Ameliorative Effects of Caffeic Acid Phenethyl Ester on an Eccentric Exercise-Induced Skeletal Muscle Injury by Down-Regulating NF-κB Mediated Inflammation

Pharmacology ◽  
2013 ◽  
Vol 91 (3-4) ◽  
pp. 219-228 ◽  
Author(s):  
Yuh-Chiang Shen ◽  
Jiin-Cherng Yen ◽  
Kuo-Tong Liou
Keyword(s):  
Skeletal Muscle ◽  
Caffeic Acid ◽  
Eccentric Exercise ◽  
Muscle Injury ◽  
Caffeic Acid Phenethyl Ester ◽  
Skeletal Muscle Injury ◽  
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

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.

P4420Is exercise-induced cardiac troponin release caused by skeletal muscle injury?

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
T Paana ◽  
S Jaakkola ◽  
E Tuunainen ◽  
S Wittfooth ◽  
K Bamberg ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Troponin ◽  
Muscle Injury ◽  
Troponin I ◽  
Troponin T ◽  
Skeletal Muscle Injury ◽  
Coronary Syndrome ◽  
Marathon Race ◽  
Recreational Runners ◽  
Exercise Induced

Abstract Background Cardiac troponins (cTn) are highly sensitive and specific markers for cardiac injury and a key element in the diagnosis of acute coronary syndrome. Strenuous exercise is known to induce increases in cTn, but the causative factors remain ambiguous. It is also equivocal whether exercise induced skeletal muscle injury is associated with cTn elevation. Purpose The aim of this study was to identify independent predictors for the rise in cardiac troponin T (cTnT) and I (cTnI) concentration and to focus on the relationship between skeletal muscle injury measured by skeletal troponin I (skTnI) and cTn elevations after a marathon race in a large group of male recreational runners. Methods A total of 40 recreational runners participating in the marathon in our city were recruited. The study included baseline visit (prerace) and immediate post-race sampling. Results The post-marathon cTnT concentration rose above the reference limit in 38 (95%) participants and the detection limit for cTnI was exceeded in 34 (85%) participants. Similarly, a 10-fold increase in skTnI concentration was observed and elevated post-race values were seen in all participants. There was no significant correlation between the post-race cTnT or cTnT change and post-race skTnI (Spearman's rho = 0.249, p=0.122, rho = 0.285, p=0.074). However, post-race cTnI and change in cTnI were associated with post-race skTnI (rho = 0.404, p=0.01, rho = 0.460, p=0.003) and creatine kinase (r=0.368, p=0.019) concentration. Subjective exertion or self-reported muscle symptoms did not correlate with post-race cTnT, cTnI or skTnI levels. Post-Race cTnT <40 Post-Race cTnT ≥40 p-value n=18 n=22 Age, years 53.3±12.2 44.0±11.9 0.002 Active training, years 12.0 (9.3) 17.0 (15.8) 0.190 Muscle symptoms 7 (38.9) 11 (52.4) 0.523 Creatinine kinase, ug/l 406 (137) 399 (319) 0.163 N-terminal proBNP ng/l 137±168 158±277 0.783 Skeletal Troponin I, ng/ml 28.6 (41) 56.7 (143) 0.199 Figure 1 Conclusions Cardiac troponin became abnormal in almost all runners after marathon race. The exercise-induced rise in cardiac troponin I is related to simultaneous release of skeletal troponin I. The mechanism of this association remains uncertain, but clinicians should be cautious when interpreting post-exercise troponin levels without clinical symptoms and signs of myocardial ischemia.

Astaxanthin Supplementation Does Not Attenuate Muscle Injury Following Eccentric Exercise in Resistance-Trained Men

2005 ◽  
Vol 15 (4) ◽  
pp. 401-412 ◽  
Author(s):  
Richard J. Bloomer ◽  
Andrew Fry ◽  
Brian Schilling ◽  
Loren Chiu ◽  
Naruhiro Hori ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Eccentric Exercise ◽  
Muscle Injury ◽  
Muscle Performance ◽  
Safflower Oil ◽  
Similar Response ◽  
Post Exercise ◽  
Skeletal Muscle Injury ◽  
Treatment Groups ◽  
Exercise Muscle

This investigation was designed to determine the effects of astaxanthin on markers of skeletal muscle injury. Twenty resistance trained men (mean ± standard error of the mean: age, 25.1 ± 1.6 y; height, 1.79 ± 0.02 m; weight, 86.8 ± 4.4 kg) were assigned to either a placebo (1732 mg safflower oil, n = 10) or astaxanthin (BioAstin; 1732 mg safflower oil; haematococcus algae extract [contains 4 mg astaxanthin and 480 mg lutein], n = 10). Subjects consumed their assigned treatment for 3 wk prior to eccentric exercise (10 sets of 10 repetitions at 85% of one repetition maximum) and through 96 h post-exercise. Muscle soreness, creatine kinase (CK), and muscle performance was measured before and through 96 h post-exercise. A similar response was observed for both treatment groups for all dependent variables, indicating that in resistance trained men, astaxanthin supplementation does not favorably affect indirect markers of skeletal muscle injury following eccentric loading.

Lovastatin increases exercise-induced skeletal muscle injury

Metabolism ◽  
1997 ◽  
Vol 46 (10) ◽  
pp. 1206-1210 ◽  
Author(s):  
Paul D. Thompson ◽  
Joseph M. Zmuda ◽  
Leslie J. Domalik ◽  
Richard J. Zimet ◽  
Joan Staggers ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Injury ◽  
Skeletal Muscle Injury ◽  
Exercise Induced
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