17 10 / 2014

Pharmacology is the study of drugs and their effects. Anabolic pharmacology is the study of drugs that have a growth-promoting effect in muscle. This column will explore anabolic pharmacology by profiling a different anabolic drug and its effects each month. The focus of discussion this month will be the anabolic androgenic steroid, Equipoise.

Boldenone is a 1-dehydro derivative of testosterone that has been sold as a veterinary preparation under the name Equipoise, and is largely known by this name. The formation of a double-bond in the 1,2 position changes the shape of the molecule slightly. This also changes the potency and characteristics of the molecule. Boldenone has a lower affinity than testosterone for the androgen receptor, making it less potent on a milligram-for-milligram basis. This steroid can be converted to estrogen, but less so than testosterone. In addition, boldenone is metabolized to 1,4 dienedione, which is a potent aromatase inhibitor.

Boldenone is converted by 5-alpha reductase to 1-testosterone, a more potent steroid, as well as to the 5-beta isomer— which is thought to be an inactive metabolite. Binding to sex hormone-binding globulin (SHBG) is much lower with boldenone than with testosterone, meaning a larger free plasma concentration but a shorter half-life in plasma. There is little-to-no binding to progesterone or glucocorticoid receptors, and no real data on the interaction of boldenone with the different enzyme systems.

The undecyclenate ester of boldenone was the ester marketed under the original trade name. In recent years, the free base and other esters have become available as underground preparations. On the street, Equipoise is erroneously considered to have the same activity as Deca and is often substituted for Deca in a stack. Dan Duchaine, if not the originator of this myth, at the very least propagated it in his book Underground Steroid Handbook II. If you look at the structure, you can see that boldenone is structurally identical to dianabol without the C-17 alkylation.

Most people experience much less side effects with boldenone, compared to methandrostenolone. This is because boldenone converts to estradiol, while methandrostenolone converts to methylestradiol. Methylestradiol is a much more potent and long-lasting estrogen than plain estradiol. Since there is no C-17 alkylation, there is no liver toxicity associated with boldenone. Boldenone is rumored to be very good at increasing red blood cell production. While all androgens stimulate erythropoiesis, there is no evidence in the scientific literature that boldenone is superior in producing this effect.

Boldenone undecyclenate is generally injected every four or five days, but some people will inject every day while others will inject once per week. The longer half-life of the undecyclenate ester would dictate an injection frequency of every 10-14 days, but there has been a trend toward more frequent dosing by anabolic steroid users, even with drugs known to have long half-lives. Dosing is generally kept pretty low (300-500 milligrams per week), but the low binding affinity would argue for twice that dosage, taken with testosterone.

The anabolic-to-androgenic ratios are favorable for boldenone, but people do not consider boldenone a particularly potent steroid— possibly due to the low doses that are utilized. Also, boldenone does not cause much water retention— so many people assume it is not working if they do not put on 10 pounds in one week. Boldenone is said to cause an increase in vascularity, although there is no mechanism to explain why boldenone would do this more than any other anabolic steroids.

10 10 / 2014

Testosterone is responsible for normal growth and development of male sex organs and maintenance of secondary sex characteristics. It is the primary androgenic hormone, and its production and secretion are the end product of a series of hormonal interactions. Gonadotropin-releasing hormone (GnRH) is secreted by the hypothalamus and controls the pulsatile secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) by the anterior pituitary. Luteinizing hormone regulates the production and secretion of testosterone by the Leydig cells of the testes, and FSH stimulates spermatogenesis.

When the testes fail to produce normal levels of testosterone, testosterone deficiency results. Hypergonadotropic hypogonadism is caused by primary testicular failure. Testosterone levels are low and pituitary gonadotropins are elevated. In secondary, or hypogonadotropic hypogonadism, there is inadequate secretion of pituitary gonadotropins. In addition to a low testosterone level, LH and FSH levels are low or low-normal. While pre-pubertal hypogonadism is generally characterized by infantile genitalia and lack of virilization, the development of hypogonadism after puberty frequently results in complaints such as diminished libido, erectile dysfunction, infertility, gynecomastia, impaired masculinization, changes in body composition, reductions in body and facial hair, and osteoporosis. In addition to these complaints, mood inventory scores indicate that hypogonadal men report levels of anger, confusion, depression, and fatigue that are significantly higher than those reported by men with normal testosterone levels.

