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During the injury of skeletal muscle, mononuclear muscle precursors, satellite cells, become activated then divide and fuse to form new multinucleated myotubes, which eventually become the mature muscle fibers.
The process of muscle regeneration is regulated by locally produced growth factors that control cellular proliferation and differentiation. Several polypeptide growth factors have been implicated as regulators of myogenic cell proliferation and differentiation during development and after injury. [1]
There are five main cytokines known to regulate the inflammation process that occurs during muscle regeneration. The most effective, being leukemia inhibitory factor (LIF). LIF has been shown to significantly increase the rate of muscular regeneration in transgenic mice. LIF stimulated the formation of larger muscle fibers, while not stimulating proliferation of resident fibroblasts. [1]
However, some cytokines display properties not so appealing to the average weight lifter. These include but are not limited to such cytokines as: alpha-tumor necrosis factor (a-TNF), Interlukin-1 (IL-1) and Interlukin-6 (IL-6).
"Cytokines may function either systemically or locally within muscle per se. Lipopolysaccharide and other pathogen-associated molecules stimulate cytokine expression in muscle. The failure to clear pathogen-associated molecules or the introduction of muscle damage may initiate a protracted activation of enzymes and transcription factors that orchestrate a genetic program that ultimately produces muscle wasting. [2]"
Now for the interesting part: During chronic low-grade systemic inflammation cardiovascular disease and Type 2 diabetes mellitus may result. During this chronic low-grade inflammation several cytokines have been show to be three to four fold elevated with in the body. Adipose tissue contributes to one of these cytokines, alpha-tumor necrosis factor (TNF-a).
During exercise, IL-6 is produced by muscle fibers via a TNF-independent pathway. IL-6 stimulates the appearance in the circulation of other anti-inflammatory cytokines such as IL-1ra and IL-10 and inhibits the production of the proinflammatory cytokine TNF-alpha. In addition, IL-6 enhances lipid turnover, stimulating lipolysis as well as fat oxidation. [2]
In conclusion, regular exercise will inhibit TNF-a via the IL-6 pathway within skeletal muscle. IL-6 has been introduced recently as a myokine (defined as a cytokine that is produced and released by contracting skeletal muscle fibers, exerting its effects in other organs of the body) and may be involved in mediating the health-beneficial effects of exercise Myokines may also be important in the protection from such chronic diseases associated with low-grade inflammation such as diabetes and cardiovascular diseases.
References:--------------------------------------------------------------
1. John B Kurek, John J. Bower. Leukaemia Inhibitory Factor and Other Cytokines as Factors Influencing Regeneration of Skeletal Muscle. Basic Appl. Myol. 8 (5): 347-360, 1998
2.Petersen AM, Pedersen BK. The anti-inflammatory effect of exercise. Appl Physiol. 2005 Apr;98(4):1154-62.
The process of muscle regeneration is regulated by locally produced growth factors that control cellular proliferation and differentiation. Several polypeptide growth factors have been implicated as regulators of myogenic cell proliferation and differentiation during development and after injury. [1]
There are five main cytokines known to regulate the inflammation process that occurs during muscle regeneration. The most effective, being leukemia inhibitory factor (LIF). LIF has been shown to significantly increase the rate of muscular regeneration in transgenic mice. LIF stimulated the formation of larger muscle fibers, while not stimulating proliferation of resident fibroblasts. [1]
However, some cytokines display properties not so appealing to the average weight lifter. These include but are not limited to such cytokines as: alpha-tumor necrosis factor (a-TNF), Interlukin-1 (IL-1) and Interlukin-6 (IL-6).
"Cytokines may function either systemically or locally within muscle per se. Lipopolysaccharide and other pathogen-associated molecules stimulate cytokine expression in muscle. The failure to clear pathogen-associated molecules or the introduction of muscle damage may initiate a protracted activation of enzymes and transcription factors that orchestrate a genetic program that ultimately produces muscle wasting. [2]"
Now for the interesting part: During chronic low-grade systemic inflammation cardiovascular disease and Type 2 diabetes mellitus may result. During this chronic low-grade inflammation several cytokines have been show to be three to four fold elevated with in the body. Adipose tissue contributes to one of these cytokines, alpha-tumor necrosis factor (TNF-a).
During exercise, IL-6 is produced by muscle fibers via a TNF-independent pathway. IL-6 stimulates the appearance in the circulation of other anti-inflammatory cytokines such as IL-1ra and IL-10 and inhibits the production of the proinflammatory cytokine TNF-alpha. In addition, IL-6 enhances lipid turnover, stimulating lipolysis as well as fat oxidation. [2]
In conclusion, regular exercise will inhibit TNF-a via the IL-6 pathway within skeletal muscle. IL-6 has been introduced recently as a myokine (defined as a cytokine that is produced and released by contracting skeletal muscle fibers, exerting its effects in other organs of the body) and may be involved in mediating the health-beneficial effects of exercise Myokines may also be important in the protection from such chronic diseases associated with low-grade inflammation such as diabetes and cardiovascular diseases.
References:--------------------------------------------------------------
1. John B Kurek, John J. Bower. Leukaemia Inhibitory Factor and Other Cytokines as Factors Influencing Regeneration of Skeletal Muscle. Basic Appl. Myol. 8 (5): 347-360, 1998
2.Petersen AM, Pedersen BK. The anti-inflammatory effect of exercise. Appl Physiol. 2005 Apr;98(4):1154-62.
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