubation with cooked turkey meat in simulated gastric fluid (SGF). Polyphenols in the human diet, as an integral part of the meal prevent the generation and absorption of cytotoxic compounds and the destruction of essential nutrients, eg. antioxidants vitamins during the meal. Polyphenols act as antioxidants in the gastrointestinal tract; they scavenge free radicals and may interact with reactive carbonyls, enzymes and proteins. These all reactions results in decreasing the absorption of reactive carbonyls and possible other cytotoxic compounds into the plasma. Consumptions of diet high in fat and red meat are contributory risk factors partly due to an increase production of cytotoxic oxidized lipid products eg. MDA. However, the simultaneously consumption of polyphenols rich foods reduce these factors. Locating the biological site of action of polyphenols in the in the gastrointestinal tract may explain the paradox between the protective effect of a highly polyphenols rich diet and the low bioavailability of these molecules in human plasma. It may also explain the "French paradox" and the beneficial effect of Mediterranean and Japanese diets, in which food products with high antioxidants content such as polyphenols are consumed during the meal.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Muscle damage' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography