While injecting Testosterone increases protein synthesis by roughly 50 times, depending on dose and time, most bodybuilders forget that it will reduce collagen synthesis by more than 50% — more like 80%, giving you the collagen synthesis rate of a senior citizen. Since collagen makes up tendons, bros are very prone to injury if they continue to lift very heavy, unless they cycle off Testosterone and let their collagen synthesis get back to normal. It’s like having the skeletal muscle of a gorilla with the tendons of a very old man.
Winstrol increases collagen synthesis. It will give you bigger tendons. However, your body compensates for this by making them more brittle, weaker, and more prone to injury. I can’t tell you how many bros work out anaerobically and become injured while on winstrol. Guys who lift in the 1-5 rep range while on winstrol, to baseball players who sprint all out from a stationary position — winstrol should be the LAST drug they choose. Most of them like winstrol because they don’t get the weight gain from it but it is very detrimental to bros who train for any sport anaerobically. Tendons tear easily on it.
Also, the drugs I mention increase collagen synthesis while also increasing collagen cross-linking integrity, making for a much stronger tendon.
Winstrol, on the other hand, will dramatically increase collagen syn, but ironically it decreases collagen cross-linking integrity, thus making a much weaker tendon.
You can plan a cycle of anabolic steroids which will increase collagen synthesis and skeletal muscle growth at the same time. The key is the drug(s) you choose.
Deca, Equipoise, Anavar, and Primobolan will ALL increase skeletal muscle while at the same time dramatically increase collagen syn and bone mass and density, leaving you with a substantially reduced chance of becoming injured than if you choose to use anabolic steroids like Sustanon, Cypionate, or Enanthate.
While Testosterone will increase bone mass and density, even at supra-physiological levels, the result is weaker tendons due to inhibition of collagen syn.
To plan a cycle where the goal is to increase skeletal muscle mass/strength while at the same time increase joint/tendon/ligament strength, enough to keep up with the dramatic increase in skeletal muscle, you must choose drugs like Equipoise, Deca, Anavar, or Primo as the base of your cycle. Testosterone and its esters can be added to your cycle to keep levels within a ‘normal’ physiological range (ie, 100-200 mg/wk) but must not go above this. Since drugs like Equipoise, Deca, Anavar and Primo will reduce endogenous, natural levels of test, these levels may be maintained with exogenous test in the 100-200 mg/wk range. Test at this dose will not inhibit collagen syn, but paradoxically, will help increase it. It is when exogenous testosterone is used > 200 mg/wk that collagen syn is inhibited.
Deca at 3 mg/kg a week(about 270 mg/wk for a 200 lb male) will increase procollagen III levels by 270% by week 2. Procollagen III is a primary indicator used to determine the rate of collagen syn. As you can see, deca is a very good drug at giving you everything you want — an increase in collagen syn, an increase in skeletal muscle, and increases in bone mass and density. The one thing it does not give you is wood.
Primobolan, at 5 mg/kg, will increase collagen synthesis by roughly 180% — less than Deca and Equipoise but still substantial.
Equipoise at 3 mg/kg will increase procollagen III by approximately 340% — slightly better than Deca.
Oxandrolone has over a hundred studies documenting its effectiveness at treating patients needing rapid increases in collagen syn to enhance healing.
These drugs have longer half-lives than most other anabolic steroids, so this should be considered when timing your post cycle clomid use. Here they are:
Deca: 15 days
Equipoise: 14 days
Primobolan: 10.5 days
Anavar has a half-life of only 8 hours so it should not pose a problem.
GH is probably the most remarkable drug at increasing collagen synthesis. It increases collagen syn in a dose dependant manner — the more you use, the more you will increase collagen syn. It has also demonstrated this ability in short and long term studies. From what I’ve read, hGH at 6 iu/day increased the collagen deposition rate by around 250% in damaged collagen structures. This result indicates that the increased biomechanical strength of wounds to collagen structures treated with biosynthetic human growth hormone was produced by an increased deposition of collagen in the collagen structures.
Equipoise, Primo, Anavar, and Deca are all good — they increase several biomakers of collagen syn — ie, type III, II, I, procollagen markers. GH just seems to do so most dramatically.
Use of any of these drugs at supra-physiological levels with a maintenance dose of test will increase collagen syn while at the same time increase skeletal muscle mass. Skeletal muscle mass gains will not be as dramatic as with large testosterone doses but you have to weigh the risk/reward basis for yourself. Also, these drugs do not satisfy the libido like testosterone, but that is not the point of this thread. It is only to demonstrate that you can increase skeletal muscle and collagen syn at the same time with certain anabolic steroids
Clenbuterol (Clen) is a beta-2 agonist/antagonist bronchodialator. What this means, is that it stimulates your beta-2 receptors. And this in turn stimulates you (Clenbuterol has stimulant effects which will make you feel….well…stimulated). All of this serves to increase your body temperature a bit, increase your basal metabolic rate, and decrease your appetite. Clenbuterol also can decrease insulin sensitivity.
Clenbuterol is a very effective repartitioning agent, and this is what it’s most often used for. What this means is that it will increase your ratio of Fat Free Mass (FFM) to Fat Mass, by decreasing your Fat and possibly increasing your FFM. Want me to quantify that a bit? In one study, horses given a reasonable dose of Clenbuterol (slightly over 1mcg/lb) and excercised for 20mins, 3x a week had significant decreases in %fat (-17.6%) and fat mass (-19.5%) at week 2, which was similar to Clenbuterol given to horses who didn’t excretes; however, the exercised group had a different FFM response, which significantly increased (+4.4%) at week 6. Week 6! Clenbuterol and Clenbuterol + exercise produce roughly the same results for the first 2 weeks! Remember the old 2 weeks-on/2weeks-off schedule? It’s officially dead and buried. If you want the quasi-anabolic effect from the Clenbuterol, it’ll take more than 2weeks on (6 weeks apparently). And in fact, since Clenbuterol alone is similar to Clenbuterol + exercise for those first 2 weeks…why would you ever use a 2on/2off protocol? Keep in mind that animal responses to beta-agonist/antagonists differ a bit from ours…but you get the picture. 2on/2off? Ha ha…
Clenbuterol has a biphastic elimination, which means that it is technically reduced in your body in 2 different stages. This isn’t particularly important, as a recent study has shown that for most intents and purposes, clen concentrations in the body decline with a ½ life (approximately) equivalent to 7-9.2 hours and again up to as much as 35 hours later. If you’re really interested, though, Clenbuterol technically declines biphastically at 10 and then 36 hours. But really, in our little world, where we use ½ life to tell us when to take our next dose, who the hell is going to take Clenbuterol, then a dose 10 hours later, then a dose 36 hours later. We’ll stick with the earlier 7-9 hour ½ life for dosing purposes, and take our Clenbuterol every 3.5-4.5 hours that we’re awake, stopping early enough to still be able to get to bed. Clenbuterol can, in some people, cause insomnia (and as with all stimulants, can cause anxiety in some).
Clenbuterol can also cause a down-regulation in testicular androgen receptors and in pulmonary, cardiac and central nervous system beta-adrenergic receptors…possibly making steroids less effective while you are on Clenbuterol, but definitely making clen less effective as time goes on and you keep taking it. To counteract this, you can take some ketotifen or periactim every 3rd or 4th week that you remain on Clenbuterol. Both of these are prescription anti-histimines, so they’ll make you drowsy (take before bedtime). Basically, the way both of these work is to reduce beta-2 receptor activity.
A lot of people claim that Clenbuterol is quite anti-catabolic and/or anabolic. This hasn’t been confirmed in human studies. And the doses given to the animals in these studies where Clenbuterol is shown to be very anti catabolic or highly anabolic are so absurdly high that no human could ever take them (1mg/kg of bodyweight and higher).
Oh yeah…I guess I should get around to the proper dosing of Clenbuterol. My recommendations are the same for both men and women. You’ll need to take 20mcgs upon rising, and then repeat that same dose again later in the day, and then once again in that day (if you find you can tolerate the effects). So you’ll start with 20mcgs, and then repeat that dose 2 more times that same day if you can tolerate it (side effects will determine this…hand shaking, sweating, etc…classic stimulant sides). Then you can start increasing the dose gradually. Personally, I wouldn’t work my way up to more than 200mcg/day. 60-120mcg/day is an average dose.
Also, bear in mind that Clenbuterol isn’t great for your heart, and can cause some issues there (enlargement of ventricles, etc…) but most studies showing Clenbuterol to cause heart problems are with animals, and even though the dosing is similar to what humans take (in some studies) it’s important to remember that animals have more beta-2 receptors and they cause certain event chains that humans’ beta-2 receptors may not. Clenbuterol causes cardiac hypertrophy to some degree, in some cases. Again though, many studies showing more significant heart problems are with mg dosing. We humans take Clenbuterol in mcg doses.
If we want to duplicate the “therapeutic” levels of Clenbuterol in the more conservative studies, we’d be taking just over 1mcg/lb of bodyweight. I’d suggest a bit less, though.
Performance issues with Clenbuterol also vary. Some studies show reduced exercise (cardiovascular) performance with Clenbuterol, while some show that clen can alleviate exercise induced asthma. Sometimes you feel like a nut…sometimes you don’t, I guess. What this means, to me, is that you’ll need to figure out how Clenbuterol affects your performance individually.
Which brings me to the issue of cramps while on clen. I don’t get them. My friends don’t get them. Most of us are athletes who use Clenbuterol during the season as well as the off season, and one of my friends even claims that it gives him more “wind” (cardiovascular stamina). Take on enough water every day and you should be fine. If you’re really concerned, you can take some extra minerals and taurine, since Clenbuterol depletes taurine as do most if not all beta-agonists. I don’t take anything more than my usual vitamins and minerals.
Well…there it is…pretty much all I know about Clenbuterol. I hope this answers some questions and clears up some misconceptions.
It has been well-established that gains in muscular hypertrophy are best when multiple sets are utilized in conjunction with high-intensity. The only problem when doing high volume is that with each set, the number of reps performed usually goes down. For example, powerlifters - give them anything less than a five-minute rest period, and they are dying. In an earlier study that examined bodybuilders compared to powerlifters after a high-intensity bodybuilding protocol, many of the powerlifters felt nauseous, wanted to puke, and were lightheaded, because it was not how they typically trained. The bodybuilders demonstrated greater fatigue resistance because of metabolic muscle adaptations associated with the bodybuilding style of training (e.g., moderate-to-high-rep sets, with shorter rest intervals). These adaptations may have included development of the fast glycolytic energy system, with higher activities of anaerobic enzymes (e.g., phosphorylase, phosphofructokinase, and lactate dehydrogenase), thus delaying lactate accumulation.
Previous research has demonstrated significant reductions in repetition performance when 1 minute or less is utilized between sets. Squats are definitely the worst in my personal opinion; I remember many days almost puking after doing multiple sets of squats, trying to maintain a set repetition criteria. In a previous study, researchers examined repetition performance for the back squat over 4 sets with a constant 8-rep maximum (8RM) load and 1-minute rest intervals between sets. Subjects performed 7.9 % reps on the first set, followed by 5.9 %, 4.5 %, and 4.2 % reps on the second, third, and fourth sets, respectively.
With each set of squats, they were not able to maintain the work capacity with a minute rest period. Another study examined bench press load reductions over 5 sets of the bench press exercise when performed at two different intensities (i.e., 10RM and 5RM) and with five different rest intervals between sets (i.e., 30 seconds, 1, 2, 3, 5 minutes). Load reductions of 2.3 to 6.9 kg were instituted when necessary to maintain repetition performance.
The findings demonstrated that, irrespective of the intensity, the load significantly decreased with each set in succession, when resting 30 seconds or 1 minute between sets. So if you have to drop the weight, what is the correct amount to drop by?
Drop sets are a common tool used by bodybuilders to stimulate muscle growth and are especially utilized during the pre-competition phase when bodybuilders are trying to by maintaining a high intensity workout. In bodybuilding and weight training, using drop sets is a technique for continuing an exercise with a lower weight once muscle failure has been achieved at a higher weight. Other names for drop sets include breakdowns, descending sets, down the rack or strip sets. Whatever you want to call them, they are painful… but the results are nothing short of astounding— if you can bear the pain.
One thought I have always wondered was how do you know what weight to drop down to? Some people, when they do drop sets may drop the pin one slot down, while others drop the pin maybe five or six notches down. So if you are doing let’s say 5 sets of 10 with 405 on squats with 1-minute rest periods, how much do you have to drop the weight to maintain 10 reps? Researchers from Eastern Illinois University set out to determine what was the exact drop in weight that had to occur in order to maintain repetition volume during leg training.
The researchers had the subjects go to the lab and perform a set of squats to determine their 10-rep maximum on squats. The subjects in the study came back for four different experiments:
- Constant load for all sets.
- 5 percent load reduction after each set
- 10 percent load reduction after each set
- 15 percent load reduction after each set
The subjects performed the following leg exercises: back squats, leg curls, and leg extensions. The subjects were allowed 1-minute rest between sets and 2 minutes rest between exercises. The subjects rated their fatigue levels after each set as well.
The 15 Percent Rule
The researchers found that if you want to maintain the same amount of reps for back squat for a given workload with 1 minute rest periods between sets, a 15 % reduction in weight was needed after each set, to maintain 10 reps in both the back squat and leg curl.
Interestingly, despite the fact that leg extensions were performed last, there was no need to drop the weight after leg extensions, as subjects demonstrated greater fatigue resistance for the leg extensions than for back squats and leg curls. So you may be asking how come there was not a decline in strength for the leg extensions when the squats predominantly utilize quadriceps?
The researchers hypothesized that since squats exhaust multiple body parts, (i.e., legs, lower back, abs, quadriceps) the lower back or abs could have fatigued to the point where the subjects could not squat further, which caused them to stop before the point in which the quadriceps were fully fatigued. So if you are squatting with 405 for 10 reps, the load needs to be dropped by 15 % per set to maintain the workout per set.
After training this way for several weeks, you may notice that the amount of weight will be less as your anaerobic enzymes increase in your body as you develop a higher lactate threshold, but for those just trying this routine, 15 % seems to be the starting number. No more randomly dropping the pin between sets, now that you have a starting reference point.
Your thyroid gland secretes two hormones that are going to be of primary importance in understanding Thyroid/GH interaction. The first is thyroxine (T4) and the second is triiodothyronine (T3). T3 is frequently considered the physiologically active hormone, and consequently the one on which most athletes and bodybuilders focus their energies on. T4, on the other hand, is converted in peripheral tissue into T3 by the enzymes in the deiodinase group, of which there are three types- the three iodothyronine deiodinase either catalyze the initiation (D1, D2) or termination (D3) of thyroid hormone effects. The majority of the body’s T3 (about 80%) comes from this conversion via the first two types of deiodinase, while conversion to an inactive state is accomplished by the third type.
It’s important to note that not all of the body’s T4 is converted to T3, however- some remains unconverted. The secretion of T4 is under the control of Thyroid Stimulating Hormone (TSH) which is produced by the pituitary gland. TSH secretion is in turn controlled through release of Thyrotropin Releasing Hormone which is produced in your hypothalamus. So, when T3 levels go up, TSH secretion is suppressed, due to the body’s self regulatory system known as the “negative feedback loop” . This is also the mechanism whereby exogenous thyroid hormone suppresses natural thyroid hormone production. However, it should be noted that thyroid stimulating hormone (like all other hormones) can not work in a vacuum. TSH also requires the presence of Insulin or Insulin-like Growth Factor to stimulate thyroid function. When thyroid hormone is present without either insulin or IGF-1, it has no physiological effect.
Most people think that T3 is just a physiologically active hormone that regulates bodyfat setpoint and has some minor anabolic effects, but in actuality, in some cases of delayed growth in children, T3 is actually too low, while GH levels are normal, and this has a growth limiting effect on several tissues. This could be due to T3’s ability to stimulate the proliferation of IGF-1 mRNA in many tissues (which would, of course, be anabolic), or it could be due to the synergistic effect T3 has on GH, specifically on regulation of the growth hormone gene. Although it is largely overlooked in the world of performance enhancement, regulation of the growth hormone response is predominantly determined by positive control of growth hormone gene transcription which is proportional to the concentration of thyroid hormone-receptor complexes, which are influenced by T3 levels.
Your body’s GH is regulated by many internal factors, such as hormones and enzymes. hormones. A change in the level of your body’s GH output begins in the hypothalamus with somatostatin (SS) and growth hormone-releasing hormone (GHRH). Somatostatin exerts its effect at the pituitary to decrease GH output, while GHRH acts at the pituitary to increase GH output. Together these hormones regulate the level of GH you have in your body. In many cases, GH deficiency presents with a low level of T3, and normal T4. This is of course because conversion of T4-T3 is partially dependant on GH (and to some degree GH stimulated IGF-1), and it’s ability to stimulate that conversion process of T4 into T3.
Interestingly, the hypothalamus isn’t the only place where SS is contained; the thyroid gland also contains Somatostatin-producing cells. This is of interest to us, because in the case of the thyroid, it’s been noted that certain hormones which were previously thought only to govern GH secretion can also influence thyroid hormone output as well. SS can directly act to inhibit TSH secretion or it may act on the hypothalamus to inhibit TRHsecretion. So when you add GH into your body from an outside source, you are triggering the body into releasing SS, because your body no longer needs to produce its own supply of GH…and unfortunately, the release of SS can also inhibit TSH, and therefore limit the amount of T4 your body produces.But that’s not the only interaction we see between the thyroid and Growth Hormone.
As we learned in high-school Biology class, the body likes to maintain homeostasis, or “normal” operating conditions. This is the body’s version of the status quo, and it fights like hell to maintain the comfort of the status quo (much like moderators on most steroid discussion boards). What we see with thyroid/GH interplay is that physiological levels of circulating thyroid hormones are necessary to maintain normal pituitary GH secretion, due to their directly stimulatory actions. However, when serum concentrations of thyroid hormone increase above the normal range we see an increase in hypothalamic somatostatin action, which suppresses pituitary GH secretion and overrides any stimulatory effects that the thyroid hormone may have had on GH. The suppression of GH secretion by thyroid hormones is probably mediated at the hypothalamic level by a decrease in GHRH release.
In addition, as IGF-I production isincreased in the hypothalamus after T3 administration and T3 may participate in IGF-1 mediated negative feedback of GH by triggeringeither increased somatostatin tone and/or decreased GHRH production. IGF, interestingly, has the ability to mediate some of T3’s effects independent of GH, but not to the same degree GH can. In fact, IGF-I production isincreased in the hypothalamus after T3, administration it may plausibly participate in negative feedback by triggeringeither increased somatostatin tone and/or decreasedGHRHproduction. So we know that GH lowers T4 (more about this in a sec), but an increase in T3 upregulates GH receptors as well as IGF-1 receptors.
As can be previously stated, and due to the ability of GH to convert inactive T4 into active T3, GH administration in healthy athletes shows us an entirely predicatble increase in mean free T3 (fT3), and a decrease in mean free T4 (fT4)levels.
Heavy steroid using athletes, particularly weight lifters, bodybuilders, football players, hockey players, shotputters etc., are subject to many adverse consequences from continuous steroid use without a break. Adverse cardiovascular effects, liver stress, HPTA downregulation, excessive virilization (women) and psychological disturbances or dependency, are some of the major problems that may develop in these individuals. Additionally, users may develop a tolerance for anabolic steroids that can only be overcome by increasing the dosage or by ceasing the use altogether. The latter, of course, is a much healthier course of action than the former.
Coming off of steroids, particularly long-term usage, is certainly not easily done without considerable loss of muscle mass. Additionally, there can be psychological effects that include depression and loss of motivation. For many athletes, especially those with schedules that do not allow prolonged periods away from competition completely coming off of steroids is not considered an option. However, if these athletes knew how to take the right approach they just might be able to cycle off and have a good chance at maintaining much of their physical condition. This could enable them to increase their ultimate potential in their sports as well as their longevity in the competitive arena.
The off cycle regimen must consist of proper drug, nutritional, and training protocols. The primary goals to achieve are the following:
- Minimization of protein catabolism
- Maintenance of muscle glycogen levels
- Maintenance of high-normal red blood cell levels
- Minimization of fat deposition
- Avoidance of injury, or injury aggravation
- Maintenance of healthy attitude and psychological state
This is an off steroids cycle and most certainly not an off drugs cycle. In fact, the proper use of non-steroidal drugs is the mainstay of this program and is vital to its success. I will describe the drugs to be used, why they are used, and how they should be used.
GH is probably the single most important drug to maintain muscle mass and bodyweight off of steroids. While GH is not known to be great for anabolic effects, it is very effective for anti-catabolism. Anti-catabolism, or minimization of muscle mass loss, is after all what we are most interested in here. GH has an overall anti-proteolytic effect on the body and shifts the body’s metabolism away from the utilization of amino acids and glucose for energy, and towards the use of fat. The end result will be a protective effect upon muscle protein and glycogen, and a mobilizing effect upon body fat.
Many bodybuilders have discovered how wonderful GH, at the proper dosages, is in maintaining their muscle mass off of steroids. Former IFBB pro Gary Strydom once commented that he didn’t care if the IFBB tested for steroids, as long as they didn’t test for GH.
Notice how I said “at the proper dosages”. That’s right, small dosages just won’t cut it. For most people a minimum of 4 i.u. a day is required to impart a proper ********* response in the body. Some may go as high as 18 i.u. a day but at this levels many problems can occur (i.e. edema, nerve impingement).
There probably is no great advantage to taking GH more than once a day, though some may inject twice a day. GH primarily works through its conversion to IGF-1 and the half-life of IGF-1 in the body is plenty long (8-16 hours). So once a day administration will be good enough to maintain pretty constant levels of IGF-1 in the blood. Furthermore, evidence is also mounting that GH breaks down to certain active peptide fragments with specific biological functions (i.e. lipolysis) and that these have prolonged half lives. Therefore, the active lifetime of the intact GH molecule itself in the blood might be pretty irrelevant.
GH is not cheap through most channels. However, good GH can be obtained from Asia at a fraction of the cost (10 – 20%) that it is available elsewhere.
I think I should also mention now that there is a big misconception amongst people as to what the shelf life of GH is, and that most people grossly underestimate it. To freeze dried GH products (unreconstituted) are quite stable under refrigerated conditions, and a 24-month shelf-life is typical at this temperature. Also, although solutions of GH at neutral pH readily deamidate (lose ammonia group from end of molecule), and storage of the reconstituted product is limited to a few weeks under refrigerated conditions, biological activity is relatively unaffected even after prolonged storage. So the stuff really stays pretty active in the ‘frig for a considerable time. By the way, reconstituted solutions of GH should NEVER be frozen (this will be the death of it).
Boldenone is a popular anabolic steroid, manufactured as Boldenone Undecylenate in several veterinary drug. Structurally Boldenone (1,4-androstadiene-3-one,17b-ol) is a close derivative of testosterone (4-androstene-3-one,17b-ol), differing from this androgen only by the addition of a second double bond in the A-ring of the structure (between carbons one and two). Likewise its direct precursor 1,4-androstadienedione differs from testosterone’s direct precursor 4-androstenedione only by this same alteration, and converts to active form via the same widely distributed body enzyme (17-beta hydroxysteroid dehydrogenase, which interconverts these hormones between inactive 17-keto and active 17-beta hydroxy form). Although similar in structure, boldenone’s second double carbon bond creates a hormone with activity that differs from testosterone in a number of significant ways.
Rate of Aromatization
One such difference is manifest in the rate in which this compound will aromatize (convert to an estrogen). Upon incubation with human placental microsomal aromatase (a standard assay for aromatase activity), the ability of 1,4-androstadienedione to aromatize to estrogenic form appears to be roughly half that of androstenedione. An equal activity level is present with our active target hormones Boldenone and Testosterone, as our active 17beta hydroxyl group will not to alter aromatase activity toward the substrate (as is noted by the equal rates of aromatization between androstenedione and testosterone). As testosterone is the primary substrate for the synthesis of estradiol in men, cutting this ability in half amounts to quite a considerable reduction in the estrogenic activity of our 1,4-androstadien hormones. It is for this reason boldenone is usually not associated with estrogen related side effects such as gynecomastia, obvious subcutaneous water retention and enhanced fat deposition, and athletes likewise consider it to be more of a steroid to promote lean muscular growth than raw bulk.