Men with primary hypogonadism (congenital or acquired) or hypogonadotropic hypogonadism are candidates for testosterone replacement therapy, and there are now a variety of products available to treat these disorders. Successful management of testosterone replacement therapy requires appropriate evaluation and an understanding of the benefits and risks of treatment.

Testosterone Replacement Therapy

Testosterone replacement should in theory approximate the natural, endogenous production of the hormone. The average male produces 4-7 mg of testosterone per day in a circadian pattern, with maximal plasma levels attained in early morning and minimal levels in the evening. However, the subtleties of pulsatile and diurnal rhythms are potentially difficult to imitate, and evidence suggests that different dose response curves exist for different androgen-dependent functions. The clinical rationale for treatment of testosterone deficiency may include:

  • stabilizing or increasing bone density 
  • enhancing body composition by increasing muscle strength and reducing adipose 
  • improving energy and mood 
  • maintaining or restoring secondary sexual characteristics, libido and erectile function

Types of Testosterone Replacement Therapy

Ideal testosterone replacement therapy produces and maintains physiologic serum concentrations of the hormone and its active metabolites without significant side effects or safety concerns. Several different types of testosterone replacement are currently marketed, including tablets, injectables, and transdermal systems.

Oral agents

Although elevations in liver function tests and abnormalities at liver scan and biopsy are relatively common in patients receiving oral testosterone, these preparations still constitute roughly a third of the testosterone prescriptions filled in the United States. Both modified and unmodified oral testosterone preparations are available. Unmodified testosterone is rapidly absorbed by the liver, making satisfactory serum concentrations difficult to achieve. Modified 17-alpha alkyltestosterones, such as Methyltestosterone or Fluoxymesterone, also require relatively large doses that must be taken several times a day.

Intramuscular injection

Testosterone cypionate and Testosterone enanthate are frequently used parenteral preparations that provide a safe means of hormone replacement in hypogonadal men. Testosterone is esterified to inhibit degradation and to make it soluble in oil-based injection vehicles that retain the drug in muscle tissue. In men 20-50 years of age, an intramuscular injection of 200 to 300 mg testosterone enanthate is generally sufficient to produce serum testosterone levels that are supranormal initially and fall into the normal ranges over the next 14 days. Fluctuations in testosterone levels may yield variations in libido, sexual function, energy, and mood. Some patients may be inconvenienced by the need for frequent testosterone injections. Increasing the dose to 300 to 400 mg may allow for maintenance of eugonadal levels of serum testosterone for up to three weeks, but higher doses will not lengthen the eugonadal period.

Transdermal systems

Currently, three testosterone transdermal systems are marketed: a system applied to the scrotum that has no permeation enhancers and two systems that contain permeation enhancers for application to appendage or torso skin. Scrotal patches produce high levels of circulating dihydrotestosterone (DHT) due to the high 5-alpha-reductase enzyme activity of scrotal skin.

Benefits of Testosterone Replacement Therapy

A number of benefits of testosterone replacement therapy have been demonstrated, including effects on mood, energy levels, and libido. Long-term follow-up of testosterone replacement in hypogonadal males and a control group indicates that self-assessment of libido was significantly higher (p<0.0001) in the testosterone-treated group. Testosterone replacement has also been shown to enhance libido and the frequency of sexual acts and sleep-related erections. Transdermal testosterone replacement therapy, in particular, has been linked to positive effects on fatigue, mood, and sexual function, as well as significant increases in sexual activity. More specifically, testosterone replacement therapy has been shown to improve positive mood parameters, such as feelings of wellness and friendliness, while reducing negative mood parameters, such as anger, nervousness, and irritability. Testosterone replacement is an effective treatment for some depressive symptoms in hypogonadal men and may effectively augment treatment in selective serotonin reuptake inhibitor (SSRI)-refractory major depression. Relative to eugonadal men, hypogonadal men in one study were impaired in their verbal fluency and showed improvement in verbal fluency following testosterone replacement therapy.

