scholarly journals PO-214 DDAH1 knockout has a protective effect on muscle damage caused by downhill running

2018 ◽  
Vol 1 (5) ◽  
Author(s):  
Hui Song ◽  
Xin Xu
Keyword(s):  
Skeletal Muscle ◽  
Grip Strength ◽  
Muscle Damage ◽  
Eccentric Exercise ◽  
Time Of Day ◽  
Control Group ◽  
Dimethylarginine Dimethylaminohydrolase ◽  
Warm Up ◽  
Downhill Running ◽  
Access To Water

Objective Purpose：Downhill running can causes muscle damage, called delayed muscle damage and induced oxidative stress and inflammatory reaction, causing abnormity of skeletal muscle morphology, changing in blood biochemical indexes, and decreasing in function of skeletal muscle systolic. Asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase (NOS) inhibitor, is degraded by dimethylarginine dimethylaminohydrolase 1 (DDAH1). There were new evidences demonstrated that DDAH1 is an important regulator of cell redox state and apoptosis. In summary, the study shown that DDAH1 is an important regulator of cell redox state and apoptosis. Emerging evidences suggests that DDAH1 controls cellular oxidative stress and apoptosis via a miR-21-dependent pathway. However, the effect and mechanism of DDAH1 on damage of skeletal muscle caused by downhill running is not clear enough. Thus，the purpose of this experiment was to determine the effect and mechanism of DDAH1 in downhill running. Keys: downhill running; delayed onset muscle soreness(DOMS); eccentric exercise; skeletal muscle. Methods Method: The experimental mice were 24 female C57 mice of 10 weeks old and 24 female DDAH1 hybrid knockout mice of 10 weeks old. DDAH1 KO mice used for this study was knockout of dimethylarginine dimethylaminohydrolase 1 compared with WT mice. Animals were fed standard laboratory chow and had access to water ad libitum. C57 mice were divided into 3 groups: C57 control, C57 48H, C57 120H; DDAH1 KO mice were divided into 3 groups: DDAH1 control, DDAH1 48H, DDAH1 120H. C57 and DDAH1 KO mice used for this study completed a single bout of downhill running exercise (20°, 17 m/min, 60 min), and gastrocnemius muscle, soleus muscle and quadriceps femoris muscle were collected 48 and 120 hours (H) postexercise (PE). C57control group and DDAH1 KO control group dose not exercise. Speed on the treadmill was gradually increased from 10 to 17m/min during a 7-min warm-up period (increased of 1m/min every minute). All experiments were conducted at approximately the same time of day. Maximal grip strength was measured ifor each groups. Grip strength testing was completed to detect post-eccentric exercise injury in C57 and DDAH1 KO mice. All results were analyzed by means of methods of histological and molecular biological. Results Method: The experimental mice were 24 female C57 mice of 10 weeks old and 24 female DDAH1 hybrid knockout mice of 10 weeks old. DDAH1 KO mice used for this study was knockout of dimethylarginine dimethylaminohydrolase 1 compared with WT mice. Animals were fed standard laboratory chow and had access to water ad libitum. C57 mice were divided into 3 groups: C57 control, C57 48H, C57 120H; DDAH1 KO mice were divided into 3 groups: DDAH1 control, DDAH1 48H, DDAH1 120H. C57 and DDAH1 KO mice used for this study completed a single bout of downhill running exercise (20°, 17 m/min, 60 min), and gastrocnemius muscle, soleus muscle and quadriceps femoris muscle were collected 48 and 120 hours (H) postexercise (PE). C57control group and DDAH1 KO control group dose not exercise. Speed on the treadmill was gradually increased from 10 to 17m/min during a 7-min warm-up period (increased of 1m/min every minute). All experiments were conducted at approximately the same time of day. Maximal grip strength was measured ifor each groups. Grip strength testing was completed to detect post-eccentric exercise injury in C57 and DDAH1 KO mice. All results were analyzed by means of methods of histological and molecular biological. Conclusions Conclusion: The DDAH1 knockout has a protective effect on delayed onset muscle soreness(DOMS) caused by downhill running, and accelerate the injury recovery.     

