Posts Tagged ‘steroids’

Lou Ferigno.

When I was a teenager just getting started in bodybuilding, I used to marvel at the biceps of Larry Scott. They were the best I’d ever seen, and to me they still rank as the best ever.

Scott’s biceps heads were incredibly long, reaching past his elbows, and they were very thick and full, too. In studying my own biceps early on, I realized that Scott would be a good role model for me because I also had long muscle bellies. As much as I was amazed by the high peaks of Freddy Ortiz (Mr. America short-class champion in 1963 and ’64), I knew that there was no way I could ever attain arms that looked like his because our basic structures were too different.

In time, my upper arms stretched the tape at 22 3/4″ cold–no pump at all. This was when I was at my biggest, 325 pounds, for the 1994 Masters Olympia, in which I finished second. For that contest, I used the same biceps routine that I had applied in preparation for the 1975 Mr. Olympia [in which he placed third in the heavyweight division]. In fact, I’ve been so pleased with the results that I still use pretty much the same workout to this day.

PYRAMID PRINCIPLE There’s a general misconception about biceps training that more is better. For more than 30 years, I’ve been doing three or four exercises, two to four sets apiece and with a strict rep range of eight to 10. That’s usually a total of about 14 sets, give or take, which takes me less than a half-hour to perform.

I pyramid up in weight for each exercise, although I don’t necessarily lower my reps to accommodate the increase. No matter how hard it may be to bump up your poundage from set to set, it is important that you do so. I firmly believe that you get the most growth activation and strength improvement out of the last set or two of an exercise, when your muscles are pushed to their limits.

For example, let’s say I’m doing barbell curls, which is usually my first biceps exercise. I’ll start with a light weight and do 10 quick reps (still using good form) just to get the biceps warmed up. My next set will again be 10 reps, with a weight that gets difficult to lift on the seventh or eighth rep. For my third set, I’ll add another 20 pounds and shoot for eight reps. Then, for my final set, I’ll add another 20 pounds and go for eight again. I struggle to get eight on the third set, so when the fourth set comes around, it’s a real test of will, after having increased the weight, to try to equal the same number of reps.

When I move on to incline dumbbell curls, I stick with eight reps for all four sets, but I keep increasing the weight for each set, from 50s to 60s to 70s to 80s. A lot of people assume that pyramiding means increasing weight while dropping reps. If you set a goal of keeping the reps the same set after set while increasing weight, you bring a whole new level of intensity and mind over matter to the equation.

INCLINED TO CURL Incline dumbbell curls are my favorite biceps exercise. I like the full range of motion and the stress in the biceps from the bottom of the movement all the way to the top. I get a really good stretch at the bottom, although I never let my elbows lock out. I believe you can do damage to your elbow joint if you let it lock each time you lower the weight. I also like to lift with my arms in unison, as opposed to alternating them, as there’s too much opportunity to cheat when doing them one arm at a time.

In the movie Pumping Iron, I do incline dumbbell curls with a pair of 100s. I don’t go quite that heavy anymore, but I can still get 80s up for reps. This exercise is a great overall biceps builder.

Barbell curls and incline dumbbell curls are basic mass movements. I try to go as heavy as I can for these, while maintaining strict form. My third exercise, however, will be an isolation movement, such as standard preacher curls or spider curls, which are done hanging over the end of a high bench. I lighten the weight and return to an eight- to 10-rep range, concentrating on slow, steady motion and really contracting my biceps at the very top of the movement.

For my last exercise, I like either 21s or concentration curls, both of which give me a great burn to end my workout. If you’ve never heard of 21s, they’re an old standby. Not many people do them anymore, but I’ve always liked them.

To perform 21s, choose a barbell that’s about half the heaviest weight you normally use for your final set of regular barbell curls. For the first seven reps, curl the weight as you would a barbell curl, but instead of going all the way up, stop when your forearms are parallel with the floor (i.e., the bottom half of the full range of motion). When you’ve finished the seventh rep, perform another seven reps beginning with your forearms parallel to the floor and curling to the apex (i.e., the top half of the full range of motion). Finally, after you’ve completed those seven reps, do seven more, this time going all the way down and all the way up. It’s a killer. By the time you’ve finished a set, your arms feel like Jell-O.

If I choose one-arm dumbbell concentration curls instead, I like to do them leaning on a bench or holding on to a dumbbell rack. I’ll only do two sets of the final exercise, which makes a total of 14 sets. The biceps aren’t a big muscle group–they don’t require the same number of sets as for chest, back or thighs. For me, 14 sets or so does the trick for biceps.

TUNING UP Although I have a few favorites I stick with time after time, I do inject variety from workout to workout by changing up the order. The sample workout I just outlined is the default order for my biceps training. If I were to do the same routine every workout, my biceps would eventually adapt to the exact kind of stresses I’m putting on them and not respond. To combat that, I’ll reverse the order, swap out different exercises for my usual ones or just mix up the entire workout on occasion. Joe Weider calls it the Muscle Confusion Training Principle, and I’m a strong believer in it.

I can’t emphasize enough how important it is to use good form. It’s just not worth the risk of injury to compromise form to try moving a weight that’s too heavy. For example, when doing barbell curls, you want to take a shoulder-width grip, keep your chest high, your shoulders back and, as with seated inclines, never completely straighten your elbows at the bottom of the movement. You also want to keep the motion steady throughout. A mental trick I’ve used is thinking of the motion as if I were playing a violin, keeping the same pace both in the positive and negative portions of each rep. You should also make sure that you are squeezing the biceps throughout; there should never be a point during a set when your muscles relax.

Some people pair biceps with back because the two groups work synergistically. Others put tris and bis together in an arm day. I prefer the latter, because I find that back training incorporates the biceps so much that they’re burned out by the time I get to them. When I train arms as a whole, however, I get a great pump and the biceps workout actually prepares my triceps for their training by pushing blood into the entire upper arm.

Train your biceps twice a week following my suggested routine (see the sidebar), keep the intensity high and the form solid, and I’m confident you’ll maximize your arms’ growth potential just as I have my own.

PHOTOGRAPHY BY CHRIS LUND

FERRIGNO'S
BICEPS WORKOUT

EXERCISE                        SETS  REPS

Standing barbell curls          1 *    10

                                 1     10

                                 2     8

Incline dumbbell curls           4     8

Preacher-bench or spider curls   4    8-10

Concentration curls or           2    8-10

  Barbell-curl 21s               2     21

* Warm-up set

Tamoxifen Nolvadex

Nolvadex is very comparable to Clomid, behaves in the same manner in all tissues, and is a mixed estrogen agonist/antagonist of the same type as Clomid. The two molecules are also very similar in structure.

It is not correct that Nolvadex reduces levels of estrogen: rather, it blocks estrogen from estrogen receptors and, in those tissues where it is an antagonist, causes the receptor to do nothing.

The claim that Nolvadex reduces gains should not be taken too seriously. The fact is that any number of bodybuilders have made excellent gains while using Nolvadex. The belief that it reduces gains seems to stem from the fact that the scientific literature reports a slight reduction in IGF-1 (individuals using anabolic steroids were not studied though) from use of Nolvadex. Thus, Dan Duchaine reported that it reduces IGF-1 and therefore reduces gains. However, if this effect exists at all, it must be very minor, due to the excellent gains that many have made, and from the fact that no one has noticed any such thing from Clomid, which has the same activity profile.

However, I would not be surprised if one were to tell a steroid user that Clomid reduced his gains, he would immediately become afraid that Clomid reduced his gains (please note that no one I have ever heard of has noticed this.) Not having been so misled, however, he would not conclude this from his results. But if an authority publishes that such an effect occurs, whether it does or not it can become self-fulfilling by biasing the user.

The fact that Nolvadex will reduce water retention may result in the user agreeing that gains are less, since weight gain is less, thus reinforcing the bias.

Tamoxifen citrate is the chemical name of active ingredient in Nolvadex. Nolvadex is a registered trademark of AstraZeneca UK Limited in the United States and/or other countries.

Clomid

Clomid is not an anabolic/androgenic steroid. Since it is a synthetic estrogen it belongs, however, to the group of sex hormones. In school medicine Clomid is normally used to trigger ovulation. Clomid also has a strong influence on the hypothalamohypophysial testicular axis. It stimulates the hypophysis to release more gonadotropin so that a faster and higher release of FSH (follicle stimulating hormone) and LH (luteinizing hormone) occurs. This results in an elevated endogenous (body’s own) testosterone level. Clomid is especially effective when the body’s own testosterone production, due to the intake of anabolic/androgenic steroids, is suppressed. In most cases Clomid can normalize the testosterone level and the spermatogenesis (sperm development) within 10- 14 days. For this reason Clomid is primarily taken after steroids are discontinued. At this time it is extremely important to bring the testosterone production to a normal level as quickly as possible so that the loss of strength and muscle mass is minimized. Even better results can be achieved if Clomid is combined with HCG or when Clomid is used after the intake of HCG.

Paradoxically, although Clomid is a synthetic estrogen it also works as an anti-estrogen. The reason is that Clomid has only a very low estrogenic effect and thus the stronger estrogens which, for example, form during the aromatization of steroids, are blocked at the receptors. These would include those that develop during the aromatizing of steroids. This does not prevent the steroids from aromatizing but the increased estrogen is mostly deactivated since it cannot at-tach to the receptors. The increased water retention and the possible signs of feminization can thus be reduced or even completely avoided. Since the antiestrogenic effect of Clomid is lower than those found in Proviron, Nolvadex, and Teslac it is mainly taken as a testosterone stimulant. Clomid is a medication that promotes the production of the body’s own stimulating hormone, gonadotropin, which in turn increases the testosterone level. It is, for example, administered to women as a so-called anti-estrogen to trigger ovulation (“ovulation stimulator”).

Side effects of Clomid are very rare if reasonable dosages are taken. Possible side effects are climacteric hot flashes and occasional visual disturbances, which can manifest themselves in blurred vision, giving flickering or flashing. Should visual disturbances occur, the manufacturer recommends discontinuing Clomid treatment. Inadequate liver functions cannot be excluded; however, they are very unlikely. In women enlargement of the ovaries and abdominal pain can occur since Clomid stimulates the ovaries. When taking Clomid multiple pregnancies are possible as well. As for the dosage, 50-100 mg/day (1 -2 tablets) seems to be sufficient. The tablets are usually taken with fluids after meals. If several tablets are taken it is recommended that they be administered in equal doses distributed throughout the day. The duration of intake has been rumored to not be taken for longer than 10-14 days. This is incorrect. Clinical studies with male patients have shown clomid to be used for up to a year or longer. Most athletes begin with 100 mg/day, taking one 50 mg tablet every morning and evening after meals. After the fifth day the dosage is often reduced to only one 50 mg tablet per day. It is normally not necessary to take the compound for more than ten days in order to increase the endogenous testosterone production. Clomid is relatively expensive. A package with 10 tablets costs approx. $35 – 45 on the black market.

