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11 months ago #1
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All profiles taken with permission from Marky's board... Thanks bro!

Testosterone Enanthate

Testosterone enantate is an ester of the naturally occurring andro-gen, testosterone. It is responsible for the normal development of the male sex characteristics. In the event of insufficient testosterone production an almost complete balance of the functional, anatomic, and psychic deficiency symptoms can be achieved by substituting testosterone." (Excerpt from the package insert of the German phar-maceutical group, Jenapharm GmbH for its compound Testosteron--Depot.)

The decisive advantage of Testosterone enanthate, however, is that this substance has a very strong androgenic effect and is coupled with an intense anabolic component. This allows almost everyone, within a short time, to build up a lot of strength and mass. The, rapid and strong weight gain is combined with distinct water reten-tion since a retention of electrolytes and water occurs. A pleasant effect is that the enormous strength gain goes hand in hand with the water retention. Weightlifters and powerlifters, especially in the higher weight classes, appreciate this characteristic. In this group, Testosterone enanthate, Testosterone cypionate, and Sustanon (see also Sustanon) are the number one steroids; this is also clearly re-flected in the dosages. Dosages of 500 mg, 1000 mg or even 2000 mg per day are no rarity-mind you, per day, not per week. Sports disciplines requiring a high degree of raw power, aggressiveness, and stamina offer an excellent application for Depot-Testosterone. The distinct water retention has also other advantages. Those who have problems with their joints, shoul-der cartilages or whose intervertebral disks, due to years of heavy training, show the first signs of wear, can get temporary relief by taking testosterone.

For the bodybuilder, the water retention that goes hand in hand with Testosterone enanthate cuts both ways. Certainly, one gets rap-idly massive and strong; however, one's reflected image after a few weeks often shows completely flat, watery, and puffy muscles. The muscles appear as if they have been pumped up with air' to new dimensions, yet during flexing nothing happens. Those who do not believe this should bother to go visit the so-called "bodybuilding champions" during the OFF-season when these exaggerated quanti-ties of "Testo" come in. A look at the now defunct bodybuilding magazine WBF makes it even clearer. An additional problem when taking Testosterone enanthate is that the conversion rate to estrogen is very high. This, on one hand, leads the body to store more fat; on the other hand, feminization symptoms (gynecomastia) are not unusual. However, it must be clearly stated that this depends on the athlete's predisposition. By all means, there are athletes who even with 1000 mg +/week do not show feminization symptoms or fat deposits and who suffer very low water retention. Others, however, develop pain in their nipples by simply looking at a Testoviron-De-pot ampule. Yet the additional intake of Nolvadex and Proviron should be considered at a dosage level of 500 mg+ /week. As already men-tioned, Testo is effective for everyone, whether a beginner or Mr. Olympia.

Testosterone enanthate also strongly promotes the regen-eration process. This leads to distinctly shorter overcompensation phases, an increased feeling of well-being, and a distinct energy in-crease. This is also the reason why several athletes are able to work out twice daily for several hours six times a week and continue to build up mass and strength. Those who can work out again two hours after a hard leg workout know that Testo works. Athletes who take Testosterone enanthate report an excessively strong pump effect during training. This "steroid pump" is attributed to an in-creased blood volume with a higher oxygen supply and a higher quantity of red blood cells. Those who take megadoses of Testoster-one enanthate will already feel an enormous pump in their upper thighs and calves when climbing stairs. Despite this we recommend that steroid novices stay away from all testosterone compounds. To make it very clear: Those who have never taken steroids do not yet need any testosterone and should wait until later when the "weaker" steroids begin to have little effect. For the more advanced, Testoster-one enanthate can either be taken alone or in combination with other compounds.

For adding mass Testosterone enanthate combines very well with Anadrol 50, Dianabol, Deca-Durabolin, and Parabolan. As an ex-ample, a stack of 100 mg Anadrol 50/day, 200 mg Deca-Durabolin/ week, and 500 mg Testosterone enanthate/week works well. After six weeks of intake the Anadrol 50, for example, could be replaced by 40 mg Dianabol/day. Principally, Testosterone enanthate can be combined with any steroid in order to gain mass. Apparently a synergetic effect between the androgen, Testosterone enanthate, and the anabolic steroids occurs which results in their bonding witli sev-eral receptors.Those who draw too much water with Testosterone enanthate and Dianabol or Anadrol, or who are more intere6ted in strength without gaining 20 pounds of body weight should take Testosterone enanthate together with Oxandrolone or Winstrol. The generally taken dose-as already mentioned-varies from 250 mg/ week up to 2000 mg/day. In our opinion the most sensible dosage for most athletes is between 250-1000 mg/week. Normally a higher dosage should not be necessary When taking up to 500 mg/week the dosage is normally taken all at once, thus 2 ml of solution are injected. A higher dosage should be divided into two injections per week. The quantity of the dose should be determined by the athlete's developmental stage, his goals, and the quantity of his previous steroid intake. The so called beach- and disco bodybuilders do not need 1000 mg of Testosterone enanthate/week. Our experience is that the Testosterone enanthate dosage for many, above all, depends on their financial resources. Since it is not, by any means, the most economic testosterone, most athletes do not take too much. Others switch to the cheaper Omnadren and because of the low price con-finue "shooting" Omnadren.

Testosterone enanthate has a strong influence on the hypothalamohypophysial testicular axis. The hypophysis is inhib-ited by a positive feedback. This leads to a negative influence on the endogenic testosterone production. Possible effects are described by the German Jenapharm GmbH in their package insert for the com-pound Testosteron Depot: " In a high-dosed treatment with test-osterone compounds an often reversible interruption or reduction of the spermatogenesis in the testes is to be expected and conse-quently also a reduction of the testes size." Consequently, after reading these state-ments, additional intake of HCG should be considered. Those who take Testosterone enanthate should consider the intake of HCG ev-ery 6-8 weeks. An injection of 5000 I.U. every fifth day over a period of 10 days (a total of 3 injections) helps to reduce this problem. At the end of the testosterone treatment the administration of HCG, Clomid, Nolvadex and Clenbuterol is now quite common. To some extent the use of these compounds helps absorb the catabolic phase and helps elevate the endogenic testosterone level. By this method the strength and mass loss which occur in any event can be reduced. Those who go off Testosterone enanthate 6cold turkey6 after several weeks of use will wonder how rapidly their body weights and former voluminous muscles will decrease. Even a slow tapering-off phase, that is reducing the dosage step by step, will not prevent a notice-able reduction. The only options available to the athlete consist of taking testosterone-stimulating compounds (HCG, Clomid, Cyclofenil), anti-catabolic substances (Clenbuterol, Ephedrine), or the very expensive growth hormones, or of switching to milder steroids (Deca-Durabolin, Winstrol, Primobolan). Most can get mas-sive and strong with Testosterone enanthate. However, only very few are able to retain their size after discontinuing the compound. This is also one of the reasons why really good bodybuilders, powerlifters, weightlighters, and others take the "stuff " all year long.

The side effects of Testosterone enanthate are mostly the distinct androgenic effect and the increased water retention. This is usually the reason for the frequent occurrence of hypertony (3). Those who have a predisposition for high blood pressure or whose blood pres-sure is elevated when they begin taking Testosterone enanthate should have it periodically checked by a physician. If necessary the intake of an antihypertensive drug (4) such as Catapresan is advisable. Many athletes experience a strong acne vulgaris with Testosterone enanthate which manifests itself on the back, chest, shoulders, and arms more than on the face. Athletes who take large quantities of Testo can often be easily recognized because of these characteristics. It is interesting to note that in some athletes these characteristics only occur after use of the compound has been discontinued, which implies a rebound effect. In severe cases the medicine Accutane can help. The already discussed feminization symptoms, especially gynecomastia, require the intake of an anti-estrogen. Sexual overstimulation with frequent erections at the beginning of intake is normal. In young athletes, "in addition to virilization,testosterone can also lead to an accelerated growth and bone maturation, to a premature epiphysial closing of the growth plates and thus a lower height" (Jenapharm GmbH, package insert for Testosteron-Depot).' Since mostly taller athletes are successful in bodybuilding, young adults should reflect carefully before taking any anabolic/andro-genic steroids, in particular, testosterone.

Doses: 250 mg - 1000 mg a week
Side effects: Medium
Strength & Mass gains: Good and solid

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10 months ago #26
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SPIRONOTHIAZ- Spironolactone/Hydrochlorthiazide

Spironothiazide is a diuretic. it is a combination of a potassium sparing diuretic, spironolactone (see also aldactone) and a thiazide. Thiazides, from their type, are similar to loop diuretics (see also Lasix). The main difference from loop diuretics is that thiazides lead to a lower release of calcium and have a less pronounced
and less drastic dehydrating effect.

Spironothiazide combines an aldosterone antagonist (see also Aldactone) with the stronger thiazid diuretic, making it a favorite and effective remedy for many competing body-builders to reduce excessive water. The advantage of this combina-tion, on the one hand, is that potassium reabsorption by the spironolactone can be compensated by the thiazide. This usually leads to a suspension of the potassium-linked side effects.

On the other hand, a good overall effect can also be obtained at lower dosages. Thus many use it as an alternative to the stronger and higher risk furosemides (Lasix). Spironothiazide is usually taken by athletes during the last days before a competition. Generally a dosage of 2-3 tablets of 50mg per day is taken and divided into 2-3 indi-vidual doses. The side effects are mostly caused by the expected imbalances in the fluids and electrolytes. These can manifest them-selves in muscle cramps, irregular pulse rate (especially at an increased potassium level) and dizziness.

In men, due to the antiandrogenic
characteristics of spironolactone, gynecomastia and impotence are also possible but unlikely due to the short intake (see also Aldactone). As a preventive measure, the additional adminis-tration of potassium should be avoided and the period of intake should be as short as possible. Spironothiazide must be prescribed and is usually difficult to find on the black market since most athletes get prescriptions from their physicians. Fifty tablets of 50/50 mg cost approximately $40 on the black market

10 months ago #27
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What is Clenbuterol?

Clenbuterol is a beta-2 agonist and is used in many countries as a broncodilator
for the treatment of asthma. Because of it's long half life, clenbuterol is not
FDA approved for medical use. It is a central nervous system stimulant and acts
like adrenaline. It shares many of the same side effects as other CNS stimulants
like ephedrine. Contrary to popular belief, Clenbuterol has a half life of 35
hours and not 48 hours.

Dosing and Cycling

Clenbuterol comes in 20mcg tablets, although it is also available in syrup, pump
and injectable form. It's also available as a powder in some areas. Doses are
very dependent on how well the user responds to the side effects, but somewhere
in the range of 4-8 tablets per day for men and 2-4 tablets a day for women is
most common. Clenbuterol loses its thermogenic effects after around 8 weeks when
body temperature drops back to normal. Its anabolic/anti-catabolic properties
fade away at around the 18 day mark. Taking the long half life into
consideration, the most effective way of cycling clen is 2 weeks on/ 2 weeks off
for no more than 12 weeks. Ephedrine or Yohimbine can be used in the off weeks.

Clenbuterol vs Ephedrine vs DNP

Ephedrine will raise metabolic levels by about 2-3 percent and 200mg of DNP
raises metabolic levels by about 30 percent. Clenbuterol raises metabolic levels
about 10 percent and it can raise body temperature several degrees.

DNP is by far the most effective fat burner but many people will never use it
because of the risks associated with it. It also offers no anti-catabolic
benefit. Although it does have anti-catabolic effect, ephedrine's short
half-life prevents it from being all that effective.

As far as side effects, Clenbuterol's are certainly milder than DNP's, and some
would even say milder than an ECA stack. There is no ECA-style crash on
Clenbuterol and many users find it easier on the prostate and sex drive. This
may in part be due to the fact that Clen is generally used for only 2 weeks at a
time.

Side effects

NAUSEA
NERVOUSNESS
DIZZINESS
DROWSINESS
DRY MOUTH
FACIAL FLUSHING
HEADACHE
HEARTBURN
INCREASED BLOOD PRESSURE
INCREASED SWEATING
INSOMNIA
LIGHTHEADEDNESS
MUSCLE CRAMPS
TREMORS
VOMITING
CHEST PAIN

The most significant side effects are muscle cramps, nervousness, headaches, and
increased blood pressure.

Muscle cramps can be avoided by drinking 1.5-2 gallons of water and consuming
bananas and oranges or supplementing with potassium tablets at 200-400mg a
day taken before bed on an empty stomach. Taurine at 3-5grams is a necessity in
minimizing cramps.

Headaches can easily be avoided with Tylenol Extra Strength taking at the first
signs of a headache.

Common Uses

Post-Cycle Therapy: Clen is used post cycle to aid in recovery. It allows the
user to continue eating large amounts of food, without worrying about adding
body fat. It also helps the user maintain more of his strength as well as his
intensity in the gym. Diet: Roughly the same as on cycle.

Fat loss: The most popular use for Clen, it also increases muscle hardness,
vascularity, strength and size on a caloric deficit. For the most significant
fat loss, Clen can be stacked with T3. Diet: A high protein(1.5g per lb of
bodyweight), moderate carb(0.5g to 1g per lb of bodyweight), low fat diet(0.25g
per lb of bodyweight) seems to work best with Clen.