Testosterone replacement therapy is also associated with potentially positive changes in body composition. In hypogonadal men, testosterone replacement therapy has demonstrated a number of effects, including an increase in lean body mass and decrease in body fat, an increase in weight, and increases in muscle size. Parenteral testosterone replacement in hypogonadal men resulted in improved strength and increased hemoglobin compared to controls. In another study by Urban and colleagues, testosterone administration also increased skeletal muscle protein synthesis and strength in elderly men. Testosterone replacement with transdermal testosterone delivery systems in HIV-infected men with low testosterone levels has been associated with statistically significant gains in lean body mass (p=0.02), increased red cell counts, and improvements in emotional distress. Transdermal testosterone has also been administered to HIV-positive women, yielding positive trends in weight gain and quality of life.

Improvements in bone density have also been shown with testosterone replacement therapy. Increases in spinal bone density have been realized in hypogonadal men, with most treated men maintaining bone density above the fracture threshold. Testosterone replacement in hypogonadal men improves both trabecular and cortical bone mineral density of the spine, independent of age and type of hypogonadism. In addition, a significant increase in paraspinal muscle area has been observed, emphasizing the clinical benefit of adequate replacement therapy for the physical fitness of hypogonadal men.

Contraindications to Testosterone Replacement Therapy

Testosterone replacement is contraindicated in men with carcinoma of the breast or known or suspected carcinoma of the prostate, as it may cause rapid growth of these tumors. Hormone therapy is also inappropriate in men with severe benign prostatic hypertrophy (BPH)-related bladder outlet obstruction. Use of testosterone to improve athletic performance or correct short stature is potentially dangerous and inappropriate. In addition, the hormone does not correct ambiguous genitalia resulting from androgen deficiency during fetal development and should not be administered at dosages high enough to inhibit spermatogenesis.

03 10 / 2014

Let’s face it; today’s professional bodybuilders are light years ahead of the typical steroid user when it comes to physique development. For most aspiring bodybuilders, their efforts in the gym are more likely to be rewarded with a level of musculature on par with a local bodybuilding competitor or the neighborhood gym rat, than the physiques which grace the Mr. Olympia stage. This contrast in development is often so wide that many are left asking the question…”What’s the secret?” From their perspective, because they struggled to build even a moderate amount of muscle size, they cannot begin to fathom how anyone could build such an extreme amount of muscle mass without using either a death-defying amount of drugs…and/or some drug combination privy only to the pros.

The promise of the existence of a missing link between themselves and the physiques they idolize keeps the fire burning by providing a “hope” that they too can one day attain a similar level of development. If they could only find out the drug “secrets” of the pros, they would surely earn their pro cards as well, right? Wrong.

The only secret is that there are no secrets. All the same knowledge utilized by professional bodybuilders to forge their physiques into the show-stopping specimens we see in the magazines is available to all of us. There are no designer drugs responsible for catapulting the pros into the upper echelon of the sport, nor are there any secret drug combinations known only by a chosen few. Even more revealing is that there are no specific dosing guidelines which must be followed in order to build a pro-worthy physique. Of course, high-dose use has certainly taken up residence in the pro ranks, but what is considered “high-dose” for one person can be interpreted to mean something completely different by another. Just as opinions on this subject differ, there is also significant variance regarding the dosing amounts among professional bodybuilders. Frequently, the uneducated individual will automatically assume that the larger bodybuilder must be using larger doses of drugs in comparison to his smaller peers, but this is not necessarily the case. Often, the size of the bodybuilders is not an accurate indicator of total drug intake.