Oral Turanabol.

Background

Turinabol was developed in the 1960’s when East German’s were looking for an edge for their Olympic and competitive athletes.  It is currently only obtainable through underground labs.

Steroid Action

This is a slower acting steroid.  When using Turinabol, weight, strength and muscle mass increases will not be overly dramatic; however, they will be of good quality. Turinabol also does not typically create risk for estrogenic side effects, so there is limited water retention or risk for gynecomastia. The user can obtain a hard look to their muscles due to limited water retention.

It is 17-alpha alkylated which means it can be toxic to the liver. Turinabol can also lower the clotting ability of blood. 

Negative side effects are rare but can occur from cycles that are too long or high in dosage.  Shutting off of one’s own natural testosterone production and testicular tumors (extremely rare) are both side effects of such extreme cycles.

Technical Data

In studies done on male athletes that were given 10 mg OT/day over six weeks, no negative health effects or side effects were reported. It was also used in low doses to reduce the binding of SHBG to other steroids.(1)  Oral Turinabol was found to have the ability to reduce SHBG and allow testosterone to be more readily used.

There was one case reported where a male experienced negative side effects from 5 years of using Oral Turinabol at a high dosage (2)(3). It was found to be effective at extremely high dosages by those looking to gain strength and mass, yet athletes looking to obtain gains more quickly and more proficiently in their game were very successful with lower doses of Oral Turinabol.  Olympic level male Shot-putters were able to add 2.5-4m to their shot throws, 10-12m on their Discus throw, and 6-10m to their Hammer throws with in four years of training. Female athletes gained even more.  One female athlete improved her throw from under 18m to over 20m (4).

Women experienced increased and more severe and sometimes intolerable side effects than male users.  Although, sometimes the women were taking doses that surpassed the men’s by almost double (5).

User Notes

Recently, Oral-Turinabol has found its way back into the hands of athletes all over the world. It’s the “new” sexy drug that’s actually very old. It was the East German secret weapon when their sports doping program was at it’s height.

O-T, or T-bol as it’s sometimes called, is a very nice strength and mass drug, and since it can’t convert to estrogen, can even be used on a cutting diet. For this reason, it gets my “most versatile oral” award.

Most users do fairly well with doses between 40 and 60 milligrams per day, taken in divided doses.

Steroid Effectivness Chart.

This is a steroid effectivness chart.  Which ones work the best and the worst. You could start planning your cycle according to the chart.  But remember people who gain 25lbs on winstroll may not gain on dball.  Everyone is diffrent. But this is a general idea of how well each Steroid works.

 

HIGH  10
LOW    1

Trade Name Chemical Name Weight Gain Strength Gain Fat Loss Side Effects
Anadrol Oxymetholone 10 10 2 10
Anavar Oxandrolone 2 8 8 2.5
Andriol Testosterone Undecanoate 3 4 4 2
Androgel Testosterone (Crème) 3 4 3 2
Boldenone (esterless) Boldenone 5 7 5 4
Cheque Drops Mibolerone 1 5 1 6
Deca-Durabolin Nandrolone Decanoate 7 6 5 6
Durabolin          
Equipoise Boldenone Undeclynate 5 7 5 4
Halotestin Fluoxymesterone 1 6 5 6
Laurabolin Nandrolone Laurate 7 6 5 6
Masteron Drostanolone Propionate 3 6 6.5 3
Masteron Enanthate Drostanolone Enanthate 3 6 6.5 3
Methyltestosterone Methyltestosterone 2 6 4 7
Omnadren Testosterone Blend 8 8 4 6
Oral-Turinabol 4-chlorodehydro methyltestosterone        
Parabolan Trenbolone Hexahydrobencylcarbonate 5 7 8 7
Primobolan (Injectable) Methenolone Enanthate 4 6 7 1
Primobolan (oral) Methenolone Acetate 4 5 5 3
Proviron Mesterolone 2 4 4 2
Sten Testosterone Blend 8 8 4 6
Sustanon Testosterone Blend 8 8 4 6
Test 400 (T400) Testosterone Blend 8 8 4 6
Testolent Testosterone Phenylpropionate 8 8 4 6
Testosterone Cypionate Testosterone Cypionate 8 8 4 6
Testosterone Enanthate Testosterone Enanthate 8 8 4 6
Testosterone Propionate Testosterone Propionate 8 8 4 6
Testosterone Suspension Testosterone Suspension 9 8 4 6
Testoviron Testosterone Blend 8 8 4 6
Trenbolone Acetate Trenbolone Acetate 5 7 8 7.5
Trenbolone Enanthate Trenbolone Enanthate 5 7 8 7
Winstrol Stanozolol 4 6.5 7 6.5

