TheGame46
Member
IGF-1 is another critical player in muscle growth. Muscle growth from weight training is the result of IGF-1 being produced by the muscle cells themselves, not the liver. In fact, IGF-1 from the liver is genetically different from IGF-1 produced in your muscles. This is the reason why using IGF-1 systemically (from the blood stream) has been a hit and miss proposition.
IGF-1 formation in muscle tissue is absolutely critical if significant muscle hypertrophy is to occur. IGF-1 produced inside muscle cells that have been damaged by heavy training, oozes out of the cell and activates satellite cells. These satellite cells then donate nuclei to the damaged muscle cell, thereby allowing it to grow larger than before. There is a limit to the size of a muscle cell, and it depends largely on the number of nuclei it has. If you prevent a muscle cell from getting more nuclei from satellite cells, it simply will not grow, no matter how heavy things get. (1,2,3) The reduction in IGF binding protein-4 (IGFBP-4) leads to increased IGF-1 activity.(4) [Note: IGFBP-"3" also binds IGF-1 but in a good way. IGFBP-3 is the main carrier of IGF-1 and prolongs the half-life of IGF-1]
Could cell mediated IGF simply be the IGF that the muscle regulates itself?
IGF-1 formation in muscle tissue is absolutely critical if significant muscle hypertrophy is to occur. IGF-1 produced inside muscle cells that have been damaged by heavy training, oozes out of the cell and activates satellite cells. These satellite cells then donate nuclei to the damaged muscle cell, thereby allowing it to grow larger than before. There is a limit to the size of a muscle cell, and it depends largely on the number of nuclei it has. If you prevent a muscle cell from getting more nuclei from satellite cells, it simply will not grow, no matter how heavy things get. (1,2,3) The reduction in IGF binding protein-4 (IGFBP-4) leads to increased IGF-1 activity.(4) [Note: IGFBP-"3" also binds IGF-1 but in a good way. IGFBP-3 is the main carrier of IGF-1 and prolongs the half-life of IGF-1]
Could cell mediated IGF simply be the IGF that the muscle regulates itself?
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