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.
Post-cycle discussion
Post-cycle has been touted as critical in the process of complete and total recovery. Here too I?m basing myself on certainties from a few studies and making my conclusions accordingly. That is why I offer the advice I offer. This does not mean you should conclude that anything else will necessarily be detrimental, but I cannot guarantee as good an outcome.
The choice of a Tamoxifen/clomiphene/spironolactone combination
The choice for a tamoxifen/Clomiphene combo is primarily because of two factors. Only one relevant study (1) came up as far as recovery after a stack of products (testosterone and nandrolone ) was used for twelve weeks, utilized HCG and both clomiphene and tamoxifen to achieve a complete recovery of the HPTA to acceptable levels in 45 days. The second reason is the raging war over which is the better post-cycle drug, clomiphene or tamoxifen has lead to several conclusions. The first is that while 150 mg of clomiphene and 20 mg of tamoxifen have lead to roughly a similar increase in LH levels (17) , but that with the high dosing of clomiphene over time there are certain disadvantages. Such as that it may damage eyesight and may act as a weak estrogen (18) in undesirable places (like the pituitary). So using tamoxifen alongside it will allow us to lower the dose and decrease the chance of these side-effects and add the distinct benefit that Tamoxifen (being the stronger of the two) will prevent the clomiphene from exerting any much influence at the pituitary, and that it will increase LH responsiveness to GnRH (17) where Clomiphene does not. Clomiphene is still used as it seems to offer other advantages, such as an increase in SHBG (19), which may seem like a bad thing at first, but which may decrease androgen-related negative feedback and may thus be in our advantage.
Regardless of the final outcome I feel I have settled the dispute, at least in my own head. Why bother figuring it out when we can use both, limit any negative effects and reap the proven benefits of full recovery ? I used to run tamoxifen slightly less long than clomiphene, but given the suppressive effects of the latter at the pituitary, I later decided it wiser to continue running tamoxifen as long as the clomiphene.
The addition of spironolactone is one of personal choice. It is a systemic anti-androgen that will reduce androgen-related negative feedback. Lack of androgens may also increase a loss of muscle tissue however, so whether or not you run it and for how long I leave up to you. I can only offer you personal findings, no studies. But in my experience the use of spironolactone during the first two weeks of clomiphene treatment offered a significant advantage in the amount of recovery post-cycle without any significant amount of muscle loss. But since I have no actual verifiable data on this, I will not attempt to push this too hard. The use of clomiphene alone should already aid in this by increase SHBG.
The use of HCG and the things you need to know
Human Chorionic Gonadotrophin acts as an LH analogue. That means it plays no active role in increasing hypothalamic or pituitary activity after suppression, but that it will act on LH receptors such as in the Leydig cells and activate the process of natural manufacture of testosterone and estrogen in the testes. This may counter or help quicker recovery of any testicular atrophy that may have occurred during a cycle, and since it increases the capacity to produce natural hormones, will also in the end speed up recovery because the response to increase LH will be greater.
What you do need to realize is that because it acts as LH, high doses of lengthy use will decrease receptor affinity for LH and increase negative feedback, thus countering the purpose of the post-cycle. For that reason it is not used during, but rather after the cycle, and intermittent rather than continually. Since it will also increase estrogen directly and via aromatase conversion, further shutdown may be created but this should in large part be covered by your co-administration of Tamoxifen and Clomiphene. Because of its inhibitory effects on the hypothalamic-pituitary axis, we will use it during the last part of the cycle and the weeks following, when the steroids have not yet cleared our body. And cease use several weeks prior to cessation of the Clomiphene/Tamoxifen combo so as not to let it interfere with our recovery at the hypothalamus and pituitary.
I should also inform you that practical experience has taught me that while most people respond better to the intermittent administration as described above, some have responded better to more frequent administration (ed to every three days).
