scholarly journals Potential role of exercise-induced glucose-6-phosphate isomerase in skeletal muscle function

2019 ◽  
Vol 23 (2) ◽  
pp. 28-33 ◽  
Author(s):  
Seong Eun Kwak ◽  
Hyung Eun Shin ◽  
Di Di Zhang ◽  
Jihyun Lee ◽  
Kyung Jin Yoon ◽  
...  
2016 ◽  
Vol 6 ◽  
Author(s):  
Erick O. Hernández-Ochoa ◽  
Stephen J. P. Pratt ◽  
Richard M. Lovering ◽  
Martin F. Schneider

2007 ◽  
Vol 103 (3) ◽  
pp. 1093-1098 ◽  
Author(s):  
Bente Klarlund Pedersen ◽  
Thorbjörn C. A. Åkerström ◽  
Anders R. Nielsen ◽  
Christian P. Fischer

During the past 20 yr, it has been well documented that exercise has a profound effect on the immune system. With the discovery that exercise provokes an increase in a number of cytokines, a possible link between skeletal muscle contractile activity and immune changes was established. For most of the last century, researchers sought a link between muscle contraction and humoral changes in the form of an “exercise factor,” which could mediate some of the exercise-induced metabolic changes in other organs such as the liver and the adipose tissue. We suggest that cytokines and other peptides that are produced, expressed, and released by muscle fibers and exert either paracrine or endocrine effects should be classified as “myokines.” Since the discovery of interleukin (IL)-6 release from contracting skeletal muscle, evidence has accumulated that supports an effect of IL-6 on metabolism. We suggested that muscle-derived IL-6 fulfils the criteria of an exercise factor and that such classes of cytokines should be named “myokines.” Interestingly, recent research demonstrates that skeletal muscles can produce and express cytokines belonging to distinctly different families. Thus skeletal muscle has the capacity to express several myokines. To date the list includes IL-6, IL-8, and IL-15, and contractile activity plays a role in regulating the expression of these cytokines in skeletal muscle. The present review focuses on muscle-derived cytokines, their regulation by exercise, and their possible roles in metabolism and skeletal muscle function and it discusses which cytokines should be classified as true myokines.


2019 ◽  
Vol 10 (4) ◽  
pp. 929-949 ◽  
Author(s):  
Matthew J. Myers ◽  
Danielle L. Shepherd ◽  
Andrya J. Durr ◽  
David S. Stanton ◽  
Junaith S. Mohamed ◽  
...  

2019 ◽  
Vol 125 (Suppl_1) ◽  
Author(s):  
Somik Chatterjee ◽  
Shumin Li ◽  
Aijun Zhang ◽  
Indira Vedula ◽  
Judy A AlRukby ◽  
...  

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Veronica Granatiero ◽  
Gaia Gherardi ◽  
Matteo Vianello ◽  
Elsa Salerno ◽  
Erika Zecchini ◽  
...  

1999 ◽  
Vol 20 (6) ◽  
pp. 423-430 ◽  
Author(s):  
R.A. Sabbadini ◽  
D. Danieli-Betto ◽  
R. Betto

2012 ◽  
Vol 303 (3) ◽  
pp. R321-R331 ◽  
Author(s):  
Kate T. Murphy ◽  
Andrew M. Allen ◽  
Annabel Chee ◽  
Timur Naim ◽  
Gordon S. Lynch

The role of the renin-angiotensin system (RAS) in vasoregulation is well established, but a localized RAS exists in multiple tissues and exerts diverse functions including autonomic control and thermogenesis. The role of the RAS in the maintenance and function of skeletal muscle is not well understood, especially the role of angiotensin peptides, which appear to contribute to muscle atrophy. We tested the hypothesis that mice lacking the angiotensin type 1A receptor (AT1A−/−) would exhibit enhanced whole body and skeletal muscle function and improved regeneration after severe injury. Despite 18- to 20-wk-old AT1A−/−mice exhibiting reduced muscle mass compared with controls ( P < 0.05), the tibialis anterior (TA) muscles produced a 25% higher maximum specific (normalized) force ( P < 0.05). Average fiber cross-sectional area (CSA) and fiber oxidative capacity was not different between groups, but TA muscles from AT1A−/−mice had a reduced number of muscle fibers as well as a higher proportion of type IIx/b fibers and a lower proportion of type IIa fibers ( P < 0.05). Measures of whole body function (grip strength, rotarod performance, locomotor activity) were all improved in AT1A−/−mice ( P < 0.05). Surprisingly, the recovery of muscle mass and fiber CSA following myotoxic injury was impaired in AT1A−/−mice, in part by impaired myoblast fusion, prolonged collagen infiltration and inflammation, and delayed expression of myogenic regulatory factors. The findings support the therapeutic potential of RAS inhibition for enhancing whole body and skeletal muscle function, but they also reveal the importance of RAS signaling in the maintenance of muscle mass and for normal fiber repair after injury.


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