Journal articles: 'Muscle damage'

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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

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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.

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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.

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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.

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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.

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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.

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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)

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Hamilton-Craig, Ian. "Statins and muscle damage." Australian Prescriber 26, no. 4 (August 1, 2003): 74–75. http://dx.doi.org/10.18773/austprescr.2003.054.

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12

Evans, William J. "Muscle Damage: Nutritional Considerations." International Journal of Sport Nutrition 1, no. 3 (September 1991): 214–24. http://dx.doi.org/10.1123/ijsn.1.3.214.

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Most exercise results in some skeletal muscle damage. However, unaccustomed exercise andlor eccentric exercise can cause extensive damage. This exercise-induced muscle damage causes a response that can be characterized by a cascade of metabolic events. Within 24 to 48 hours, delayed onset muscle soreness and weakness, the most obvious manifestations of the damage, peak. Increased circulating neutrophils and interleukin-1 occurs within 24 hours after the exercise, with skeletal muscle levels remaining elevated for a much longer time. There is a prolonged increase in ultrastructural damage and muscle protein degradation as well as a depletion of muscle glycogen stores. These metabolic alterations may result in the increased need for dietary protein, particularly at the beginning of a training program that has a high eccentric component such as strength training. The delay in muscle repair and glycogen repletion following damaging exercise should cause coaches and athletes to allow an adequate period of time between competition for complete recovery.

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Kuipers, H. "Exercise-Induced Muscle Damage." International Journal of Sports Medicine 15, no. 03 (April 1994): 132–35. http://dx.doi.org/10.1055/s-2007-1021034.

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PIZZA, FRANCIS X., JOEL B. MITCHELL, BRUCE H. DAVIS, RAYMOND D. STARLING, ROBERT W. HOLTZ, and NANCY BIGELOW. "Exercise-induced muscle damage." Medicine & Science in Sports & Exercise 27, no. 3 (March 1995): 363???370. http://dx.doi.org/10.1249/00005768-199503000-00012.

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Mirzayev, Javid A. "Muscle damage: Scientific fundamentals." Journal of Applied Physiology 122, no. 4 (April 1, 2017): 1052. http://dx.doi.org/10.1152/japplphysiol.00010.2017.

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Endoh, Takashi, Tsuyoshi Nakajima, Masanori Sakamoto, Toshiki Tazoe, Hideoki Ogawa, Tsugutake Yoneda, and Tomoyoshi Komiyama. "Exercise-Induced Muscle Damage Exacerbates Muscle Fatigue." Medicine & Science in Sports & Exercise 38, Supplement (May 2006): S343—S344. http://dx.doi.org/10.1249/00005768-200605001-02340.

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Locke, Marius, and Stephanie A. Salerno. "Ovariectomy alters lengthening contraction induced heat shock protein expression." Applied Physiology, Nutrition, and Metabolism 45, no. 5 (May 2020): 530–38. http://dx.doi.org/10.1139/apnm-2019-0212.

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Estrogen appears to play a role in minimizing skeletal muscle damage as well as regulating the expression of the protective heat shock proteins (HSPs). To clarify the relationship between estrogen, muscle HSP content, and muscle damage, tibialis anterior (TA) muscles from ovary-intact (OVI; n = 12) and ovariectomized (OVX; 3 weeks, n = 12) female Sprague–Dawley rats were subjected to either 20 or 40 lengthening contractions (LCs). Twenty-four hours after stimulation, TA muscles were removed, processed, and assessed for HSP25 and HSP72 content as well as muscle (damage) morphology. No differences in muscle contractile properties were observed in TA muscles between OVI and OVX animals for peak torque during the LCs. In unstressed TA muscles, the basal expression of HSP72 expression was decreased in OVX animals (P < 0.05) while HSP25 content remained unchanged. Following 20 LCs, HSP25 content was elevated (P < 0.05) in TA muscles from OVX animals but unchanged in muscles from OVI animals. Following 40 LCs, HSP25 content was elevated (P < 0.01) in TA muscles from both OVI and OVX animals while HSP72 content was elevated only in TA muscles from OVI animals (P < 0.05). Taken together, these data suggest the loss of ovarian hormones, such as estrogen, may impair the skeletal muscle cellular stress response thereby rendering muscles more susceptible to certain types of contraction induced damage. Novelty Ovariectomy alters muscle HSP72 content. Muscle contractile measures are maintained following ovariectomy.