Oral Tren

Methyltrienolone (MT) is a very potent, reasonably toxic, non-aromatizing steroid. Ok. Let´s go over those three points again. First of all, MT is potent. It binds so strongly to the AR (androgen receptor) that it is often used in studies on other androgens to measure how strongly they bind. In other words, this stuff binds onto the AR receptor so strongly that it is pretty much the benchmark for that quality. If you´ve read my profile on Trenbolone Acetate (TA), you´ll note that I said TA is the most potent injectable weapon in our arsenal with regards to ability to bind to the Androgen receptor. That´s still true, because this particular compound is not in our arsenal, and it´s not injectable… it´s simply the oral version of TA (i.e. it is Trenbolone which has undergone modification to become orally active, via the addition of a 17-alph-methyl group). So why is it important that this stuff binds so tightly to the AR? Well, Androgen Receptors are found in both fat cells as well as muscle cells; they act on the AR in muscle cells to promote growth, and in the fat cells to affect fat burning. The stronger the androgen binds to the A.R, the higher the lipolytic (fat burning) effect on adipose (fat)tissue. Unfortunately, that strong binding doesn´t also automatically mean that it will elicit the strongest possible anabolic response, nor that the weakest bind will elicit a weak anabolic response. Anadrol (oxymetholone) has the weakest bind to the AR possible (too low to be measured), and it produces a profound anabolic response, for example. Dianabol is simarly low, and produces a very good anabolic response. AR´s are found in both muscle tissue as well as adipose tissue. When a muscle´s AR is stimulated, it can induce hypertrophy. When an adipose tissue´s AR is stimulated, through various related mechanisms, fat is lost. This is a gross oversimplification. Whatever. All we need to know is that when you have a steroid that binds to the AR, it builds muscle and burns fat. And a steroid that binds very tightly to the AR will stimulate a lot of muscle synthesis and burn a lot of fat. A good example of this is Trenbolone. And since I mentioned Trenbolone, its worth further mentioning that MT is basically a 17aa (oral) version of (injectable) Trenbolone. AR binding and AR stimulation is not the only mechanism which stimulates anabolism, however. It is important to note that dbol has a very low AR binding ability and A50 has an AR binding ability which is too low to even measure! Both are very potent oral steroids, though. So while it´s important, AR binding/stimulation is not the end all & be all of anabolism, although it is an important part. Don´t be fooled by the anabolic/androgenic ratio of this (or any steroid), either. The anabolic/androgenic ratio of MT would suggest that it produces 120(+)x the anabolic and 60(+)x androgenic effect of Test-osterone (which has a score of 100 and 100 respectively). If one were able to get a bottle of this stuff, I believe it would be best used as part of a cutting cycle, stacked with some injectables (testo-steron, etc… ), but certainly no other orals. It´s just too toxic. Negma (the French company who brought Parabolan to the market, and then discontinued it) never pushed MT to gain approval as a commercially released item, since their original studies showed it to be highly toxic. Methyltrienolone is, of course, a 19Nor compound (as is Trenbolone)…Thus, it will effect your sexual drive and performance in a similar way to both Tren and Nandrolone, meaning that Temporary Impotence and/or a lack of libido is highly possible.(10). Another problem with MT is that it is a progestin, and binds shockingly well to the progesterone receptor also (PgR) . As we know, progestins amplify estrogenic effects of Aromatizing drugs. Although MT doesn´t aromatize, you will still need to worry about its ability to cause side-effects by amplifying the estrogenic issues caused by the other compounds you may be taking. How toxic is this stuff? Well, it was never commercially marketed for use in humans, and has been relegated to Steroid-Purgatory, to be used only in studies. I´d probably rate it on around the same level as taking very high doses of halotestin or methyltestosteron.

Man gets 8 months Steroid Charges.

TAMPA, Fla. (AP) – A Lakeland man claiming involvement in the sale of steroids to professional athletes has been sentenced to eight months in federal prison.

A U.S. district judge sentenced 36-year-old Richard Andrew Thomas on Wednesday. He pleaded guilty in November to possession of steroids with intent to distribute. He could have faced up to five years in prison, but Thomas received leniency after helping build a case against 50-year-old Douglas Owen Nagel. Thomas told authorities that the Virginia chiropractor sold steroids to professional athletes, including players for the Washington Capitals hockey team and the Washington Nationals baseball team.

Thomas also told authorities about a Polk County corrections officer selling steroids. The female officer was prosecuted in state court.

Mike Tyson Workout Routine.

Mike Tyson is kind of an legend to a lot of bodybuilders. Many have expressed the desire to know about “Iron Mike’s” daily routine. According to what we found out, you’ll have to be an early bird if you want to follow in his footsteps!

This routine was listed on several websites and while I’m not 100% sure of its validity, it appears to be what is considered to be his daily schedule.

o 5am: Wake up and go for a 3 mile jog
o 6am: Back home for a shower and then back to bed (great workout for those huge legs of his)
o 10am: Wake up and eat oatmeal
o 12pm: Do ring work (10 rounds of sparring)
o 2pm: Eat another meal (steak and pasta with fruit juice drink)
o 4pm: More ring work and 60 mins on the exercise bike (again working those legs for endurance and

power)
o 5pm: Floor exercises: 2000 sit ups; 500-800 ‘dips’; 500 press ups and 500 shrugs with a 30kg barbell

and 10 mins of neck exercises (working the biceps, triceps, chest, abs and shoulders)
o 7pm: Eat steak and pasta meal again with fruit juice (probably orange juice)
o 8pm: Another 30 minutes on the exercise bike
o 9:30 Watch TV and then go to bed

Mike Tyson’s training program may or may not be for you. In fact, some bodybuilders don’t like to run since it uses up nutrients and energy they want to save for building muscle. If you do both without a long rest in between you may end up losing muscle when you burn through the nutrients. There are body builders who do run, don’t get me wrong. Running builds up muscle fiber in the legs, it just best to get a rest after your workout before you run.