Alternative to Steroids: Clenbuterol has mild steroid-like properties and can be
used by non-AS using bodybuilder to increase LBM as well as strength and muscle
hardness. Diet: A moderate carb, high protein, moderate fat diet work well.

Stimulant/Performance Enhancement: It can be used as a stimulant, but an ECA
stack may be a better choice because of it's much shorter half-life. Diet: To
take full advantage of the stimulatory effects of Clen, carbohydrates must be
included in the diet. Ketogenic diets do not work well in this case.

Precautions: Is Clen for you?

The same precautions that apply to Ephedrine must be applied to Clen, although
some people find ECA stacks are harsher than Clen. It should not be stacked
with other CNS stimulants such as Ephedrine and Yohimbine. These combinations
are unnecessary and potentially dangerous. Caffeine can be used in moderation
before a workout for an extra quick. burst of energy.

A word on Ketotifen

Ketotifen is safe antihistamine used extensively some European countries to
treat asthma and allergies. It can up regulate beta-2-receptors that Clen down
regulates. Basically, it allows users to extend their use of Clen for 6-8 weeks
at a time. 2-3mg a day is ideal, 10mg as found in "superclen" can make users
extremely drowsy. It also increases the effectiveness of Clen so doses must be
adjusted accordingly. The downfall of this drug is its ability to induce
extreme hunger is some people, which is not a desirable state to be in when
dieting.

Cycling Clenbuterol

Most users that report bad side effects and discontinue use are those who use
high doses right at the start of the cycle. The worst side effects occur within
the first 3-4 days of use.

A first time user should not exceed 40mcg the first day. Increase by one tab
until the side effects are not tolerable

Example of a first cycle:

Day1: 20mcg
Day2: 40mcg
Day3: 60mcg
Day4: 80mcg
Day5: 80mcg(Note: Increase the dose only when the side effects are tolerable)
Day6-Day12: 100mcg
Day13: 80 mcg (Tapering is not necessary, but it helps some users get back to
normal gradually)
Day14: 60 mcgs
Day15: off
Day16: off
Day 17: ECA/ NYC stack

Example of a second cycle:

Day1: 60mcg
Day2: 80mcg
Day3: 80mcg
Day4: 100mcg
Day5: 100mcg
Day6-Day12: 120mcg
Day13: 100 mcg
Day14: 80 mcgs
Day15: off
Day16: off
Day 17: ECA/ NYC stack

What else do I need to know?

Taurine MUST be used with Clen at 3-5g daily. Clenbuterol depletes taurine
levels in the liver which stops the conversion of T4 to T3 in the liver.
Taurine allows the user to avoid the dreaded rebound effect and painful muscle
cramps. It's a must with Clen.

Clenbuterol should not be taken too close to a workout. It can interfere with
your breathing and complete ruin your workout. When doing cardio, it's
advisable to stay at a consistent pace and avoid HIIT style routines.

Do not take Clen Past 4pm and drink plenty of water; 1.5-2 gallons a day.
Q: Will Clenbuterol show up on a drug test?

A: Only if you are being tested by a body that bans it. This is generally
international competition such as the Olympics. Employment, doctors physicals, military does NOT test for this

Drug Approximate Detection Time in Urine:
Alcohol 1-2 days
Amphetamines (crystal, Ice, crank, methamphetamines) 5-7 days
Barbituates Short-Acting (ie. secobarbital) 1-2 days
Barbituates Long-Acting (ie. phenobarbital) 2-3 weeks
Benzodiazepines (Librium®,Valium®,Serax,Xanax®) 2-30 days
Cannabinoids (THC,Marijuana) 20-90 days
Clenbuterol 2-4 days
Cocaine (Crack) 3-5 days
Codeine 2-5 days
Euphorics (MDMA, Ecstasy) 3-7 days
LSD 1-4 days
Methadone 3-5 days
Methaqualone (Quaalude) l-14 days
Opiates (heroin, Vicode, morphine, codeine) 2-7 days
Phencyclidine (PCP, Angel Dust) 1-30 days
Phenobarbital 10-20 days
Propoxyphene (Darvon) 1-3 days
Psilocybin (mushrooms) 3-5
Steroids (anabolic) oral 14 days

Courtousy of BIG ANDY & SWOLE

10 months ago #28
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Excellent info in a single thread. Appreciate it

10 months ago #29
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Ketotifen

I see a lot of newbie people trying to find good info on this so I thought it would be best to put it all in one place. I patched this from a wide range of sources as well as my own experience (also thanks to FONZ). This truly is a wonderdrug for BB.

What Is It?
Ketotifen is very safe antihistamine used extensively in Europe to treat bronchial asthma and allergies. It is also being studied as a treatment for colitis. When used for asthma, weight gain and an increase in appetite are among the most frequent side effects. Ketotifen also protects the cells in the stomach, small intestine and perhaps the rest of the gut from a number of toxins. A number of case studies suggest that it may be helpful treating skin problems such as acne. Ketotifen also reduces edema (swelling and puffiness caused by water retention) around sores.

Ketotifen Studies
German researchers have published data showing that ketotifen lowers tnf-alpha in the test tube. One study used ketotifen in combination with oxymethadone, a steroid like Megace that helps people gain weight, so it is hard to gauge what effect ketotifen had (the study notes a 14% reduction in TNF-alpha levels and weight gains of 11-12 pounds in less than four weeks). A larger placebo controlled study of this combination is underway. The other study used ketotifen by itself in eight patients with elevated TNF-alpha, (but no wasting). Taking ketotifen for 12 weeks, these patients gained an average of six pounds, had increases in their body cell mass and reductions in their TNF-alpha levels.

Side Effects and Toxicity
Ketotifen is virtually non-toxic (although it is not advised for patients with epilepsy). People who took twenty times the recommended dose (in suicide attempts) suffered no serious consequences (other than embarrassment). Its primary side effects seem to be temporary drowsiness, dry mouth,(and other mucuos membranes) appetite stimulation and weight gain.

Dosing and side effects
No studies have been done to find the most effective dose but the German researchers used 4 mg ED. Dan Duchaine (who discovered ketos use for BB) suggested 10mg ED but in my experience this much is not needed and makes u far too sleepy. I find that 3-4mg ED seems ideal. However, much higher doses have been shown to be quite safe with no adverse affects other than increased drowsiness and appetite – it will make u hungry for solid foods. You can take it divided in the day or all at once.

Ketotifen and Clen
Clenbuterol is a beta 2 agonist which has a limited anabolic effect during its first few days of use and afterward is normally used to fight fat. At higher doses, however, it can be catabolic to muscle and it must be cycled on a 2 week on, 2 week of basis or the beta 2 receptors that clen binds to become saturated and down regulate.