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Azizi, Emanuel, and Emily M. Abbott. "Anticipatory motor patterns limit muscle stretch during landing in toads." Biology Letters 9, no. 1 (February 23, 2013): 20121045. http://dx.doi.org/10.1098/rsbl.2012.1045.

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To safely land after a jump or hop, muscles must be actively stretched to dissipate mechanical energy. Muscles that dissipate energy can be damaged if stretched to long lengths. The likelihood of damage may be mitigated by the nervous system, if anticipatory activation of muscles prior to impact alters the muscle's operating length. Anticipatory motor recruitment is well established in landing studies and motor patterns have been shown to be modulated based on the perceived magnitude of the impact. In this study, we examine whether motor recruitment in anticipation of landing can serve a protective function by limiting maximum muscle length during a landing event. We use the anconeus muscle of toads, a landing muscle whose recruitment is modulated in anticipation of landing. We combine in vivo measurements of muscle length during landing with in vitro characterization of the force–length curve to determine the muscle's operating length. We show that muscle shortening prior to impact increases with increasing hop distance. This initial increase in muscle shortening functions to accommodate the larger stretches required when landing after long hops. These predictive motor strategies may function to reduce stretch-induced muscle damage by constraining maximum muscle length, despite variation in the magnitude of impact.

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Balnave, C. D., and M. W. Thompson. "Effect of training on eccentric exercise-induced muscle damage." Journal of Applied Physiology 75, no. 4 (October 1, 1993): 1545–51. http://dx.doi.org/10.1152/jappl.1993.75.4.1545.

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Eccentric muscle contractions generate delayed onset muscle soreness (DOMS), possibly as a result of the high tensions involved causing muscle damage. Muscle function, serum indicators of muscle damage, and DOMS were investigated throughout a training regimen that involved a 40-min eccentric walk down a 25% gradient on a treadmill at 6.4 km/h once a week for 8 wk. Serum creatine kinase and myoglobin concentrations were used as indicators of muscle damage, and both demonstrated a delayed increase after the exercise protocol. The muscles that contracted eccentrically exhibited low-frequency fatigue, as well as decreases in muscle fatigability and maximal voluntary contraction force, which were greatest immediately postexercise. Although the results show that training reduces DOMS, the serum muscle protein response, and muscle function impairment, the time courses of these adaptations are different. It is suggested that the function of the muscle can be impaired without apparent muscle damage.

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Roth, Stephen M., Gregory F. Martel, Frederick M. Ivey, Jeffrey T. Lemmer, E. Jeffrey Metter, Ben F. Hurley, and Marc A. Rogers. "High-volume, heavy-resistance strength training and muscle damage in young and older women." Journal of Applied Physiology 88, no. 3 (March 1, 2000): 1112–18. http://dx.doi.org/10.1152/jappl.2000.88.3.1112.

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To determine possible age differences in muscle damage response to strength training, ultrastructural muscle damage was assessed in seven 20- to 30-yr-old and six 65- to 75-yr-old previously sedentary women after heavy-resistance strength training (HRST). Subjects performed unilateral knee-extension exercise 3 days/wk for 9 wk. Bilateral muscle biopsies from the vastus lateralis were assessed for muscle damage via electron microscopy. HRST resulted in a 38 and 25% increase in strength in the young and older women, respectively ( P < 0.05), but there were no between-group differences. In the young women, 2–4% of muscle fibers exhibited damage before and after training in both the trained and untrained legs ( P = not significant). In contrast, muscle damage increased significantly after HRST, from 5 to 17% of fibers damaged ( P < 0.01), in the older women in the trained leg compared with only 2 and 5% of fibers damaged in the untrained leg before and after training, respectively. The present results indicate that older women exhibit higher levels of muscle damage after chronic HRST than do young women.

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Van der Meulen, J. H., H. Kuipers, and J. Drukker. "Relationship between exercise-induced muscle damage and enzyme release in rats." Journal of Applied Physiology 71, no. 3 (September 1, 1991): 999–1004. http://dx.doi.org/10.1152/jappl.1991.71.3.999.

