TweetWhat type of testosterone ?
There are many different types of testosterone. Long esters, short esters, methyltest, andriol, and mixes like sustanon and omnadren. First of all we need to state that methyltest is not testosterone. The 17-alpha-methylation makes quite a few alterations. It will express less androgen binding, lower conversion to mestanolone (Methyl-DHT), and despite lower aromatization, also a heavier amount of estrogenic action because it converts to methyl-DHT, a much stronger and efficient type of estrogen. So methyltestosterone is not a valid choice. Andriol uses a rather ineffective delivery system based on lipophillic absorption in the ductus thoracicus of the lymphatic system. Fine in theory, but appears to be less effective than hoped, and the amounts needed to make andriol of use to us are not affordable.
We will also include sustanon and omnadren, these are combinations of long and short esters (structures attached to slow the release of the compound into the blood), usually injected over wide time-spans. This creates a very unstable blood-level, contrary to popular belief. Imagine if you will a product of 3 esters, one that releases over 3 days, one that releases over 6 days and one that releases over 9 days. 100 mg of each injected once every 9 days. The first three days the first ester would release 100 mg of testosterone. The second ester would release 50 mg and the last ester would release 33.3 mg of testosterone. The next three days the first is already gone, the second releases only 50 mg and the last only 33.3 mg. And on the last three days only 33.3 mg of testosterone from the last ester is released. At the beginning I have the massive dose of 183.3 mg in my blood, and at the end only 33.3 mg … you do the math.
The saner thing to do is to use a single ester and inject as soon as levels taper off to levels upon injection. The three most widely used esters and their frequency of injection are propionate (every 2 days), enanthate (every 6-7 days) and cypionate (every 7 days). There is also the longer undecanoate, but that is rather hard to find, and the esterless suspension. The latter is great for mass, but seems to cause a great deal of water retention and needs to be injected once or twice a day, which is not wishful for a long term plan. So which of these should we use ?
Well, the propionate is my first choice, because its release patterns seems to be the most beneficial in keeping water weight under control, and it clears faster than the other two allowing for faster recuperation. For lean gains, I would certainly make the choice for propionate, also because it has a lighter, shorter ester and thus more testosterone per mg. But not many people appreciate injecting every 2 days, and with the concomitant use of boldenone undecylenate the fast clearance time seems to be a non-factor. So if you can tolerate a little more water weight, enanthate or cypionate allow for weekly injections.
In defense of boldenone
Boldenone differs from testosterone only in that it has an extra double-bond on it’s a-ring at the 1 position. This changes the conformation of the A-ring and its affinity for certain structures. As such it is only half as androgenic as testosterone because of lower affinity to the androgen receptor, and it does not form a more potent androgen in androgen-specific tissue, because it has particularly low affinity for the 5-alpha-reductase enzyme (10) (that converts test to DHT). Eventhough its conversion product is quite potent (1-testosterone).
Boldenone’s affinity for the aromatase is roughly reduced by the same percentage, and so it only creates about half as much estrogen. So in essence, boldenone offers us many of the same characteristics that testosterone does, but because of its lessened affinity poses less of a threat for the acute, visible side-effects. So by dividing our doses over testosterone and boldenone, we can reduce both acute and long-term side-effects.
Boldenone is patented as a veterinary drug, but the high demand has made a wide range of affordable human grade products available to us and the use of boldenone is now quite wide-spread among recreational athletes. It is touted as the successor to the mighty Deca-Durabolin. Deca is nandrolone decanoate. Nandrolone has the benefit of being deactivated by the 5-alpha-reductase enzyme and being even less of a threat for acute androgenic side-effects. But alas, it is a very suppressive hormone that severely interferes with endogenous production of testosterone and it has been concluded that both nandrolone (11) and several of its metabolites (12) exhibit progestagenic activity (which causes gyno through estrogen mediated pathways) and seems to cause more bloat because it acts as an aldosterone agonist (13), resorbing more salts from the urinary tract. On top of that it seems to have a terrible effect on our libido (can you say limp dick ?).
Boldenone gives us none of the aforementioned problems, and despite being a much, much weaker androgen than nandrolone, it seems to exhibit the same level of anabolism in vivo. Which again points in the direction of the non-AR and non-ER mediated pathways to muscular hypertrophy we discussed with testosterone. Boldenone offers two other distinct benefits that have been noted by many a user, despite lack of scientific backing so far. The first is that boldenone seems to increase the appetite. This too is most likely a non-AR mechanism, since many of its inactive metabolites like androstadiendione exhibit the same property and to the same extent, but in low doses. This could be crucial since we steroids can build our muscles, but they need something to build with. That something is amino acids derived from our protein intake, hence our high-protein diets. But to have ample amino acids left to build muscle, we must first eat sufficient calories, more calories than our maintenance of metabolism requires. And in that case it can be of huge benefit to increase your appetite.
The second advantage is that it causes an uncharacteristic rise in aerobic fitness. It is well known that androgen binding increases Erythropoetin release from the kidneys, which increases red blood cell count. Red blood cells carry oxygen through the blood stream, so we have a greater aerobic capacity. But boldenone seems to exhibit an increase in aerobic capacity, far greater than its androgenic affinity would allow us to suspect. Which is probably why this veterinary hormone gained so much human attention in the first place. Along with the increase in respiratory capacity from beta-adrenrgic stimulation (discussed later in this article) could lead us to new heights in any type of sports we practice that require endurance.
So in light of its safety and efficacy, the choice for boldenone as our secondary drug is a quite easy one.