Ketotifen’s magic is that it upregulates the beta-receptors including the beta 2s that clen uses. As long as you are taking ketotifen, it will continue to clean these receptors, never allowing them to downregulate – even while on a heavy clen cycle. That means you can continue to take clen indefinitely without having to cycle off to regenerate the receptors. 2-3mg ED can upregulate even severely shut down receptors within a week.

It also means that you don’t need as much clen to get the same benefits. It seems u can take about 30-40% less clen and it be equally effective. FONZ posted that it also increases the number of receptor sites on the surface of the cell, allowing more clen to attach and perhaps this is the reason for the increased efficacy. Ketotifen also seems to lessen the sides of clen including the jitters.

Ketotifen and ECA
Perhaps an even better use for ketotifen is taking it with the ECA stack. While the thermogenic effect of ephedrine is not as potent as clen because it doesn't have a high receptor affinity, and it is not limited to beta-2 receptors. In fact it seems to have a good effect on beta 3 receptors as well, which act as a type of thermogenic messenger and over half of ephedrine effect is from beta-3 stimulation. Clen has almost no effect on beta 3 however. So by keeping the beta 2 receptors up, ketotifen can allow the benefits of continuous beta 2 and beta 3 stimulation from ephedrine.

10 months ago #30
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SPIRONOTHIAZ- Spironolactone/Hydrochlorthiazide

Spironothiazide is a diuretic. it is a combination of a potassium sparing diuretic, spironolactone (see also aldactone) and a thiazide. Thiazides, from their type, are similar to loop diuretics (see also Lasix). The main difference from loop diuretics is that thiazides lead to a lower release of calcium and have a less pronounced
and less drastic dehydrating effect.

Spironothiazide combines an aldosterone antagonist (see also Aldactone) with the stronger thiazid diuretic, making it a favorite and effective remedy for many competing body-builders to reduce excessive water. The advantage of this combina-tion, on the one hand, is that potassium reabsorption by the spironolactone can be compensated by the thiazide. This usually leads to a suspension of the potassium-linked side effects.

On the other hand, a good overall effect can also be obtained at lower dosages. Thus many use it as an alternative to the stronger and higher risk furosemides (Lasix). Spironothiazide is usually taken by athletes during the last days before a competition. Generally a dosage of 2-3 tablets of 50mg per day is taken and divided into 2-3 indi-vidual doses. The side effects are mostly caused by the expected imbalances in the fluids and electrolytes. These can manifest them-selves in muscle cramps, irregular pulse rate (especially at an increased potassium level) and dizziness.

In men, due to the antiandrogenic
characteristics of spironolactone, gynecomastia and impotence are also possible but unlikely due to the short intake (see also Aldactone). As a preventive measure, the additional adminis-tration of potassium should be avoided and the period of intake should be as short as possible. Spironothiazide must be prescribed and is usually difficult to find on the black market since most athletes get prescriptions from their physicians. Fifty tablets of 50/50 mg cost approximately $40 on the black market

10 months ago #31
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Thyroid Hormone for Weight Loss: Physiologic and Metabolic Effects

by Karl Hoffman

Introduction

It has been over 100 years since the discovery by Magnus-Levy that thyroid hormones play a central role in energy homeostasis, and 75 years since the hormones were first used for weight loss. Despite this great length of time, the precise mechanisms by which thyroid hormones exert their calorigenic effect are not completely characterized, and still actively debated. Despite numerous clinical studies having shown that the administration of thyroid hormone induces weight loss, it is not currently indicated as a weight loss agent. This is probably due to the number of side effects observed during thyroid hormone use at the relatively high doses used in the majority of obesity treatment studies. These deleterious effects include cardiac problems such as tachycardia and atrial arrhythmias, loss of muscle mass as well as fat, increased bone resorption and muscle weakness. Nevertheless, thyroid hormones, particularly triiodothyronine (T3) are a mainstay in the arsenal of drugs used by bodybuilders for fat loss. The widespread underground use of T3 warrants an understanding of its mechanism of action, as well as a knowledge of how it is most effectively and safely used, with an eye to minimizing side effects.

Thyroid Function and Physiology

Before jumping right into a discussion of the use of thyroid hormone for fat loss, a little review of thyroid function and physiology might be in order. The thyroid gland secretes two hormones of interest to us, thyroxine (T4) and triiodothyronine (T3). T3 is considered the physiologically active hormone, and T4 is converted peripherally into T3 by the action of the enzyme deiodinase. The bulk of the body's T3 (about 80%) comes from this conversion. 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 the hypothalamus. This is analogous to testosterone production, where GnRH from the hypothalamus causes the pituitary to release LH, which in turn stimulates the testes to produce testosterone.

In addition to T3, it has recently been recognized that there exist two additional active metabolites of T3: 3,5 and 3,3' diiodothyronines, which we will collectively call T2. Studies have shown that 3,3'-T2 may be more effective in raising resting metabolic rate when hypothyroid subjects are treated with T3, than when normal (euthyroid) subjects are given T3. Therefore in normal subjects 3,5-T2 may be the principal active metabolite of T3 (1)

Like the hypothalamic-pituitary-gonadal axis, the thyroid gland is under negative feedback control. When T3 levels go up, TSH secretion is suppressed. This is the mechanism whereby exogenous thyroid hormone suppresses natural thyroid hormone production. There is a difference though between the way anabolic steroids suppress natural testosterone production and the way T3 suppresses the thyroid. With steroids, the longer and heavier the cycle is, the longer your natural testosterone is suppressed. This is not the case with exogenous thyroid hormone.

An early study that looked at thyroid function and recovery under the influence of exogenous thyroid hormone was undertaken by Greer (2). He looked at patients who were misdiagnosed as being hypothyroid and put on thyroid hormone replacement for as long as 30 years. When the medication was withdrawn, their thyroids quickly returned to normal.

Here is a remark about Greer's classic paper from a later author:

"In 1951, Greer reported the pattern of recovery of thyroid function after stopping suppressive treatment with thyroid hormone in euthyroid [normal] subjects based on sequential measurements of their thyroidal uptake of radioiodine. He observed that after withdrawal of exogenous thyroid therapy, thyroid function, in terms of radioiodine uptake, returned to normal in most subjects within two weeks. He further observed that thyroid function returned as rapidly in those subjects whose glands had been depressed by several years of thyroid medication as it did in those whose gland had been depressed for only a few days" (3)

These results have been subsequently verified in several studies.(3)(4) So contrary to what has been stated in the bodybuilding literature, there is no evidence that long term thyroid supplementation will somehow damage your thyroid gland. Nevertheless, most bodybuilders will choose to cycle their T3 (or T4 which in most cases works just as well) as part of a cutting strategy, since T3 is catabolic with respect to muscle just as it is with fat. As previously mentioned, long term T3 induced hyperthyroidism is also catabolic to bone as well as muscle.