As far as Mike’s diet goes, the oatmeal is a good choice. The steak, if it is lean, is also good. The pasta? Well, there’s mixed opinions about eating pasta, but you should definitely avoid pasta made from white flour. Whole wheat is a good carb for a body builder. According to the list provided he is missing essential fats. He should be consuming healthy, unsaturated fats like fatty fish, nuts, seeds, olive oil and flax seed oils. It’s also been proven that eating 5 – 7 small meals throughout the day is a much better plan than just having three meals.

HGH

There are primarily two theories as to how GH exerts its growth promoting effects. The first theory is called the Dual Effector theory. The second theory is called the Somatomedin (“mediator of growth”) Hypothesis. Both theories are fairly strait forward. Let?s start with the Dual Effector theory.

The Dual Effector theory states that GH itself has anabolic effects directly on body tissues. This theory has been supported by studies looking at the effects of injecting GH directly into growth plates. Genetically altered strains of mice have also help to support this theory. When comparing mice that genetically over express GH and mice that over express insulin-like growth factor-1 (IGF-1), GH mice are larger. Those who support the dual effector theory site this evidence. Interestingly, when IGF-1 antiserum (it destroys IGF-1) is administered concomitantly with GH, all of the anabolic effects of GH are abolished. Clearly IGF-1 has got to be involved somewhere between the pituitary and the target tissue (i.e. muscle). The Somatomedin hypothesis clears things up somewhat.

The Somatomedin hypothesis states that GH exerts its growth promoting effects through IGF-1. More specifically, GH is first released from the pituitary and then travels to the liver and other peripheral tissues where it causes the synthesis and release of IGFs. IGFs work as endocrine growth factors, meaning that they travel in the blood to the target tissues after being released from cells that produced it, specifically the liver in this case. Many studies have been performed showing that animals that are GH deficient, systemic IGF-1 infusions lead to normal growth. Admittedly, the effects are similar to those observed after GH administration. In fact, additional studies have shown IGF-1 to be greatly inferior as an endocrine growth factor requiring almost 50 times the amount to exert that same effects of GH. Recently rhIGF-1 has become widely more available and is currently approved form the treatment of HIV associated wasting. This increased availability allowed testing of this hypothesis in humans. Studies in human subjects with GH insensitivity (Laron syndrome) have consistently validated the somatomedin hypothesis (Rank, 1995; Savage, 1993). These results indicate that although IGF-1 might be the mediator of GH effects, it’s not as simple as just getting the liver to release IGF-1.

So the main difference between these two theories is that the Dual effector theory states that GH doesn?t necessarily need IGF-1 to work, the Somatomedin hypothesis insists it does. In reality both theories are correct. It?s just that the Somatomedin hypothesis focuses on “circulating” IGF-1, the Dual Effector theory recognizes that although IGF-1 is still the active hormone, it doesn’t have to come from the blood (liver), it can be produced on location by the very cells that use it.

In summary, by combining the Dual Effector theory and the Somatomedin hypothesis there are three main mechanisms by which GH makes things grow. First, the effects of GH on bone formation and organ growth are mediated by the endocrine action of IGF-1. As stated in the Somatomedin hypothesis, GH, released from the pituitary, causes increased production and release of IGF-1 into the general circulation. IGF-1 then travels to target tissues such as bones, organs, and muscle to cause anabolic effects.

Second, GH regulates the activity of IGF-1 by increasing the production of binding proteins (specifically IGFBP-3 and another important protein called the acid-labile subunit) that increase the half-life of IGF-1 from minutes to hours. Circulating proteases then act to break up the binding protein/hormone complex thereby releasing the IGF-1 in a controlled fashion over time. GH may even cause target tissues to produce IGFBP-3 increasing its effectiveness locally.

Third, GH may influence the activity of IGF-1 on an autocrine/paracrine level. Autocrine means that a hormone has an effect on the cell that produced it, paracrine means to have an effect on the “cell(s)” next to it as well. This is a completely localized effect, not dependent on the blood stream to carry things where you want them. Muscle growth from weight training is the result of IGF-1 being produced by the muscle cells themselves, not the liver. In fact, IGF-1 form the liver is genetically different from IGF-1 produced in your muscles. This information should explain why using IGF-1 systemically (from the blood stream) has been a hit and miss proposition.

In order to sufficiently address the role of GH and IGF-1 in muscle growth, we need to explore the mechanism of not only IGF-1?s autocrine/paracrine actions, but also the mechanisms of muscle growth itself.