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The relationship between the amount of exercise-induced muscle damage and the release of creatine kinase (CK), aspartate aminotransferase (AST), and lactate dehydrogenase (LD) was studied. Gender differences in enzyme release and histological damage were also studied. Serial pre- and postexercise blood samples were drawn from untrained male and female catheterized Wistar rats that ran 1.5 or 2.5 h on a treadmill (incline 10 degrees). Three days postexercise, muscle damage was quantified morphometrically in five different hindlimb and forearm muscles. The 1.5 and 2.5 h of exercise elicited histological damage only in the soleus muscle. Significant plasma CK, AST, and LD elevations were found immediately postexercise both in male and female rats. However, the enzyme release was significantly greater in males than in females. Part of this could be explained by differences in clearance rates between males and females. No gender difference in amount of histological damage was found. The actual volume of histological muscle damage was significantly less than the calculated muscle damage based on enzyme release. An increase in the exercise duration from 1.5 to 2.5 h resulted in a disproportional increase in both histological muscle damage and muscle enzyme release. From the present study it is concluded that muscle enzyme release is not clearly reflected in histological muscle damage.

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Dessem, Dean, and Richard M. Lovering. "Repeated Muscle Injury as a Presumptive Trigger for Chronic Masticatory Muscle Pain." Pain Research and Treatment 2011 (June 12, 2011): 1–13. http://dx.doi.org/10.1155/2011/647967.

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skeletal muscles sustain a significant loss of maximal contractile force after injury, but terminally damaged fibers can eventually be replaced by the growth of new muscle (regeneration), with full restoration of contractile force over time. After a second injury, limb muscles exhibit a smaller reduction in maximal force and reduced inflammation compared with that after the initial injury (i.e., repeated bout effect). In contrast, masticatory muscles exhibit diminished regeneration and persistent fibrosis, after a single injury; following a second injury, plasma extravasation is greater than after a single injury and maximal force is decreased more than after the initial injury. Thus, masticatory muscles do not exhibit a repeated bout effect and are instead increasingly damaged by repeated injury. We propose that the impaired ability of masticatory muscles to regenerate contributes to chronic muscle pain by leading to an accumulation of tissue damage, fibrosis, and a persistent elevation and prolonged membrane translocation of nociceptive channels such as P2X3 as well as enhanced expression of neuropeptides including CGRP within primary afferent neurons. These transformations prime primary afferent neurons for enhanced responsiveness upon subsequent injury thus triggering and/or exacerbating chronic muscle pain.

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Kholodnyi, R. D. "MODELING THE SKELETAL MUSCLE INJURY IN RATS." International Journal of Veterinary Medicine, no. 3 (October 18, 2022): 253–57. http://dx.doi.org/10.52419/issn2072-2419.2022.3.253.

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Muscles are the most important executive organs - effectors. Both according to morphological and functional characteristics, muscles are divided into two types - striated and smooth. Striated muscles, in turn, are usually divided into skeletal and cardiac. Striated muscles form the motor apparatus of the skeleton, oculomotor, chewing and other motor systems in animals. The striated muscles, with the exception of the heart muscle, are completely controlled by the central nervous system, they are devoid of automatism.The problem of damage to skeletal muscles is very relevant and widespread. These injuries disrupt the musculoskeletal function of animals, up to its complete loss. To search for methods for restoring the structure and function of muscles, experiments are being carried out on laboratory animals. This article is devoted to the selection of the optimal model of skeletal muscle injury, performed on laboratory rats. The study was conducted on Wistar rats. The choice of the muscle on which the models will be worked out, as well as the surgical access to it, is substantiated. Three options for inflicting damage to muscle tissue (cut wounds directed parallel to muscle fibers; cut wounds directed across muscle fibers; crushed wounds of muscle tissue) and the timing of healing of these injuries are proposed. The result of the study showed that the gastrocnemius muscle is the most suitable for modeling damage to muscle tissue in rats, and a crushed wound has the longest healing time.

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Yamane, Akira, Satonari Akutsu, Thomas G. H. Diekwisch, and Ryoichi Matsuda. "Satellite cells and utrophin are not directly correlated with the degree of skeletal muscle damage in mdx mice." American Journal of Physiology-Cell Physiology 289, no. 1 (July 2005): C42—C48. http://dx.doi.org/10.1152/ajpcell.00577.2004.

