Anabolic-Androgenic Steroid Cycle Planning

In previous issues, we have discussed the pharmacology of anabolic steroids somewhat. However, ultimately, most are interested in having and understanding the answers to very simple questions, such as, “Which steroids should I use? How much of them should be used, and for how long? What other drugs are needed in combination with the steroids?” However there is no single correct answer for everyone.I do need to stress that there is no recommendation that anyone “should” use these drugs. We are discussing use by those who have already made that decision for themselves.

The first thing to be considered is, “What are the goals?” And perhaps the second thing to be considered is, “Are those goals reasonable or should they be changed?” All too often I am asked questions from people who wish to add a lot of muscle and cut a lot of fat simultaneously and who want to use the mildest and safest drugs and they want to know what they should do. What they should do is to come up with some goals that do not contradict each other. In this article, we will consider goalsand how to achieve them. In all cases we refer to use by male users. Females must use much lower doses to avoid virilization problems, and in fact even low dose use may lead to irreversible lowering of voice, increase of facial hair, etc. Therefore, use by women is a separate issue which is not being addressed here.

Muscle Mass

Let us consider the first goal mentioned: gaining muscle mass. Now this goal depends highly on how advanced one already is as a trainer and/or steroid user. Someone who is already 40 lb. more muscular than he could achieve naturally, and who wishes to add still more for the purposes of competitive bodybuilding, will simply find no use from a recommendation to use 500 mg/week of Sustanon. At best such a dose might allow him to maintain what he has, instead of slowly losing muscle while off drugs. Such an athlete will probably not achieve his goals with less than a gram per week of injectables, stacked with at least 50 mg/day of orals. And he may need more than this. He is already far beyond what he could attain naturally, and more yet will not come easily.

What of the person who, after several years of hard, quality training, is probably fairly close to his genetic limit under natural conditions? He would probably achieve excellent results with this same 500 mg/week dose of Sustanon, and undoubtedly would do so with some Dianabol added as well.

Another person may not even be close to his natural genetic limit in the first place, due to inconsistent or poor training, or novice status. Such a person can make excellent gains without anabolic/androgenic steroids (AAS) at all, and while AAS can increase the rate of gains, one cannot say that any particular drug regimen is necessary or advisable.

Yet another person, who simply wishes to have an attractive physique and appearance by conventional standards, and highly values the condition of his skin and hair, would be poorly served by the advice to use Sustanon or Dianabol at any dose. The likely worsening of his skin and possible acceleration of hair loss would not be worth it. He would be better served with a milder drug, which would allow him to achieve his goals with minimal cosmetic or health risk.

Fat Loss

And what about the second goal: losing fat? Well, this goal is at cross-purposes with gaining muscle. One simply cannot gain nearly as much muscle on reduced calories as on higher calories allowing a fat gain of perhaps 1 lb/week. The person would be best advised to divide muscle gains and fat loss into separate phases. If a person is not at a level of muscularity beyond what he can attain naturally, AAS really are not necessary for dieting down to moderate bodyfat levels such as 8%. However, AAS use can make the dieting easier and faster, especially for natural endomorphs. It does not seem that much of a dose is required in this application. 250 mg/week Sustanon or 400 mg/week Primobolan will be effective. That however is not the case for individuals who are well beyond their natural limits. They will shrink much faster on low dose steroids than on high dose steroids while dieting, and anything less than a gram per week would be obviously much less effective than doses actually used (2-4 grams per week not being unusual in elite circles.)


Estrogenic effects are one of the serious problems with AAS use. Most AAS either convert to estrogen or even if they may not, act to increase the effect of estrogen. Testosterone, Dianabol, and Anadrol® are particularly noted bad performers in this regard, and nandrolone (Deca) is not by any means immune to conversion to estrogen. Methenolone (Primobolan), trenbolone, oxandrolone, stanozolol (Winstrol), and dromostanolone (Masteron) are AAS which do not convert to estrogen at all and which avoid the problem entirely.

For those compounds which do convert to estrogen, the problems experienced include increased inhibition of natural hormone production (which however is not mediated only by the estrogen receptor, so the problem is not entirely solved by blocking estrogen), possible gynecomastia (abnormal development of breast tissue), liver problems, and water retention. We have previously discussed anti-estrogenic agents.

The other main area of concern with safety of these drugs is hepatotoxicity of oral anabolics. Primobolan oral does not have this problem, but on the other hand, is essentially useless for a male bodybuilder at 5 mg/tab. At least 100 mg/day would be needed even for mild effect, and this simply would be cost prohibitive. Oxandrolone has minimal liver toxicity, but is not known for greatly increasing gains, and is expensive. Stanozolol has some toxicity and is not particularly effective. This leaves methandrostenolone (Dianabol) and oxymetholone (Anadrol®.) Dianabol is rather mild in its liver toxicity, at least if it is not used for many weeks consecutively. Anadrol® can make some users feel rather ill rather quickly. In my opinion, if Dianabol will do the job, and it will in most cases, it is the better drug of the two. If nothing else, it is simply more pleasant for the user.

