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GXR64
04-19-2010, 05:01 AM
Understanding Post Cycle Therapy Recovery
O.K. You have been on an awesome 4-month cycle of Sustanon and Dianabol. You?ve gained a massive 20 lbs, and are extremely pleased with your results. You can?t stop looking in the mirror. But there is a problem now starting to eat away at you. You are going to run out of steroids very soon (you know you need a break anyway), and your testicles are the size of raisins. Your body is producing less testosterone than a 9-year-old girl, and you are scrambling to figure out what to do to avoid a nasty post-cycle crash that could potentially strip away some of your hard-earned muscle. The opinions on how to restore endogenous testosterone production post-cycle seem to be different everywhere you look. What option is best? Without an understanding of exactly what is going on in your body, and why certain compounds help to correct the situation, choosing the right post-cycle program can be quite confusing. In this article I would therefore like to discuss the role of Anti-estrogens and HCG during this delicate window of time, while detailing an effective strategy for their use.

The Axis
The Hypothalamic-Pituitary-Testicular Axis, or HPTA for short, is the thermostat for your body?s natural production of testosterone. Too much testosterone and the furnace will shut off. Not enough, and the heat is turned up, to put it very simply. For the purposes of our discussion here we can look at this regulating process as having three levels. At the top is the hypothalamic region of the brain, which releases the hormone GnRH (Gonadotropin-Releasing Hormone) when it senses a need for more testosterone. GnRH sends a signal to the second level of the axis, the pituitary, which releases Luteinizing Hormone in response. LH for short, this hormone stimulates the testes (level three) to secrete testosterone. The same sex steroids (testosterone, estrogen) that are produced serve to counter-balance things, by providing negative feedback signals (primarily to the hypothalamus and pituitary) to lower the secretion of testosterone when too much of this hormone is sensed. Synthetic steroids, of course, suppress testosterone the same way. This quick background of the testosterone-regulating axis is necessary to furthering our discussion, as we need to first look at the underlying mechanisms involved before we can understand why natural recovery of the HPTA post-cycle is a slow process. Only then can we implement an ancillary drug program to effectively deal with it.

Testicular Desensitization
Although steroids suppress testosterone production primarily by lowering the level of gonadotropic hormones discussed above, the big roadblock to a restored HPTA after we come off the drugs is surprisingly not the level of LH itself. This problem is made clearly evident in a study published in Acta Endocrinologica back in 1975(1). Here blood parameters, including testosterone and LH levels, were monitored in male subjects whom were given testosterone enanthate injections of 250mg weekly for 21 weeks. Subjects remained under investigation for an additional 18 weeks after the drug was discontinued. At the start of the study, LH levels became suppressed in direct relation to the rise in testosterone, which is to be expected. Things looked very different, however, once the steroids had been withdrawn (see Figure I). LH levels went on the rise quickly (by the 3rd week), while testosterone barely budged for quite some time. In fact, on average it was more than 10 weeks before any noticeable movement started. This lack of correlation makes clear that the problem in getting androgen levels restored is not the level of LH, but in fact testicular atrophy and desensitization to this hormone. After a period of inactivation the testes have apparently lost mass (atrophied), making them unable to perform the workload required by heightened levels of LH.


Post Cycle testosterone Levels
Figure I. LH and testosterone measurements starting 1 week after the last injection of 250mg of testosterone enanthate (pretreated measures were 5 mU/ml and 4.5 ng/ml respectively). Note that between weeks 1 and 5, as testosterone levels are declining due to the cessation of exogenous androgen administration, LH levels are already rebounding. From weeks 5 to 10 testosterone levels are at or very near baseline, to spite the substantial LH levels by this point. No significant increase in testosterone is noted until after the 10-week mark.

The Role of Anti-estrogens
It is important to understand that Anti-estrogens alone do not do much to restore endogenous testosterone release after a cycle. Normally they only foster LH by blocking the negative feedback of estrogens, and we now see that LH rebounds quickly without help anyway. Plus, post cycle there is not an elevated level of estrogen for Anti-estrogens to block, as testosterone (now suppressed) is a major substrate used for the synthesis of estrogens in men. Serum estrogen levels will actually be lower here as a result, not higher. Any estrogen rebound that occurs post-cycle likewise happens concurrently with a rebound in testosterone levels, not prior to it (note there is an imbalance in the ratio post cycle, but this is another topic altogether). We are seeing no mechanism in which anti-estrogenic drugs can really help here. We can see why this fact would not be difficult to overlook, however. The medical literature is filled with references showing anti-estrogenic drugs like Clomid and Nolvadex to increase LH and testosterone levels, and in normal situations these drugs do indeed increase endogenous androgen production by blocking the negative feedback of estrogens. Combine this with the fact that just as many studies can be found to show that steroid use lowers LH levels when suppressing testosterone, and we can see how easy it would be to jump to the conclusion that post-cycle we need to focus on restoring LH. We would miss the true problem of testicular desensitization unless we were really looking into the actual recovery rates of the hormones involved. When we do, we immediately see little value in using anti-estrogenic drugs.