Effects of oat protein supplementation on skeletal muscle damage, inflammation and performance recovery following downhill running in untrained collegiate men

2018 ◽  
Vol 9 (9) ◽  
pp. 4720-4729 ◽  
Author(s):  
Z. Xia ◽  
J. M. Cholewa ◽  
D. Dardevet ◽  
T. Huang ◽  
Y. Zhao ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Damage ◽  
Eccentric Exercise ◽  
Protein Supplementation ◽  
Protective Effects ◽  
Skeletal Muscle Damage ◽  
Downhill Running ◽  
Performance Recovery ◽  
And Performance

Oat protein supplementation exhibits protective effects on muscles during eccentric exercise, but more research is needed to clarify the mechanism.

Polymethoxyflavones in orange peel extract prevent skeletal muscle damage induced by eccentric exercise in rats

2020 ◽  
Vol 85 (2) ◽  
pp. 440-446
Author(s):  
Toshihide Suzuki ◽  
Makoto Shimizu ◽  
Yoshio Yamauchi ◽  
Ryuichiro Sato
Keyword(s):  
Skeletal Muscle ◽  
Muscle Damage ◽  
Eccentric Exercise ◽  
Vastus Lateralis ◽  
Orange Peel ◽  
Skeletal Muscle Damage ◽  
Downhill Running ◽  
Exercise Induced ◽  
Orange Peel Extract ◽  
Peel Extract

ABSTRACT Polymethoxyflavones (PMFs) contained in the peel of citrus fruits have anti-inflammatory, anticancer, and antidepressant effects. However, their effects on skeletal muscle are unknown. We investigated whether PMFs could prevent skeletal muscle damage induced by eccentric exercise in rats. Downhill running for 90 min increased the levels of the inflammatory cytokines, monocyte chemotactic protein-1 (MCP-1), and interleukin-1β (IL-1β) in skeletal muscles, especially in vastus lateralis, and the plasma creatine kinase levels. These increases were attenuated by a single oral administration of orange peel extract (OPE) 30 min before downhill running. A mixture of nobiletin, sinensetin, 3,5,6,7,8,3′,4′-heptamethoxyflavone, and tangeretin, which are the major PMFs of OPE, also showed similar effects on muscle damage. These results suggest that OPE has a protective effect against eccentric exercise-induced skeletal muscle damage, and that the effects may be attributed to the 4 major PMFs.

scholarly journals Hormone therapy attenuates exercise-induced skeletal muscle damage in postmenopausal women

2009 ◽  
Vol 107 (3) ◽  
pp. 853-858 ◽  
Author(s):  
Christina M. Dieli-Conwright ◽  
Tanya M. Spektor ◽  
Judd C. Rice ◽  
E. Todd Schroeder
Keyword(s):  
Skeletal Muscle ◽  
Hormone Therapy ◽  
Mrna Expression ◽  
Postmenopausal Women ◽  
Muscle Damage ◽  
Exercise Bout ◽  
Control Group ◽  
Skeletal Muscle Damage ◽  
Tnf Α ◽  
Exercise Induced

Hormone therapy (HT) is a potential treatment to relieve symptoms of menopause and prevent the onset of disease such as osteoporosis in postmenopausal women. We evaluated changes in markers of exercise-induced skeletal muscle damage and inflammation [serum creatine kinase (CK), serum lactate dehydrogenase (LDH), and skeletal muscle mRNA expression of IL-6, IL-8, IL-15, and TNF-α] in postmenopausal women after a high-intensity resistance exercise bout. Fourteen postmenopausal women were divided into two groups: women not using HT (control; n = 6, 59 ± 4 yr, 63 ± 17 kg) and women using traditional HT (HT; n = 8, 59 ± 4 yr, 89 ± 24 kg). Both groups performed 10 sets of 10 maximal eccentric repetitions of single-leg extension on the Cybex dynamometer at 60°/s with 20-s rest periods between sets. Muscle biopsies of the vastus lateralis were obtained from the exercised leg at baseline and 4 h after the exercise bout. Gene expression was determined by RT-PCR for IL-6, IL-8, IL-15, and TNF-α. Blood draws were performed at baseline and 3 days after exercise to measure CK and LDH. Independent t-tests were performed to test group differences (control vs. HT). A probability level of P ≤ 0.05 was used to determine statistical significance. We observed significantly greater changes in mRNA expression of IL-6, IL-8, IL-15, and TNF-α ( P ≤ 0.01) in the control group compared with the HT group after the exercise bout. CK and LDH levels were significantly greater after exercise ( P ≤ 0.01) in the control group. Postmenopausal women not using HT experienced greater muscle damage after maximal eccentric exercise, indicating a possible protective effect of HT against exercise-induced skeletal muscle damage.

