scholarly journals A semiquantitative scoring tool to evaluate eccentric exercise-induced muscle damage in trained rats

2015 ◽  
Vol 59 (4) ◽  
Author(s):  
D. Rizo-Roca ◽  
J.G. Ríos-Kristjánsson ◽  
C. Núñez-Espinosa ◽  
A. Ascensão ◽  
J. Magalhães ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Damage ◽  
Muscle Fibre ◽  
Eccentric Exercise ◽  
Muscle Injury ◽  
Time Course ◽  
Intraclass Correlation ◽  
Post Injury ◽  
Exercise Induced ◽  
Scoring Tool

Unaccustomed eccentric exercise is a well-documented cause of exercise-induced muscle damage. However, in trained subjects muscle injury involves only light or moderate tissue damage. Since trained rats are widely used as a model for skeletal muscle injury, here we propose a semiquantitative scoring tool to evaluate muscle damage in trained rats. Twenty male Sprague-Dawley rats were trained fortwo weeks following a two-week preconditioning period, and randomly divided into two groups: control rats (CTL; n=5) and rats with eccentric exercise-induced muscle damage (INJ; n=15). Injured rats were sacrificed at three time points: 1, 3 and 7 days post injury (n=5 each). Transverse sections from the right soleus were cut (10 µm) and stained with haematoxylin-eosin. Samples were evaluated by two groups of observers (four researchers experienced in skeletal muscle histopathology and four inexperienced) using the proposed tool, which consisted of six items organised in three domains: abnormal fibre morphology, necrotic/(re)degenerating fibres (<em>muscle fibre domain</em>), endomysial and perimysial infiltration (<em>inflammatory state domain</em>) and endomysium and perimysium distension (<em>interstitial compartment domain)</em>. We observed the expected time course in the six evaluated items. Furthermore, agreement among observers was evaluated by measuring the Intraclass Correlation Coefficient (ICC). Within the experienced group, items from the <em>muscle fibre</em> and <em>interstitial compartment</em> domains showed <em>good</em> agreement and the two items from the <em>infiltration compartment domain</em> showed <em>excellent</em> agreement. in conclusion, the proposed tool allowed quick and correct evaluation of light to moderate muscle damage in trained rats with good agreement between observers.

Honokiol protects rats against eccentric exercise-induced skeletal muscle damage by inhibiting NF-κB induced oxidative stress and inflammation

2009 ◽  
Vol 610 (1-3) ◽  
pp. 119-127 ◽  
Author(s):  
Jasson Chiang ◽  
Yuh-Chiang Shen ◽  
Yea-Hwey Wang ◽  
Yu-Chang Hou ◽  
Chien-Chih Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Muscle Damage ◽  
Eccentric Exercise ◽  
Skeletal Muscle Damage ◽  
Exercise Induced

scholarly journals MRI Quantitative Analysis of Eccentric Exercise-induced Skeletal Muscle Injury in Rats

2020 ◽  
Vol 27 (4) ◽  
pp. e72-e79 ◽  
Author(s):  
Congcong Fu ◽  
Yu Xia ◽  
Fan Meng ◽  
Fei Li ◽  
Qiang Liu ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Quantitative Analysis ◽  
Eccentric Exercise ◽  
Muscle Injury ◽  
Skeletal Muscle Injury ◽  
Exercise Induced

Cellular adaptation to repeated eccentric exercise-induced muscle damage

2001 ◽  
Vol 91 (4) ◽  
pp. 1669-1678 ◽  
Author(s):  
N. Stupka ◽  
M. A. Tarnopolsky ◽  
N. J. Yardley ◽  
S. M. Phillips
Keyword(s):  
Skeletal Muscle ◽  
Protein Content ◽  
Muscle Damage ◽  
Eccentric Exercise ◽  
Muscle Protein ◽  
Vastus Lateralis ◽  
Relative Magnitude ◽  
Knee Extension ◽  
Proteolytic Pathway ◽  
Exercise Induced

