bananafeet
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Some more data:
Source: The Growth Hormone/Insulin-Like Growth Factor Axis during Development
TLDR they made mice with low circulating IGF1 and they still grew muscle just fine.....
TLDR HGH is anabolic in skeletal muscle but it hasn't been established if this is caused by HGH itself or IGF1.
Page 132Two mice models of liver IGF-I deficiency, in which body growth
remained unaltered challenged the somatomedin hypothesis that
circulating IGF-I levels mediated by GH secretion are the principal effectors of body growth. These results pointed out the importance of
autocrine/paracrine IGF-I secretion in extrahepatic tissues to mediate
growth. These data may be also interpreted to suggest that IGF-I may
function alone in certain tissues, whereas it may mediate the effects of GH in other tissues as in bone. As we mentioned earlier, gene targeting studies of the IGF-I system in skeletal muscle have clearly shown the role of skeletal muscle IGF-I and its receptor in mediating proliferation and differentiation as well as anabolic actions. Since GH binding in skeletal muscle cells has been very difficult to assess46, it may be possible that the autocrine/paracrine effects of IGF-I and its receptor are exerted in a GH-independent manner.
Page 122GH is primarily an anabolic hormone and in skeletal muscle it induces
positive nitrogen balance and protein synthesis. Treatment with GH
reduces fat mass and increases lean body weight by enhancing protein
synthesis, with no effect on protein degradation. In elderly patients,
rhGH treatment had similar effects. Infusion of GH, IGF-I, and insulin into the forearm showed that GH and IGF-I increased amino acid uptake, whereas IGF-I and insulin, but not GH, inhibited amino acid release.
Moreover, IGF-I is capable of inhibiting proteolysis. Although there is no consensus as to whether IGF-I may or may not mediate the effects of GH on nitrogen balance and protein synthesis in muscle, these studies strongly support the suggestion that many of the anabolic effects of GH in muscle may be IGF-I dependent. GH has a lipolytic action on fat and muscle. Acute GH administration causes a rise in the levels of circulating FFAs and glycerol by inhibition of lipoprotein lipase. Long-term effects of GH include decreased deposition of fat and increased fat mobilization. The acute insulin-like activity of GH on carbohydrate metabolism has been seen both in vitro and in vivo and is independent of both IGF-I and insulin. GH-induced tyrosine phosphorylation of ERS-1 and/or IRS-2 may be responsible for this effect.
Prolonged GH stimulation also enhances hepatic gluconeogenesis and
glycogenolysis, resulting ultimately in hyperglycemia. This inhibitory effect on insulin activity may be indirectly caused by the GH-induced lipolysis and elevated plasma FFA levels that inhibit insulin activity at its target tissues
Source: The Growth Hormone/Insulin-Like Growth Factor Axis during Development
TLDR they made mice with low circulating IGF1 and they still grew muscle just fine.....
TLDR HGH is anabolic in skeletal muscle but it hasn't been established if this is caused by HGH itself or IGF1.