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

EFFECTS OF WARM-UP PRIOR TO ECCENTRIC EXERCISE ON INDIRECT MARKERS OF MUSCLE DAMAGE

2001 ◽  
Vol 33 (5) ◽  
pp. S122
Author(s):  
R K. Evans ◽  
A C. Parcell ◽  
K L. Knight ◽  
S S. Schulthies ◽  
D O. Draper
Keyword(s):  
Muscle Damage ◽  
Eccentric Exercise ◽  
Warm Up

scholarly journals Liver kinase B1 inhibits the expression of inflammation-related genes postcontraction in skeletal muscle

2016 ◽  
Vol 120 (8) ◽  
pp. 876-888 ◽  
Author(s):  
Ting Chen ◽  
Timothy M. Moore ◽  
Mark T. W. Ebbert ◽  
Natalie L. McVey ◽  
Steven R. Madsen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Inflammatory Response ◽  
Muscle Contraction ◽  
Muscle Damage ◽  
Treadmill Running ◽  
Gene Markers ◽  
Downhill Running ◽  
Liver Kinase B1 ◽  
Increased Susceptibility

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.

Gender differences in muscle inflammation after eccentric exercise

2000 ◽  
Vol 89 (6) ◽  
pp. 2325-2332 ◽  
Author(s):  
N. Stupka ◽  
S. Lowther ◽  
K. Chorneyko ◽  
J. M. Bourgeois ◽  
C. Hogben ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Creatine Kinase ◽  
Muscle Damage ◽  
Eccentric Exercise ◽  
Kinase Activity ◽  
Morphological Changes ◽  
Vastus Lateralis ◽  
Creatine Kinase Activity ◽  
Blue Staining ◽  
Positive Staining

Unaccustomed exercise is followed by delayed-onset muscle soreness and morphological changes in skeletal muscle. Animal studies have demonstrated that women have an attenuated response to muscle damage. We studied the effect of eccentric exercise in untrained male ( n = 8) and female ( n = 8) subjects using a unilateral exercise design [exercise (Ex) and control (Con) legs]. Plasma granulocyte counts [before (Pre) and 48 h after exercise (+48h)] and creatine kinase activity [Pre, 24 h after exercise (+24h), +48h, and 6 days after exercise (+6d)] were determined before (Pre) and after (+24h, +48h, +6d) exercise, with biopsies taken from the vastus lateralis of each leg at +48h for determination of muscle damage and/or inflammation. Plasma granulocyte counts increased for men and decreased for women at +48h ( P < 0.05), and creatine kinase activity increased for both genders at +48h and +6d ( P < 0.01). There were significantly greater areas of both focal ( P < 0.001) and extensive ( P < 0.01) damage in the Ex vs. Con leg for both genders, which was assessed by using toluidine blue staining. The number of leukocyte common antigen-positive cells/mm2 tissue increased with exercise ( P< 0.05), and men tended to show more in their Ex vs. Con leg compared with women ( P = 0.052). Men had a greater total (Ex and Con legs) number of bcl-2-positive cells/mm2 tissue vs. women ( P < 0.05). Atrophic fibers with homogeneous bcl-2-positive staining were seen only in men ( n = 3). We conclude that muscle damage is similar between genders, yet the inflammatory response is attenuated in women vs. men. Finally, exercise may stimulate the expression of proteins involved in apoptosis in skeletal muscle.

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.

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