T Nation

Test E, Tri-Tren 200, Dbol, Winstrol Cycle


test enanthate @500mg W1-12
Tri-tren @400mg W5-12
dbol @40mg ED W1-4
Winstrol @50mg ED W9-12
Vitamin B6 @300mgED W5-12
letrozole @.25 EOD (Incase of gyno)

HCG @250iu 2x Week W1-12
HCG @500iu for 10 days (Day after last test injection)


HCG @250iu 2x Week W1-12 (or start when balls start shrinking)

HCG @500iu EOD W15-18(Day 8-26)

PCT (2weeks after last pin)
clomid @50mg x2/day W14 (Day 1-7)

Liquid Stane @20mg ED (Day 8-34)

Tamox @20mg ED (Day 8-34)

I re-wrote up a cycle that i will be doing at the end of the year does it look fine should i change anything what do you guys think any help is apreciated. was just wondering if i should start the tren from week 1 or week 5? the tren is 50mg hex, 50mg ace and 100 enanthate


You need caber and to loose the HCG untill post cycle pre PCT. What are your stats? What do you want to get out of this cycle? PCT looks funky. 20mg Aromasin is a lot for during PCT, I know people who use less than that when they are on a gram of test.


You don't necessarily need caber. You should instruct people to make the decision based on the available evidence, not just blindly tell them to use a dopamine agonist.

HCG is used throughout the cycle, but not during PCT.


HCG during can cause problems with PCT. Using it as a kickstart to reactivate the Leydig Cells is probably the only thing I would recommend it for. The reason why I recommend caber is to improve the chances of not having negative effects from the Tren as he has long lasting esters of Tren in his cycle, he cant just stop it have the sides leave in a few days like with Tren Ace.


I have heard this once and once only, and that was you writing this. Give me a reason why. And just to be clear, I think you are completely wrong.

Tren doesn't necessarily create increased prolactin levels - this is what you forgot to mention as being the reason why someone might use caber with tren.


A single injection of 75 IU of human chorionic gonadotropin (hCG) into adult male rats caused a dramatic reduction in the concentration of membrane receptors for luteinizing hormone (LH) in the testis. The mean receptor level reached a nadir which was 5--10% of that in the control testes, 3 days after the injection, after which it gradually returned toward normal.

This cannot be due to increased competition caused by the injected hCG since no decrease was observed at a time when the circulating levels of hCG were at a maximum (2--24 h after injection). Furthermore, at a time when receptor levels had been maximally reduced, circulating hCG was at or below the level of detection.

Reduction in the number of LH binding sites in the testis was associated with a decreased responsiveness of the testicular tissue to hCG as measured by hCG-stimulated testosterone production in vitro. This inhibitory effect of large quantities of LH on its own receptor is suggested as a possible explantation for the previously observed low concentrations of LH receptor in the testis of the testicular feminized male (tfm) rat. This syndrome is characterized by high endogenous levels of plasma LH (Sherins et al., 1971).

Took me about 30 seconds to find this.

HCG does not directly affect the pituitary or hypothalamus. However, in large enough amounts, it can desensitize your body's LH receptors.

Even if you take it in lower doses to avoid receptor desensitization, it suppresses in two ways:

1)Testosterone inhibits GnRH at the hypothalamus.
2)Estrogen inhibits gonadotropin secretion at the pituitary.

Maybe you should do more research.

I also have first hand experience with a person I know who shutdown his test using HCG even post Tamoxifen PCT and further use of Clomid and AIs.


On the other side there is little study on this, whats your take?


I was going to applaud your actual use of a scientific study until you said this line, acting like a child.

On cycle it does not matter if your LH receptors are desensitized as the body is not attempting to produce its own testosterone due to the abundant amount of exogenous test supplied. HCG however will keep that signal sent to the testes so the testes remain in working condition throughout the cycle. This is highly advantageous for post cycle as they have never fully "stopped working".

I don't understand this - are you saying that we should not have any testosterone or estrogen in the body so that there is no suppression? This doesn't make sense - rewrite the sentence: "HCG supresses in two ways; testosterone inhibits..... Estrogen inhibits...." These are not even statements about HCG.

Again, acting like a little child.

First off all, how did he use HCG? You didn't explain that at all. Was he on cycle? Did he use it throughout the cycle? Did he use it post cycle? Did he use it during PCT? Was his cycle abnormally long? What did his cycle consist of? Has he had blood tests done to source the problem of this "shutdown" you say? Has he tried using HCG since this "shutdown" occurred to ascertain whether or not the problem lies in the pituitary or the testes themselves?

And second, however he used it, how can you prove this shutdown is specifically from using HCG? Anytime you supply the body with exogenous testosterone, you are running the risk of permanently shutting down natural production. Of the countless people that have used HCG on cycle as this is COMMON DOSING PROTOCOL, I doubt that more than a very small number of them or none of them have permanent shutdown, especially when it comes to specifically being caused by HCG.

EDIT: i just noticed your second comment saying there was little study and asking for my opinion. I apologize for the child comments and retract them. I explained my opinion above; the use of HCG continues to artificially supply the signal from the pituitary to the testes so the testes continue to "think" they need to produce testosterone, thus keeping them active for the duration of the cycle and almost as if they were never really shut-off in the first place.


I was more annoyed you didnt take the small amount of time it took me to find that and instead just said "your wrong". Which I thought was childish.

Im sorry how poorly worded the second part was. I was in a rush, I was burning something in the kitchen :s.

It was meant to read as:
HCG does not directly affect the pituitary or hypothalamus. However, in large enough amounts, it can desensitize your body's LH receptors.

Testosterone suppresses in two ways:

1)Testosterone inhibits GnRH at the hypothalamus.
2)Biproduct Estrogen inhibits gonadotropin secretion at the pituitary.

The guy I know whe shutdown his test used HCG from week 2 till 1 week after his last shot of Test E. He used 500iu twice a week. He maintained testicular size untill he came off. He used a large amount of TC, more than what I would have recommended for his PCT (I think it was something like 60/60/40/40/20/20). He had zero effect from it. We ended up getting his Test back using a mix of GH, TC and small amounts of HCG.


1000 iu of hcg seems a bit high, always heard half that . Thus, it's what I've alway done and it has worked beautifully. Of course there always a chance of weird shit happening to different people. Sucks about your boy, but he seems more like an exception than the rule.


Thank you for the information guys. my stats are:

Age: 25
Weight: 83kg
Height: 5"7

My goals for this cycle are to bulk to 90kg and add some good muscle.


But what about the bad muscle?