Test enanthate to sust 250

[Woodes Rogers]

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[Matt20385]

I can't remember asking for your approval Or to be called an idiot! So can you please explain what Ronnie Colman like size has anything to do with the question I asked.

If you don't approve the use of steroid or use them what are you doing posting in this forum at all?

 

[Matt]

The following comments since my last beg the question, does anybody on this site do research or even take steroids. Spartacus touched on some valid points, however, those posting with the attitude “OMG 1000 mgs is crazy”, fuck, slap yourself. I just can’t be any more direct than that.

Some would argue you need be to slightly mentally unbalanced to be a true professional bodybuilder. Dosages around these numbers 1000mg – 3000mg are not uncommon (even in your average gym) those who dispute that well…….say hello to Alice or Mary Poppins or whoever the fuck it is that know in the fantasy land you come from.

Look at the final top ten of the 1992 Mr Olympic two of them are dead (Mohammed Benaziza Algeria, Sonny Schmidt) and the all mighty Ronnie Coleman placed a mere 16th. And people want to tell me that a couple of 250mg jabs a week will allow you to compete at that level.

All that aside, I don’t give rip nor want to enter a debate about what pro’s do or do not take.

So revisiting the original point I raised in my last post. If little fucken Johnny jumps on the forum and says I want decent gains and some Muppet tells him a 200mg jab once a week will have you looking like Arnold, this forum is not serving its purpose.

So I ask once again, if some on here can provide me with concrete evidence that a running a 1000mg test (any ester) a week is detrimental I will take back all I have said and concede that I am provided poor information.

For example, Dorian Yates Off season consisted of:

Test -750mg,
Deca- 500mg,
Daily Anavar- 50mg.

Lee Priest has given this as his 16 week steroid cycle

16 to 9 weeks out. 250ml Test Cyp, 350ml Test Enth, 200ml Decca every 6 days, 2-4ius Gh a day, 50mlg Anapolan a day, 20mlg Nolvadex a day.

14 weeks out start Clen, taking 6 tabs a day, 2 days on, 2 days off and so on.

9 to 7 weeks 200ml Decca, 200ml Test Enth, every 6 days, 200ml Mastron every 4 days, 1 Anapolon a day, 1 Nolvadex a day, Keep Clen as normal. 1 proviron morning, 1 at night.

7-3 weeks out 150ml Test Prop Mon, Wed, Fri, 50ml Win-V Tues, Thurs, Sat, 200ml Tren Ace every 3 days, 1 Anapolon a day, 20mlg Nolvadex aday, 1 proviron morning, 1 at night. Clen as normal eg. 6 a day 2 on 2 off.

3-2 weeks out, 100ml Test Prop Mon, Wed, Fri, 50mlg Win-V Tues, Thurs, Sat, 200ml Tren Ace every 4 days, 1 Proviron Morning, 1 night, 1 Arimadex a day, 20mlg Nolvadex a day. 25mlg Anavar a day, 25-30mg Halo a day. Clen as normal

2 weeks out Stop GH.

10 days out Stop Tren and Prop. Keep every thing else the same

7 days out Stop Win-V and swap over to Oral win 30mlg a day, keep all other orals the same, right up to show day.

I may use a little T-3 3-4 WEEKS OUT 30-40MCG A DAY.

And David Palumbo has written that this was his pre-contest cycle:

Test: 1200mg per week
Deca: 600mg per week
Parabolin: 76mg amp 3x per week
Winstrol: 50mg every other day
Halosten: 20mg per day
GH: 6IU per day
Teslac: 20 pills per day (anti-aromatase)
Proviron 20mg 4x per day
6IU Humulin-R 2x per day

Source: Mike Arnold, Muscular Development and RX Muscle.


even at Palumbo's levels, it is still considerably lower then the 5g you suggested as the norm for pro's. add to that the fact that you're giving recommendations to newbies, not seasoned veterans who have been using gear for years and training even longer.

also:

This thread has been created because of the discussion over the last few days over the use of anti estrogen drugs or SERMS in post cycle therapy when you have not made use of HCG during a steroid cycle or at the end of the cycle.

This article explains why SERMS and anti estrogen drugs do very little for you post cycle if you have not used HCG as part of your cycle or PCT plan. It also explains how to use SERMS and anti estrogen drugs if you have made use of HCG as part of your PCT.


Understanding Post Cycle “T” Recovery

Posted
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.

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.

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 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

 

[Woodes Rogers]

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