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To determine whether muscle satellite cells and utrophin are correlated with the degree of damage in mdx skeletal muscles, we measured the area of the degenerative region as an indicator of myofiber degeneration in the masseter, gastrocnemius, soleus, and diaphragm muscles of mdx mice. Furthermore, we analyzed the expression levels of the paired box homeotic gene 7 ( pax7), m-cadherin (the makers of muscle satellite cells), and utrophin mRNA. We also investigated the immunolocalization of m-cadherin and utrophin proteins in the muscles of normal C57BL/10J (B10) and mdx mice. The expression level of pax7 mRNA and the percentage of m-cadherin-positive cells among the total number of cell nuclei in the muscle tissues in all four muscles studied were greater in the mdx mice than in the B10 mice. However, there was no significant correlation between muscle damage and expression level for pax7 mRNA ( R = −0.140), nor was there a correlation between muscle damage and the percentage of satellite cells among the total number of cell nuclei ( R = −0.411) in the mdx mice. The expression level of utrophin mRNA and the intensity of immunostaining for utrophin in all four muscles studied were greater in the mdx mice than in the B10 mice. However, there also was not a significant correlation between muscle damage and expression level of utrophin mRNA ( R = 0.231) in the mdx mice, although upregulated utrophin was incorporated into the sarcolemma. These results suggest that satellite cells and utrophin are not directly correlated with the degree of skeletal muscle damage in mdx mice.

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Yang, Yongfen, and Zhenting Chen. "NEUROMUSCULAR INJURY METHOD IN DIFFERENT STRENGTH SPORTS DAMAGE." Revista Brasileira de Medicina do Esporte 27, no. 8 (August 2021): 767–69. http://dx.doi.org/10.1590/1517-8692202127082021_0366.

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ABSTRACT Introduction: Sports muscle injury is a common phenomenon in sports, and most of it is caused by intense exercise done for a long time. Objective: The effect of high intensity mode (HI) speed endurance training on the muscle injury of athletes. Methods: 14 sprinters were recruited; the muscle injury indexes of the subjects were tested 15 min before and 24 h, 48 h and 72 h after speed endurance training in HV mode and HI mode (high volume mode and high intensity mode, respectively). Results: The results of this study showed that both high amount and HI mode speed endurance training caused a certain degree of injury to the subjects’ muscles, but the injury caused by HI mode speed endurance training to the muscles was more serious than that caused by high amount (P < 0.05). Conclusions: HI mode speed endurance training causes a certain degree of injury to the subjects’ muscle, but it causes more serious injury than high volume mode speed endurance training. Level of evidence II; Therapeutic studies - investigation of treatment results.

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Manfredi, T. G., W. Ding, W. J. Evans, R. A. Fielding, J. G. Cannon, H. Y. Lee, and S. L. Verdon. "Quantification of ultrastructural damage in human skeletal muscle." Proceedings, annual meeting, Electron Microscopy Society of America 49 (August 1991): 126–27. http://dx.doi.org/10.1017/s0424820100084934.

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Qualitative microscopic analysis of muscle architecture provides information about cellular markers of muscle fiber disruption in myopathic, aging, and experimentally damaged muscle. However, this approach does not provide sensitive information regarding the extent of muscle damage and has serious limitations when research protocols address tissue remodeling. The purpose of this study was to quantitatively assess the extent of muscle damage in young and older adults before and after exercise-induced damage. The older adults in this study had lower aerobic capacities and muscle mass than their younger counterparts, suggesting greater vulnerability toward muscle damage produced by physiologic stress.Five young males, ages 20 to 29 years and five older males, age 60 to 75 years had percutaneous needle biopsies taken from the vastis lateralis muscle before and after (N=9) exercise consisting of reverse cycling or downhill treadmill running at a prescribed physiologic effort. Muscle samples were prefixed in 3.0% gluteraldehyde in cacodylate buffer and post-fixed in VL OSO4. This was followed by routine procedures for TEM.

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Böge, Veysel, and Süleyman Patlar. "Muscle fatique and muscle damage in strength training." Physical education of students 26, no. 3 (June 30, 2022): 136–44. http://dx.doi.org/10.15561/20755279.2022.0304.

