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Originally Posted by Mr. Masse Would there be any advantage or disadvantage in runnning GH and IGF EOD opposite each other?? |
No advantage IMO.....a possible disadvantage though. I'll cut and paste what I wrote about the potential of using
GH concurrent with IGF-1, which may allow you to run IGF-1 longer and still see results.
Satellite cell regulation
originally posted by einstein1905
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Satellite cells are the cells that are "recruited" by IGF-1 to mature and become part of functional muscle fibers, thus increasing the number of "muscle cells", functional ones at least.
It has been shown in rats that overexpression of IGF-1, intramuscularly, promotes great increases in muscle mass and strength for several weeks, but eventually the rate of above average growth plateaus. Researchers hypothesized that this was due to a decreased supply of satellite cells (i.e. the rate of satellite cell mitosis was slower than the rate of IGF-1 mediated satellite cell "recruitment").
What regulates the rate of satellite cell mitosis?.....
One thing to note, in rats overexpressing IGF-1, their
GH will be greatly inhibited due to negative feedback by IGF-1 on the hypothalamus, so thier endogenous
GH production/release would be nearly nonexistent.
Here are two studies....the first shows that myostatin has a distinct adverse effect on satellite cell replication (mitosis)...the second study shows that
GH has a distinct effect on decreasing the expression of myostatin. If you put these two results together, you can conclude that
GH has a positive effect on satellite cell mitosis. So, since the mice overespressing IGF-1 had their endogenous
GH production suppressed, their rates of satellite cell mitosis was also greatly reduced, and therefore the limiting factor was the inability of rate of satellite cell mitosis to provide an adequate supply of satellite cells for IGF-1 recruitment, so growth eventually stopped.
For those of use using LR3 and noticing gains decreasing after 4-5 weeks, this could very well be due to LR3's suppression of our endogenous
GH, which is occuring with use of exogenous IGF-1, and therefore a decreased rate of satellite cell mitosis. The first time I used LR3 I was not using
GH at the time, and my gains seemed to slow at the 4 week mark. I'd heard others having the same effects, so I wrote it off as a fact that 4 week cycles were the best, beyond which, gains were harder to achieve. On subsequent cycles of LR3, I have always been using
GH with them but have stopped the cycles after 4 weeks due to my earlier conclusion that gains slowed substantially after 4 weeks.
My theory now is that using
GH with LR3 can allow one to cycle for a longer duration with LR3 and continue to gain......I hadn't before given this the chance to work, by cutting my cycles at 4 weeks.
Next cycle will be as long as I continue to see good gains, since I'll be using
GH along with it again.
Here are the studies:
J Cell Biol. 2003 Sep 15;162(6):1135-47. Epub 2003 Sep 08. Related Articles, Links
Myostatin negatively regulates satellite cell activation and self-renewal.
McCroskery S, Thomas M, Maxwell L, Sharma M, Kambadur R.
Animal Genomics, AgResearch, Hamilton 2015, New Zealand.
Satellite cells are quiescent muscle stem cells that promote postnatal muscle growth and repair. Here we show that myostatin, a TGF-beta member, signals satellite cell quiescence and also negatively regulates satellite cell self-renewal. BrdU labeling in vivo revealed that, among the Myostatin-deficient satellite cells, higher numbers of satellite cells are activated as compared with wild type. In contrast, addition of Myostatin to myofiber explant cultures inhibits satellite cell activation. Cell cycle analysis confirms that Myostatin up-regulated p21, a Cdk inhibitor, and decreased the levels and activity of Cdk2 protein in satellite cells. Hence, Myostatin negatively regulates the G1 to S progression and thus maintains the quiescent status of satellite cells. Immunohistochemical analysis with CD34 antibodies indicates that there is an increased number of satellite cells per unit length of freshly isolated Mstn-/- muscle fibers. Determination of proliferation rate suggests that this elevation in satellite cell number could be due to increased self-renewal and delayed expression of the differentiation gene (myogenin) in Mstn-/- adult myoblasts. Taken together, these results suggest that Myostatin is a potent negative regulator of satellite cell activation and thus signals the quiescence of satellite cells.
J Clin Endocrinol Metab. 2003 Nov;88(11):5490-6. Related Articles, Links
Myostatin is a skeletal muscle target of growth hormone anabolic action.
Liu W, Thomas SG, Asa SL, Gonzalez-Cadavid N, Bhasin S, Ezzat S.
Department of Medicine, Mount Sinai Hospital and University of Toronto, Ontario, Canada.
Myostatin is a cytokine that has recently been shown to selectively and potently inhibit myogenesis. To investigate the mechanisms of anabolic actions of
GH on skeletal muscle growth, we examined the in vitro and in vivo effects of
GH on myostatin regulation. Twelve
GH-deficient hypopituitary adult subjects were treated with recombinant
GH (5 micro g/kg.d) in a double-blind, placebo-controlled fashion. Body composition and physical function were assessed and skeletal muscle biopsies from the vastus lateralis performed at 6-monthly intervals during 18 months of treatment. Myostatin mRNA expression was significantly inhibited to 31 +/- 9% (P < 0.001) of control by
GH but not by placebo administration (79 +/- 11%) as determined by quantitative real-time PCR normalized for the housekeeping glyceraldehyde-3-phosphate dehydrogenase gene. The inhibitory effect of
GH on myostatin was sustained after 12 and 18 months of
GH treatment. These effects were associated with increases in lean body mass and translated into enhanced aerobic performance as determined by maximal oxygen uptake and ventilation threshold. Parallel in vitro studies of skeletal muscle cells demonstrated significant reduction of myostatin expression by myotubes in response to
GH, compared with vehicle treatment. Conversely,
GH receptor antagonism resulted in up-regulation of myostatin in myoblasts. Given the potent catabolic actions of myostatin, our data suggest that myostatin represents a potential key target for
GH-induced anabolism.
06-12-2004, 09:02 PM
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