For example, one pro bodybuilder in particular, who weighs about 190 lbs in contest shape, routinely administers over 3 grams of anabolic steroids per week, while another pro bodybuilder who carries significantly more lean muscle mass (over 70 pounds more) only uses about 2 grams per week. As a 2nd example, one very popular pro bodybuilder has been known to use massive doses of steroids, as well as large doses of GH, insulin, and other bodybuilding drugs. Taking 500 mg of Anadrol per day, on top of 5+ grams of injectables weekly, is commonplace in this bodybuilder drug regimen. In contrast, another pro, who carries roughly the same amount of lean mass, uses no insulin, a moderate amount of GH, and about 2-3 grams of anabolic steroids per week.

The point here is that drug intake can vary considerably. While I have found that most pro bodybuilders tend to stay within a certain dosing “range”, there are those who take much less than one might think…and there are those who take much more than one might think. Several other factors, aside from total drug intake, play a significant role in determining the ultimate size potential of a bodybuilder, such as genetics, nutrition, and training. Today, more than ever, the importance of the training component has been vastly undermined by a certain segment of the drug culture, which basically claims that attaining pro-level size has little to do with nutrition &amp; training, and is almost completely attributable to one’s drug intake. Of course, this is miles from the truth, as nutrition is the catalyst which allows BB’ing drugs to capitalize on their muscle-building properties. If nutritional intake is inadequate, growth either slows or stops altogether. One cannot emphasize enough how important nutrition is for the steroid user wishing to build his physique to its greatest potential.

Aside from the direct influence that nutrition has on a steroid’s ability to build muscle, many bodybuilders have been led to believe that they must use a particular combination of drugs or certain drugs in specific quantities, if they ever want to turn pro. For example, it has often been claimed that all professional bodybuilders use between 15-20 IU of GH on a daily basis and that a bodybuilder couldn’t possibly turn pro without it. Both of these statements are untrue and there are numerous examples confirming each. In reality, only a small percentage of pro bodybuilders use between 15-20 IU of GH per day, as the cost involved is considerable and quite frankly, most pro bodybuilders don’t earn shit. Just meeting the basic needs of the pro bodybuilder lifestyle can cause a substantial hit to the pocket book, let alone purchasing large amounts of GH on top of it. Needless to say, only the financially well off are able to utilize chemical enhancement to its fullest advantage.

It is also commonly claimed that Insulin is partially responsible for the recent increase in size witnessed among today’s bodybuilders. No doubt, insulin (especially when combined with GH) has contributed greatly and in many cases has added a significant amount of bodyweight to an already monstrous physique. However, many wrongly assume that just because Insulin is easy to source that it necessarily means every pro bodybuilders is using it in massive quantities. This is not so. While insulin use may be widespread, dosages and frequency of use are personalized, with some bodybuilders choosing to abstain completely. Readers might be surprised to learn that one popular pro, who recently placed in the Top 10 of this year’s Mr. Olympia contest, has never used insulin in his life.

As mentioned above, genetics will ultimately determine not only the potential for growth, but also the appearance of that’s musculature as it sits on the frame. Many pro bodybuilders are exceedingly gifted in terms of shape &amp; structure, allowing their muscles to look even bigger than they really are. With enough hard work, the right diet, and adequate drug use, even a man with average genetics can usually build enough size to stand on the national stage, but what that muscle will look like once he’s built it is purely up to genetics…and this is what separates the pros from the non-pros. In conclusion, the next time someone tells you that all the pros are doing this or that, you can reliably discount such talk as nonsense. Drug use among the pros is as diverse as it is in any other sport, with each individual selecting a PED protocol based on their needs, personal preferences, and willingness to assume risks.

26 9 / 2014

What would you say if I told you that your level of “self-discipline” might not be quite “up to snuff” when it comes to your bodybuilding endeavors? Before you answer, consider this: no matter whether you’re an elite body builder or a “couch potato,” you still have the same amount of self-discipline.

How is this possible? The difference lies in which habits you’re disciplined to.