The ability of muscle tissue to constantly regenerate in response to activity makes it unique. Its ability to respond to physical/mechanical stimuli depends greatly on what are called satellite cells. Satellite cells are muscle precursor cells. You might think of them as “pro-muscle” cells. They are cells that reside on and around muscle cells. These cells sit dormant until called upon by growth factors such as IGF-1. Under the influence of IGF-1 these cells divide (proliferate) and genetically change (differentiation) into cells that have nuclei identical to those of muscle cells. These new satellite cells with muscle nuclei are critical if not mandatory to muscle growth.

Without the ability to increase the number of nuclei, a muscle cell will not grow larger and its ability to repair itself is limited. The explanation for this is quite simple. The nucleus of the cell is where all of the blue prints for new muscle proteins come from. The larger the muscle, the more nuclei you need to maintain protein synthesis. There is a “nuclear to volume” ratio that cannot be overridden. Whenever a muscle grows in response to mechanical overload (i.e. weight training) there is a positive correlation between the increase in the number of myonuclei and the increase in muscle cell’s cross sectional area (CSA). When satellite cells are prohibited from donating new nuclei, overloaded muscle will not grow. So you see, one important key to exercise induced muscle growth is the activation of satellite cells by growth factors such as IGF-1.

Few people realize that you can inject a muscle with IGF-1 and it will grow! Studies have shown that, when injected locally, IGF-1 increases satellite cell activity, muscle DNA content, muscle protein content, muscle weight and muscle cross sectional area.

Scientists are now figuring out the signaling pathway by which mechanical stimulation and IGF-1 activity leads to all of the above changes in satellite cells, muscle DNA content, muscle protein content, muscle weight and muscle cross sectional area just outlined above. This research is stemming from studies done to explain cardiac hypertrophy. It involves a muscle enzyme called calcineurin which is a phosphatase enzyme activated by high intracellular calcium ion concentrations (Dunn, 1999). Note that overloaded muscle is characterized by chronically elevated intracellular calcium ion concentrations. Other recent research has demonstrated that IGF-1 increases intracellular calcium ion concentrations leading to the activation of the calcineurin signaling pathway, and subsequent muscle fiber hypertrophy. I am by no means a geneticist so I hesitated even bringing this research up. To avoid confusion I will enlist the help of the people doing the research. The researchers involved in these studies have explained it this way, IGF-1 as well as activated calcineurin, induces expression of the transcription factor GATA-2, which accumulates in a subset of myocyte nuclei, where it associates with calcineurin and a specific dephosphorylated isoform of the transcription factor nuclear factor of activated T cells or NF-ATc1. Thus, IGF-1 induces calcineurin-mediated signaling and activation of GATA-2, a marker of skeletal muscle hypertrophy, which cooperates with selected NF-ATc isoforms to activate gene expression programs leading to increased contractile protein synthesis and muscle hypertrophy. Simple huh?

I’m not really sure why someone would choose to inject oil instead of IGF-1. Oil gives you lumps and causes your peers to make jokes about you behind your back. IGF-1 just makes the muscle grow and leaves people wondering how you brought up those lagging rear delts. There are primarily two theories as to how GH exerts its growth promoting effects. The first theory is called the Dual Effector theory. The second theory is called the Somatomedin (“mediator of growth”) Hypothesis. Both theories are fairly strait forward. Let?s start with the Dual Effector theory.

The Dual Effector theory states that GH itself has anabolic effects directly on body tissues. This theory has been supported by studies looking at the effects of injecting GH directly into growth plates. Genetically altered strains of mice have also help to support this theory. When comparing mice that genetically over express GH and mice that over express insulin-like growth factor-1 (IGF-1), GH mice are larger. Those who support the dual effector theory site this evidence. Interestingly, when IGF-1 antiserum (it destroys IGF-1) is administered concomitantly with GH, all of the anabolic effects of GH are abolished. Clearly IGF-1 has got to be involved somewhere between the pituitary and the target tissue (i.e. muscle). The Somatomedin hypothesis clears things up somewhat.

The Somatomedin hypothesis states that GH exerts its growth promoting effects through IGF-1. More specifically, GH is first released from the pituitary and then travels to the liver and other peripheral tissues where it causes the synthesis and release of IGFs. IGFs work as endocrine growth factors, meaning that they travel in the blood to the target tissues after being released from cells that produced it, specifically the liver in this case. Many studies have been performed showing that animals that are GH deficient, systemic IGF-1 infusions lead to normal growth. Admittedly, the effects are similar to those observed after GH administration. In fact, additional studies have shown IGF-1 to be greatly inferior as an endocrine growth factor requiring almost 50 times the amount to exert that same effects of GH. Recently rhIGF-1 has become widely more available and is currently approved form the treatment of HIV associated wasting. This increased availability allowed testing of this hypothesis in humans. Studies in human subjects with GH insensitivity (Laron syndrome) have consistently validated the somatomedin hypothesis (Rank, 1995; Savage, 1993). These results indicate that although IGF-1 might be the mediator of GH effects, it’s not as simple as just getting the liver to release IGF-1.

So the main difference between these two theories is that the Dual effector theory states that GH doesn?t necessarily need IGF-1 to work, the Somatomedin hypothesis insists it does. In reality both theories are correct. It?s just that the Somatomedin hypothesis focuses on “circulating” IGF-1, the Dual Effector theory recognizes that although IGF-1 is still the active hormone, it doesn’t have to come from the blood (liver), it can be produced on location by the very cells that use it.