HCG
So we now see, contrary to the dominating opinion of the times, that Anti-estrogens alone will do little to raise testosterone levels in the early weeks of the post-cycle window. This leaves us to focus on a very different level of the HPTA in order to hasten recovery: the testes. For this we will need the injectable drug HCG. If you are not familiar with it, HCG, or Human Chorionic Gonadotropin, is a prescription fertility agent that mimics the bodies own natural LH. Although the testes are equally desensitized to this drug as LH (they both work through the same mechanism), we are administering it as a measured drug and are therefore not constrained by the limits of our own LH production. We similarly can use HCG to provide a bolus dose of LH (of our choosing), which works only to augment the recovering LH levels we already have in the body. In essence we are looking to shock them with an overwhelmingly high level of LH activity, coming from both endogenous and exogenous sources. We want it to reach a level far above what our body, even when supported by Anti-estrogens, could possibly do on its own. The result can be a rapid restoration of original testicular mass and functioning, which would allow normal levels of testosterone to be output much sooner than without such an ancillary program. What we are looking at now is HCG actually being the pivotal post-cycle drug, while Anti-estrogens are relegated to a supportive role at best.

Finalizing the Program
An ideal post-cycle recovery program will focus on two things really. The first is hitting the testes hard with HCG. It is important, however, not to overuse this drug. Taken for too long, or at too high a dosage, the LH receptor will actually become desensitized to LH(2) , which may further exacerbate our post-cycle problem instead of helping it (this is why I am not in favor of regular HCG use on-cycle). My experience with HCG has led me to feel comfortable using it for a course of three weeks, at a dosage of maybe 5000-7500IU weekly. Often the last week I limit the dose to 2,500IU, unless the cycle has been particularly long or potent. This is timed so at least half of the total administered drug dosage will be given when there is still exogenous steroid in the body. On our graph above this would be at about the 3-week mark after the last injection of testosterone. This will give the testes some time to get back into shape before the baseline is actually hit with T levels. Secondly, Anti-estrogens are used to play a supportive role at the same time, so 20mg of Nolvadex or 50-100mg of Clomid would typically be added (my last article for Mind and Muscle discusses the comparative differences with these two agents). This is to combat the suppressive effects of estrogen as testosterone levels start to go back up, as well as potential side effects (HCG has been shown to increase testicular aromatase activity as well (3)). Although in the first couple of weeks the anti-estrogen does little, it may indeed be helpful when testosterone levels actually start to get back up near normal. To further stimulate the HPTA, and support continuingly high LH levels, the anti-estrogen remains to be used for 2 to 3 weeks after the HCG therapy has been stopped. A sample program, as it would be instituted in our sample post-cycle window, is provided below.

GXR64
04-19-2010, 05:02 AM
Sample post-cycle Plan:
Week
Amount

Week 3:
5000IU HCG total + 20mg Nolvadex daily

Week 4:
5000IU HCG total + 20mg Nolvadex daily

Week 5:
2500IU HCG total + 20mg Nolvadex daily

Week 6:
20mg Nolvadex daily

Week 7:
20mg Nolvadex daily

Week 8:
20mg Nolvadex daily

In Closing
I hope this article provided a well-needed new look at the mechanisms involved in post-cycle testosterone recovery. Indeed I believe it should debunk a commonly held belief these days, as we seen now that those advocating the sole use of Clomid post cycle are sorely missing the mark. The problem goes much deeper than just getting LH levels back. In fact, we see that LH doesn?t even need much help kicking back into gear, and a drug like Clomid will do very little to help this anyway in the absence of significant estrogen levels anyway. HCG is a drug with undeniable usefulness during the post-cycle window, and many bodybuilders have been much too quick to abandon it. It is truly fundamental to an effective recovery program, and would not consider any dose or combination of Anti-estrogens or aromatase inhibitors capable of doing the job without it.


References:
1. Effect of long-term testosterone enanthate administration on male reproductive function: Clinical evaluation, serum FSH, LH, testosterone and seminal fluid analysis in normal men. J. Mauss, G. Borsch et al. Acta Endocrinol 78 (1975) 373-84

2. Desensitization to gonadotropins in cultured Leydig tumor cells involves loss of gonadotropin receptors and decreased capacity for steroidogenesis. Freeman DA, Ascoli M Proc Natl Acad Sci U S A 1981 Oct;78(10):6309-13

3. Acute stimulation of aromatization in Leydig Cells by Human Chorionic Gonadotropin In-vitro. Proc Natl Acad Sci USA 76:4460-3,1079

by William Llewellyn

Lonniebatt
11-26-2010, 08:54 PM
Man thanks alot for this advice this is the first time that I have read anyones advice and was able to totally understand it I am due to cycle of very soon and I will use your method, it is very simple to understand and I want to thank you for breaking it down to a point where it is so easy to understand

RonnyT
11-29-2010, 04:50 PM
This is a very bad PCT. The use of HCG post cycle works contra productive. This is an old concept that is no longer in use by anyone that knows a little bit about the human body. From an other forum in reaction on the same article from llewellyn. Recently new insights came to light, I'll post about it later.