An elite bodybuilder is disciplined to working out regularly, eating frequent and nutritionally-dense meals, taking quality bodybuilding supplements, and getting plenty of rest. All of these habits propel him/her towards the goal of gaining muscle and losing fat. On the other hand, a “couch potato” is disciplined towards his habits of watching endless hours of TV and stuffing down as much junk food as his artery-plugged heart desires.

Everyone is already disciplined to their current habits. The real breakthrough comes when we can alter our habits to push us towards our desired goals! But you first must set a specific bodybuilding goal! Question: Right this second do you know what your current physique goal is? If not, how are you ever supposed to attain it? Good question, right?

Adopt These Habits and Double The Bodybuilding Gains From Your Program. So here’s the first part of your weekly “assignment.”

1)Write down your specific physique goal and the date it will be accomplished by.

Example:

I will gain 5 lbs. of muscle and lose 5 lbs. of fat by July 1st.

(Grab a pen and paper and actually do this. C’mon - you want bodybuilding results don’t you?)

2) Next, identify and write down four of your “bad” habits that are keeping you from achieving your bodybuilding goals.

Example:

  • Skipping meals because I don’t take the time to prepare healthy meals during the week.
  • Hitting the snooze button on the alarm clock in the morning until it’s too late for me to get in my morning workout.
  • Forgetting to take my supplements at the correct times during the day.
  • Robbing my body of sleep by staying up late watching the boob tube. (Could this have something to do with hitting the snooze button?)

Now it’s time to replace these “bad” habits with “good” ones by identifying and writing down four new habits.

Example:

  • Spend one hour on Wednesday and Sunday nights preparing healthy meals to eat during the week. (Try freezing meals in advance.)
  • Be asleep by 10 PM each night so I can get the rest I need to recuperate from my work outs.
  • Skip hitting the snooze button so I can make my workout before work each morning.
  • Create a supplement schedule so I can “check-off” each time I take my bodybuilding supplements.

3) Once you have completed writing down your new habits, hang them somewhere where you can read them everyday. (Otherwise you will slip back into your old habits in a day or two.)

You will experience tremendous resistance (from yourself!) when trying to develop your new habits.

Warning: It’s not easy. Good habits are hard to form, but easy to live with. Bad habits are easy to form but hard to live with. Remember that successful people do things that unsuccessful people aren’t willing to do.

It will take you one month to form a new habit, but once it’s “ingrained” it feels more uncomfortable not doing the activity than doing it.

Remember how uncomfortable it was when you first started working out with weights? But soon this discomfort turned into pleasure when you started becoming stronger and more muscular? Believe me, the same thing happens when you stick to new habits!

Start your new habit list now, and make the commitment to those habits that will pay you in rich dividends for years to come.

18 9 / 2014

Those who are fans of this highly beneficial for core and lower body exercise tend to think that it is generally for vagrancy, but can you hide something behind that average repetition?

Yes, it is very possible that it is a problem of mobility in certain joints, and can identify carefully observing the execution of the exercise. This is a job that personal trainers make in every move: identify the weak links in the various movements. And where are these weak links in the squat?

The two joint weaknesses when performing a squat usually found in the ankle and hip. If we have a good ROM (range of movement) of these joints, movement execution will be incomplete or deficient.

Ankle dorsiflexion

If we do not have good mobility of the ankle joint, in this case the tibia closer to the toes, is very likely to occur two things. The first is that the weight you are moving to move forward with the corresponding lumbar risk. The second is that our knees, instead of keeping in line with the toes, moving inward.

The first thing to do is find out why our mobility is reduced: usually due to muscle shortening in the posterior tibial and flexor of the fingers, but can also be caused by poorly cured strains.

Flexion and internal rotation of hip

The other most common when running a squat weak link is the lack of mobility in the hip joint; we can observe that it tends to raise the heels. In the case of poor flexion is usually due to shortened hip flexors, so we will focus on stretching them.

In the case of internal rotation of the hip, we come in handy some yoga postures especially dedicated to the opening of hips and the stretching tensor fascia lata, gluteus minimus and gluteus medius, which are the involved in this movement.