5-alpha Reduction of Boldenone
Boldenone also differs from testosterone in its ability to interact with the 5-alpha reductase enzyme. This is the enzyme responsible for forming dihydrotestosterone from testosterone, which is a much more potent activator of the androgen receptor. The 5AR enzyme is predominantly found in androgen target tissues such as the skin, scalp, prostate, pituitary, hypothalamus, and other regions of the central nervous system, and as such causes a notable increase in the androgenic potency of testosterone in these tissues. Although the 5-alpha reduction of boldenone (to dihydroboldenone) also results in the formation a more potent androgen, the C1-2 double bond on this hormone almost completely inhibits such interaction in the human body. Dihydroboldenone is likewise produced in small amounts at best in humans, allowing this hormone to be much less androgenic in nature compared to testosterone. On the plus side we see why athletes using boldenone injectables usually find them much more tolerable in terms of not promoting androgenic side effects such as acne, body/facial hair growth and hair loss. On the minus, of course we pay for reduced androgenic potency in terms of expected strength and mass gains (androgens are known to support neuromuscular functioning and development), which will be lower (though probably of higher quality) compared to that achieved with testosterone.
Comparative effectiveness of Nandrolone and Boldenone
The closest steroid in appearance (obvious effect to the user) to Boldenone would probably be Nandrolone. Most athletes use these two drugs under similar conditions, typically when there is a need for lean muscle tissue gain or a drug with fewer side effects in general. For these purposes both are well suited, however there are still some noticeable variances in the effects of both hormones. For example, at promoting overall muscle and strength gains Boldenone is often proported to be more effective than Nandrolone. This may be because Boldenone is somewhat more androgenic in nature than Nandrolone, due to the fact that it goes primarily unaltered by the 5-alpha reductase enzyme whereas Nandrolone is actually reduced to less active form (dihydronandrolone). While this allows Nandrolone to be slightly milder in terms of side effects (except for interfering with libido, which can be much stronger with Nandrolone as it is too weak an androgen), the lack of strong activity in crucial areas of the central nervous system may also act to lessen its effectiveness as a muscle and strength promoting anabolic. As Boldenone is almost fully resistant to 5-alpha reductase, it retains an equal level of potency in both muscle and androgen target tissues.
We also see that in their respective rates of estrogen conversion both Nandrolone and Boldenone are similar in that they aromatize much more slowly than does testosterone. That is not to say that are equally resistant to this process however. In fact we see than Nandrolone actually converts to estrogen at an even lower rate than Boldenone does. One might automatically think that this is a more beneficial trait, however this would be assuming estrogen serves us no purpose in terms of muscle growth. Indeed this would be ignoring quite a bit of evidence showing just the opposite. For example, we find Primobolan (methenolone, a non-aromatizable steroid) and nandrolone activate the androgen receptor with near equal affinity, and more avidly than does testosterone. Yet we know that testosterone is more effective at building muscle size. Were 5-alpha reductase the only cause for this disparity, we would think methenolone would be a similarly or more potent steroid than nandrolone, as it is more androgenic (due to the fact that similar to boldenone, methenolone remains unaltered in the presence of the 5-AR enzyme).
But Primobolan is notably weaker as an anabolic compared to Nandrolone, making one question if its inability to convert to estrogen is also a key factor mediating its ability to promote growth. We see an interesting trend here. Testosterone (easily aromatized and the least effective AR agonist of the group) is the most potent muscle builder, whereas nandrolone (weakly aromatized, strong AR agonist) is thought to be roughly half as effective. Methenolone (not aromatizable at all, AR agonist potency near equal to nandrolone) is further known to possess even lower anabolic potency next to nandrolone, to spite its near equal effectiveness at the level of the androgen receptor.
We do know a couple of important things about estrogen and muscle growth. This first is that its sodium and water retaining effects of estrogen can greatly enhance the size of muscle tissue. The bulk you see from highly estrogenic steroids is in large part due to intercellular and intracellular water retention, and makes agents like testosterone, Dianabol and Anadrol rapidly acting agents. We also know that the conversion of androgens to estrogens is responsible for enhancing glucose-6-phosphate-dehydrogenase enzyme levels in muscle tissue. G6PD is an important regulator of glucose utilization, and plays a vital role in muscle growth and recuperation. Clearly the athlete today knows that if you want to put on size, you don’t want to get away from estrogen completely. Likewise the low rate of estrogen conversion we see with boldenone may be ideal in that it allows for enough estradiol buildup to help foster muscle growth, yet it should reach a point where we see strong side effects like gynecomastia and excess fat retention.
Boldenone and Dianabol
It is also interesting to point out that boldenone is also structurally almost identical to methandrostenolone (Dianabol), barring that the latter hormone contains an added c-17alpha methyl group to allow for optimal survival during oral administration. The principal achievement with both steroids was again the C1-2 double bond, which markedly increases the ratio of anabolic to androgenic effect in each case. Athletes however usually fail to notice the relationship between these two anabolics, the two drugs varying in outward appearance so much that use of methandrostenolone is usually isolated to bulking cycles while boldenone is accepted as a mild anabolic for cutting phases. Clearly the more active estrogenic nature of methandrostenolone is the cause for such discrepancy, a trait due to the added methyl group. Although we find that c-17 alpha methylation moderately decreases the affinity of this substrate for the aromatase enzyme, the product here is a different form of estradiol (17-alpha methylestradiol). When we look at testosterone for example, we find that a 17alpha-methylated version (methyltestosterone) represents a more potent form of this hormone. This is because the methyl group does not greatly interfere with the ability of the hormone to activate the androgen receptor, however it does allow it have a lower affinity for the serum binding protein SHBG and exist in a more free and active state. Sharing use of the same binding protein (SHBG is also referred to as Testosterone-Estradiol Binding Globulin) and knowing that 17-methylestradiol is near in potency to estradiol , it seems logical to conclude that 17-methylestradiol would be similarly more active (and explain the greater estrogenic potency of drugs such as methyltestosterone, methandrostenolone and norethandrolone). The structural and characteristic similarities between these two hormones however remain evident.
High Oral Efficacy and Legal Status:
Although one might think 1,4-androstadienedione would be a synthetic hormone at first glance, it has clearly been demonstrated to occur in nature. This allows it to be is protected by the Dietary Supplement Health and Education Act (DSHEA), and legal for sale as a nutritional supplement in the U.S. To support the belief that a 1,4-androstadienedione supplement really works as an effective precursor to boldenone in humans and not just on paper, we can take note of a 1971 study in which an unusually high amount of 17beta hydroxylated metabolites (as high as 22% of the given dose) were recovered in urine after oral administration of 100mg (10). Remember that in order to become active its 17-keto group must be converted to a 17-beta hydroxyl group. In fact 7.1% and 11.1% of the given dose was actually recovered in the form of intact boldenone in the two subjects of this investigation, indicating an extremely notable capacity for this hormone to convert to active form in the human body after oral dosing. It also demonstrates the ability for the C1-2 double bond to resist 17-ketosteroid reduction, a trait far different from testosterone, which produces 17-hydroxy metabolites in much smaller amounts.
Clearly Boldenone has a firmly rooted place in the world of bodybuilding pharmaceuticals, standing out as a mild yet potent anabolic for the promotion of lean muscle tissue growth. It has likewise always been in high demand on the black market. The inclusion of a highly efficient steroidal precursor to this potent anabolic steroid in the world of legally available nutritional supplements will undoubtedly come to represent a welcome expansion in choices for the consumer.
Actually developed as a vet steroid, Equipoise has come a long way to become one of the most recommended body building steroids. This long-acting injectable anabolic is a steroid ester that is recognized by anabolic qualities and little androgenic activity. One of the best things about Equipoise is that it allows users to stay away from regular oral dosing or recurring injections since it has a lengthy active life of 14-16 days.
The molecular weight of Boldenone is 286.4132 g/mol at the base and its chemical name is 1,4-androstadiene-3-one,1 7b-ol). Its framework is similar to the natural testosterone. Also known as Boldenone Undecylenate, Equipoise is ranked very high by athletes, gym trainers, and doctors all over the world. The efficiency enhancing medication can be made a part of both a cutting cycle and a bulking cycle. Moreover, the use of this effective steroid does not lead to estrogenic adverse reactions like greasy skin and gynecomastia unless misused or of a low quality. If that was not all, top quality Equipoise can be purchased online, with or without healthcare prescription, cheaply.