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Background and Study Aim. The aim of this study is to investigate the effects of different types of contractions on muscle damage and muscle fatigue in sedentary individuals. Material and Methods. Thirty healthy male sedentary individuals participated in the study. Strength training in different types of contractions applied in the study was applied 3 times a week for 8 weeks. Before the study, the training loads were determined by making maximal force measurements of all subjects. The 30 subjects participating in the study were divided into 3 groups: isometric (n = 10), concentric (n = 10) and eccentric (n = 10) contraction group. Appropriate amount of blood samples was taken from the elbow vein 2 times from all subjects, before the studies and at the end of the 8-week strength training. Results. It was observed that eight-week strength training did not cause muscle fatigue in all groups and did not create a statistically significant difference (P> 0.05). Strength training with isometric and concentric contractions for eight weeks significantly increased serum lactate dehydrogenase (LDH), C-reactive protein (CRP), myoglobin (Mb), interleukin 6 (IL-6) levels, while concentric strength training significantly reduced serum aspartate amino transferase (AST) levels. Strength training with eccentric contractions significantly increased serum LDH, CRP, AST, Mb and IL-6 levels, while significantly reducing serum tumor necrosis factor alpha (TNF-α) levels. Strength training with eccentric contractions significantly increased serum creatine kinase (CK), CRP, AST, IL-6 and Mb levels compared to strength training with isometric and concentric contractions at the end of the eight-week study period, but did not show the same significant effect in other parameters. Conclusions. As a result, it can be said that eccentric strength training performed in sedentary individuals leads to more muscle damage than isometric and concentric strength training.

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Pidlisetskyi, A. T. "Damages of Neuromuscular System After Mechanical-Induced Limb Ischemia (Experimental Study)." Visnyk Ortopedii Travmatologii Protezuvannia, no. 2(109) (October 12, 2021): 58–62. http://dx.doi.org/10.37647/0132-2486-2021-109-2-58-62.

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Relevance. Traumatic and ischemic injury of the limbs is accompanied by damage of the skeletal muscles and peripheral nerves of the limbs. The dynamics and consequences of ischemic lesions remain poorly understood and need to be corrected. Objective: using quantitative morphological and sonographic methods, to study the dynamics of skeletal muscle damage of the limb after traumatically induced ischemia with and without the injection of platelet-rich plasma, bone marrow aspirate, and adipose tissue fraction. Materials and Methods. In 3 experiments, rabbits were modeled with 6-hour limb ischemia by applying an elastic tourniquet. After compartment syndrome detection, based on the assessment of subfascial pressure, cell suspensions were injected into the leg muscles. Sonographic and histological examination of the muscles was performed on days 5, 15, and 30. The results of sonography and morphometry were evaluated by statistical methods. Results. The developed model of ischemia consists of 6-hour immobilization of the limb, on тwhich medical elastic tourniquets were imposing. The action of the tourniquets causes high subfascial pressure and necrosis of the superficial muscle groups of the lower third of the thigh and lower leg. According to sonography, the δ-entropy of damaged tissues on day 5 is reduced relative to the intact limb, as in the case of administration of bone marrow aspirate cells. On days 15 and 30, sonography showed no difference between the comparison groups. The dynamics of morphological features of limb tissue damage consist of necrosis of superficial muscle groups, atrophy in the middle layers, and almost intact deep muscle groups. Necrosis was replaced by scar tissue, the density of which increases 11-14 times, and does not differ in the period 5-30 days. The administration of platelet plasma, bone marrow aspirate, and adipose tissue fraction did not change the dynamics of fibrotic changes in ischemic damaged muscles. Muscle atrophy is accompanied by activation of endogenous repair of single muscle fibers, which tended to intensify after injection of bone marrow aspirate. The sciatic nerve of the injured limb was not structurally damaged according to the deep topography, while the nerves of the tibia develop degenerative changes from the 15th day.

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Norman, A. "Adaptive changes in locust kicking and jumping behaviour during development." Journal of Experimental Biology 198, no. 6 (June 1, 1995): 1341–50. http://dx.doi.org/10.1242/jeb.198.6.1341.