This has been gone over so many times that my head is spinning......H.C.G should be used DURING the cycle to prevent testicular atrophy in the first place! At the very least it should be used during the last two weeks of a cycle. Dose needs to be low and at 500iu's per day there in NO desensitization issue.

Bill Roberts has a cow when he hears Llewellyn talk about HCG use post cycle and so does my endocrinologist. The use of HCG post cycle will cause such a sharp rise in test levels that the high test levels will be inhibitory in and of itself and thus further inhibit recovery of HPTA.
Again I repeat .....it is far better to prevent testicular atrophy in the first place with prudent use of HCG during the cycle than to try to bring them back after the fact.

Both nolvadex and clomid stimulate the LH to cause the testes to produce! That is ancient history and you take them DURING the cycle to prevent atrophy in the first place.

HCG stands for Human Chorionic Gonadotrophin and is not a steroid, but a natural peptide hormone which develops in the placenta of pregnant women during pregnancy to controls the mother's hormones. (Incidentally, this is the reason you may hear of people testing for growth hormone (HGH) with a pregnancy testing kit - If their HGH shows 'pregnant', they've been ripped-off with cheaper HCG - but we digress slightly).

Its action in the male body is like that of LH, stimulating the Leydig cells in the testes to produce testosterone even in the absence of endogenous LH. HCG is therefore used during longer or heavier steroid cycles to maintain testicular size and condition, or to bring atrophied (shrunken) testicles back up to their original condition in preparation for post-cycle Clomid therapy. This process is necessary because atrophied testicles produce reduced levels of natural testosterone, this situation should be rectified prior to post-cycle Clomid therapy.

HCG administration post-cycle is common practice among bodybuilders in the belief that it will aid the natural testosterone recovery, but this theory is unfounded and also counterproductive. The rapid rise in both testosterone, and thus oestrogen due to aromatisation, from the administration of HCG causes further inhibition of the HPTA (Hypothalamic/Pituitary/Testicular Axis - feedback loop discussed above); this actually worsens the recovery situation. HCG does not restore the natural testosterone production.

The typically observed dosing of 2000 to 5000IU every 4 to 5 days causes such an increase in oestrogen levels via aromatisation of the natural testosterone that this has been responsible for many cases of gynecomastia.

From the above discussion it is clear that HCG is best used during a cycle, either to:

1) Avoid testicular atrophy, or
2) Rectify the problem of an existing testicular atrophy.

Doses of HCG
Smaller doses, more frequently during a cycle will give best overall results with least unwanted side effects. Somewhere between 500iu and 1000iu per day would be best over about a two-week period. These doses are sufficient to avoid/rectify testicular atrophy without increasing oestrogen levels too dramatically and risking gynecomastia. This dosing schedule also avoids the risk of permanently down-regulating the LH receptors in the testes.

Male Hypogonadism Caused by Homozygous Deletion of Exon 10 of the Luteinizing Hormone (LH) Receptor: Differential Action of Human Chorionic Gonadotropin and LH
J. Gromoll ? U. Eiholzer ? E. Nieschlag ? M. Simoni

JayDiesel
06-14-2011, 05:24 AM
Another great read! Thanks man

Guest
07-13-2011, 11:20 PM
I'm TorN!Jsos

atavist
07-13-2011, 11:59 PM
So what is your recommendation on HCG dosing for say a 17 week cycle... which is what I'm planning on next (Test C 750 and EQ 600 EW)....

how about something like 500iu ed every 3rd week, then at the end wrap up with taking 500iu ed for three weeks starting two weeks before the last inject??

I just want to make sure I don't take to much and desencitize myself to LH which is why I think maybe one week out of every 3 instead of 2 or 3 on at a time...

thoughts?

Test-ee!
07-14-2011, 11:26 PM
Mod fight!?!

ODB
07-30-2011, 07:43 PM
lets throw HGH in the mix;

one of the best anti-catabolics out there is good old growth hormone. Just ask Pro football players who juices in the off-season and they will tell you that GH is a savior to them. In addition to GH, there is the drug called Trental (pentoxyfilline), which blocks many of the pathways related to muscle atrophy and can really help maintain mass during catabolic conditions. Other supplements of mention are the 7-oxygenated DHEA derivatives, which are known to antagonize many of the negative effects of cortisol in the body, as well as suppress catabolic inflammatory cytokines.