Eccentrically biased exercise results in skeletal muscle damage and stimulates adaptations in muscle, whereby indexes of damage are attenuated when the exercise is repeated. We hypothesized that changes in ultrastructural damage, inflammatory cell infiltration, and markers of proteolysis in skeletal muscle would come about as a result of repeated eccentric exercise and that gender may affect this adaptive response. Untrained male ( n = 8) and female ( n = 8) subjects performed two bouts ( bout 1and bout 2), separated by 5.5 wk, of 36 repetitions of unilateral, eccentric leg press and 100 repetitions of unilateral, eccentric knee extension exercises (at 120% of their concentric single repetition maximum), the subjects' contralateral nonexercised leg served as a control (rest). Biopsies were taken from the vastus lateralis from each leg 24 h postexercise. After bout 2, the postexercise force deficit and the rise in serum creatine kinase (CK) activity were attenuated. Women had lower serum CK activity compared with men at all times ( P < 0.05), but there were no gender differences in the relative magnitude of the force deficit. Muscle Z-disk streaming, quantified by using light microscopy, was elevated vs. rest only after bout 1 ( P< 0.05), with no gender difference. Muscle neutrophil counts were significantly greater in women 24 h after bout 2 vs. rest and bout 1 ( P < 0.05) but were unchanged in men. Muscle macrophages were elevated in men and women after bout 1 and bout 2 ( P < 0.05). Muscle protein content of the regulatory calpain subunit remained unchanged whereas ubiquitin-conjugated protein content was increased after both bouts ( P < 0.05), with a greater increase after bout 2. We conclude that adaptations to eccentric exercise are associated with attenuated serum CK activity and, potentially, an increase in the activity of the ubiquitin proteosome proteolytic pathway.

The cytokine response to strenuous exercise

1998 ◽  
Vol 76 (5) ◽  
pp. 505-511 ◽  
Author(s):  
Bente Klarlund Pedersen ◽  
Kenneth Ostrowski ◽  
Thomas Rohde ◽  
Helle Bruunsgaard
Keyword(s):  
Muscle Damage ◽  
Eccentric Exercise ◽  
Time Course ◽  
Close Association ◽  
Serum Levels ◽  
Strenuous Exercise ◽  
Necrosis Factor Alpha ◽  
Sequential Release ◽  
Systemic Endotoxemia ◽  
Exercise Induced

Strenuous exercise is accompanied by an increase in circulating proinflammatory and inflammation responsive cytokines, having some similarities with the response to sepsis and trauma. The sequential release of tumour necrosis factor-alpha, interleukin (IL)1beta, IL-6, and IL-1 receptor antagonist (IL-1ra) in the blood is comparable to that observed in relation to bacterial diseases. Eccentric exercise is associated with an increase in serum IL-6 concentrations and is significantly correlated with the concentration of creatine kinase (CK) in the following days, whereas no changes are found after the concentric exercise; this demonstrates a close association between exercise-induced muscle damage and increased serum levels of IL-6. The time course of cytokine production, the close association with muscle damage, and the finding of mRNA-IL-6 in skeletal muscle biopsies after intense exercise all support the idea that during eccentric exercise myofibers are mechanically damaged and that this process stimulates the local production of inflammatory cytokines. It remains to be shown whether systemic endotoxemia during exercise is also a cause of elevated levels of cytokines in the plasma. The present review also discusses the possible roles of protein breakdown, delayed onset muscle soreness, and clinical implications of the acute-phase response following exercise.Key words: exercise, sport, trauma, sepsis, cytokines, interleukin, muscle.

