Proud Pangolin
Member
Hey guys so im on a diet for the last 2-3 months. Now, as I had some GHRP-2 + CJC no dac from last autum still laying around (delivery took to long and then I went on vacation) I thought “Why not use it, if you have it anyways”. So I started taking it like a little more than one month ago.
So my routine was 100mcq 3x a day of each.
-First in the morning on empty stomache
-directly after the gym (meaning before even drinking my shake I went to the bathroom to pin it)
-right before going to sleep
Now what I personally noticed after like 2 weeks was some significant weight loss, like out of the sudden I could see my abbs (and that way faster than I had expected based on my weightjourny till then) but I didn’t thought much about it.
Now in the last 1-2 weeks I got a lot of compliments about my physique. Even from my coach. So I looked at some pictures from last year. And im not shitting you I look right now basically the same as last year on 600mg of test + 600mg of DHB!!
I mean I look great right now, especially considering the fact that my total test was at 270 a couple of weeks ago.
Some people have asked me if im on gear right now. Im lean, my venes pop and well I look just great.
However there are some “confounding variables”:
-last year at this time I had massive stress due to my ex girlfriend. Meaning fights the whole day, I often had no focus in the gym because of course we fought a lot via phone. Generally I was very stressed out due to the fights and big exams I had, probably raised my cortisol signfificantly.
-I also had high E2 sides (because I got so scared from crashed E2 storys that I didn’t want to risk it before my exams) which meant insomnia especially in the last weeks (woke up after 2h and couldn’t fall back to sleep) and no hunger
-du to the E2 sides and the stress I also couldn’t get enough food in. I mean tbf with DHB you can eat incredible amounts of food, like seriously it was crazy and the reduced appetite really didn’t help.
=> so as you can see these are all factors that will influence the muscle building effect signfificantly. But did it really matter THAT much??
Im especially surprised because it seems like the general opinion is that 2-4IU of GH is neglectiable in the context of muscle growth especially without the usage of ASS.
Now after reading in GH and muscle building, it seems a lot more complictated:
“I’ve mentioned this quite a few times already but, in an attempt to further drive this point home, autocrine levels of IGF-1 appear to be far more important than endocrine levels of IGF-1 as it relates to muscle mass regulation. Further to this point, overexpression of autocrine IGF-1 within muscle causes fiber hypertrophy [374]. Overexpression of autocrine IGF-1 has also shown anti-catabolic effects, with animal models tending to demonstrate an overall resistance to the muscle atrophy normally observed with aging [375]. Localized IGF-1 also provides age-independent regenerative capacity in skeletal muscle cells [376].
There is also some compelling evidence that suggests endocrine IGF-1 acts directly as a negative feedback regulator on autocrine IGF-1 production. This negative feedback mechanism is PI3K/Akt pathway dependent [377-378]. In addition, elevated endocrine IGF-1 levels may also act indirectly to stifle autocrine IGF-1 production. So, in other words, not only does endocrine IGF-1 have minor direct impacts on skeletal muscle mass regulation itself, but it also possibly suppresses the autocrine IGF-1 that has major impacts on hypertrophy.
Elevated levels of circulating IGF-1, and specifically elevated free IGF-1, act in a negative regulatory manner on GH ultimately resulting in a suppressed rate of downstream autocrine IGF-1 production [379]. It is not entirely clear, however, if IGF-1 negative regulation changes the half-life of IGF-1 mRNA or directly affects IGF-1 gene expression. Further to this, it has also been demonstrated that autocrine IGF-1 expression is downregulated in muscle cells following IGF-1 treatment [366]. Hepatic expression of IGF-1 mRNA has also been shown to be downregulated by acute IGF-1 exposure [127]. So ensuring we keep endocrine levels as suppressed as possible for a respective rHGH dose, while simultaneously elevating autocrine levels, is going to be a priority for the stack design.
GH is pulsatile by nature in all species. So it would stand to reason that many of the body’s built in processes are going to thereby be designed in a manner which will be optimized to exposure to GH in a similar manner. In accordance with this statement it has been shown that only pulsatile GH administration, and not continuous infusion, has the ability to maximally stimulate IGF-1 mRNA expression in skeletal muscle [366,380-381]. Pulsatile delivery has also been shown to lead to increased overall postnatal growth potential, as compared to continuous delivery [89,382]. Pulsatile administration may also lead to comparable, or even decreased, serum endocrine IGF-1 levels [383] which is advantageous due to the potential negative regulatory capabilities it possesses on autocrine IGF-1 expression which were discussed earlier. Evidence also suggests that the peak itself, and not necessarily the number of peaks, may be of utmost importance to target tissues [384]. For maximal growth and hypertrophy potential the evidence tends to suggest that getting GH elevated, and then back to baseline multiple times per day, may be preferable as compared to keeping them elevated for longer periods of time.”
