Few questions about first cycle :)

^^I am quite sure that it does keep test production alive. Pointless as it may be to your cycle, it makes recovery a walk in the park. If I'm wrong I'm sorry, but I'm almost positive I'm not
Really bro? I give u more credit than to think u believe the body can still be producing test while on gear...
 
Really bro? I give u more credit than to think u believe the body can still be producing test while on gear...

I think Bill Roberts says something to this effect on multiple occasions, or at least it sounds like that's what he's getting at. Which is wrong of course; but I have a feeling that's where this is coming from most of the time.
 
If I'm wrong I'm wrong. I thought that it sided in keeping the precursors to test at least not entirely shit down. I realize it takes more than one thing to produce test, but the precursors do not remain present? I don't know. I've never read studies so I'm going on info I was told on this forum. This is why I said I may be wrong...
 
If a few of u guys really believe that HCG or any compound can aid the body in natural test production while on gear u are sadly mistaken... I shouldn't even be wasting time commenting on this as it's newbie knowledge to be aware of this fact

It's an honest question. I am asking you why. I'm here to learn just as much as the next guy.
 
It's an honest question. I am asking you why. I'm here to learn just as much as the next guy.

Why? Because when your brain detects test in the body from an outside source it sends a signal to your nuts to stop producing natty test... at least that's how I was lead to believe over the years. I could be wrong, but I think there is some method to that madness
 
If a few of u guys really believe that HCG or any compound can aid the body in natural test production while on gear u are sadly mistaken... I shouldn't even be wasting time commenting on this as it's newbie knowledge to be aware of this fact

Why wouldn't it aid in natural production? Test suppresses the HPTA at the hypothalamus which ceases production of GnRH. Without GnRH the pituitary does not produce LH. No LH no test production on cycle. Introducing HCG which is a direct analog to LH bypasses the suppression at the hypothalamic level and the inhibited production of LH At the pituitary level. It goes straight to the testes and tells them to produce the test.
 
Why wouldn't it aid in natural production? Test suppresses the HPTA at the hypothalamus which ceases production of GnRH. Without GnRH the pituitary does not produce LH. No LH no test production on cycle. Introducing HCG which is a direct analog to LH bypasses the suppression at the hypothalamic level and the inhibited production of LH At the pituitary level. It goes straight to the testes and tells them to produce the test.

Not possible bro... believe it or not, the testes are not that smart. Bottom line is when the body detects synthetic test it will immediately stop producing testosterone
 
Interesting talk here about the test-feedback mechanism(s) and their regulation. DreDay´s comment is in line with what I have learned, but I am curious about your comments as well China_Wall. You got any litterature on that?
 
Interesting talk here about the test-feedback mechanism(s) and their regulation. DreDay´s comment is in line with what I have learned, but I am curious about your comments as well China_Wall. You got any litterature on that?

Just my experience and that of many other bodybuilders I've been around over the last 20 years
 
Not possible bro... believe it or not, the testes are not that smart. Bottom line is when the body detects synthetic test it will immediately stop producing testosterone

Then why does the addition of HCG increase test levels of those on TRT?

The testes don't have to be smart. They can be stupid as much as they want but if they're prevented from atrophying and they haven't been desensitized (like in the case of primary hypogonadism) like HCG would accomplish then the testes WILL react to the analog LH and start producing some endogenous test.

I explained in my first post why the body stops producing test when it senses exogenous sources...the hypothalamus stops making GnRH which is the precursor to the pituitary production of LH which is a precursor to the Ledyig cells making endogenous testosterone. The signal gets cut off at the top.

When you use HCG the signal is cut off at the top still, and cut off at the middle at the pituitary bc HCG is suppressive at the level of the pituitary BUT since HCG acts as a LH analog it doesn't matter if the brain and pituitary are shut down...HCG acts as a direct messenger to the testes to produce testosterone.


The following is from Dr. Crisler, if you don't believe me believe him.