Other problems that may prevent us perform the squat correctly can be a bad body alignment, weak core, poor thoracic mobility, poor weight set, a starting position shoddy… Look around you and try to discover why people do not go down.

12 9 / 2014

WEEK 1.

Set Rep Range Weight
Set 1 5 reps 60% of W1RM
Set 2 5 reps 65% of W1RM
Set 3 5 reps 75% of W1RM
Set 4 5 reps 75% of W1RM

WEEK 1

Day 1
Warm-Up: Dynamic Stretch, Foam Roll
Barbell Bench Press
4 sets of 5 reps, 2.5 minutes rest
Perform 5 reps with 60% of W1RM, 5 reps with 65%, and 2 sets of 5 reps with 75%.
Dumbbell Shoulder Press
4 sets of 10 reps, 1 minute rest
Behind-The-Neck Press
4 sets of 10 reps, 1 minute rest
Cuban Press
3 sets of 10 reps, 30 seconds rest
SUPERSET
Triceps Dips
3 sets of 10 reps, 15 seconds rest
Triceps Push-Downs
3 sets of 12 reps, 60 seconds rest
SHOULDER CIRCUIT: 4 ROUNDS
Lateral Raise
8 reps
Front Raise
8 reps
Rear Flyes
8 reps
Overhead Press
8 reps, rest 60 seconds

Day 2

Warm-Up: Dynamic Stretch, Foam Roll
Barbell Back Squat
4 sets of 5 reps, 2.5 minutes rest
Perform 5 reps with 60% of W1RM, 5 reps with 65%, and 2 sets of 5 reps with 75%.
Front Squat
4 sets of 10 reps, 1 minute rest
Single-Leg Press
4 sets of 10 reps per side, 1 minute rest
SUPERSET
Calf Raise
4 sets of 12 reps, 1 minute rest
Hanging Leg Raises
4 sets of 12 reps, 1 minute rest
Ab Wheel Roll-Outs
4 set of 10 reps, 1 minute rest
Flexibility Work: Static Stretching, Foam Roll

Day 3

Warm-Up: Dynamic Stretch, Foam Roll
Weighted Pull-Ups
4 sets of 5 reps, 2.5 minutes rest
Perform 5 reps with 60% of W1RM, 5 reps with 65%, and 2 sets of 5 reps with 75%.
Dumbbell Single-Arm Row
4 sets of 12 reps, 1 minute rest
Bodyweight Row
4 sets of 10 reps, 1 minute rest
Incline Dumbbell Curl
4 sets of 10 reps, 1 minute rest
BICEPS CIRCUIT: 4 ROUNDS
Zottman Curl
8 reps
Cross-Body Curl
8 reps
Pronated Curl
8 reps, rest 60 seconds
Flexibility Work: Static Stretching, Foam Roll

Day 4

Warm-Up: Dynamic Stretch, Foam Roll
Incline Dumbbell Bench Press
4 dropsets of 6+6 reps, 2.5 minutes rest
Incline-Drop Dumbbell Bench Press
4 sets of 6+6+6 reps, 1 minute rest

Start on a steep incline. Perform 6 reps, reduce incline, perform another 6 reps, and then perform 6 reps from the flat bench.
High-to-Low Cable Flyes
4 sets of 10 reps, 1 minute rest
Narrow-Grip Bench Press
4 sets of 10 reps, 1 minute rest
TRICEPS CIRCUIT: 4 ROUNDS
Triceps Push-Downs
8 reps
Triceps Dips
8 reps
Narrow Push-Ups
8 reps, rest 60 seconds
Flexibility Work: Static Stretching, Foam Roll

Day 5

Warm-Up: Dynamic Stretch, Foam Roll
Deadlift
4 sets of 5 reps, 2.5 minutes rest
Perform 5 reps with 60% of W1RM, 5 reps with 65%, and 2 sets of 5 reps with 75%.
Romanian Deadlift
4 sets of 10 reps, 1 minute rest
Zercher Squat
4 sets of 12 reps, 1 minute rest
Weighted Incline Sit-Up
4 sets of 10 reps, 1 minute rest
Barbell Landmine
4 sets of 20 reps, 1 minute rest
Flexibility Work: Static Stretching, Foam Roll

