Important HPTA and HCG question

[Gambale]

Hello, I have some doubt about HCG and HPTA someone kindly can help me with these doubts? Now I try to explain.

What I know is that HCG mimics leutenizing hormone (LH). LH stimulates the Leydig cells in the testicles to produce testosterone . This action also causes the testicles to return to normal size and function if they were suppressed due to exogenous testosterone.
There is a problem, HCG at high doses or for long periods down-regulate and/or desensitize Leydig cell receptors to LH so when you stop HCG your testicles will atrophize again. The question is: is this true? and if yes, how can we avoid this? What dosages and times should be followed?

Second, when you are on AAS or TRT your hypothalamus stops producing GnRH, → your pituitary stops producing LH and FSH, → Leydig cells stop producing Testosterone and sertoli cells stop producing sperm → your testicles atrophy.

When I use SERMs in PCT the pituitary gland restarts LH and FSH production and this should induce the testicles to restart testosterone and sperm production as before. The question is: Do the testicles after an AAS cycle respond to the LH / FSH that are reproduced by the pituitary gland as before the cycle and slowly resume their previous sizes and functionality or since they have become atrophied they have become less sensitive to LH/FSH and to bring them back to size and functionality before the cycle, should HCG be used?
Then I should use SERM for a short time to raise own LH/FSH and maintain the sensitivity and sizes/functionality obtained from HCG.
What do you think?

Thank you very much to all those who will answer my questions.

[Gambale]

Hello, I have some doubt about HCG and HPTA someone kindly can help me with these doubts? Now I try to explain.

What I know is that HCG mimics leutenizing hormone (LH). LH stimulates the Leydig cells in the testicles to produce testosterone . This action also causes the testicles to return to normal size and function if they were suppressed due to exogenous testosterone.
There is a problem, HCG at high doses or for long periods down-regulate and/or desensitize Leydig cell receptors to LH so when you stop HCG your testicles will atrophize again. The question is: is this true? and if yes, how can we avoid this? What dosages and times should be followed?

Second, when you are on AAS or TRT your hypothalamus stops producing GnRH, → your pituitary stops producing LH and FSH, → Leydig cells stop producing Testosterone and sertoli cells stop producing sperm → your testicles atrophy.

When I use SERMs in PCT the pituitary gland restarts LH and FSH production and this should induce the testicles to restart testosterone and sperm production as before. The question is: Do the testicles after an AAS cycle respond to the LH / FSH that are reproduced by the pituitary gland as before the cycle and slowly resume their previous sizes and functionality or since they have become atrophied they have become less sensitive to LH/FSH and to bring them back to size and functionality before the cycle, should HCG be used?
Then I should use SERM for a short time to raise own LH/FSH and maintain the sensitivity and sizes/functionality obtained from HCG.
What do you think?

Thank you very much to all those who will answer my questions.

Any opinions?

[kelkel]

Normal doses of HCG will not desensitize anything. There is no need to run high doses.
There's always a risk when running cycles but yes, your testicals will once again respond to endogenous LH stimulation. If HCG is used during cycle then atrophy will not be an issue.

[Gambale]

Normal doses of HCG will not desensitize anything. There is no need to run high doses.
There's always a risk when running cycles but yes, your testicals will once again respond to endogenous LH stimulation. If HCG is used during cycle then atrophy will not be an issue.

Ok, what doses do you consider normal? I was thinking about 200IU x3 per week or 250IU x2 per week. Also, what do you think about the HMG during or after the cycle?
Thanks