The proviso about T4 vs T3 for weight loss alluded to above needs some elaboration. There have been a number of studies that have shown that during starvation, or when carbohydrate intake is reduced to approximately 25 to 50 grams per day, levels of deiodinase decline, hindering the conversion of T4 to the physiologically active T3.(5) From an evolutionary standpoint this makes sense: during periods of starvation the body, teleologically speaking, would like to reduce its basal metabolic rate to preserve fat and especially muscle stores. However, a recent study demonstrating the effectiveness and safety of the ketogenic diet for weight loss recorded no change in circulating T3 levels.(6) So this issue not completely settled. Nevertheless, persons contemplating thyroid supplementation during ketogenic dieting might prefer T3 over T4 since the bulk of the research does suggest a decline in the peripheral conversion of T4 to T3 during low carb dieting.

Now that we have reviewed a little about thyroid function, let's consider just how it is that thyroid hormone exerts its fat burning effects.

Increased Oxidative Energy Metabolism

Thyroid hormone has long been recognized as a major regulator of the oxidative metabolism of energy producing substrates (food or stored substrates like fat, muscle, and glycogen) by the mitochondria. The mitochondria are often called the "cell's powerhouses" because this is where foodstuffs are turned into useful energy in the form of ATP. T3 and T2 increase the flux of nutrients into the mitochondria as well as the rate at which they are oxidized, by increasing the activities of the enzymes involved in the oxidative metabolic pathway. The increased rate of oxidation is reflected by an increase in oxygen consumption by the body.

T3 and T2 appear to act by different mechanisms to produce different results. T2 is believed to act on the mitochondria directly, increasing the rate of mitochondrial respiration, with a consequent increase in ATP production. T3 on the other hand acts at the nuclear level, inducing the transcription of genes controlling energy metabolism, primarily the genes for so-called uncoupling proteins, or UCP (see below). The time course of these two actions is quite different. T2 begins to increase mitochondrial respiration and metabolic rate immediately. T3 on the other hand requires a day or longer to increase RMR since the synthesis of new proteins, the UCP, is required (1).

There are a number of putative mechanisms whereby T2 is believed to increase mitochondrial energy production rates, resulting in increased ATP levels. These include an increased influx of Ca++ into the mitochondria, with a resulting increase in mitochondrial dehydrogenases. This in turn would lead to an increase in reduced substrates available for oxidation. An increase in cytochrome oxidase activity has also been observed. This would hasten the reduction of O2, speeding up respiration. These and a number of other proposed mechanisms for the action of T2 are reviewed by Lannie et al.(7)

What is the fate of the extra ATP produced during hyperthyroidism? There are a number of ways by which the increased ATP promotes an increase in metabolic activity, including the following:

Increased Na+/K+ATPase. This is the enzyme responsible for controlling the Na/K pump, which regulates the relative intracellular and extracellular concentrations of these ions, maintaining the normal transmembrane ion gradient. Sestoft(7) has estimated this effect may account for up to to 10% of the increased ATP usage.

Increased Ca++-dependent ATPase. The intracellular concentration of calcium must be kept lower than the extracellular concentration to maintain normal cellular function. ATP is required to pump out excess calcium. It has been estimated that 10% of a cell's energy expenditure is used just to maintain Ca++ homeostasis. (1)

Substrate cycling. Hyperthyroidism induces a futile cycle of lipogenesis/lipolysis in fat cells. The stored triglycerides are broken down into free fatty acids and glycerol, then reformed back into triglycerides again. This is an energy dependent process that utilizes some of the excess ATP produced in the hyperthyroid state (8). Futile cycling has been estimated to use approximately 15% of the excess ATP created during hyperthyroidism (8)

Increased Heart Work. This puts perhaps the greatest single demand on ATP usage, with increased heart rate and force of contraction accounting for up to 30% to 40% of ATP usage in hyperthyroidism (9)

10 months ago #32
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Thyroid Hormone for Weight Loss: Physiologic and Metabolic Effects - Continued

Mitochondrial Uncoupling

As mentioned, the mitochondria are often characterized as the cell's powerhouse. They convert foodstuffs into ATP, which is used to fuel all the body's metabolic processes. Much research suggests that T3, like another much more potent agent DNP, has the ability to uncouple oxidation of substrates from ATP production. T3 is believed to increase the production of so called uncoupling proteins. Uncoupling protein (UCP) is a transporter family that is present in the mitochondrial inner membrane, and as its name suggests, it uncouples respiration from ATP synthesis by dissipating the transmembrane proton gradient as heat. Instead of useful ATP being produced from energy substrates, heat is generated instead. There are conflicting studies about the importance of T3 induced uncoupling. Animal studies have demonstrated an actual increase in ATP production commensurate with increased oxygen consumption as we discussed above. Other studies in humans have shown that in fact uncoupling in skeletal muscle does occur. This would contribute to T3 induced thermogenesis, with a resulting increase in basal metabolic rate.(10)

To make up for the deficit in ATP production (as well as provide fuel for the extra ATP production discussed above) more substrates must be burned for fuel, resulting in fat loss. Unfortunately, along with the fat that is burned, some protein from muscle is also catabolized for energy. This is the downside of T3 use, and the reason many people choose to use an anabolic steroid or prohormone during a T3 cycle to help preserve muscle mass. Studies have shown this to be an effective strategy (11). (Muscle glycogen is also more rapidly depleted, and less efficiently stored during hyperthyroidism. This may account for some of the muscle weakness generally associated with T3 use.)

Countering T3 induced muscle loss with AAS or prohormones makes sense from a physiological viewpoint as well. Thyroid hormone muscle protein breakdown is mainly mediated via the so-called ubiquitin-proteasome pathway. (12). (There are several independent metabolic pathways of protein breakdown in the body. For instance, another pathway, the lysosomal pathway, is responsible for the accelerated rate of muscle protein breakdown during and after exercise.) Testosterone administration has been shown to decrease ubiquitin-proteasome activity. (13) So AAS specifically target the muscle protein breakdown process stimulated by T3.

What may not be an effective strategy to maintain muscle mass during a T3 cycle is the use of exogenous growth hormone (GH). Studies have shown that when GH and T3 are administered concurrently, the increased nitrogen retention normally associated with GH use is abolished. This has been attributed to the observation that T3 increases levels of insulin like growth factor binding protein, reducing the bioavailability of igf-1 (14). Nevertheless, GH has fat burning properties independent of igf-1, so using GH with T3 would act additively to speed fat burning, but with little if any preservation of lean body mass. So again, if GH is used in conjunction with T3, anabolic steroid/prohormone use would be indicated.