04 9 / 2014

Because of their ability to promote gains in lean muscle mass, increases in strength and the ability to “cut” fat effectively, many bodybuilders and strength athletes use anabolic steroids Winstrol and Equipoise. Depending on your training goals, the dosage will differ and will also affect other substances you use to “stack” with either Winstrol, Equipoise or both. If you decide to use these drugs without consulting a physician, be forewarned that they may have very harmful side effects.

Winstrol is the brand name for the steroid hormone Stanozolol and comes in two forms: oral pills and an injectable form suspended in water, which some users claim yields better results while costing less. Winstrol is most often used as a drug to “lean out” or improve strength gains, and Winstrol is not known as a steroid that greatly adds muscle mass. Therefore, steroid experts recommend using 50 mg daily. This amount requires five tablets of 10 mg each; if you decide to inject, that will require one daily shot, and users suggest rotating injection sites. By itself, Winstrol promotes fast and dramatic gains in strength at the recommended dosage. Dianabol provides a good complementary drug for promoting strength gains.

For those looking to gain mass while using Winstrol, try using a product containing nandrolone (like Deca-Durabolin), using 25-50 mg of Winstrol for 6 to 8 weeks.

For those looking to lean out (drop fat while retaining as much muscle as possible), try stacking 25-50 mg of Winstrol with Boldenone, Masteron or Trenbolone for 6 weeks. As Winstrol does not aromatize (convert through chemical breakdown) into estrogen, you will not need to take an antiestrogen while using Winstrol, and you would not need to use any Clomid or Nolvadex after your cycle.

Equipoise is the brand name for the steroid hormone Boldenone, a product used mostly in cows and horses to improve their lean body mass. Equipoise has a number of uses for bodybuilders and athletes, from stimulating EPO (erythropoietin) production to increase the number of red blood cells (thereby increasing endurance), to gaining muscle mass easily (indirectly by increasing the appetite), to allowing a user to “cut” bodyweight by leaning out the muscle tissue. Equipoise comes in injectable form only.

By itself Equipoise promotes an increase in muscle mass and muscle hardness at dosages of 300 to 400 mg/week for 8 to 10 weeks. Users recommend “front-loading” this steroid, that is, using an increased dosage in the first 2 weeks (say 600 to 800 mg/week) and then tapering off to 200 to 400 mg/week for the next 6 to 8 weeks.

To keep your existing muscle mass while increasing muscle hardness and losing fat, you can combine Equipoise with Winstrol, taking 300 to 400 mg/week of Equipoise and 25-50 mg of Winstrol daily for 8 to 10 weeks. To lean out, you can also try stacking normal doses of Equipoise with trenbolone, using 76 mg of the latter every other day to increase lean muscle mass.

Those looking to greatly increase muscle mass and keep their gains after they stop using the drugs might try stacking Equipoise with testosterone. This stack will enable users to maximize the appetite increases that accompany Equipoise usage, as testosterone is a strong anabolic (muscle-building) drug. Along with normal dosages of Equipoise, try using 500 mg/week of Sustanon (a multi-form testosterone) or 500 mg/week of testosterone enanthate.

Like Winstrol, Equipoise by itself does not aromatize into estrogen. Therefore, users only using Equipoise will not need to take anti-estrogens during the dosing period and will not have to use any anti-estrogens (like Clomid or Nolvadex) after the dosing period has ended.

28 8 / 2014

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

15 8 / 2014

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.

08 8 / 2014

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:

  1. Constant load for all sets.
  2. 5 percent load reduction after each set
  3. 10 percent load reduction after each set
  4. 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.

24 7 / 2014


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.

17 7 / 2014

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 Strategy

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

Drugs

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.

Growth Hormone

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).

11 7 / 2014

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.

03 7 / 2014

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.

26 6 / 2014

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.”