06-16-2004, 12:51 AM #1
Just wondering on timing of these, going to start at 2iu per day of hgh, and was thinking 1iu in morning when i get up, and 1iu with my igf shot after workout. I will be spot injecting the IGF, so second shot of HGH will not be SUB Q. Is it cool to mix both igf and hgh with some extra bact water? I know these things are fragile so wanted to double check Thanks for any info!
06-16-2004, 09:54 AM #2
LR3 isn't as fragile as rIGF-1 so I don't see a problem.
06-16-2004, 04:42 PM #3
Should i start both at same time? I know igf starts working right away, but what about hgh? I plan to run GH for atleast 6 months, not in a rush for it to kick in, just want to know if i should hold off on the IGF for now.
06-16-2004, 05:36 PM #4
I started my HGH and will run LR3 in 4-6 weeks, I think your cycle should be at peak levels before starting the LR3. I did my first 1 by itself to see how it'd work for me, that's why this time I'm waiting for the cycle to reach peak levels before starting.
06-16-2004, 06:27 PM #5
Bets timing IMO for GH is at 8:00am and at 2:00pm that's when cortisol levels are at there peak, also this will not interupt with your nocturnal release of GH...Taking the second shot PWO with your LR3 will probably be alright though...Are you taking slin as well?
06-16-2004, 08:32 PM #6
****, i only get outta bed at around 2 for my first shot I'm not taking slin yet, i'm going to read up on it though, and probably run it later on. Thanks for the replies guys!
06-16-2004, 10:42 PM #7
I need to look into the effects of hgh on cortisol or does someone have something I can read on it?
06-17-2004, 10:29 AM #8Originally Posted by JohnnyB
06-17-2004, 10:50 PM #9Originally Posted by Mallet
06-17-2004, 10:53 PM #10Originally Posted by JohnnyB
This interests me as well because I want to know how I can adjust my training frequency, volume, and intensity with GH and slin while not on a steroid cycle. If you send JB a PM, can you hook me up as well?
06-18-2004, 01:30 PM #11
Cortisol increases GH receptor expression
High levels of glucocorticoids are well known to cause osteoporosis, and physiological levels of growth hormone (GH) are required for a normal bone remodeling. It has been suggested that glucocorticoids regulate the GH-response via a regulation of GH-receptor expression. The aim of the present study was to investigate whether or not cortisol regulates growth hormone receptor expression in cultured human osteoblasts.
The effect of serum starvation and cortisol on GH-receptor expression was tested in human osteoblast-like cells. Serum starvation for 24h resulted in an increase in GH-receptor mRNA levels (90±1% over control culture). Cortisol increased GH-receptor mRNA levels in a dose-dependent manner with a maximal effect at 10-6 M. The stimulatory effect of cortisol on GH-receptor mRNA levels was time dependent, reaching a peak after 12 h (126±29% over control culture) and the effect was still present 12 h later. The increase in GH-receptor mRNA levels was accompanied by an increase in 125I-GH binding with a maximal effect at 24 h (196±87% over control culture).
In conclusion, glucocorticoids increase GH-receptor expression in human osteoblast-like cells. Further studies are needed to clarify whether or not a glucocorticoid-induced regulation of the GH- receptor is of importance to human bone physiology.
06-18-2004, 01:37 PM #12
Dual mode of cortisol action on GH/IGF-1/IGFBP's
Glucocorticoids are known to impede somatic growth in a wide range of vertebrates. In order to clarify the mechanisms through which they may act in an advanced teleost fish, we examined the effects of cortisol administration on the growth hormone (GH)/insulin -like growth factor-I (IGF-I)/IGF-binding protein (IGFBP) system in the tilapia (Oreochromis mossambicus). In a short-term experiment, fish were injected intraperitoneally with cortisol (2 or 10 mg/g), and sacrificed at 2, 4, 8 and 24 h after the injection. In a longer-term experiment, fish were sacrificed 24 and 48 h after cortisol injection (2, 10 and 50 mg/g). Cortisol at doses of 2 and 10 mg/g increased four different sizes of IGFBPs (24, 28, 30, and 32 kDa) significantly in the plasma within 2 h without altering the plasma levels of IGF-I or GH. On the other hand, cortisol at doses of 10 and 50 mg/g significantly reduced plasma IGF-I levels after 24 and 48 h. IGF-I mRNA levels in the liver were also significantly reduced by cortisol at doses of 10 and 50 mg/g after 48 h, suggesting that a decrease in plasma IGF-I levels is mediated through the attenuation of IGF-I gene expression in the liver. In contrast, no significant change was observed in plasma or pituitary contents of GH at any time point examined, which would appear to indicates that cortisol reduces IGF sensitivity to GH (GH- resistance). These results clearly indicate that cortisol induces a rapid increase in plasma IGFBPs and a more delayed decrease in IGF-I production. The dual mode of cortisol action may contribute to the inhibitory influence of cortisol on somatic growth in teleosts.
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