Equipoise is an excellent medication for athletes who want to keep muscle mass during bulking cycle and stack it with Winstrol allows athletes drop fat and keep muscles without limiting on muscular description and durability profits. It is for these reasons that Equipoise discovers a special place among athletes owed to Major League Soccer, Australian Rules football, mixed martial arts, athletics, body building, boxing, and cycling. This very successful steroid is, generally, used to activate efficiency, endurance, aggression, and muscle mass and definition improvements moreover to help athletes restore early from extreme exercises and accidents. It is also efficient for solving bodyweight loss and enhancing appetite besides promoting the sense of well being to a significant level. Along with that, Equipoise is also beneficial to promote durability and enable greater restoration after heavy training times or classes since it stimulates the production of red blood cells by facilitating the production of erythropoietin (EPO) by the kidneys.
Mouse muscles treated with steroids (right) grow bigger than ones in undrugged animals(left). Steroids increase the number of nuclei in a muscle cell, which may help the muscle pump back up long after the steroids are gone.
Steroids may continue to boost muscle-building capacity long after a person stops taking the drugs, a new study of mice suggests. The finding could mean that athletes who cheat by taking anabolic steroids should be suspended from competition for a decade or longer. The research also suggests that building muscles in youth may have benefits that last into old age.
In the new study, researchers led by Kristian Gundersen, a physiologist at the University of Oslo, tested the effect of steroids on female mice. The team had previously shown that exercise builds new nuclei in muscle cells (SN: 9/11/10, p. 15). Nuclei are the cellular compartments where DNA is stored, and muscle cells typically have multiple nuclei. Increasing the number of nuclei gives muscles the capacity to build more proteins.
Doses of the steroid testosterone caused the mice to add nuclei to their muscles. After two weeks of steroid treatment, the muscle cells had up to 66 percent more nuclei per muscle fiber. Mice that didn’t get steroids, but had surgery that cut one muscle to make another work harder, had 51 percent more nuclei in the overworked muscle. Mice that got both steroids and surgery built 92 percent more nuclei in their uncut muscle.
The mice’s muscle cells also bulked up, but eventually shrank back to pre-steroid size after the drugs were stopped. The new nuclei didn’t go away, though, Gundersen’s team found. Steroid-treated muscles kept their ill-gotten nuclei for at least three months, which corresponds to about a decade in humans’ life span. The effect may last even longer, but the researchers did not extend the experiment to find out. When muscles were worked three months after the steroid treatment stopped, the muscle mass of animals that previously took testosterone bounced back right away, bulking up 31 percent in the first six days. Mice that never took steroids only added about 6 percent to their muscle mass during that time. “In my career it has been rare to see such clear results,” Gundersen says. “It is more dramatic than I thought it would be.”
Other researchers are also impressed with the results. “There’s no question it’s very interesting data and it’s very strong,” says Bengt Saltin, a physiologist at the University of Copenhagen. “This should be a hotter topic in muscle research and physiology,” he says. Elderly people often have trouble with muscle wasting, and the new study suggests that working out in young adulthood could help old muscles regain vigor with exercise later.
Lawrence Schwartz, a cell biologist at the University of Massachusetts Amherst, agrees. “The implication is once you have these nuclei, you never lose them.”
Both researchers also say that before antidoping agencies can decide how long cheating athletes should be barred from competition, similar research to see how long steroids exert their influence would need to be done on humans.
“I suspect the basics of muscle physiology are going to be very similar,” Schwartz says of mice and humans. But given the side effects of steroids and the difficulty of studying large samples of muscle in living people without causing harm, “I don’t see any easy, or even an ethical way of doing this in humans.”
Depending on your budget, a nice pre contest cycle will consist of various compounds, while slowly ramping down the test near the end, and increasing Trenbolone/Masterone combo alongside a nice hardening agent, like Winstrol, while dropping your water weight pre show. Use this layout as a guide; adjust where you see fit, and where permits budget. HGH and various peptides can also be used, Leave a comment below, and let me know your goals, and I will do my best to tailor any cycles to your current state, and budget.
Phase One: 8 weeks – Carb Cycle – and Re-feeds. This phase is concentrated on gaining as much muscle as you can, while keeping fat at a minimum. 3-4 HIIT Cardio Sessions Weekly.
- 1-8 Testosterone Propionate 75mg/ed
- 1-8 NPP 150mg/eod
- 1-5 Choice of Oral, I’d suggest, Dianabol
- T3 (Cytomel) Protocol
Starting at week 2
- Day 1-3 25mcg Daily
- Day 4-7 50mcg Daily
- Day 8-11 75mcg Daily
- Day 12-24 100mcg Daily
- Day 25-27 75mcg Daily
- Day 28-31 50mcg Daily
- Day 32-35 25mcg Daily End,
- Take a 20-30 day break, repeat.
You can add a bit of Clenbuterol in, but I would save that for Phase 2.
Phase 2 weeks: 12-18 – Continue Dialing in your Diet, and Increase your cardio to at least 6 Sessions of Hiit Per Week. Continue Lifting Hard, Focusing on Every Movement.
- 12-18 Testosterone Propionate 75/mg EOD
- 12-18 Trenbolone Acetate 75mg/ed
- 12-18 Masterone 100mg/ed
- 16-18 Winstrol 50mg/ed Continue
- T3 (Cytomel), Alongside 50-75mcg Clenbuterol Daily
Phase 3 Weeks: 19-22 – This is Make or Break time, Cardio is now increased to 9 Sessions Weekly, FASTED, Keep Protein Intake high, Carbs should still be cycled but cut out close to 2 -3 days before show time, I’m sure others can chime in on diet a bit further for you.
- 19-22 Drop the Propionate, and continue on your TRT Cruise Dose 200-250mg/wk
- 18-22 Trenbolone Acetate – 75/mg ED
- 19-22 Masterone 100mg/ed
- 19-21 Winstrol 100mg/ed
- T3 (Cytomel)/Clenbuterol protocol should still be running.
Of course throughout this cycle, you’re going to want a solid AI, keeping water and estro related sides away, constant blood work needs to be done. You can play with some Halotestin near the end at 40 – 50mg /ed if you like, but honestly, The Trenbolone on this re-comp is king. T3 (Cytomel) protocol is not a said in stone deal, you can run it a variety of ways that is just one way. Get a good multi, fish oil, and all protective measures ready and on hand. A liv support should be taken midpoint at the latest, alongside a well-rounded multivitamin and fish oil you’re going to find it hard to do cardio on tren, but push through it, focus each movement contracting every muscle, shaping your body.
This is just a guideline, adjust to what you know works for your body, pre comp cycles can get even more intricate than this one, but this should be a nice guide on your road to glory!
Equipoise is the popularly referenced brand name for the veterinary injectable steroid Boldenone Undecylenate. Specifically it is a derivative of testosterone, which exhibits strong anabolic and moderately androgenic properties. The undecylenate ester greatly extends the activity of the drug (the undecylenate ester is only one carbon atom longer than decanoate), so that clinically injections would need to be repeated every three or four weeks. In veterinary medicine Equipoise is most commonly used on horses, exhibiting a pronounced effect on lean bodyweight, appetite and general disposition of the animal. This compound is also said to shows a marked ability for increasing red blood cell production, although there should be no confusion that this is an effect characteristic of newly all anabolic/androgenic steroids. The favorable properties of this drug are greatly appreciated by athletes, Equipoise being a very popular injectable in recent years. It is considered by many to be a stronger, slightly more androgenic Deca Durabolin. It is generally cheaper, and could replace Deca Durabolin in most cycles without greatly changing the end result.
The side effects associated with Equipoise are generally mild. The structure of boldenone does allow it to convert into estrogen, but it does not have an extremely high affinity to do so. To try and quantify this we can look toward aromatization studies, which suggest that its rate of estrogen conversion should be roughly half that of testosterones. The tendency to develop a noticeable amount of water retention with this drug would therefore be slightly higher than that with Deca Durabolin (with an estimated 20°/a conversion), but much less than what would be expected with a stronger agent such as Testosterone. While one does still have a chance of encountering an estrogen related side effect as such when using this substance, it is not a common problem when taken at a moderate dosage level. Gynecomastia might theoretically become a concern, but is usually only heaved of with very sensitive individuals or (again) those venturing high in dosage. Should estrogenic effects become troublesome, the addition of Nolvadex and/or Proviron should of course make the cycle more tolerable. An antiaromatase such as Arimidex would be stronger options, however probably not indicated with a mild drug as such.