Ephedrine and the point of beta-adrenergic stimulation
I have been referring to the beta-adrenergic system all throughout this article and I know a lot of you are dying to find out what the hell I?m talking about. Most of you who know the term beta-adrenergic have heard in relation to certain fat loss supplements. And that will be a key part of what we discuss here. But beta-adrenergic stimulation offers both catabolic benefits (lipolysis in adipocytes) and anabolic benefits (increased protein synthesis in muscle tissue). Naturally our high calorie diet will prohibit us from losing a great deal of fat and in most cases we may not lose any. But if we can prevent adding fat, the consequent increase in lean muscle tissue will lower our body-fat percentage favourably.
I will explain the mechanism of the beta-adrenergic system in a minute, but first we need to understand that we have beta-adrenoreceptors on fat cells, that will initiate the release of fatty acids for oxidation (fat loss) and that we also have them on muscle cells, where they will increase protein synthesis (20). That means muscular hypertrophy will be greater with adequate caloric intake while restricting fat loss. The combination should result in a lower body-fat percentage since lean body mass will increase and fat storage remains status quo.
The beta-adrenergic system in a nutshell
Imagine the end of a nerve, then a space and then a fat cell (adipocyte). The space between the nerve and the adipocyte is called the synapse or the synaptic space. The nerve stimulates the adipocyte via electrical charges (ion streams) or neurotransmitters. Among the neurotransmitters is a hormone called noradrenaline (NA). When NA is released into the synapse, it has several receptors it can bind to on the adipocyte. They are classified into two categories, alpha and beta. The alpha receptors will inhibit fat loss (or protein synthesis in the muscle cell) while the beta receptors will increase fat loss (or protein synthesis in the muscle cell).
When a beta-receptor is engaged it will release a stimulatory G-protein into the cell, the alpha variation will release an inhibitory G-protein into the cell. These proteins will activate or deactivate the enzyme adenylate cyclase which splits ATP molecules into cyclic AMP (cAMP) molecules. cAMP is what we call the second messenger, the transporter of the signal in the cell. Without cAMP stimulation would not occur. cAMP activates the catalytic subunit of protein Kinase A, which activates Hormone sensitive Lipase (HSL) by phosphorylating it to HSL-P. HSL-P in turn will initiate a three step process by which it removes fatty acids that are bound to an alcohol function (normal storage of fat is triacylglycerides). These free fatty acids can be transported outside the cell by certain proteins and then used as fuel for the body, completing the oxidation of fat.
In muscle cells the process is similar, with stimulation, cAMP etc, but will obviously differ in the last few steps, leading to protein synthesis.
Beta agonists and the diet : losing fat AND gaining muscle ?
The main regulator of the system is insulin , which has the exact opposite effect as noradrenaline. So obviously we will have to keep insulin under control as much as possible. That will allow us to use the beta-adrenergic system to its maximum potential. Now noradrenaline has been touted as anti-catabolic, but this effect is observed because it causes protein synthesis and thus less protein is released from the cell to be burned. The effect is in other words anabolic . Which is why it may serve us as far as increasing lean muscle mass, especially since we have demonstrated effectively that testosterone and most likely boldenone will upregulate beta-adrenoreceptors. By using beta stimulators later in the cycle and post-cycle (provided adequate calories in diet) we can insure maximum muscle gain and muscle maintenance post-cycle, while keeping the fat off.
Because we need to eat a certain amount of calories to grow it is unrealistic to expect a great deal of fat loss capacity from the use of these products. But it should go a long distance in preventing the addition of further fat mass, which, combined with a significant increase in lean body mass, will decrease body-fat percentage. However, some fat loss is not unthinkable, since we are eating a high protein diet and the body will prefer the available free fatty acids, especially if we can bring them into circulation.