Investigation of serum creatine kinase variability after muscle-damaging exercise

1988 ◽  
Vol 75 (3) ◽  
pp. 257-261 ◽  
Author(s):  
Priscilla M. Clarkson ◽  
Cara Ebbeling
Keyword(s):  
Creatine Kinase ◽  
Muscle Damage ◽  
Eccentric Exercise ◽  
Muscle Injury ◽  
Serum Creatine Kinase ◽  
Blood Levels ◽  
Large Variability ◽  
Exercise Induced

1. The present study examined if the presence of creatine kinase (CK) inhibitors might explain the large variability in blood levels of CK among subjects after exercise-induced muscle damage. 2. Twenty-four women performed an eccentric exercise with the forearm flexors and were then classified as no CK responders, low CK responders and high CK responders. High CK responders repeated the exercise two weeks later (bout two). 3. Sera from high CK responders were mixed with sera from no CK responders or low CK responders. Also, serum from high CK responders obtained after bout one was mixed with the same subject's serum from after bout two. 4. In all cases, the differences between the expected and observed CK activity for the mixes were within the expected variability for the assay. 5. Although CK inhibitors have been previously observed in sera from patients with muscle injury or disease, we were unable to demonstrate the presence of CK inhibitors in the sera from subjects who showed evidence of exercise-induced muscle damage.

scholarly journals Vitamin D Promotes Skeletal Muscle Regeneration and Mitochondrial Health

2021 ◽  
Vol 12 ◽  
Author(s):  
Christine M. Latham ◽  
Camille R. Brightwell ◽  
Alexander R. Keeble ◽  
Brooke D. Munson ◽  
Nicholas T. Thomas ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Vitamin D ◽  
Muscle Damage ◽  
Muscle Regeneration ◽  
Muscle Injury ◽  
Time Course ◽  
Active Form ◽  
Skeletal Muscle Regeneration ◽  
Optimal Timing

Vitamin D is an essential nutrient for the maintenance of skeletal muscle and bone health. The vitamin D receptor (VDR) is present in muscle, as is CYP27B1, the enzyme that hydroxylates 25(OH)D to its active form, 1,25(OH)D. Furthermore, mounting evidence suggests that vitamin D may play an important role during muscle damage and regeneration. Muscle damage is characterized by compromised muscle fiber architecture, disruption of contractile protein integrity, and mitochondrial dysfunction. Muscle regeneration is a complex process that involves restoration of mitochondrial function and activation of satellite cells (SC), the resident skeletal muscle stem cells. VDR expression is strongly upregulated following injury, particularly in central nuclei and SCs in animal models of muscle injury. Mechanistic studies provide some insight into the possible role of vitamin D activity in injured muscle. In vitro and in vivo rodent studies show that vitamin D mitigates reactive oxygen species (ROS) production, augments antioxidant capacity, and prevents oxidative stress, a common antagonist in muscle damage. Additionally, VDR knockdown results in decreased mitochondrial oxidative capacity and ATP production, suggesting that vitamin D is crucial for mitochondrial oxidative phosphorylation capacity; an important driver of muscle regeneration. Vitamin D regulation of mitochondrial health may also have implications for SC activity and self-renewal capacity, which could further affect muscle regeneration. However, the optimal timing, form and dose of vitamin D, as well as the mechanism by which vitamin D contributes to maintenance and restoration of muscle strength following injury, have not been determined. More research is needed to determine mechanistic action of 1,25(OH)D on mitochondria and SCs, as well as how this action manifests following muscle injury in vivo. Moreover, standardization in vitamin D sufficiency cut-points, time-course study of the efficacy of vitamin D administration, and comparison of multiple analogs of vitamin D are necessary to elucidate the potential of vitamin D as a significant contributor to muscle regeneration following injury. Here we will review the contribution of vitamin D to skeletal muscle regeneration following injury.

scholarly journals Exercise promotes α7 integrin gene transcription and protection of skeletal muscle

2008 ◽  
Vol 295 (5) ◽  
pp. R1623-R1630 ◽  
Author(s):  
Marni D. Boppart ◽  
Sonja E. Volker ◽  
Nicole Alexander ◽  
Dean J. Burkin ◽  
Stephen J. Kaufman
Keyword(s):  
Skeletal Muscle ◽  
Muscle Damage ◽  
Muscle Injury ◽  
Rapid Change ◽  
Myotendinous Junction ◽  
Wild Type ◽  
Integrin Gene ◽  
Exercise Muscle ◽  
Exercise Induced ◽  
Response To Exercise

