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  1. I've started reading what is considered one of the main references for muscle hypertrophy: One very interesting issue described is IGF-1 and its Isomorphs, I'm trying to summarize here. In humans have been identified 3 different isoforms of IGF-1: IGF-1Ea, IGF-1Eb, IGF-1Ec Ea and Eb are produced mainly in the liver and then released into the systemic circulation However, muscle contraction produces the majority of systemic IGF-1 during intense exercise and much of the circulating IGF-1 is taken up by active myofibers IGF-1Ec is also called mechano growth factor (MGF) since it si stimulated by mechanical load on muscles; its peptide sequence is different from the systemic isoform. MGF acts locally as opposed to systemically Sarcopenia is caused by the age-related decrease in serum IGF-1 and this suggests the existence of a threshold below which muscle mass is compromised. IGF-1 is a potent signal for the PI3K/Akt pathway which stymulates the mTOR pathway but it is not clear if it has a primary role in the anabolic response to exercise Serum concentrations of IGF-1 are not necessarily correlated with postworkout increases in muscle protein synthesis and IGF-1 impaired mice (only 20% of normal values) do not exhibit a compromised hypertrophic response to exercise. Systemic IGF-1 upregulation after exercise is delayed in coincidence with satellite cell regulation and this may be related to its ability to stimulate differentiation and fusion following myotrauma. Obviously, the issue has a degree of complexity which is usually not discussed. There is systemic IGF-1 released by the liver, but also systemic IGF-1 upregulated by intense exercise, which is sequestered by muscle cells themselves so maybe the net effect on the system is not so significant. In addition, there is local IGF-1 in its isoform Ec or MGF which is released by exercise.
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