Andregenic Receptor Modulation

Administration of T3 has been shown to upregulate the so-called beta 2 adrenergic receptor in fat tissue. What is the significance of this effect for fat loss? Before fat can be used as fuel, it must be mobilized from the fat cells where it is stored. An enzyme called Hormone Sensitive Lipase (HSL) is the rate-controlling enzyme in lipolysis, or fat mobilization. The body produces two catecholamines, epinephrine and norepinephrine, which bind to the beta 2 receptor and activate HSL. The upregulation of the beta 2 receptor due to T3 results in an increased ability of catecholamines to activate HSL, leading to increased lipolysis.

Bodybuilders often use drugs like clenbuterol, which bind to the beta 2 receptors and activate them in the same way as the body's endogenous catecholamines. The use of clenbuterol along with T3 can produce an additive lipolytic effect: T3 increases the number of receptors, while clenbuterol binds to the receptors activating HSL and increasing lipolysis. Since clenbuterol itself downregulates the beta 2 receptor, most bodybuilders use clenbuterol in a two week on/ two week off cycle, the rationale being that this minimizes downregulation and allows receptor recovery. Another option is to use the antihistamine ketotifen concurrently with the clenbuterol. Studies have shown that ketotifen attenuates the beta 2 receptor downregulation caused by clenbuterol (15). Moreover, research in AIDS patients has shown that ketotifen blocks the production of the proinflammatory and catabolic cytokine TNF-alpha (16). This may be of relevance to bodybuilders since there is evidence showing TNF lowers both testosterone and IGF-1 levels quite significantly (17) (18), while strenuous exercise elevates TNF levels. (19)

Besides increasing beta 2 receptor density in adipose tissue, T3 upregulates this receptor in human skeletal muscle (12). This has some very intriguing if somewhat speculative implications for the combined use of clenbuterol and T3. Animal studies have shown that catecholamines, particularly clenbuterol, inhibit Ca++ dependent skeletal muscle proteolysis (20). Like the lysosomal and ubiquitin-proteasome pathways discussed above, Ca++ regulated proteolysis is yet another way for the body to degrade muscle protein. Again the implications are enticing: Increased beta 2 receptor density from T3 use, coupled with the beta 2 agonist clenbuterol, could slow this pathway of muscle catabolism.

Another adrenergic receptor important to lipolysis is the alpha 2 receptor, which impedes fat mobilization by counteracting the effects of the beta 2 receptor. There are some conflicting studies about the effects of T3 on the alpha 2 receptor, with studies showing either a downregulation (21) or no effect (22). If T3 does in fact downregulate alpha 2 receptors, this would further aid lipolysis.

Studies in rats have shown that inducing hyperthyroidism increases the lipolytic beta 3 receptor density in white adipose tissue by 70% (23). Beta 3 receptors are abundant in human white adipose tissue as well, and if T3 administration has the same effect in humans, this could could contribute significantly to T3 induced fat loss. This might also argue for taking a currently available beta 3 agonist such as octopamine along with T3 and perhaps clenbuterol.

Decreased Phosphodiesterase Expression

In hyperthyroid patients as well as in normal subjects given T3, levels of the enzyme phosphodiesterase are lowered in fat cells (20). When lipolytic hormones like epinephrine (adrenaline) bind to the beta 2 receptor described above, they initiate a signaling cascade mediated by the so called “second messenger” cyclic AMP (cAMP). cAMP in turn acts on other cellular enzymes to initiate and maintain lipolysis. The original signal is terminated when cAMP is degraded by the enzyme phosphodiesterase. Clearly, maintaining elevated cAMP levels, by lowering phosphodiesterase concentrations with T3, will prolong lipolysis.

As an aside, caffeine is thought to exert at least a portion of its lipolytic action by lowering phosphodiesterase in fat cells. Interestingly, Viagra and Cialis are also phosphodiesterase inhibitors but their action seems to be limited to relaxing vascular smooth muscles.

Increased Growth Hormone Secretion

In vitro, animal, and human studies have all demonstrated that T3 administration increases growth hormone production. (24)(25) Since GH is calorigenic aside from any increase in igf-1, elevated GH may contribute to some of the fat burning associated with T3 administration. This effect may obviate the need for the use of expensive recombinant HGH, as mentioned above.

Decreased Insulin Secretion

Insulin is well known as a lipogenic hormone. It promotes fat storage by facilitating the uptake of fatty acids by adipocytes, and reducing lipid oxidation in muscle tissue. Several studies have shown that thyroid hormone is associated with glucose intolerance resulting from decreased glucose stimulated insulin secretion (26).

This defect in insulin secretion is believed to result from an increase in the rate of apoptosis (programmed cell death) of pancreatic beta cells as a direct effect of thyroid hormone excess.(27) This process is reversible, since when thyroid hormone is withdrawn the rate of beta cell replication increases until homeostasis returns. However, there are conflicting studies regarding the effects of T3 on insulin. For example, Dimitriadis et al (28) showed a decrease in glucose stimulated insulin secretion, consistent with (25), but an increase in basal insulin. They also observed increased insulin clearance, with a compensatory increase in basal insulin secretion.

So if in fact the hyperthyroid state is associated with lower insulin levels, this could explain a portion of hyperthyroid stimulated lipolysis. The obvious downside here is that insulin is also an anabolic hormone. Basal insulin concentration is thought to limit the action of the ubiquitin-proteasome degradative pathway of muscle protein breakdown (29). Of course supplementing with insulin during T3 use would be counterproductive. However, as mentioned above, anabolic steroids inhibit ubiquitin-proteasome activity, so their use could counter any loss in muscle anabolism resulting from a drop insulin levels.

10 months ago #33
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Thyroid Hormone for Weight Loss: Physiologic and Metabolic Effects - Continued

The Future

As mentioned at the beginning of this article, a major roadblock in the adoption of T3 by the medical community as an antiobesity agent is its deleterious effect on the heart. Recent research has identified two isoforms of the thyroid hormone receptor, TRalpha and TRbeta. The TRalpha-form may preferentially regulate the heart rate, and an experimental agent, GC-1, has been developed that selectively binds the TRbeta receptor, with minimal effects on the heart (30). The distribution and actions of TRalpha and TRbeta throughout the body are not yet well characterized. However should it turn out that TRalpha is specific to the heart, then drugs like GC-1 may turn out to be effective fat burning agents with a much safer profile that T3 or T4.