In defense of Stanozolol
Stanozolol is a methylated drug. That means it can be taken orally and be quite effective, but also displays a certain level of liver toxicity. We need to relativate these findings, toxicity is often overstated and it was found (14) that many cases where liver toxicity was determined based on aminotransferase levels were false positives when we looked at the CGT levels. Nonetheless some care should be taken. In general we advise no more than 6-8 weeks on any hepatoxic drug within normal doses (for stanazolol that is 50-100 mg per day) when taken orally and up to 10 weeks when injected (50-75 mg per day). After that ample time should be given to the liver to recover.
Stanozolol has no 3-keto group, which is in most cases essential for androgen binding. So it is far from the heavy androgen some would have you believe it is. But it does appear to exhibit good binding in some places. Like its parent, DHT, it seems to reduce some aromatase activity and it may guard against some progestagenic binding (15) as well (from nandrolone or trenbolone) although it is unlikely its affinity for the PR is strong enough to play a crucial role in that. It has been suggested that stanozolol may have good binding to the microsomal AR, which may explain its benefits as far as energy utilization. Both aerobic and anaerobic, stanozolol seems to exhibit a large increase in performance. Strength and explosiveness increase, and athletes seem to tire less fast. It has therefore been a favourite of many runners, both in shorter and longer distances. The main use here for us will then also be to assist in the maintaining and gaining of strength, rather than sheer mass, although its light anti-aromatase properties will also aid us in attaining a more fat-free body.
One reason, with regards to safety, why I chose to include stanozolol and not a more potent bulk-up agent as the oral component of this cycle, is because of its effects on tendons. It has long been a concern that steroid usage causes tendon damage. Directly it doesn’t of course, but as muscle size increases and strength increases, so does pressure on tendons. And since the tendons do not have a large degree of vascularity they cannot adapt as quickly as the muscle. Repeated strain causes microtraumata, and when enough microtraumata have built up, eventually the tendon will rupture. Stanozolol however, has been found to increase collagen synthesis (16) where testosterone did not. Collagen is a key component in fibrous tissue such as cartilage and tendons, and may therefore offer us the bonus effect of maintaining tendon health or even repairing damage of microtrauma, and keep our cartilage healthy so we can resist the pressure on our joints.
The Goal and the diet
The goal we are pursuing with this, is to create a stable long-term plan for cycling steroids that will not only not jeopardize our health, but actually improve it. The reason we choose to use steroids however is to look better or perform better. It would therefore be unwise for a long-term plan to include excess body-fat, too much water retention etc. On the other hand, muscle growth is reliant on sufficient calories.
Our primary goal is to eat enough. If we consider what we do in a day and the calories we need to achieve that, we need to eat at the very least 20% more to see sufficient growth. Preferably 30% more. Our secondary goal is to keep fat off. The prime mover there is insulin. Insulin stores glucose in the muscle as glycogen and increases the shuttling of nutrients into fat cells. So naturally our goal is to keep insulin low. Insulin is a very anabolic hormone, but that does not mean we cannot achieve growth without it. In order to keep insulin low, we need to eat as little as possible high-glycemic carbs. Any type of carbs that contain glucose (and can therefore increase insulin rapidly) must be avoided. That increases most types of pasta, white bread, an excess amount of starches like potatoes, anything that has added sugar in it, regular table sugar, dextrose, maltodextrin, maltose and several oligosaccharides. A little fruit here and there is fine, as fructose does not appear to be so drastic in insulin levels, and low Glycemic carbs are fine as well (such as the lactose in milk and such). Our diet will probably be moderate to low-carb because of this. More importantly our diet should be high protein. Because first of all protein is what we require to build muscle. Secondly because the body can burn protein, but most likely will not if other means are available. And since we will be manipulating our beta-adrenergic system, we will have plenty of free fatty acids at our disposal. That means the amount of protein in our diet needs to be so great that with it we are eating at least 20% above maintenance, and without it we are eating at least 20% below maintenance. I would keep fat around 20-25% of your diet (from clean sources of course) and then fill the rest in as you please : high-protein and no high GI carb sources.
Because this will allow us to keep insulin low, we cannot only keep fat off, we can also maximally manipulate the beta-adrenergic system, meaning we could potentially lose fat, or at least lower body-fat percentage by keeping fat off and increasing lean body mass.
The take home message : A high-protein diet that contains little or no high GI carb sources, and that meets the demand of being at least 20% over maintenance (around 18 kcals per pound of bodyweight, but that is just an estimate).
The actual cycle
Now we need to put the cycle together. Below I will outline one good way to use these products and then offer some explanations to my reasoning. I will also already include the post-cycle regimen, eventhough we will discuss that at a later point in time.
Week 1-12 : Testosterone enanthate / cypionate 400-500 mg/week
Or : Testosterone propionate 150 mg every other day
Week 1-2 : Boldenone Undecylenate 600-800 mg/week
Week 3-12 : Boldenone Undecylenate 300-400 mg/week
Week 6-13 : Stanozolol 50-100 mg/day
Week 12-14 : HCG 3000/3000/1500/1500 IU / 5days
Week 12-17 : Tamoxifen Citrate 20 mg/day
Week 14-15 : Clomiphene Citrate 100 mg/day
Week 16-17 : Clomiphene Citrate 50 mg/day
Week 14-15 : (Spironolactone) 50 mg/day
Week 7-18 : Beta-adrenergic mix with eph as described.
You may notice the dose of boldenone is larger the first two weeks, that’s because longer esters tend to need some time to accumulate before showing their best effects, and by front-loading with a higher dose, we can achieve accumulation faster and see results sooner. I ran the stanozolol a week longer in this example, which should be fine considering it would take at least 2 weeks after the cycle to clear all boldenone, so the stanazolol beyond this point should cause no further suppression.
The patterns for post-cycle will be discussed at a later time.