Dr. Crisler said:
But there’s another metabolic reason to employ this protocol. The P450 Side Chain Cleavage enzyme, which converts CHOL into pregnenolone at the initiation of all three metabolic pathways CHOL serves as precursor (the sex hormones, glucocorticoids and mineralcorticoids), is actively stimulated, or depressed, by LH concentrations. It is intuitively consistent that during conditions of lowered testosterone levels, commensurate increases in LH production would serve to stimulate this conversion from CHOL into these pathways, thereby feeding more raw material for increased hormone production. And vice versa. Thus the addition of HCG (which also stimulates the P450scc enzyme) helps restore a more natural balance of the hormones within this pathway in patients who are entirely, or even partially, HPTA-suppressed.

It is important that no more than 500IU of HCG be administered on any given day. There is only just so much stimulation possible, and exceeding that not only is wasteful, doing so has important negative consequences. Higher doses overly stimulate testicular aromatase, which inappropriately raises estrogen levels, and brings on the detrimental effects of same. It also causes Leydig cell desentization to LH, and we are therefore inducing primary hypogonadism while perhaps treating secondary hypogonadism. 250IU QD is an effective, and safe, dose. After all, we are merely replacing that which is lost to inhibition.

In my previous report I recommended 250IU of HCG twice per week for all TRT patients, taken the day of, along with the day before, the weekly test cyp injection. After looking at countless lab printouts, listening to subjective reports from patients, and learning more about HCG, I am now shifting that regimen forward one day. In other words, my test cyp TRT patients now take their HCG at 250IU two days before, as well as the day immediately previous to, their IM shot. All administer their HCG subcutaneously, and dosage may be adjusted as necessary (I have yet to see more than 350IU per dose required).

I made this change after realizing that the previous HCG protocol was boosting serum testosterone levels too much, as the test cyp serum concentrations rise, approaching its peak at roughly the 72 hour mark. The original goal of supporting serum androgen levels with HCG had overshot its mark.


^^^shows that even when suppressed HCG will STILL help you produce some endogenous testosterone.
 
Then why does the addition of HCG increase test levels of those on TRT?

The testes don't have to be smart. They can be stupid as much as they want but if they're prevented from atrophying and they haven't been desensitized (like in the case of primary hypogonadism) like HCG would accomplish then the testes WILL react to the analog LH and start producing some endogenous test.

I explained in my first post why the body stops producing test when it senses exogenous sources...the hypothalamus stops making GnRH which is the precursor to the pituitary production of LH which is a precursor to the Ledyig cells making endogenous testosterone. The signal gets cut off at the top.

When you use HCG the signal is cut off at the top still, and cut off at the middle at the pituitary bc HCG is suppressive at the level of the pituitary BUT since HCG acts as a LH analog it doesn't matter if the brain and pituitary are shut down...HCG acts as a direct messenger to the testes to produce testosterone.


The following is from Dr. Crisler, if you don't believe me believe him.




^^^shows that even when suppressed HCG will STILL help you produce some endogenous testosterone.
If this were true then bodybuilders would use it all the time at higher dosages in order to increase test levels, thus giving more muscle growth... but they don't, so is it some sort of secret?
 
If this were true then bodybuilders would use it all the time at higher dosages in order to increase test levels, thus giving more muscle growth... but they don't, so is it some sort of secret?

The testes have only a limited amount of Ledyig cells to stimulate and the cells present can only be stimulated so much before desensitization or primary hypogonadism occurs.

^^^tbis part is explained in the Crisler quote in the part that I did not bold or color. It talks about maximal stimulation and desensitization.

It is a suppressive compound so it will shut you down at the pituitary regardless of if you're on cycle or not but bc it's a bio identical copy to LH it still stimulates production in the testes. Running HCG for extended periods of time or excessively high doses will cause desensitization so bodybuilder's cannot run it all the time for practical reasons.
 
The testes have only a limited amount of Ledyig cells to stimulate and the cells present can only be stimulated so much before desensitization or primary hypogonadism occurs.

^^^tbis part is explained in the Crisler quote in the part that I did not bold or color. It talks about maximal stimulation and desensitization.

It is a suppressive compound so it will shut you down at the pituitary regardless of if you're on cycle or not but bc it's a bio identical copy to LH it still stimulates production in the testes. Running HCG for extended periods of time or excessively high doses will cause desensitization so bodybuilder's cannot run it all the time for practical reasons.

I see what ur gettin at... nearly sold haha
 
Okay. Thanks dre. This is similar to my reading in steroid profiles and on forums, but wasn't one hundred percent on it. Thanks for clarifying.
 
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