Equipoise can also produce distinct androgenic side effects. Incidences of oily skin, acne, increased aggression and hair loss are likewise all possible with this compound, although will typically be related to the use of higher doses. Women in fact find this drug quite comfortable, virilization symptoms usually unseen when taken at low doses. Boldenone does reduce to a more potent androgen (dihydroboldenone) via the 5alpha reductase enzyme (which produces DHT from testosterone), however its affinity for this interaction in the human body is low to nonexistent”.
Although it stays active for a much longer time, Equipoise is injected at least once per week by athletes. It is most commonly used at a dosage of 200-400 mg (4-8 ml, 50 mg version) per week for men, 50-75 mg per week for women. Should a 25 mg version be the only product available, the injection volume can become quite uncomfortable. The dosage schedule can be further divided, perhaps injections given every other day to reduce discomfort. One should also take caution to rotate injection sites regularly, so as to avoid irritation or infection. Should too large an oil volume be injected into one site, an abscess may form that requires surgical draining. To avoid such a problem, athletes will usually limit each injection to 3 ml and reuse each site no more than once per week, preferably every other week. With Equipoise this may require using not only the gluteus, but also the outer thighs for an injection site. Of course all problems associated with 25 mg and 50 mg dosed products are eliminated with the newer 100 mg and 200 mg/ml versions of this steroid, which clearly give the user much more dosage freedom and injection comfort.
Not a rapid mass builder, instead Equipoise will be looked at to provide a slow but steady gain of strength and quality muscle mass. The most positive effects of this drug are seen when it is used for longer cycles, usually lasting more than 8-10 weeks in duration. The muscle gained should not be the smooth bulk seen with androgens, but very defined and solid. Since water bloat is not contributing greatly to the diameter of the muscle, much of the size gained on a cycle of Equipoise can be retained after the drug has been discontinued. It is interesting to note that structurally Equipoise and the classic bulking drug Dianabol are almost identical. In the case of Equipoise the compound uses a l7beta ester (undecylenate), while Dianabol is 17 alpha alkylated. Aside from this the molecules are the same. Of course they act quite differently in the body, which goes to show the 17-methylation effects more than just the oral efficacy of a steroid.
As discussed earlier, Equipoise is a very versatile compound. We can create a number of drug combinations with it depending on the desired result. For mass, one may want to stack it with Anadrol 50(oxymetholone) or an injectable testosterone such as Sustanon 250. The result should be an incredible gain of muscle size and strength, without the same intensity of side effects if using the androgen (at a higher dose) alone. During a cutting phase, muscle hardness and density can be greatly improved when combining Equipoise with a non-aromatizable steroid such as Trenbolone acetate, or Winstrol Depot (Stanozolol). For some however, even the low buildup of estrogen associated with this compound is enough to relegate its use to bulking cycles only.
Equipoise is not an ideal steroid for the drug tested athlete however. This drug has the tendency to produce detectable metabolites in the urine months after use, a worry most commonly associated with Deca Durabolin. This is of course due to the high oil solubility of long chain esterified injectable steroids, a property which enables the drug to remain deposited in fatty tissues for extended periods of time. While this will reliably slow the release of steroid into the blood stream, it also allows small residual amounts to remain present in the body far after the initial injection. The release of stubborn stores of hormone would no doubt also be enhanced around contest time, a period when the athlete drastically attempts to mobilize unwanted body fat. If enough were used in the off-season, the athlete may actually fail a drug screen for boldenone although many months may have past since the drug was last injected.
The debate on the effect of anabolic steroids on the structure of the heart reached another phase, since Finnish scientists studied twenty local bodybuilders who had just finished their cycles. Anabolic steroids don’t damage the heart, the researchers found. But the combination of anabolic steroids and growth hormone does.
Context Since the eighties scientists have been discussing whether anabolic steroids enlarge the heart, when several sports investigators learned anabolic steroids use was associated with enlargement of the left ventricular mass – the part of the heart that pumps oxygenated blood through the body. An overdeveloped left ventricle causes arrhythmia and, in severe cases, death. In 2001 Australian physicians found the hypertrophy in clean strength athletes and postulated that this condition was caused by weight training, not anabolic steroids use. They also found that the hypertrophy didn’t impair their subjects’ health. The new Finnish study doesn’t contradict the Australian study. Nevertheless, it provides insight into the relationship between anabolic steroids and heart hypertrophy.
Study The Finnish ran an advertorial in a bodybuilding magazine on their project. Twenty bodybuilders, who had planned to do a cycle and bought their medication on the black market, responded. Before their cycle started the bodybuilders had their medication checked and analysed by the pharmacological department of the university. Not unnecessary, because up to fifty percent of the European black steroids may be counterfeited, according to the latest estimates. Sixteen bodybuilders used anabolic steroids only. The weekly doses varied from a few hundred milligrams to more than thousand milligrams. Four athletes stacked their anabolic steroids with HGH. All four used moderate dosages of two, three or four IU’s during four to six weeks. The HGH was injected once daily, mostly in the evening. In this group steroid doses were 1,3 times higher than in the anabolic steroids only group. When their cycles ended, the bodybuilders had their hearts examined. The table below summarizes some results. The control group consisted of fifteen young males with active life styles who didn’t engage in weight training.
Anabolic steroids and the combination of anabolic steroids and HGH change the structure of the heart, the table suggests. But that doesn’t have any consequences for the cardiovascular health of at least the anabolic steroid users. Their diastolic blood pressure – reported to rise phenomenally in some anabolic steroid related medical horror-stories – was fine, and more interestingly, their E/A ratio improved. Cardiologists use the E/A ratio to measure the hearts efficiency. According to the table, in the anabolic steroids only group deterioration of the heart muscle didn’t occur. But HGH, well, that is another story. The higher anabolic steroid doses that the HGH-users took can only explain a small part of the serious ventricular hypertrophy, the Finnish stress. They suspect that the lowering effect of androgens on the IGF-1-binding protein 3 concentrations causes the ventricular growth. Discussion So far not so good. But there is more. The Finnish discovered something very interesting about the nature of the relationship between anabolic aids and hypertrophy of the heart: it’s direct. For example, the Finnish asked their subjects for how many years they had been using anabolic steroids. The answers varied from one to twelve years. Statistically the relationship between lifetime anabolic steroids use and the E/A ratio was weak. On the other hand, the mean anabolic steroids dose of the present cycle was a strong predictor of variables like E/A ratio, ventricular weight of relative wall thickness.
This means that cycles don’t have a cumulative effect on heart hypertrophy. The Finnish discovered that even the pronounced impact of cycles with added HGH wears off. That became evident when they investigated an athlete three times: when he just finished a five weeks cycle of anabolic steroids and HGH, after a wash out period of 237 days, and just after he completed a anabolic steroids only cycle. Of course a study with twenty users is not conclusive. But the study suggests that just like the Australians proved before, anabolic steroids are not as disastrous for the heart morphology as some agencies want you to believe; the combination with HGH does however add considerable cardiovascular risks to steroid cycles; and the deleterious effects wear off during wash out periods. Especially athletes in their late thirties and older should take their wash out periods seriously. The age of the subjects in the Finnish study ranged from 25 to 43. In this population age was the strongest predictor of the E/A ratio. The older they were, the lower their ratio ratio. (The Pearson’s correlation coefficient was –0.70. The coefficient of mean steroid dose and E/A ratio was –0.42.)
Equipoise was actually created while attempting to make a product which would be be a long acting injectable d-bol (Methandrostenolone). What was actually created was a product which, in the real world acts nothing like Dianabol, despite its similarity to it chemically. A simple way to think of Equipoise, chemically at least, is simply as Dianabol without the 17-alpha-methyl group (thats the thing which makes Dianabol able to be ingested orally and not be destroyed by your liver). However, having had first hand experience with both Equipoise as well as Dianabol, I can tell you that the results from each are vastly different.
To make Equipoise, a double bond was added between carbon atoms 1 and 2 of the Steran Nucleus of Testosterone. What does this mean? Well, first of all, since Equipoise was created by one simple modification in the testosterone molecule, you could rightly suspect that it shares many similarities with it.
Equipoise is just as anabolic as testosterone (as you can tell by its anabolic rating above), but only half asandrogenic. Those ratings can be quite deceiving though, as I don’t know anyone who would claim that you can gain as much weight on Equipoise as you can gain on an equal amount of testosterone (even though strength gains from the two compounds are very similar).