In summary, by combining the Dual Effector theory and the Somatomedin hypothesis there are three main mechanisms by which GH makes things grow. First, the effects of GH on bone formation and organ growth are mediated by the endocrine action of IGF-1. As stated in the Somatomedin hypothesis, GH, released from the pituitary, causes increased production and release of IGF-1 into the general circulation. IGF-1 then travels to target tissues such as bones, organs, and muscle to cause anabolic effects.

Second, GH regulates the activity of IGF-1 by increasing the production of binding proteins (specifically IGFBP-3 and another important protein called the acid-labile subunit) that increase the half-life of IGF-1 from minutes to hours. Circulating proteases then act to break up the binding protein/hormone complex thereby releasing the IGF-1 in a controlled fashion over time. GH may even cause target tissues to produce IGFBP-3 increasing its effectiveness locally.

Third, GH may influence the activity of IGF-1 on an autocrine/paracrine level. Autocrine means that a hormone has an effect on the cell that produced it, paracrine means to have an effect on the “cell(s)” next to it as well. This is a completely localized effect, not dependent on the blood stream to carry things where you want them. Muscle growth from weight training is the result of IGF-1 being produced by the muscle cells themselves, not the liver. In fact, IGF-1 form the liver is genetically different from IGF-1 produced in your muscles. This information should explain why using IGF-1 systemically (from the blood stream) has been a hit and miss proposition.

In order to sufficiently address the role of GH and IGF-1 in muscle growth, we need to explore the mechanism of not only IGF-1?s autocrine/paracrine actions, but also the mechanisms of muscle growth itself.

The ability of muscle tissue to constantly regenerate in response to activity makes it unique. Its ability to respond to physical/mechanical stimuli depends greatly on what are called satellite cells. Satellite cells are muscle precursor cells. You might think of them as “pro-muscle” cells. They are cells that reside on and around muscle cells. These cells sit dormant until called upon by growth factors such as IGF-1. Under the influence of IGF-1 these cells divide (proliferate) and genetically change (differentiation) into cells that have nuclei identical to those of muscle cells. These new satellite cells with muscle nuclei are critical if not mandatory to muscle growth.

Without the ability to increase the number of nuclei, a muscle cell will not grow larger and its ability to repair itself is limited. The explanation for this is quite simple. The nucleus of the cell is where all of the blue prints for new muscle proteins come from. The larger the muscle, the more nuclei you need to maintain protein synthesis. There is a “nuclear to volume” ratio that cannot be overridden. Whenever a muscle grows in response to mechanical overload (i.e. weight training) there is a positive correlation between the increase in the number of myonuclei and the increase in muscle cell’s cross sectional area (CSA). When satellite cells are prohibited from donating new nuclei, overloaded muscle will not grow. So you see, one important key to exercise induced muscle growth is the activation of satellite cells by growth factors such as IGF-1.

Few people realize that you can inject a muscle with IGF-1 and it will grow! Studies have shown that, when injected locally, IGF-1 increases satellite cell activity, muscle DNA content, muscle protein content, muscle weight and muscle cross sectional area.

I’m not really sure why someone would choose to inject oil instead of IGF-1. Oil gives you lumps and causes your peers to make jokes about you behind your back. IGF-1 just makes the muscle grow and leaves people wondering how you brought up those lagging rear delts.

Scientists are now figuring out the signaling pathway by which mechanical stimulation and IGF-1 activity leads to all of the above changes in satellite cells, muscle DNA content, muscle protein content, muscle weight and muscle cross sectional area just outlined above. This research is stemming from studies done to explain cardiac hypertrophy. It involves a muscle enzyme called calcineurin which is a phosphatase enzyme activated by high intracellular calcium ion concentrations (Dunn, 1999). Note that overloaded muscle is characterized by chronically elevated intracellular calcium ion concentrations. Other recent research has demonstrated that IGF-1 increases intracellular calcium ion concentrations leading to the activation of the calcineurin signaling pathway, and subsequent muscle fiber hypertrophy. I am by no means a geneticist so I hesitated even bringing this research up. To avoid confusion I will enlist the help of the people doing the research. The researchers involved in these studies have explained it this way, IGF-1 as well as activated calcineurin, induces expression of the transcription factor GATA-2, which accumulates in a subset of myocyte nuclei, where it associates with calcineurin and a specific dephosphorylated isoform of the transcription factor nuclear factor of activated T cells or NF-ATc1. Thus, IGF-1 induces calcineurin-mediated signaling and activation of GATA-2, a marker of skeletal muscle hypertrophy, which cooperates with selected NF-ATc isoforms to activate gene expression programs leading to increased contractile protein synthesis and muscle hypertrophy. Simple huh?

Winstrol Depot Profile

Winstrol

(stanozolol)

Winstrol – Stanozolol is a very commonly used anabolic steroid for cutting cycles. While many people will attempt to use Dianabol or even Anadrol for cutting cycles, I´ve really never heard of anyone using Stanozolol for anything except a cutting cycle. It´s a bit of a one-trick-pony in this respect. Let me repeat that: Stanozolol is a cutting drug. Not many people will argue for its use in a bulking cycle. It´s certainly not a very effective compound for treating anemia (1) and thus, one could rightly assume that its role in bulking cycles is very limited. One novel use for Winstrol in any cycle (perhaps even bulking) would be to use it at a very limited dose, in order to lower SHBG. (2) One of the properties of Winstrol is it´s profound ability to lower SHBG much more than other steroids. A dose of .2mg/kg lowered SHBG significantly, which would in turn, raise the amount of free testosterone circulating in the body. As with 99% of steroids, however, it´s important to note that suppression of your natural hormonal levels will occur (though perhaps not to the extent that it will with many other steroids).(10) As with running virtually any compound, testosterone supplementation (i.e. running test in a cycle containing Winstrol) is warranted to avoid possible sexual dysfunction.