Ephedrine Hcl
Our first goal in this endeavour should be to have a product that stimulates noradrenaline. Now some may think it is wiser to opt for other methods of fat loss, but DNP , T3 and corticosteroids will make it increasingly difficult to preserve lean mass. Other still may profer that the use of stronger specific beta-2 or beta-3 agonists like clenbuterol , salbutamol, albuterol or octopamine should be used, but because of their potency they will quickly render the beta-adrenrgic system useless, and only make use of part of the available systems to us (either beta-2 or beta-3 instead of both). The beta-2 receptor is most certainly the prime mobilizer here, where the beta-3 only has minimal if any activity, but has been deemed crucial to continuation of cathecholamine responses under sustained sympathetic activity (21). Most likely it maintains a certain amount of beta-adrenergic stimulation, but without increasing metabolism, so as to spare calories but continue the use of fatty acids for survival. As much as 40% of the activity of ephedrine has been attributed to the beta-3 stimulatory effects (22).
Since ephedrine acts by increasing natural noradrenaline release, it serves our purpose the best. It is also the more natural approach and less taxing on our system than some other fat loss preparations (T3 causes rebound by TSH shutdown, clenbuterol is very strong in increasing heart rate, and the list goes on). As opposed to more specific beta-2 agonists such as the likes of clenbuterol, ephedrine actually seems to have improved effects on thermogenisis after continual use (23). Ephedrine Hcl is our best choice here, although some will no doubt opt for standardized preparations using ma huang. This herb, depending on preparation will contain more or less than the actual 8% ephedra from dose to dose and is hence unreliable. If this is the only thing available to you, it is better than nothing however, but pure ephedrine Hcl should be preferred.
Yohimbine Hcl
Yohimbine is quite critical in the equation. It acts as a potent alpha-adrenoreceptor blocker (strong on alpha2, mild on alpha1). The alpha receptors inhibit adenylate cyclase activity in the cell, increase its breakdown and thus prohibit fat loss. In normal people with normal diets, there is a certain level of adrenergic action. But noradrenaline seems to have greater affinity for alpha receptors, so not enough beta receptors get filled to cause fat loss / protein synthesis. By increasing the noradrenaline release we have already filled all alpha receptors and a greater number of beta-receptors. But if we could block the alpha receptors, then that would lead not only to more potency from the existing noradrenaline / beta-latches, but it would create MORE noradrenaline / beta-latches since less NA is taken up by the alpha receptors. Thus a major strike in the right direction.
A second factor we need to consider is the alpha-2 receptor concentration on our nerve as well, which, when activated, will increase the re-uptake of noradrenaline into the nerve. By blocking this receptor we prevent re-uptake and again, more NA is available to us. So yohimbine interferes with the NA?s auto-regulated negative feedback loop by acting as an alpha receptor antagonist, pre-synaptic and post-synaptic.
This is also very crucial in fat loss or prevention of fat gain in predisposed areas (abdomen and obliques in men, gluteo-femoral region in women), because these area?s have adipocytes that are extremely rich in alpha receptors, but rather poor in beta receptors (ever tried getting rid of those love handles ?).
Caffeine
Apart from the well-documented findings that the combination of ephedrine and caffeine far outperformed either alone (24) in terms of lipolysis, caffeine acts very distinctly as a phospho-diesterase inhibitor. PDE?s are released in the cell as a response to continual beta-adrenergic stimulation and commences the breakdown of cAMP and creates adenosine from it. Adenosine travels outside the cell and has its own receptor, that acts very similarly to the alpha-receptor to block adenylate cyclase activity and stop fat loss. Caffeine has also been shown to prevent this process by blocking the adenosine receptor and seems to offer some benefit in preventing noradrenaline reuptake (25), like yohimbine does. Possibly via the same mechanism (adenosine receptor blockade).
Caffeine also decreases insulin sensitivity, further helping to assure maximal aid in preserving and enhancing the beta-adrenergic system, and possibly helping to prevent wrong doing from eventual lapses in our diet.
Lastly caffeine is a potent diuretic and will reduce water retention in the body, offering us a leaner and more striated appearance.
Statistics: Posted by nextlevel — Mon Apr 14, 2014 3:34 pm