Curtis
Competitive Bodybuilder
- Lid sinds
- 26 apr 2007
- Berichten
- 1.906
- Waardering
- 113
- Lengte
- 1m95
- Massa
- 132kg
- Vetpercentage
- 11%
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Kickstarten kan idd wel maar op welke dosis ga je daarna verder dan ?

Quote Originally Posted by weltweite;
I'm wondering how much insulin is needed over what duration of time to reduce translocation of GH receptors to the cell membrane. I understand there are a lot of variables to answering that question, but thought id put my thoughts down in words.
...
To me it sounds like there is a good synergism between a long acting cjc and a long acting insulin, but wouldn't that go down the drain if insulin caused these issues with the GH receptors and the STAT5b pathway./Quote
You asked a very good question.
From: Insulin Regulation of Human Hepatic Growth Hormone Receptors: Divergent Effects on Biosynthesis and Surface Translocation, Kin-Chuen Leung, Nathan Doyle, Mercedes Ballesteros, Michael J. Waters, And Ken K. Y. Ho, The Journal of Clinical Endocrinology & Metabolism 2000 Vol. 85 No. 12 4712-4720
In the study they recognized the importance of insulin and how it interacts with growth hormone, specifically highlighting that "insulin is essential for GH stimulation of IGF-I production and growth."
They then focused on the results of their study. They found that:
- Insulin up-regulated total and intracellular GH-receptors in a concentration-dependent manner.
- The abundance of GHR messenger ribonucleic acid and protein, ... respectively, markedly increased with insulin treatment.
[So the more insulin that was used the more biosynthesis or creation of GH-receptors that occurred. Now these receptors while abundant were not necessarily moved to the surface of the cell nor where they activated. Just a pool of GHRs was created.]
CAVEAT: Parts of the GH-Receptor can move to the nucleus and mediate gene expression. See the wonderful post that follows on "Growth Hormone Receptor structure, post-biogenesis behavior and degradation"
- It increased surface GHRs in a biphasic manner, with a peak response at 10 nmol/L, and modulated GH-induced Janus kinase-2 phosphorylation in parallel with expression of surface GHRs.
[So insulin increases the number of GH-receptors that make it to the cell surface AND increase the "intensity" of activation...but up to a point. After that point is reached insulin begins to hinder both the number of GH-receptors and "intensity" of activation"]
To quote from the study on this point:
Insulin induced a concentration-dependent increase in GHR biosynthesis, but simultaneously inhibited surface translocation. However, the net effect of reducing receptor surface availability only occurred at concentrations greater than 10 nmol/L, a concentration causing 70% inhibition of surface translocation. These data suggest that up-regulation of surface GHRs can occur with as little as 30% of intracellular receptors available for translocation to the cell surface. At concentrations above 10 nmol/L, the inhibitory effect of insulin on surface translocation overrides the compensatory effect of a 4- to 5-fold increase in receptor biosynthesis.
[So this means that insulin increases GH-receptors by 400-500% but that as insulin rises it reduces the number of those GH-receptors that make it to the surface and are active. There is a point at which insulin begins to reduce the benefit of this GH-receptor creation. That point is 10 nmol/L of insulin. Just prior to that point insulin has inhibited substantially the translocation of GH-Receptors but the increased quantity made up for it and created an overall net benefit.]
So the problem becomes how to translate that pivot point (10 nmol/L) into a number we can use.
From: Correspondence Letter Regarding Article by von Lewinski et al, "Insulin Causes [Ca2+]i-Dependent and [Ca2+]i-Independent Positive Inotropic Effects in Failing Human Myocardium", Chih-Hsueng Hsu, MD; Cheng-I Lin, PhD; Jeng Wei, MD, Circulation. 2005;112:e367
...we find that "3 IU/L, equivalent to 20 nmol/L" ...so 10 nmol/L is equivalent to 1.5 IU/L
From Wiki Answers
...we find that humans have 5-6 litres of blood in general.
So 5 x 1.5 = 7.5IU
So 6 x 1.5 = 9IU
Therefore the point at which the amount of insulin in plasma becomes a negative rather then a positive is approximately 7.5 to 9 IUs.
So to arrive at a net benefit an insulin amount below that threshold point such as 5-6 ius is desirable.
dam heb je op 250 oxy gezeten? moet je wel insane bloat en kracht destijds gekregen hebben?er is zeker wel verschil tussen 150mg oxy en 250mg oxy hoor
Deca, kan ik niet zeggen nog.
Misschien een stomme vraag, maar aangezien je het voor een wedstrijd doet die niet zover weg is, ben je niet bang voor een doping controle?

dam heb je op 250 oxy gezeten? moet je wel insane bloat en kracht destijds gekregen hebben?

Laat die kerel nu is doen als hij zoveel bepaalde aas wil gebruiken is het zijn zaak. Hou het topic nu eens netjes.No offense bro, maar de Flex cup is toch een wedstrijd voor beginners? (C niveau)?
Waarom dan die grote hoeveelheden AAS?
knallen denk ik. Op die lengte ben je pas een beest op 150 KG denk ik 
No offense bro, maar de Flex cup is toch een wedstrijd voor beginners? (C niveau)?
Waarom dan die grote hoeveelheden AAS?