One alleged “futuristic” agent that is here now is T2, or 3,5-Di-iodo-L-thyronine, the T3 metabolite discussed above. Unfortunately, this product does not live up to its hype. It has been claimed to be as or more effective that T3 for fat burning with minimal suppression of endogenous thyroid production. Regarding the relative effectiveness of T2 as a lipolytic agent, and its effect on TSH, this topic was thoroughly covered in a recent article by Bryan Haycock in Muscle Monthly.

All of my research into this subject has led me to the same conclusion reached by Mr. Haycock. That is, T2 is only slightly less suppressive of TSH than is T3, and only packs a portion of the lipolytic punch of T3, with no ability to increase the expression of the UCPs, which is a major determinant of the action of thyroid hormone.

Summary

We have discussed a number of ways by which T3, and its active metabolite T2 act to increase resting energy expenditure. Also discussed were some drawbacks of T3 use, such as cardiac stress, as well as the potential loss of muscle mass. It is ironic that the latter may be of more concern to many bodybuilders that the other more serious potential impacts on health. Nevertheless, used moderately and for short periods (a couple of months or less) in people with no preexisting cardiovascular disease T3 has a relatively safe medical profile, compared to other lipolytic agents like DNP. Perhaps most importantly we have presented substantial evidence that even the long-term use of supraphysiological levels of T3 does not damage the thyroid gland.

References:

(1) Endocrinology 2002 Feb;143(2):504-10 Are the effects of T3 on resting metabolic rate in euthyroid rats entirely caused by T3 itself? Moreno M, Lombardi A, Beneduce L, Silvestri E, Pinna G, Goglia F, Lanni A.

(2)(Greer,M. N Engl J Med 244:385, 1951)

(3)N Engl J Med 1975 Oct 2;293(14):681-4 Recovery of pituitary thyrotropic function after withdrawal of prolonged thyroid-suppression therapy. Vagenakis AG, Braverman LE, Azizi F, Portinay GI, Ingbar SH.

(4) J Clin Endocrinol Metab 1975 Jul;41(1):70-80 Patterns off recovery of the hypothalamic-pituitary-thyroid axis in patients taken of chronic thyroid therapy. Krugman LG, Hershman JM, Chopra IJ, Levine GA, Pekary E, Geffner DL, Chua Teco GN

(5) Int J Obes 1983;7(2):123-31 The effect of a low-calorie diet alone and in combination with triiodothyronine therapy on weight loss and hypophyseal thyroid function in obesity. Koppeschaar HP, Meinders AE, Schwarz F.

(6) Am J Med 2002 Jul;113(1):30-6 Effect of 6-month adherence to a very low carbohydrate diet program. Westman EC, Yancy WS, Edman JS, Tomlin KF, Perkins CE.

(7) J Endocrinol Invest 2001 Dec;24(11):897-913 Control of energy metabolism by iodothyronines.
Lanni A, Moreno M, Lombardi A, de Lange P, Goglia F

(8) Clin Endocrinol (Oxf) 1980 Nov;13(5):489-506 Metabolic aspects of the calorigenic effect of thyroid hormone in mammals. Sestoft L.

(9)Annu Rev Nutr 1995;15:263-91 Thermogenesis and thyroid function. Freake HC, Oppenheimer JH.

(10) J Clin Invest 2001 Sep;108(5):733-7 Effect of triiodothyronine on mitochondrial energy coupling in human skeletal muscle. Lebon V, Dufour S, Petersen KF, Ren J, Jucker BM, Slezak LA, Cline GW, Rothman DL, Shulman GI.

(11)J Clin Endocrinol Metab 1999 Jan;84(1):207-12 Testosterone administration preserves protein balance but not muscle strength during 28 days of bed rest. Zachwieja JJ, Smith SR, Lovejoy JC, Rood JC, Windhauser MM, Bray GA.

(12) Genome Res 2002 Feb;12(2):281-91 In vivo regulation of human skeletal muscle gene expression by thyroid hormone. Clement K, Viguerie N, Diehn M, Alizadeh A, Barbe P, Thalamas C, Storey JD, Brown PO, Barsh GS, Langin D.

(13) J Clin Endocrinol Metab 2003 Jan;88(1):358-62 Related Articles, Links Differential anabolic effects of testosterone and amino Acid feeding in older men. Ferrando AA, Sheffield-Moore M, Paddon-Jones D, Wolfe RR, Urban RJ.

(14) J Hepatol 1996 Mar;24(3):313-9 Effects of long-term growth hormone (GH) and triiodothyronine (T3) administration on functional hepatic nitrogen clearance in normal man. Wolthers T, Grofte T, Moller N, Vilstrup H, Jorgensen JO.

(15) Cardiovasc Res 1998 Oct;40(1):211-22 Terbutaline-induced desensitization of human cardiac beta 2-adrenoceptor-mediated positive inotropic effects: attenuation by ketotifen. Poller U, Fuchs B, Gorf A, Jakubetz J, Radke J, Ponicke K, Brodde OE.

(16) Eur J Clin Pharmacol 1996;50(3):167-70 Ketotifen in HIV-infected patients: effects on body weight and release of TNF-alpha. Ockenga J, Rohde F, Suttmann U, Herbarth L, Ballmaier M, Schedel I.

(17)Endocrinology 1998 Jun;139(6):2863-8 Tumor necrosis factor-alpha inhibits leydig cell steroidogenesis through a decrease in steroidogenic acute regulatory protein expression. Mauduit C, Gasnier F, Rey C, Chauvin MA, Stocco DM, Louisot P, Benahmed M.

(18) Growth Horm IGF Res 2001 Aug;11(4):250-60 Tissue-specific regulation of IGF-I and IGF-binding proteins in response to TNFalpha. Lang CH, Nystrom GJ, Frost RA.

(19) Exerc Immunol Rev 2001;7:18-31 Exercise and cytokines with particular focus on muscle-derived IL-6. Pedersen BK, Steensberg A, Fischer C, Keller C, Ostrowski K, Schjerling P.

(20) Am J Physiol Endocrinol Metab 2001 Sep;281(3):E449-54 Catecholamines inhibit Ca(2+)-dependent proteolysis in rat skeletal muscle through beta(2)-adrenoceptors and cAMP. Navegantes LC, Resano NM, Migliorini RH, Kettelhut IC

(21) J Clin Endocrinol Metab 2002 Feb;87(2):630-4 Regulation of human adipocyte gene expression by thyroid hormone Viguerie N, Millet L, Avizou S, Vidal H, Larrouy D, Langin D.