Cycle Planning

The next thing to be considered, after “What drug?” and “What dose?” is how long the drug should be used, or what pattern should be used if the drugs are varied.

Now again, we must consider the goals of the user. If we are speaking of an IFBB pro it simply is not realistic in today’s age to suggest that he should ever come off the drugs at all while competing. Others are not taking time off, and he would fall behind if he did choose to take off weeks and allow his system to return to normal periodically. Therefore, I am addressing here the concerns of the more average athlete who does not desire to be on drugs perpetually, and desires to maintain most of his gains while off drugs.

If gains are to be retained, losses at the end of the cycle must be avoided. Such losses occur if the natural hormonal axis, involving the hypothalamus, pituitary, and testes, is not producing normal levels of testosterone by the time that anabolic drugs are no longer providing significant levels to the system.

Incidentally, inhibition of each of these organs is somewhat independent of the others, and different factors are involved for each. We’ll look at those issues in a future article.

The risk factors for inhibition are principally length of the cycle, choice of AAS, dosage of AAS, and in the case of orals, dosage pattern of AAS.

Very simply, the longer the cycle, the greater the chance of recovery problems. And in calculating the cycle length, one must take into account the half life of the drug, and the time required for levels to injected drug to fall below inhibitory levels. This will be several half lives. Thus, some people speak of 2 week cycles using Sustanon, with 2 weeks “off,” which is then repeated. But they are incorrect in believing that they are doing 2 week cycles. Because substantial and inhibitory amounts of Sustanon will remain in the system during the “off” weeks, there is no recovery. If a person strings 4 of these cycles together, for example, he will have been on steroids for 16 weeks and may well have a difficult time recovering natural testosterone production afterwards. Thus, this is no solution.

The same type of scheme, however, can be quite successful with testosterone propionate with use of antiestrogens, as reported for example by Alexander Filippidis in a case study. With this shorter acting drug, there is actual time off between cycles.

Single short cycles, with many weeks allowed before beginning another new cycle, don’t seem so efficient. Usually, real strength gains don’t begin coming until the third week or so. While muscular weight may be gained in the first two weeks, it seems that the body is also adapting itself in a manner which will make growth very efficient in the next few weeks: or rather it would, if AAS were still available. Thus, I can’t recommend doing isolated cycles which are shorter than four weeks at the minimum, and really five or six weeks is probably more reasonable. Only in the case of short acting drugs, with very frequent cycles, are two or three week cycles a good idea in my opinion.

While it makes little sense to cut a stand-alone cycle too short, while the body is still ready to gain rapidly, on the other hand, heavy use beyond say 10 weeks becomes fairly likely to result in recovery problems. Furthermore, after the body has already grown a good deal and has been growing for many weeks, it is less ready to grow more. Thus, long cycles are inefficient in that regard, and furthermore are likely to result in greater losses after the cycle. Perhaps 6 weeks of heavy use and two to four weeks of light use is approximately optimal for conservative users.

The choice of AAS is quite critical towards the end of the cycle, so far as inhibition is concerned, but the inhibition issue is not so vital at the beginning. In other words, if one hits the system heavily at the beginning, but then lightly at the end, recovery will be better than if the reverse strategy were employed.

Primobolan, while not an exceptionally strong anabolic per milligram, seems to have a better ratio of anabolic to inhibitory activity than any other steroid, and is my recommendation as the injectable to use in the last weeks of a cycle. It is not absolutely clear though that this is an intrinsic property of Primobolan. It may be due to the fact that Primobolan does not convert to estrogen, and perhaps (this is speculation) low dose trenbolone might give an equally favorable anabolic/inhibitory ratio.

Dosage for this use is somewhat less clear. Some have made excellent recoveries on a gram of Primobolan per week. In the US, however, such use would be quite expensive. In general, though, I don’t know if most people will recover well with that dose. 400 mg/week is still sufficient to saturate the androgen receptors (ARs) and is a more conservative approach for the last weeks of a cycle.

Where oral anabolics are concerned, once-a-day dosing results in much less inhibition than divided doses. It’s unknown what time of day is best, but morning has been used successfully, and makes sense since that timing will result in little drug being in the system at night and early morning, when LH and natural testosterone production are highest. Thus, switching to once a day dosing in the last few weeks would make sense.

Our goal throughout the cycle as a whole, however, cannot simply be to minimize inhibition. If it were, the answer would be simply to take no AAS at all, or to use very little.

In the early phases of the cycle, inhibition must simply be accepted if serious gains are desired. This is not because inhibition itself in any way leads to gains, but simply because there is inhibition mediated by the androgen receptor, and therefore high levels of androgen will cause some inhibition. And as long as inhibition is occurring anyway, gains may as well be as much as possible. I see no point in half-measures. Either be gaining as much as possible, or be setting yourself up for recovery while still making some decent gains or at least maintaining gains.