->So it seems that autocrine igf-1 levels are important for muscle growth which are again surpressed by endocrine egf1 levesls
“The GH pathways involved in anabolism are also susceptible to desensitization, which is by design as part of endogenous GH physiology [385]. Due to the inherently pulsatile nature of GH in vivo, receptors and pathways expect a pulse followed by a period of inactivity [386]. Continuous, or repeated, exposure to subsequent GH without proper refractory time will result in heavily suppressed activity levels. In fact, numerous studies have shown this to be the case over the years. Skeletal muscle cells and tissues require a somewhat lengthy refractory period before their full response to GH is recovered. After exposure to GH, muscle cells are unable to even respond to subsequent GH doses at all. In fact, it takes a full two hours just to partially regain responsiveness in cell models, with a total of 6-8 hours of GH abstinence required for full sensitivity to be restored [366]. Conversely, when GH is micro-dosed in ten minute pulses, followed by eight hour intervals, it was shown to progressively increase IGF-1 mRNA with each subsequent pulse [386].
This phenomenon is potentially a result of an overall desensitization within the JAK-STAT5 pathway, as exposure to GH in hepatic cell studies has been shown to cause resistance to subsequent activation of the STAT5 pathway for 4-8 hours [387-388]. This timeframe just so happens to sync up quite nicely with what has been seen in the myocyte cell models mentioned previously.“
-> It also seems that continuous presence of GH leads to a desensitization of the receptors responsible for the muscle building effect.
At least that’s how I understand this. Full source: The Most Effective Growth Hormone Protocol for Hypertrophy «
And this made me thinking: maybe this is why I respond “so well” to these peptides as they (compared to rHGH) act in a pulsative manner and therefore not desensitize the receptor (and maybe even will increase rather autocrine? Im just speculating here right now)
Or im just a hyperresponder to GH/igf-1 and an underresponder to ASS?
Or do you have another/better explanation?
So my routine was 100mcq 3x a day of each.
-First in the morning on empty stomache
-directly after the gym (meaning before even drinking my shake I went to the bathroom to pin it)
-right before going to sleep
Now what I personally noticed after like 2 weeks was some significant weight loss, like out of the sudden I could see my abbs (and that way faster than I had expected based on my weightjourny till then) but I didn’t thought much about it.
Now in the last 1-2 weeks I got a lot of compliments about my physique. Even from my coach. So I looked at some pictures from last year. And im not shitting you I look right now basically the same as last year on 600mg of test + 600mg of DHB!!
I mean I look great right now, especially considering the fact that my total test was at 270 a couple of weeks ago.
Some people have asked me if im on gear right now. Im lean, my venes pop and well I look just great.
However there are some “confounding variables”:
-last year at this time I had massive stress due to my ex girlfriend. Meaning fights the whole day, I often had no focus in the gym because of course we fought a lot via phone. Generally I was very stressed out due to the fights and big exams I had, probably raised my cortisol signfificantly.
-I also had high E2 sides (because I got so scared from crashed E2 storys that I didn’t want to risk it before my exams) which meant insomnia especially in the last weeks (woke up after 2h and couldn’t fall back to sleep) and no hunger
-du to the E2 sides and the stress I also couldn’t get enough food in. I mean tbf with DHB you can eat incredible amounts of food, like seriously it was crazy and the reduced appetite really didn’t help.
=> so as you can see these are all factors that will influence the muscle building effect signfificantly. But did it really matter THAT much??
Im especially surprised because it seems like the general opinion is that 2-4IU of GH is neglectiable in the context of muscle growth especially without the usage of ASS.
Now after reading in GH and muscle building, it seems a lot more complictated:
“I’ve mentioned this quite a few times already but, in an attempt to further drive this point home, autocrine levels of IGF-1 appear to be far more important than endocrine levels of IGF-1 as it relates to muscle mass regulation. Further to this point, overexpression of autocrine IGF-1 within muscle causes fiber hypertrophy [374]. Overexpression of autocrine IGF-1 has also shown anti-catabolic effects, with animal models tending to demonstrate an overall resistance to the muscle atrophy normally observed with aging [375]. Localized IGF-1 also provides age-independent regenerative capacity in skeletal muscle cells [376].
