So I think by now there’s consensus in most parts of the AAS-using universe, that a proper PCT following a more HPGA suppressive cycle should comprise of a SERM, AI & hCG. Although I have seen newbs ask if using just an AI or hCG will suffice… Rather try a SERM for 4 to 5 weeks, for a single component PCT, if your budget is that scant.
The more commonly available options for SERMs are clomiphene citrate & tamoxifen (I’m not going too deep into explanations which have been repeated to DEATH, on this site & others). SERMs work to restore HPGA function by competitively binding to ERs at the hypothalamus, thereby causing an increase in the secretion of LH. Because, elevated LH stimulates the testes to increase/ restart their production of testosterone, right?
BUT in their dormant & atrophied state, regardless of how much circulatory LH you have, your testes just aren’t fit to respond. Indeed, I’ve read studies where blood tests were taken on test subjects some time after a cycle & LH levels were found to be higher than baseline or on cycle. But testosterone levels had not yet risen. And another study where clomiphene citrate (CC) was administered to a group of young men & another of older men. Prior blood tests showed that LH & FSH were higher in the elderly men. After CC administration FSH & LH rose similarly between the 2 groups. Yet mean serum total testosterone & non-SHBG-bound levels rose by 100% & 304% respectively, in the younger men but only 32% & 8% respectively, in the elderly men (although these are age related differences, I’m sure you see my point about the testes’ ability to act upon elevated LH).
And that is my major critique of every PCT I’ve ever seen; they start you off with a SERM for the sake of increasing T levels via elevated LH when those very same testes will be highly unresponsive for sometime into your PCT (another critique is that conventional wisdom suggests waiting too late to start PCT). Cue the LH analogue known as hCG. It quickly brings your testes back to size & out of dormancy. Instant (short term) endogenous T production. And it elevates T levels for days after administering. My logic tells me that hCG should be introduced towards the end of your cycle, in anticipation of the SERM portion of your PCT. In fact if you’re using, say trenbolone or deca in your cycle, 2 to 3 weeks of hCG during your cycle would serve you well. So during, say a 5 week PCT, you’d start hCG more than a week before you start that SERM (consider day 1 of the SERM as the beginning of your PCT) & stop using it during the 4th week of PCT. Allowing for more than a full week of just the SERM (at the end of PCT) to see where you really are in your recovery & endogenous T production.
BUT you can’t just use that hCG willy nilly. 1stly, the more testosterone there is, the greater the amount of aromatizing that occurs. 2ndly hCG has the ability to increase aromatase activity in the Leydig’s cells, leading to even more oestrogen production. So for the above reasons & also for the sake of negative feedback manipulation (everything mentioned thus far has been for the sake of manipulating factors involved in negative feedback), we introduce an AI. Because basically, the body’s assumption is that high levels of oestrogen detected are a result of high levels of T which has been aromatized. Under natural conditions, more T equals more oestrogen, in the ratio applicable to each individual.
(Physiologically, 80% of circulating oestrogen in men is produced by the aromatase pathway. The remaining 20% is produced directly by the testes)
Just a quick recap: for the less suppressive or shorter cycle, a SERM should suffice. Otherwise go for a SERM, hCG & an AI. You’d then first decide which SERM to use. Followed by the toss up between urinary hCG & recombinant hCG. Then finally, the AI. Should you opt for CC, no limits. But if it’s tamoxifen you want, then your only option is exemestane.
Now for an effective PCT you need to create the smoothest transition from cycle to natural training. Besides retained water, the main culprit for loss of gains is that dip/ absence of anabolic hormones between your last injection & eventual resumption of endogenous androgen production.
So here’s what I do: besides suggesting low to moderately doses during the cycle, the very last injection of a long estered compound would be of a lower quantity eg. for TC 300mg (some people also decide to use short estered or quick acting compunds between that last injection & PCT). Then take the given half life of the compound (12 days for TC) then shave off a few days, coinciding with the day or 2 days BEFORE you would expect (from past experience) to lose strength in the gym &/ or water from decreased oestrogen. For the example of TC, I say 10 or 11 days from your last injection, is when you begin the the SERM, at a dose that will allow it to become active sooner in your body (exogenous androgen levels at this stage won’t be enough to suppress your recovery). But remember what I said earlier about not allowing that dip in your anabolic hormone levels? You’d have also began hCG more than a week before that, achieving good T levels even this far after your last injection. Simultaneously, your testes are now also more responsive to the LH being released as a result of the SERM & AI.
So for some time since your last injection until your 2nd last week of PCT, thanks to hCG, you’ve got GUARANTEED endogenous T, holding onto those gains, smoothing the transition. But using high doses of hCG, for extended periods of time, desensitizes the testes to endogenous LH. Also, using doses that are too high means that the overly elevated T will suppress its own production… Ok so, for the last 1 to 2 weeks of your +/- 5 week PCT, you’re cruising on a SERM & AI only. And at the lowest doses possible.
With a good diet, nutrition, training regimen, rest/ sleep etc I see no reason why anyone should lose anything more than retained water after a cycle, even without access to MSRP.