Winstrol & Stanozol Side Effects

Adding it to a heavy bulking cycle could be problematic, as Stanozolol is a 17aa compound, meaning that it´s been altered to endure the first pass through your liver without being destroyed. This makes it an orally active compound; so many people choose to take the pills which are available from both legitimate pharmaceutical companies as well as Underground Labs. Unfortunately, since it is 17aa, it is also liver toxic& in fact; Stanozolol has one of the worst hepatoxicity (mg for mg) of any steroid. This is the reason its addition to a bulking cycle could be problematic; generally a bulking cycle will be very heavy, dosage wise as well as toxicity-wise. It also has undesirable results on Cholesterol, and a mere 6mgs/day of Stanozolol can lower HDL by 33% and raise LDL by 29% (3). Cardiac Hypertrophy, even at lower doses could be a concern with Winstrol as well (4) Thus, many people limit their intake of Stanozolol to precontest or Summer-cutting types of cycles. It´s generally accepted that due to the toxicity issues of Stanozolol, its use should be limited to 6 weeks& as with anything though, many people have run it for up to 12 weeks with no problems.

Winstrol & Stanozol Use Effects

I ran Winstrol for about 3 months (12 weeks) at a dose of 100mgs Every Other Day (along with Test prop at 125mgs, every other day) and I suffered no ill-effects. My joints felt fine, and I can say that the only thing which was undesirable about that cycle was the injection pain. Generally, people report a “dry” and less lubricated feeling in their joints when on this drug (fluid retention is nil with Stanozolol), and also a “dry” overall look as regards contest prep. This could be due to a sort of “reverse-osmotic” effect…of course this is speculation, but people do look “dryer” on Winnie, and some even look dryer in the site they inject (more on this later). There are many conflicting reports on tendon strength and Stanozolol, even in medical journals. Some reports state that it weakens tendons, others that it strengthens them (and some speculation on the internet among many “guru´s” is that it strengthens them unevenly, leading to possible injury). For this reason, it may be best for athletes in explosive or high-impact sports to stay away from this drug. It has certainly been shown to be beneficial in some bone ailments induced by glucocorticoid induced stress (5) as well as having collagen producing properties (11), but with all of the anecdotal problems athletes have suffered with their joints while on Stanozolol, I simply can not recommend it with confidence to strength/speed athletes. I can say that personally, it was an effective compound for me and did not cause joint duress, but I can do without the discomfort of the shots, and have found other DHT based compounds to be far more effective (Masteron springs to mind).

As previously stated, this compound is unique, as it is available in both an oral form as well as an injectable form. Both forms contain the exact same compound, but injecting this compound (and yes, you can drink the injectable version, and no you shouldn´t) is superior to ingesting it orally in terms of nitrogen retention (6), and thus one would also imagine, for overall anabolism. Injecting it also has the advantage of avoiding the “first pass” through your liver, and thus places your liver under less stress.

Stanozolol (Winstrol) and Women

Stanozolol is also one of the few compounds that women can take safely, as it´s anabolic:androgenic ratio is quite skewed towards anabolism. It´s generally accepted that women can tolerate around 5-10mgs a day of this compound. Men, on the other hand can dose themselves in the .5-1.5mg/kg range. I find 100mgs injected every other Day to be sufficient, but of course, even with the injectable form, every day dosing is optimal. I tend to favor DHT based compounds, and have enjoyed great success with a Winstrol/Masteron/Testosterone cycle, but I suspect that replacing the Masteron in that cycle with Trenbolone would prove more beneficial for most bodybuilders seeking to get ripped.

Although the anabolic ratio of this product is very high as compared to its androgenic actions, not many people report huge weight gains off of Stanozolol. Also, interestingly, it has a relatively weak AR binding ability (7), which is quite unusual for a “cutting” steroid. Many of the effects of this drug, as relates to building muscle, are probably from its very high protein synthesizing ability (6) (8). In addition, since this compound is derived from DHT, it tends to promote a very nice, “quality” look to the user´s muscles, with little or no water retention. Winstrol does not aromatize at any rate and has even been speculated to have anti-progestenic properties (in at least some cases, where it may “block” that receptor) (9). If one were to run ancillary compounds with Stanozolol, perhaps Tamoxifen would be appropriate for it´s beneficial effects on blood lipids, but an anti-estrogen (in it´s classic sense) would be unwarranted; proper post cycle therapy is still needed, though.

Most underground labs produce Winstrol at very reasonable prices, in both an oral as well as injectable form. Unfortunately, production value differs vastly due to the varying size of the Stanozolol powder used to make the injectable version; the finer the powder, the smaller gauge needle it will fit through, and the easier the injection will be. Of course the opposite is also true& In any case, you should be paying under $100 for a 10ml bottle of 100mg/ml concentration, and roughly the same for 100 or so 10mg tablets

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