(22) Metabolism 1987 Nov;36(11):1031-9 Alpha 2- and beta-adrenergic receptor binding and action in gluteal adipocytes from patients with hypothyroidism and hyperthyroidism. Richelsen B, Sorensen NS

(23) Br J Pharmacol 2000 Feb;129(3):448-56 Regulation of beta 1- and beta 3-adrenergic agonist-stimulated lipolytic response in hyperthyroid and hypothyroid rat white adipocytes. Germack R, Starzec A, Perret GY

(24) Braz J Med Biol Res 1994 May;27(5):1269-72 Role of thyroid hormone in the control of growth hormone gene expression. Volpato CB, Nunes MT.

(25) Am J Physiol 1999 Aug;277(2 Pt 1):E370-9 Related Articles, Links Low-dose T(3) improves the bed rest model of simulated weightlessness in men and women. Lovejoy JC, Smith SR, Zachwieja JJ, Bray GA, Windhauser MM, Wickersham PJ, Veldhuis JD, Tulley R, de la Bretonne JA.

(26) Life Sci 2002 Jul 19;71(9):1059-70 Evidence for a deficient pancreatic beta-cell response in a rat model of hyperthyroidism. Fukuchi M, Shimabukuro M, Shimajiri Y, Oshiro Y, Higa M, Akamine H, Komiya I, Takasu N.

(27) Diabetologia 2002 Jun;45(6):851-5 Thyroxine induces pancreatic beta cell apoptosis in rats.
Jorns A, Tiedge M, Lenzen S.

(28) Am J Physiol 1985 May;248(5 Pt 1):E593-601 Effect of thyroid hormone excess on action, secretion, and metabolism of insulin in humans.= Dimitriadis G, Baker B, Marsh H, Mandarino L, Rizza R, Bergman R, Haymond M, Gerich J

(29) Curr Opin Clin Nutr Metab Care 2000 Jan;3(1):67-71 Effects of insulin on muscle tissue.
Wolfe RR.

(30) J Steroid Biochem Mol Biol 2001 Jan-Mar;76(1-5):31-42 Selective modulation of thyroid hormone receptor action. Baxter JD, Dillmann WH, West BL, Huber R, Furlow JD, Fletterick RJ, Webb P, Apriletti JW, Scanlan TS.

10 months ago #34
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More info on igf-1

To understand how IGF-1 works you have to understand how muscles grow. The ability of muscle tissue to constantly regenerate in response to activity makes it unique. It’s 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. Once this happens these cells divide and genetically change 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 come from. The larger the muscle, the more nuclei you need to maintain it. In fact there is a "nuclear to volume" ratio that cannot be overridden. Whenever a muscle grows in response to functional overload there is a positive correlation between the increase in the number of myonuclei and the increase in fiber cross sectional area (CSA). When satellite cells are prohibited from donating new nuclei, overloaded muscle will not grow (Rosenblatt,1992 & 1994; Phelan,1997). So you see, one important key to unnatural muscle growth is the activation of satellite cells by growth factors such as IGF-1.
IGF-1 stimulates both proliferation (an increase in cell number) and differentiation (a conversion to muscle specific nuclei) in an autocrine-paracrine manner, although it induces differentiation to a much greater degree. This is in agreement with the Dual Effector theory. In fact, 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 (Adams,1998).
On the very cutting edge of research scientists are now discovering 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 signaling pathway, and subsequent muscle fiber hypertrophy (Semsarian, 1999; Musaro, 1999). I am by no means a geneticist so I hesitated even bringing this new research up. In summary 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. Did you get all that?

10 months ago #35
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PGF2a

Prostoglandin Factor 2 alpha(PGF2) is not a hormone at all, but can have some interesting effects of the muscle building process, fat loss and endocrine system. This drug is used agriculture to syncrinize ovulation and induce labor or abortions. It must absolutly stay out of contact with females!!!!! It is easily trandermaly absorbed. In the male bodybuilder it can have many benifits.

  1. Anabolic: In site specific IM injections it cuases muscle size and definition to increase, it is especialy useful in getting stubborn nonresponding muscles to grow, even after treatment is over. I see it less as an anabolic and more a anti-catabolic, precontest, this stuff will save pounds of tissue.People have reported loss in strength due to pain, though I have never experienced it.
    -for this purpose I recomend 10-60 iu 5-8 times a day, starting at the lower dose/frequency working SLOWLY up to max.
  2. Fat loss: This stuff kills fat cells on contact!!! Don't beleive me, go look it up. Only compound I can think of that actually does this. Fat cells die, actually dissolve, releasing fatty acids into the blood streem, so you gotta due cartio right after(or T3,clen) On T3 you can actually save Lean tissue by using this as frequently as possible. It can be used transdermal(check Lab for recipe) or sub-cue right where you need it. I accually carved out a six pack in a week this way. Put it right in the where want cuts to form.
  3. Endocrine:I just read a whole buch of old german studies that recently were translated that showed certain Prostoglandins increased LH. The study also showed increased adrogen activity on the inter-celluar basis. I will do more research for you all on this and report back later.
    Sounds like the perfect drug right? Wrong! This **** has got more sides than a giga-gon(let me know who got that), I've seen this **** kill a horse, 20some minutes after injection. It causes asthma attacks to a degree in everybody(sometimes aysimtomatic), contractions of smooth muscle(diareaha), intense injection site pain, fever, and genneral feeling of "**** this sucks".

Prostaglandin F2{alpha} stimulates growth of skeletal muscle cells via an NFATC2-dependent pathway.

  • Horsley V, Pavlath GK
    J Cell Biol 2003 Apr 14;161(1):111-118.

Skeletal muscle growth requires multiple steps to form large multinucleated muscle cells. Molecules that stimulate muscle growth may be therapeutic for muscle loss associated with aging, injury, or disease. However, few factors are known to increase muscle cell size. We demonstrate that prostaglandin F2alpha (PGF2alpha) as well as two analogues augment muscle cell size in vitro. This increased myotube size is not due to PGF2alpha-enhancing cell fusion that initially forms myotubes, but rather to PGF2alpha recruiting the fusion of cells with preexisting multinucleated cells. This growth is mediated through the PGF2alpha receptor (FP receptor). As the FP receptor can increase levels of intracellular calcium, the involvement of the calcium-regulated transcription factor nuclear factor of activated T cells (NFAT) in mediating PGF2alpha-enhanced cell growth was examined. We show that NFAT is activated by PGF2alpha, and the isoform NFATC2 is required for PGF2alpha-induced muscle cell growth and nuclear accretion, demonstrating the first intersection between prostaglandin receptor activation and NFAT signaling. Given this novel role for PGF2alpha in skeletal muscle cell growth, these studies raise caution that extended use of drugs that inhibit COX receptors, such as nonsteroidal antiinflammatory drugs, may be deleterious for muscle growth

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