The α7β1 integrin is increased in skeletal muscle in response to injury-producing exercise, and transgenic overexpression of this integrin in mice protects against exercise-induced muscle damage. The present study investigates whether the increase in the α7β1 integrin observed in wild-type mice in response to exercise is due to transcriptional regulation and examines whether mobilization of the integrin at the myotendinous junction (MTJ) is a key determinant in its protection against damage. A single bout of downhill running exercise selectively increased transcription of the α7 integrin gene in 5-wk-old wild-type mice 3 h postexercise, and an increased α7 chain was detected in muscle sarcolemma adjacent to tendinous tissue immediately following exercise. The α7B, but not α7A isoform, was found concentrated and colocalized with tenascin-C in muscle fibers lining the MTJ. To further validate the importance of the integrin in the protection against muscle damage following exercise, muscle injury was quantified in α7−/−mice. Muscle damage was extensive in α7−/−mice in response to both a single and repeated bouts of exercise and was largely restricted to areas of high MTJ concentration and high mechanical force near the Achilles tendon. These results suggest that exercise-induced muscle injury selectively increases transcription of the α7 integrin gene and promotes a rapid change in the α7β integrin at the MTJ. These combined molecular and cellular alterations are likely responsible for integrin-mediated attenuation of exercise-induced muscle damage.

scholarly journals Adenosine A3 receptor stimulation induces protection of skeletal muscle from eccentric exercise-mediated injury

2010 ◽  
Vol 299 (1) ◽  
pp. R259-R267 ◽  
Author(s):  
Ruibo Wang ◽  
Maria L. Urso ◽  
Edward J. Zambraski ◽  
Erik P. Rader ◽  
Kevin P. Campbell ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Eccentric Exercise ◽  
Receptor Agonist ◽  
Muscle Injury ◽  
Protective Role ◽  
Blue Dye ◽  
Receptor Stimulation ◽  
Skeletal Muscle Injury ◽  
Exercise Induced ◽  
Dystrophic Mice

Effective therapy to reduce skeletal muscle injury associated with severe or eccentric exercise is needed. The purpose of this study was to determine whether adenosine receptor stimulation can mediate protection from eccentric exercise-induced muscle injury. Downhill treadmill exercise (−15°) was used to induce eccentric exercise-mediated skeletal muscle injury. Experiments were conducted in both normal wild-type (WT) mice and also in β-sarcoglycan knockout dystrophic mice, animals that show an exaggerated muscle damage with the stress of exercise. In the vehicle-treated WT animals, eccentric exercise increased serum creatine kinase (CK) greater than 3-fold to 358.9 ± 62.7 U/l (SE). This increase was totally abolished by stimulation of the A3 receptor. In the dystrophic β-sarcoglycan-null mice, eccentric exercise caused CK levels to reach 55,124 ± 5,558 U/l. A3 receptor stimulation in these animals reduced the CK response by nearly 50%. In the dystrophic mice at rest, 10% of the fibers were found to be damaged, as indicated by Evans blue dye staining. While this percentage was doubled after exercise, A3 receptor stimulation eliminated this increase. Neither the A1 receptor agonist 2-chloro- N6-cyclopentyladenosine (0.05 mg/kg) nor the A2A receptor agonist 2- p-(2-carboxyethyl)phenethylamino-5′- N-ethylcarboxamidoadenosine (0.07 mg/kg) protected skeletal muscle from eccentric exercise injury in WT or dystrophic mice. The protective effect of adenosine A3 receptor stimulation was absent in mice, in which genes for phospholipase C β2/β3 (PLCβ2/β3) and β-sarcoglycan were deleted. The present study elucidates a new protective role of the A3 receptor and PLCβ2/β3 and points to a potentially effective therapeutic strategy for eccentric exercise-induced skeletal muscle injury.

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