Effects of Rest Interval Following Eccentric Muscle Contraction Exercise on Circulating Substance, Parameters Related to Damage and Regeneration in Skeletal Muscle

2013 ◽  
Vol 15 (4) ◽  
pp. 107-115
Author(s):  
송상협
2007 ◽  
Vol 32 (2) ◽  
pp. 273-281 ◽  
Author(s):  
Michihiro Kon ◽  
Kai Tanabe ◽  
Hoseong Lee ◽  
Fuminori Kimura ◽  
Takayuki Akimoto ◽  
...  

The purpose of this study was to examine oxidative stress in skeletal muscle after eccentric and concentric muscle contractions. Eight-week-old Institute of Cancer Research (ICR) mice (n = 90) were divided into 3 groups: eccentric muscle contraction group (ECC, n = 42), concentric muscle contraction group (CON, n = 42), and control group (pre, n = 6). The tibialis anterior muscle was stimulated via the peroneal nerve to contract either eccentrically or concentrically. The tibialis anterior muscle was isolated before and 0, 6, 12, 18, 24, 72, and 168 h after muscle contraction. Immediately after muscle contractions, thiobarbituric acid reactive substances (TBARS) in skeletal muscle significantly increased (p < 0.05) in both ECC and CON conditions. However, in the ECC group alone, the TBARS level peaked at 12 and 72 h after the contractions. There was greater migration of mononuclear cells in ECC than in CON muscle. In addition, there was a correlation between TBARS in skeletal muscle and migration of mononuclear cells in ECC muscle (r = 0.773, p < 0.01), but this correlation was not apparent in CON muscle (r = 0.324, p = 0.12). The increased mononuclear cells may reflect inflammatory cells. These data suggest that eccentric muscle contraction induces greater oxidative stress in skeletal muscle, which may in turn be due to enhanced generation of reactive oxygen species (ROS) by migrating inflammatory cells.


2011 ◽  
Vol 436 (2) ◽  
pp. 437-445 ◽  
Author(s):  
Zhe Chen ◽  
Tong-Jin Zhao ◽  
Jie Li ◽  
Yan-Song Gao ◽  
Fan-Guo Meng ◽  
...  

Muscle contraction requires high energy fluxes, which are supplied by MM-CK (muscle-type creatine kinase) which couples to the myofibril. However, little is known about the detailed molecular mechanisms of how MM-CK participates in and is regulated during muscle contraction. In the present study, MM-CK is found to physically interact with the slow skeletal muscle-type MyBPC1 (myosin-binding protein C1). The interaction between MyBPC1 and MM-CK depended on the creatine concentration in a dose-dependent manner, but not on ATP, ADP or phosphocreatine. The MyBPC1–CK interaction favoured acidic conditions, and the two molecules dissociated at above pH 7.5. Domain-mapping experiments indicated that MM-CK binds to the C-terminal domains of MyBPC1, which is also the binding site of myosin. The functional coupling of myosin, MyBPC1 and MM-CK is further corroborated using an ATPase activity assay in which ATP expenditure accelerates upon the association of the three proteins, and the apparent Km value of myosin is therefore reduced. The results of the present study suggest that MyBPC1 acts as an adaptor to connect the ATP consumer (myosin) and the regenerator (MM-CK) for efficient energy metabolism and homoeostasis.


2004 ◽  
Vol 63 (2) ◽  
pp. 227-232 ◽  
Author(s):  
Yun Chau Long ◽  
Ulrika Widegren ◽  
Juleen R. Zierath

Exercise training improves glucose homeostasis through enhanced insulin sensitivity in skeletal muscle. Muscle contraction through physical exercise is a physiological stimulus that elicits multiple biochemical and biophysical responses and therefore requires an appropriate control network. Mitogen-activated protein kinase (MAPK) signalling pathways constitute a network of phosphorylation cascades that link cellular stress to changes in transcriptional activity. MAPK cascades are divided into four major subfamilies, including extracellular signal-regulated kinases 1 and 2, p38 MAPK, c-Jun NH2-terminal kinase and extracellular signal-regulated kinase 5. The present review will present the current understanding of parallel MAPK signalling in human skeletal muscle in response to exercise and muscle contraction, with an emphasis on identifying potential signalling mechanisms responsible for changes in gene expression.


2016 ◽  
Vol 7 ◽  
Author(s):  
Wan X. Yao ◽  
Zhiguo Jiang ◽  
Jinqi Li ◽  
Changhao Jiang ◽  
Crystal G. Franlin ◽  
...  

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