There is also some compelling evidence that suggests endocrine IGF-1 acts directly as a negative feedback regulator on autocrine IGF-1 production. This negative feedback mechanism is PI3K/Akt pathway dependent [377-378]. In addition, elevated endocrine IGF-1 levels may also act indirectly to stifle autocrine IGF-1 production. So, in other words, not only does endocrine IGF-1 have minor direct impacts on skeletal muscle mass regulation itself, but it also possibly suppresses the autocrine IGF-1 that has major impacts on hypertrophy.
Elevated levels of circulating IGF-1, and specifically elevated free IGF-1, act in a negative regulatory manner on GH ultimately resulting in a suppressed rate of downstream autocrine IGF-1 production [379]. It is not entirely clear, however, if IGF-1 negative regulation changes the half-life of IGF-1 mRNA or directly affects IGF-1 gene expression. Further to this, it has also been demonstrated that autocrine IGF-1 expression is downregulated in muscle cells following IGF-1 treatment [366]. Hepatic expression of IGF-1 mRNA has also been shown to be downregulated by acute IGF-1 exposure [127]. So ensuring we keep endocrine levels as suppressed as possible for a respective rHGH dose, while simultaneously elevating autocrine levels, is going to be a priority for the stack design.
GH is pulsatile by nature in all species. So it would stand to reason that many of the body’s built in processes are going to thereby be designed in a manner which will be optimized to exposure to GH in a similar manner. In accordance with this statement it has been shown that only pulsatile GH administration, and not continuous infusion, has the ability to maximally stimulate IGF-1 mRNA expression in skeletal muscle [366,380-381]. Pulsatile delivery has also been shown to lead to increased overall postnatal growth potential, as compared to continuous delivery [89,382]. Pulsatile administration may also lead to comparable, or even decreased, serum endocrine IGF-1 levels [383] which is advantageous due to the potential negative regulatory capabilities it possesses on autocrine IGF-1 expression which were discussed earlier. Evidence also suggests that the peak itself, and not necessarily the number of peaks, may be of utmost importance to target tissues [384]. For maximal growth and hypertrophy potential the evidence tends to suggest that getting GH elevated, and then back to baseline multiple times per day, may be preferable as compared to keeping them elevated for longer periods of time.”
->So it seems that autocrine igf-1 levels are important for muscle growth which are again surpressed by endocrine egf1 levesls
“The GH pathways involved in anabolism are also susceptible to desensitization, which is by design as part of endogenous GH physiology [385]. Due to the inherently pulsatile nature of GH in vivo, receptors and pathways expect a pulse followed by a period of inactivity [386]. Continuous, or repeated, exposure to subsequent GH without proper refractory time will result in heavily suppressed activity levels. In fact, numerous studies have shown this to be the case over the years. Skeletal muscle cells and tissues require a somewhat lengthy refractory period before their full response to GH is recovered. After exposure to GH, muscle cells are unable to even respond to subsequent GH doses at all. In fact, it takes a full two hours just to partially regain responsiveness in cell models, with a total of 6-8 hours of GH abstinence required for full sensitivity to be restored [366]. Conversely, when GH is micro-dosed in ten minute pulses, followed by eight hour intervals, it was shown to progressively increase IGF-1 mRNA with each subsequent pulse [386].
This phenomenon is potentially a result of an overall desensitization within the JAK-STAT5 pathway, as exposure to GH in hepatic cell studies has been shown to cause resistance to subsequent activation of the STAT5 pathway for 4-8 hours [387-388]. This timeframe just so happens to sync up quite nicely with what has been seen in the myocyte cell models mentioned previously.“
-> It also seems that continuous presence of GH leads to a desensitization of the receptors responsible for the muscle building effect.
At least that’s how I understand this. Full source: The Most Effective Growth Hormone Protocol for Hypertrophy «
And this made me thinking: maybe this is why I respond “so well” to these peptides as they (compared to rHGH) act in a pulsative manner and therefore not desensitize the receptor (and maybe even will increase rather autocrine? Im just speculating here right now)
Or im just a hyperresponder to GH/igf-1 and an underresponder to ASS?
Or do you have another/better explanation?