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The hind, or metathoracic, leg of a locust is specialised, enabling it to store energy that is used to extend the tibia rapidly during kicking and jumping; behaviours which share a common motor pattern. This study describes developmental changes in kicking and jumping behaviour and relates these changes to the development of the exoskeleton and jumping performance. In mature adults and intermoult larvae, the exoskeleton is strong and kicks can readily be elicited. Before and after the adult moult, when the exoskeleton is weak, kicks can be elicited less frequently, thus avoiding skeletal damage. At these times, animals do not generate the adult motor pattern for kicking, so that extension of the tibia is powered by direct muscle contraction, rather than through the release of stored energy. The muscles of all newly moulted animals are capable of generating sufficient force to damage the leg, but 14 days later the muscles can rarely generate sufficient force to damage the leg. To mimic the forces generated during the preparation for a kick, when the flexor and extensor tibiae muscles co-contract, the extensor muscle was stimulated electrically at a range of frequencies and the nature and occurrence of the resulting mechanical damage to components of the skeleton were assessed over a 14 day period following the adult moult. In newly moulted animals, the proximal femur partially collapses and thus protects the leg from damage before the muscles generate sufficient force to damage chronically other components of the leg. This partial collapse of the femur is reversible when the extensor muscle is activated at low frequency, but high frequencies cause permanent damage. The muscles of all animals 1 day after the moult are also capable of generating sufficient force to damage the leg, but the proximal tibia breaks most commonly in the region where the extensor muscle apodeme attaches. 5 days after the moult, the muscles in only 50 % of animals can damage the leg and most commonly the extensor muscle apodeme breaks. In mature animals, the only structure that fails is the extensor muscle apodeme, which fractures close to its point of attachment to the tibia. Damaging a metathoracic leg can significantly decrease the ability of a locust to jump and to compete for mates. Changes in the likelihood of damage to a metathoracic leg occur at predictable stages of development. Locust behaviour is modified during development, avoiding such damage.

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Zuluaga Tamayo, Marisol, Laurence Choudat, Rachida Aid-Launais, Olivier Thibaudeau, Liliane Louedec, Didier Letourneur, Virginie Gueguen, Anne Meddahi-Pellé, Anne Couvelard, and Graciela Pavon-Djavid. "Astaxanthin Complexes to Attenuate Muscle Damage after In Vivo Femoral Ischemia-Reperfusion." Marine Drugs 17, no. 6 (June 14, 2019): 354. http://dx.doi.org/10.3390/md17060354.

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(1) Background: Reperfusion injury refers to the cell and tissue damage induced, when blood flow is restored after an ischemic period. While reperfusion reestablishes oxygen supply, it generates a high concentration of radicals, resulting in tissue dysfunction and damage. Here, we aimed to challenge and achieve the potential of a delivery system based on astaxanthin, a natural antioxidant, in attenuating the muscle damage in an animal model of femoral hind-limb ischemia and reperfusion. (2) Methods: The antioxidant capacity and non-toxicity of astaxanthin was validated before and after loading into a polysaccharide scaffold. The capacity of astaxanthin to compensate stress damages was also studied after ischemia induced by femoral artery clamping and followed by varied periods of reperfusion. (3) Results: Histological evaluation showed a positive labeling for CD68 and CD163 macrophage markers, indicating a remodeling process. In addition, higher levels of Nrf2 and NQO1 expression in the sham group compared to the antioxidant group could reflect a reduction of the oxidative damage after 15 days of reperfusion. Furthermore, non-significant differences were observed in non-heme iron deposition in both groups, reflecting a cell population susceptible to free radical damage. (4) Conclusions: Our results suggest that the in situ release of an antioxidant molecule could be effective in improving the antioxidant defenses of ischemia/reperfusion (I/R)-damaged muscles.

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Pollock-Tahiri, Evan, and Marius Locke. "The cellular stress response of rat skeletal muscle following lengthening contractions." Applied Physiology, Nutrition, and Metabolism 42, no. 7 (July 2017): 708–15. http://dx.doi.org/10.1139/apnm-2016-0556.

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The cellular stress response of the rat tibialis anterior (TA) muscle was investigated following 20, 40, or 60 lengthening contractions (LCs) using an in vivo model of electrical stimulation. Muscles were removed at 0, 1, 3, or 24 h after LCs and assessed for heat shock transcription factor (HSF) activation, heat shock protein (HSP) content, and/or morphological evidence of muscle fibre damage. When compared with the first muscle contraction, peak muscle torque was reduced by 26% (p < 0.05) after 20 LCs and further reduced to 56% and 60% (p < 0.001) after 40 and 60 LCs, respectively. Following 60 LCs, HSF activation was detected at 0, 1, and 3 h but was undetectable at 24 h. Hsp72 content was elevated at 24 h after 20 LCs (2.34 ± 0.37 fold, p < 0.05), 40 LCs (3.02 ± 0.31 fold, p < 0.01), and 60 LCs (3.37 ± 0.21 fold, p < 0.001). Hsp25 content increased after 40 (2.36 ± 0.24 fold, p < 0.01) and 60 LCs (2.80 ± 0.37 fold, p < 0.01). Morphological assessment of TA morphology revealed that very few fibres were damaged following 20 LCs while multiple sets of LCs (40 and 60) caused greater amounts of fibre damage. Electron microscopy showed disrupted Z-lines and sarcomeres were detectable in some muscles fibres following 20 LCs but were more prevalent and severe in muscles subjected to 40 or 60 LCs. These results suggest LCs elevate HSP content by an HSF-mediated mechanism (60 LC) and a single set of 20 LCs is capable of increasing muscle HSP content without causing significant muscle fibre damage.