Its not very common to compare Equipoise to testosterone; however a far more common comparison is between Equipoise and Deca Durabolin. I suspect this is because when Dan Duchaine introduced this compound to the steroid using community, he made an immediate comparison to Deca, speculating that it would act similarly to Deca Durabolin but like a much stronger version of it. Equipoise doesn’t actually act much like deca at all; Deca Durabolin is actually a progestin and a 19-nor derived steroid whereas Equipoise is more closely related to testosterone (being only one double bond differ rent). Duchaine later rescinded his original statement on Equipoise and said that it was disappointing as a mass builder when compared with deca, but a far better drug than for both strength gains and vascularity. Unfortunately, the myth that Equipoises action is similar to Deca Durabolin’s has persisted for nearly 2 decades after he revised his opinion; this is most evident on internet message boards today, where many will advise against including both of them in a cycle because “they act the same way.”
The 1-2 double bond that Equipoise has is responsible for many of its characteristics. First of all, it acts to slow aromatization (conversion into estrogen). The best estimate is that it does so at roughly half the rate of testosterone. This is the best number Ive found in studies. Athletes almost never report estrogenic side effects with Equipoise, even when the dose is up to a gram per week. Side effects caused by estrogen include oily skin, acne, and gynocomastia, and as I said, those are usually not found from Equipoise. Virilization (development of male sexual characteristics in women) is almost never seen with this compound, when reasonable doses are used by female athletes. This is one of the few injectable compounds which could be successfully be used by female athletes and bodybuilders, and isn’t often faked.
Clinical Equipoise and Athletes
That double bond is also responsible for Equipoises resistance for being changed by the 5- 5-Alpha-reductase enzyme. This enzyme converts a small amount of Boldenone into Dihydroboldenone, which is a very potentandrogen (7x as anabolic as testosterone). As I said though, such a small amount of it is converted that its really of no concern to most athletes taking Equipoise. This factor, plus its low aromatization rate mean athletes don’t need to consider using ancillaries with Equipoise.
Athletes taking Equipoise often report a slow and constant buildup of quality muscle, and certainly this has been my experience with the drug. I would speculate that this slow buildup of muscle is due to the very long ester attached to the Boldenone; Boldenone Undecylenate is a longer ester than the decanoate ester by one carbon. Thus, we could expect the accumulation of muscle from Equipoise to actually occur at a slightly slower rate than that found with Deca (nandrolone decanoate). This leads me to advise that if you are considering the use of Equipoise, you should consider using it for no less than 12 weeks. Equipoise, like Deca, is also detectable in your system for a long time (although it is substantially less than Deca’s detection time).
Strangely, shorter estered versions of Boldenone are available as well. Anecdotally, many people (and manufacturers) claim that this produces less water retention…but water retention from Equipoise is virtually unheard of, so I consider this to be a silly idea.
An informal poll I took on xxx (as well as with my friends) seems to put the ideal dose of Equipoise at 600mgs/week. Most people I asked about their Equipoise experience with Equipoise seemed to think that using over 600mgs/week produced no additional results, but the jump from 400mgs/week to 600mgs/week produced noticeable additional gains, and thus was warranted. I have personally found very nice results from 400mgs-600mgs/week myself.
Equipoise Side Effects
One of the most pronounced effects in Equipoise is its ability to raise your RBCs (red blood cells). This is very typical of anabolic steroids; however, Equipoise would appear to do it to a slightly greater degree than most. One of the other effects most Equipoise users report is an increased appetite. I can say that this is true of me, also; this factor makes it impossible for me to diet on it. Its because of this ability to increase appetite that many will include Equipoise in a mass cycle, and its for the quality of muscle gained on it that many will include it in a cutting cycle. Its probably the most versatile injectable compound, next to testosterone. People even use a low dosed version of Equipoise to blend with irritating injectable drugs suck as testosterone suspension or Propionate.
Anabolic steroids are synthetic derivatives of the male hormone testosterone. They can exert strong effects on the human body that may be beneficial for athletic performance. A review of the literature revealed that most laboratory studies did not investigate the actual doses of anabolic steroids currently abused in the field. Therefore, those studies may not reflect the actual (adverse) effects of anabolic steroids. The available scientific literature describes that short-term administration of anabolic steroids by athletes can increase strength and bodyweight. Strength gains of about 5-20% of the initial strength and increments of 2-5 kg bodyweight, that may be attributed to an increase of the lean body mass, have been observed. A reduction of fat mass does not seem to occur.
Although anabolic steroids administration may affect erythropoiesis and blood haemoglobin concentrations, no effect on endurance performance was observed. Little data about the effects of anabolic steroids on metabolic responses during exercise training and recovery are available and, therefore, do not allow firm conclusions. The main untoward effects of short- and long-term anabolic steroids abuse that male athletes most often self-report are an increase in sexual drive, the occurrence of acne vulgaris, increased body hair and increment of aggressive behaviour. anabolic steroids administration will disturb the regular endogenous production of testosterone and gonadotrophins that may persist for months after drug withdrawal. Cardiovascular risk factors may undergo deleterious alterations, including elevation of blood pressure and depression of serum high-density lipoprotein (HDL)-, HDL2- and HDL3-cholesterol levels.
In echocardiographic studies in male athletes, anabolic steroids did not seem to affect cardiac structure and function, although in animal studies anabolic steroids have been observed to exert hazardous effects on heart structure and function. In studies of athletes, anabolic steroids were not found to damage the liver. Psyche and behaviour seem to be strongly affected by anabolic steroids. Generally, anabolic steroids seem to induce increments of aggression and hostility. Mood disturbances (e.g. depression, [hypo-]mania, psychotic features) are likely to be dose and drug dependent. anabolic steroids dependence or withdrawal effects (such as depression) seem to occur only in a small number of anabolic steroids users. Dissatisfaction with the body and low self-esteem may lead to the so-called ‘reverse anorexia syndrome’ that predisposes to the start of anabolic steroids use. Many other adverse effects have been associated with anabolic steroids misuse, including disturbance of endocrine and immune function, alterations of sebaceous system and skin, changes of haemostatic system and urogenital tract.
One has to keep in mind that the scientific data may underestimate the actual untoward effects because of the relatively low doses administered in those studies, since they do not approximate doses used by illicit steroid users. The mechanism of action of anabolic steroids may differ between compounds because of variations in the steroid molecule and affinity to androgen receptors. Several pathways of action have been recognised. The enzyme 5-alpha-reductase seems to play an important role by converting anabolic steroids into dihydrotestosterone (androstanolone) that acts in the cell nucleus of target organs, such as male accessory glands, skin and prostate.
Other mechanisms comprises mediation by the enzyme aromatase that converts anabolic steroids in female sex hormones (estradiol and estrone), antagonistic action to estrogens and a competitive antagonism to the glucocorticoid receptors. Furthermore, anabolic steroids stimulate erythropoietin synthesis and red cell production as well as bone formation but counteract bone breakdown. The effects on the cardiovascular system are proposed to be mediated by the occurrence of anabolic steroids-induced atherosclerosis (due to unfavourable influence on serum lipids and lipoproteins), thrombosis, vasospasm or direct injury to vessel walls, or may be ascribed to a combination of the different mechanisms. anabolic steroids-induced increment of muscle tissue can be attributed to hypertrophy and the formation of new muscle fibres, in which key roles are played by satellite cell number and ultrastructure, androgen receptors and myonuclei.
In the steroids scene Oxymetholone is known as a pretty risky oral anabolic steroid that can give users extra muscle mass and strength, but alos may lead to moisture retention and fat mass growth. An American study in which elderly men were given 50 or 100 mg Oxymetholone every day for 12 weeks confirms this reputation. But not when it comes to the effect on fat mass.
The world’s population is aging and scientific interest in substances that can maintain the elderly’s health, strength and fitness is growing. Scientists hope that these substances will enable the elderly to live longer on their own, needing less care and with a better quality of life. In 2003 sports scientists at the University of Southern California published the results of a study in which they examined whether oxymetholone was a serious candidate. At first glance this anabolic steroid didn’t do badly at all.
The researchers divided their subjects, all healthy men aged between 65 and 80, into three groups. One group was given a placebo; the second took 50 mg and the third group 100 mg Oxymetholone daily. The men consumed about 1 g protein per kg bodyweight per day and did not do any weight training.
In the 12 weeks that the experiment lasted, the lean body mass of the men who had taken 50 mg Oxymetholone increased by 3.3 kg; that of the men who had taken 100 mg increased by 4.2 kg. See the figure below. The fat mass in the two groups decreased by 2.6 and 2.5 kg respectively.
