Understand Post Cycle Recovery

Post Cycle “T” Recovery

by William Llewellyn

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 LH Levels

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.


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

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.

Sample Post-cycle Plan:



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.


1. Effect of long-term testosterone oenanthate 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

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