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Nozdrenko, D. "Fullerene C60 impact on changes of contraction speed of ischemicaly damaged rat soleus muscle." Bulletin of Taras Shevchenko National University of Kyiv. Series: Biology 68, no. 3 (2014): 11–14. http://dx.doi.org/10.17721/1728_2748.2014.68.11-14.

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The effect of water-soluble C 60 fullerene (C 60 FAS) at a dose of 1 mg/kg on ischemic damagd muscles (muscle soleus) of rat was studied. The therapeutic effect of C 60 FAS was analyzed under intravenous and intramuscular injection. An evident C 60 FAS protective effect on the dynamics of ischemic damage muscles contraction was revealed. In particular, it was found that in most cases the protective effect of С 60 FAS with intramuscular administration at 15-17% is more effective than intravenous administration of this drug. This clearly indicates that C 60 FAS can be considered as a promising therapeutic agent for the prevention and correction of contractile activity of ischemic damage muscles.

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Kim, Jeong-su, Kenneth W. Hinchcliff, Mamoru Yamaguchi, Laurie A. Beard, Chad D. Markert, and Steven T. Devor. "Exercise training increases oxidative capacity and attenuates exercise-induced ultrastructural damage in skeletal muscle of aged horses." Journal of Applied Physiology 98, no. 1 (January 2005): 334–42. http://dx.doi.org/10.1152/japplphysiol.00172.2003.

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Exercise training improves functional capacity in aged individuals. Whether such training reduces the severity of exercise-induced muscle damage is unknown. The purpose of the present study was to determine the effect of 10 wk of treadmill exercise training on skeletal muscle oxidative capacity and exercise-induced ultrastructural damage in six aged female Quarter horses (>23 yr of age). The magnitude of ultrastructural muscle damage induced by an incremental exercise test before and after training was determined by electron microscopic examination of samples of triceps, semimembranosus, and masseter (control) muscles. Maximal aerobic capacity increased 22% after 10 wk of exercise training. The percentage of type IIa myosin heavy chain increased in semimembranosus muscle, whereas the percentage of type IIx myosin heavy chain decreased in triceps muscle. After training, triceps muscle showed significant increases in activities of both citrate synthase and 3-hydroxyacyl-CoA-dehydrogenase. Attenuation of exercise-induced ultrastructural muscle damage occurred in the semimembranosus muscle at both the same absolute and the same relative workloads after the 10-wk conditioning period. We conclude that aged horses adapt readily to intense aerobic exercise training with improvements in endurance, whole body aerobic capacity, and muscle oxidative capacity, and heightened resistance to exercise-induced ultrastructural muscle cell damage. However, adaptations may be muscle-group specific.

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Ozaki, Mika, Tuan Dat Le, and Yoshihiro H. Inoue. "Downregulating Mitochondrial DNA Polymerase γ in the Muscle Stimulated Autophagy, Apoptosis, and Muscle Aging-Related Phenotypes in Drosophila Adults." Biomolecules 12, no. 8 (August 11, 2022): 1105. http://dx.doi.org/10.3390/biom12081105.

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Reactive oxygen species, generated as by-products of mitochondrial electron transport, can induce damage to mitochondrial DNA (mtDNA) and proteins. Here, we investigated whether the moderate accumulation of mtDNA damage in adult muscles resulted in accelerated aging-related phenotypes in Drosophila. DNA polymerase γ (Polγ) is the sole mitochondrial DNA polymerase. The muscle-specific silencing of the genes encoding the polymerase subunits resulted in the partial accumulation of mtDNA with oxidative damage and a reduction in the mtDNA copy number. This subsequently resulted in the production of abnormal mitochondria with reduced membrane potential and, consequently, a partially reduced ATP quantity in the adult muscle. Immunostaining indicated a moderate increase in autophagy and mitophagy in adults with RNA interference of Polγ (PolγRNAi) muscle cells with abnormal mitochondria. In adult muscles showing continuous silencing of Polγ, malformation of both myofibrils and mitochondria was frequently observed. This was associated with the partially enhanced activation of pro-apoptotic caspases in the muscle. Adults with muscle-specific PolγRNAi exhibited a shortened lifespan, accelerated age-dependent impairment of locomotor activity, and disturbed circadian rhythms. Our findings in this Drosophila model contribute to understanding how the accumulation of mtDNA damage results in impaired mitochondrial activity and how this contributes to muscle aging.