Scans showed that the men who took 50 mg Oxymetholone daily had lost 1.7 kg fat mass in the trunk area, and those who took 100 mg lost 2.2 kg. The figure above shows this. So most of the fat that was lost disappeared from the abdominal area we reckon.
The maximal strength that the men managed to develop when doing chest-press, lat-pulldown and leg press exercises increased by several tens of percent among the oxymetholone takers.
Doctors monitored the men during the experiment. They only found it necessary to intervene in the case of one man whose ALT enzyme level rose dangerously high. The man, who had taken 100 mg Oxymetholone, admitted that he had drunk four glasses of wine before the doctors took a blood sample from him. After a week without alcohol, his blood levels had returned to normal. The incident confirms what many people in doping circles know from experience. Alcohol and Oxymetholone are not a good combination for many users.
Nevertheless, other things happened to the Oxymetholone takers that are a slight cause for concern. Their ALT and AST levels rose slightly and their HDL levels went down. The effects were relatively small, but were statistically significant.
So Oxymetholone can help men to stay strong the researchers conclude. But before all over 65s start taking Oxymetholone, doctors would be well advised to examine this steroid more closely.
“The study leaves a number of issues unresolved, including the optimal formulation of androgen for supplementation in this age group, the benefits and risks of longer periods of therapy, the durability of outcomes associated with intermittent therapy, the question of whether measures of visceral adipose tissue and markers of atherosclerosis are improved, and the question of whether similar beneficial effects can be achieved in older women”, the researchers write.
Personal trainers and fitness professionals often spend countless hours reading articles and research on new training programs and exercise ideas for developing muscular fitness. However, largely because of its physiological complexity, few fitness professionals are as well informed in how muscles actually adapt and grow to the progressively increasing overload demands of exercise. In fact, skeletal muscle is the most adaptable tissue in the human body and muscle hypertrophy (increase in size) is a vastly researched topic, yet still considered a fertile area of research. This column will provide a brief update on some of the intriguing cellular changes that occur leading to muscle growth, referred to as the satellite cell theory of hypertrophy.
Trauma to the Muscle: Activating The Satellite Cells
When muscles undergo intense exercise, as from a resistance training bout, there is trauma to the muscle fibers that is referred to as muscle injury or damage in scientific investigations. This disruption to muscle cell organelles activates satellite cells, which are located on the outside of the muscle fibers between the basal lamina (basement membrane) and the plasma membrane (sarcolemma) of muscles fibers to proliferate to the injury site. In essence, a biological effort to repair or replace damaged muscle fibers begins with the satellite cells fusing together and to the muscles fibers, often leading to increases in muscle fiber cross-sectional area or hypertrophy. The satellite cells have only one nucleus and can replicate by dividing. As the satellite cells multiply, some remain as organelles on the muscle fiber where as the majority differentiate (the process cells undergo as they mature into normal cells) and fuse to muscle fibers to form new muscle protein stands (or myofibrils) and/or repair damaged fibers. Thus, the muscle cells’ myofibrils will increase in thickness and number. After fusion with the muscle fiber, some satellite cells serve as a source of new nuclei to supplement the growing muscle fiber. With these additional nuclei, the muscle fiber can synthesize more proteins and create more contractile myofilaments, known as actin and myosin, in skeletal muscle cells. It is interesting to note that high numbers of satellite cells are found associated within slow-twitch muscle fibers as compared to fast-twitch muscle fibers within the same muscle, as they are regularly going through cell maintenance repair from daily activities.
Growth factors are hormones or hormone-like compounds that stimulate satellite cells to produce the gains in the muscle fiber size. These growth factors have been shown to affect muscle growth by regulating satellite cell activity. Hepatocyte growth factor (HGF) is a key regulator of satellite cell activity. It has been shown to be the active factor in damaged muscle and may also be responsible for causing satellite cells to migrate to the damaged muscle area.
Fibroblast growth factor (FGF) is another important growth factor in muscle repair following exercise. The role of FGF may be in the revascularization (forming new blood capillaries) process during muscle regeneration.
A great deal of research has been focused on the role of insulin-like growth factor-I and –II (IGFs) in muscle growth. The IGFs play a primary role in regulating the amount of muscle mass growth, promoting changes occurring in the DNA for protein synthesis, and promoting muscle cell repair.
Insulin also stimulates muscle growth by enhancing protein synthesis and facilitating the entry of glucose into cells. The satellite cells use glucose as a fuel substrate, thus enabling their cell growth activities. And, glucose is also used for intramuscular energy needs.
Growth hormone is also highly recognized for its role in muscle growth. Resistance exercise stimulates the release of growth hormone from the anterior pituitary gland, with released levels being very dependent on exercise intensity. Growth hormone helps to trigger fat metabolism for energy use in the muscle growth process. As well, growth hormone stimulates the uptake and incorporation of amino acids into protein in skeletal muscle.
Lastly, testosterone also affects muscle hypertrophy. This hormone can stimulate growth hormone responses in the pituitary, which enhances cellular amino acid uptake and protein synthesis in skeletal muscle. In addition, testosterone can increase the presence of neurotransmitters at the fiber site, which can help to activate tissue growth. As a steroid hormone, testosterone can interact with nuclear receptors on the DNA, resulting in protein synthesis. Testosterone may also have some type of regulatory effect on satellite cells.
Muscle Growth: The ‘Bigger’ Picture
The previous discussion clearly shows that muscle growth is a complex molecular biology cell process involving the interplay of numerous cellular organelles and growth factors, occurring as a result of resistance exercise. However, for client education some important applications need to be summarized. Muscle growth occurs whenever the rate of muscle protein synthesis is greater than the rate of muscle protein breakdown. Both, the synthesis and breakdown of proteins are controlled by complimentary cellular mechanisms. Resistance exercise can profoundly stimulate muscle cell hypertrophy and the resultant gain in strength. However, the time course for this hypertrophy is relatively slow, generally taking several weeks or months to be apparent.
Interestingly, a single bout of exercise stimulates protein synthesis within 2-4 hours after the workout which may remain elevated for up to 24 hours. Some specific factors that influence these adaptations are helpful to highlight to your clients.
All studies show that men and women respond to a resistance training stimulus very similarly. However, due to gender differences in body size, body composition and hormone levels, gender will have a varying effect on the extent of hypertrophy one may possibly attain. As well, greater changes in muscle mass will occur in individuals with more muscle mass at the start of a training program.
Aging also mediates cellular changes in muscle decreasing the actual muscle mass. This loss of muscle mass is referred to as sarcopenia. Happily, the detrimental effects of aging on muscle have been shown be restrained or even reversed with regular resistance exercise. Importantly, resistance exercise also improves the connective tissue harness surrounding muscle, thus being most beneficial for injury prevention and in physical rehabilitation therapy.
Heredity differentiates the percentage and amount of the two markedly different fiber types. In humans the cardiovascular-type fibers have at different times been called red, tonic, Type I, slow-twitch (ST), or slow-oxidative (SO) fibers. Contrariwise, the anaerobic-type fibers have been called the white, phasic, Type II, fast-twitch (FT), or fast-glycolytic (FG) fibers. A further subdivision of Type II fibers is the IIa (fast-oxidative-glycolytic) and IIb (fast-glycolytic) fibers. It is worthy of note to mention that the soleus, a muscle involved in standing posture and gait, generally contains 25% to 40% more Type I fibers, while the triceps has 10% to 30% more Type II fibers than the other arm muscles (Foss and Ketyian, 1998). The proportions and types of muscle fibers vary greatly between adults. It is suggested that the new, popular periodization models of exercise training, which include light, moderate and high intensity training phases, satisfactorily overload the different muscle fiber types of the body while also providing sufficient rest for protein synthesis to occur.
Muscle Hypertrophy Summary
Resistance training leads to trauma or injury of the cellular proteins in muscle. This prompts cell-signaling messages to activate satellite cells to begin a cascade of events leading to muscle repair and growth. Several growth factors are involved that regulate the mechanisms of change in protein number and size within the muscle. The adaptation of muscle to the overload stress of resistance exercise begins immediately after each exercise bout, but often takes weeks or months for it to physically manifest itself. The most adaptable tissue in the human body is skeletal muscle, and it is remarkably remodeled after continuous, and carefully designed, resistance exercise training programs.