For the early part of the cycle, the inhibitory properties of the AAS used are of less importance than the mass-gaining properties.

Two anabolics reign supreme: testosterone and trenbolone (which is found in Parabolan or in illicit injectable preparations of Finaplix.) These AAS appear more effective for mass building than any other injectables.

They may be stacked to advantage: since one is unlikely to be able to afford or to obtain large amounts of Parabolan, it is worthwhile to add testosterone in order to obtain a higher total dose and greater results. Furthermore, there may be a synergistic effect. However, trenbolone itself, particularly in combination with Dianabol, can give excellent results. Oral AAS add their own benefits, not because of binding to different receptors, but probably because of their direct action on the liver, which produces various growth factors.

What about other injectables?

I see little point in stacking weaker injectables such as Deca or Primobolan in the heavy phase of the cycle. While on the one hand they probably won’t hurt – if they bind to the AR, they will give essentially the same action as testosterone – if the phase is heavy there is already enough AAS to saturate the receptors. There is no benefit there.

And there is little benefit from any possible non-AR-mediated activity, since these drugs do not seem to have much if any such effect. Nor can they act to reduce the side effects of the heavier anabolics. So there is little point to using them in the heavy phase of the cycle.

Side effects of testosterone are the main reason why people have been interested in weaker drugs such as Deca. However, with an effective aromatase inhibitor such as Cytadren at 250 mg/day, stacked with an effective estrogen receptor antagonist such as Clomid at 50-100 mg/day, testosterone becomes comparable to Deca in terms of side effects for equally effective doses of drug.

Some have found that Proscar acts to minimize effects of testosterone use on skin and hair. The objection that reduced conversion to DHT might reduce muscular growth may have some validity. This might be true either because of loss of DHT activity on nervous tissue, or because of possible loss of non-AR-mediated effects of androstanediol, a DHT metabolite, or an indirect effect not occurring in muscle tissue itself. DHT itself is not an effective anabolic for muscle tissue.

If one chooses to use Proscar to minimize risk of hair loss, I would suggest topical use to the scalp, or if used orally, certainly not in excess of the recommended dose for medically-indicated use.


There is one side effect cannot be blocked: if one uses heavy doses of testosterone and/or trenbolone for months, and then ends the cycle, losses of muscle will occur because of poor recovery. LH production will be low, and because it has been low for some time, very often it may take some considerable time for the pituitary to again produce normal levels. Furthermore, testicular atrophy may have occurred, although such can be avoided with occasional use of hCG during the heavy phase of the cycle.

Because of recovery problems, it is wise to limit the heavy phase to 5-8 weeks, and then switch to Primobolan for the last several weeks of the cycle, beginning two weeks after the last injection of long acting ester. Once a day dosing of orals might be concurrent with this.

If long acting esters were used, then the existing drug from the heavy phase will have significant anabolic effectiveness for 2-3 weeks after injection, depending on dose, and thus no injectables would need to be used in those weeks. After that point, if Primobolan is not available, one might wish to continue with once-a-day dosing of orals, very low dose (100 mg/week) testosterone with use of antiestrogens, or even perhaps use of androdiol or norandrodiol. A balance must be struck, however: there is a middle ground that we do not want to be in. There is a range where there is still some anabolic support yet there is fairly little inhibitory effect, but past this range, there still is not great anabolic effect, but there is substantial inhibition. One does not want to spend more time than necessary in this middle ground, but pass through it relatively quickly. Once in the light phase, the dose must remain low enough to allow recovery of natural hormone production to occur.

Clomid use should continue until the user is confident that natural testosterone levels have returned to normal.

Ultimately, there cannot be one answer for everyone. Different users will have different needs. The above is generally good advice for reasonably conservative bodybuilders who wish substantial results. Those desiring either more moderate or more extreme results would need to adjust their plans accordingly.

Article courtesy of

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About the Author:

Bill Roberts holds a bachelor’s degree in Microbiology and Cell Science, and was doctoral candidate(Ph.D.) in Medicinal Chemistry. He is working on the completion and defense of his doctoral thesis:“Synthesis, characterization, and determination of transdermal flux of 3-alkylcarbonyloxymethyl derivativesof 5-fluorouracil, and development of models for prediction of transdermal flux from physical parameters. “His education was invaluable so far as being able to design/improve nutritional supplement compounds,since it was in the field of designing drug molecules and secondarily some work in transdermal delivery.It was not specifically “geared” toward androgens other than expertise with pharmacological principles havingbroad applications. This has allow Bill to provide unique insight into the field of anabolic pharmacologywith knowledge of points which he would not have known otherwise. He is a former writer for Dan Duchaine’sDirty Dieting newsletter, and is an avid lifter.