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35

Armstrong, R. B. "Muscle Damage and Endurance Events." Sports Medicine 3, no. 5 (1986): 370–81. http://dx.doi.org/10.2165/00007256-198603050-00006.

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Appell, H. J., J. M. C. Soares, and J. A. R. Duarte. "Exercise, Muscle Damage and Fatigue*." Sports Medicine 13, no. 2 (February 1992): 108–15. http://dx.doi.org/10.2165/00007256-199213020-00006.

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37

Nosaka, Kazunori, Andrew Lavender, Mike Newton, and Paul Sacco. "Muscle Damage in Resistance Training." International Journal of Sport and Health Science 1, no. 1 (2003): 1–8. http://dx.doi.org/10.5432/ijshs.1.1.

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Koller, Arnold. "Creatine Phosphokinase and Muscle Damage." Medicine & Science in Sports & Exercise 37, no. 1 (January 2005): 166. http://dx.doi.org/10.1249/01.mss.0000149772.78950.bd.

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Saunders, Michael J. "Creatine Phosphokinase and Muscle Damage." Medicine & Science in Sports & Exercise 37, no. 1 (January 2005): 167. http://dx.doi.org/10.1249/01.mss.0000149773.82908.4b.

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40

JACKSON, M. J., A. McARDLE, R. H. T. EDWARDS, and D. A. JONES. "Muscle damage in mdx mice." Nature 350, no. 6320 (April 1991): 664. http://dx.doi.org/10.1038/350664b0.

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41

Kasper, Christine E., Laura A. Talbot, and Jean M. Gaines. "Skeletal Muscle Damage and Recovery." AACN Clinical Issues: Advanced Practice in Acute and Critical Care 13, no. 2 (May 2002): 237–47. http://dx.doi.org/10.1097/00044067-200205000-00009.

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Hughes, Chris. "Skeletal Muscle Damage and Repair." Medicine & Science in Sports & Exercise 41, no. 6 (June 2009): 1350. http://dx.doi.org/10.1249/01.mss.0000351852.73014.dc.

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43

Jackson, M. J., and S. O' Farrell. "Free radicals and muscle damage." British Medical Bulletin 49, no. 3 (1993): 630–41. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072636.

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Power, I. "Muscle damage with diclofenac injections." Anaesthesia 47, no. 5 (May 1992): 451. http://dx.doi.org/10.1111/j.1365-2044.1992.tb02256.x.

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Evans, William J. "Exercise-Induced Skeletal Muscle Damage." Physician and Sportsmedicine 15, no. 1 (January 1987): 89–100. http://dx.doi.org/10.1080/00913847.1987.11709254.

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Norman, A. T. "Succinylcholine and temporal muscle damage." Anaesthesia 55, no. 8 (August 17, 2000): 829–30. http://dx.doi.org/10.1046/j.1365-2044.2000.01629-35.x.

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&NA;. "Muscle Damage During Back Surgery." Back Letter 9, no. 10 (1994): 118. http://dx.doi.org/10.1097/00130561-199409100-00012.

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&NA;. "Reducing Muscle Damage During Surgery." Back Letter 19, no. 8 (August 2004): 91. http://dx.doi.org/10.1097/00130561-200419080-00008.

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Hodak, E., N. Gadoth, M. David, and M. Sandbank. "Muscle damage induced by isotretinoin." BMJ 293, no. 6544 (August 16, 1986): 425–26. http://dx.doi.org/10.1136/bmj.293.6544.425.

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Clarkson, P. "Eccentric Exercise and Muscle Damage." International Journal of Sports Medicine 18, S 4 (October 1997): S314—S317. http://dx.doi.org/10.1055/s-2007-972741.

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Journal articles on the topic 'Muscle damage'

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