Clenbuterol burn fat build muscle

[Mountain-Man]

Build Muscle & Burn Fat at the Same Time



Clenbuterol is a popular drug used by bodybuilders and athletes that belongs to a class of compounds known as beta-agonists that bind to the beta-adrenergic receptor embedded in the cell membrane— turning on cellular signaling cascades within the fat cell that break down body fat while in the muscle cell and activating muscle growth. These functions bestow clenbuterol with the extraordinary capability to decrease body fat while supporting muscle growth.Although clenbuterol is a powerful bodybuilding compound, it also has several drawbacks. One of those drawbacks being the rapid inhibition of clenbuterol activity within the cell that swiftly shuts down its fat-burning and muscle-building activity. In addition, recent scientific evidence has shown that clenbuterol not only loses its anabolic potency rather quickly— but it may also stimulate muscle atrophy if taken for extensive periods of time, by increasing the amount of the muscle-depleting molecule myostatin within the muscle cell.

Myostatin is a member of the transforming growth factor-beta (TGF-beta) super family of growth factors where, despite being a growth factor, it actually reduces muscle growth by initiating several pathways that inhibit muscle hypertrophy while stimulating muscle atrophy. However, certain nutritional supplements have been shown to inhibit myostatin activity, which should prevent clenbuterol-stimulated muscle loss while enhancing clenbuterol-driven muscle growth. In addition, these myostatin-inhibiting compounds should also lower the amount of clenbuterol necessary for muscle growth, which would also diminish cellular inhibition of clenbuterol within the cell— further enhancing the anabolic properties of clenbuterol.



Reducing Myostatin Function Boosts Clenbuterol’s Anabolic Activity

One key investigation clearly demonstrated that inhibiting myostatin function improved clenbuterol activity. This study by Kim et al.1 showed that clenbuterol, which has previously been shown to enhance muscle size via the mTOR pathway2, works well in combination with myostatin inhibition to additively stimulate muscle growth and strength. The researchers took normal mice and myostatin-deficient mice and fed them clenbuterol. After two weeks, muscle biopsies revealed an additive effect on mTOR activation in the myostatin-deficient mice that were also fed clenbuterol. These myostatin-deficient mice that were fed clenbuterol had an increase in muscle mass of ~25 percent. The result of this investigation demonstrates that inhibiting myostatin clearly enhances clenbuterol function.



Clenbuterol Amplifies the Level of Muscle-depleting Myostatin

Considering the previously mentioned study by Kim et al.1 which showed that clenbuterol stimulates greater muscle growth when combined with myostatin inhibition,a recent study by Abo et al.3 investigated whether this inhibitory function of myostatin on clenbuterol was induced by clenbuterol consumption. In this study, they analyzed the level and activity of myostatin in the muscle of rats that were given clenbuterol for 21 days straight. Muscle hypertrophy was induced from day 3 to 14, which corresponded to increased levels of the muscle-building growth factor IGF1. In addition, the study also showed increased levels and activity of myostatin after consuming clenbuterol for 21 days. These results show that myostatin function is induced by clenbuterol where it functions as a negative regulator in the later stages of clenbuterol use, whereas IGF1 works as a positive regulator in the earlier stages.



Creatine and Vitamin D Decrease Myostatin and Enhance Clenbuterol

Certain nutritional supplements are known to inhibit myostatin. Therefore, consuming them should negate myostatin’s hold on muscle growth directly induced by clenbuterol. Creatine is a well-characterized compound that has been unmistakably shown to enhance muscle size and strength. In addition to creatine’s obvious function as a primary energy storage molecule used to regenerate muscle ATP, thus prolonging muscle function, creatine has also been shown to stimulate muscle growth.4 More recently, however, a study by Saremi et al.5 demonstrated that creatine consumption causes a decrease in myostatin levels in muscle cells, leading to significant muscle growth. In this study, two groups of men performed resistance training with or without creatine for a total of eight weeks. Both groups showed decreased levels of myostatin, but the group that performed resistance training and consumed creatine had a considerably larger decrease in myostatin levels along with greater gains in muscle mass and strength— clearly demonstrating the ability of creatine to reduce myostatin levels, improving muscle growth and strength.

Another potent myostatin inhibitor is vitamin D. As shown in a recent study by Garcia et al.6, vitamin D exposure decreased the amount of myostatin found in isolated muscle cells, generating greater muscle growth. In addition to the decrease in myostatin, this study also showed that vitamin D triggers an increase in the powerful inhibitor of myostatin known as follistatin, which increases muscle mass by inhibiting myostatin.7 Ultimately, this study indicates that the decrease in myostatin level and activity caused by vitamin D significantly increased muscle fiber size.



Essential Amino Acids Drive Muscle Growth by Reducing Myostatin

While essential amino acids (EAAs) have been shown to potently activate mTOR-stimulated muscle protein synthesis, leading to greater muscle size8,9, a more recent study by Drummond et al.10 demonstrated that EAAs also have the uniquely powerful ability to decrease genetic expression of myostatin in muscle cells. EAAs decrease myostatin levels by stimulating the production of a class of molecules known as micro-RNA that have the ability to strongly decrease the expression level of specific genes. The unique finding in this study was that several micro-RNA molecules were produced in human skeletal muscle following the ingestion of 10 grams of EAAs, which subsequently decreased myostatin expression by approximately 50 percent. Although further work is needed to elucidate the precise role that micro-RNA has in the regulation of myostatin and muscle mass following EAA consumption, this investigation represents a completely novel way to decrease myostatin levels for enhanced muscle growth.

In summary, although clenbuterol has the extraordinary capability to stimulate fat loss while supporting muscle growth, clenbuterol directly increases myostatin levels— which may drive substantial muscle loss. On the other hand, myostatin is such an extremely responsive target that even a minor reduction of clenbuterol-increased myostatin levels should restore clenbuterol activity, boosting notable muscle growth and fat loss. As a result, clenbuterol’s ability to increase myostatin function should be mitigated by simultaneously consuming clenbuterol with the right nutritional supplements that inhibit myostatin and restore clenbuterol function that only cuts fat and not muscle growth.



For most of Michael Rudolph’s career he has been engrossed in the exercise world as either an athlete (he played college football at Hofstra University), personal trainer or as a Research Scientist (he earned a B.Sc. in Exercise Science at Hofstra University and a Ph.D. in Biochemistry and Molecular Biology from Stony Brook University). After earning his Ph.D., Michael investigated the molecular biology of exercise as a fellow at Harvard Medical School and Columbia University for over eight years. That research contributed seminally to understanding the function of the incredibly important cellular energy sensor AMPK— leading to numerous publications in peer-reviewed journals including the journal Nature. Michael is currently a scientist working at the New York Structural Biology Center doing contract work for the Department of Defense on a project involving national security.

 

[Mountain-Man]

Commonly used doses

It is well known that Clenbuterol use results in rapid down-regulation of beta 2 receptors. This is due to the powerful stimulatory effect of the drug. It is therefore pointless to use clen for long periods without a break. Some believe that a two day on, two day off dosing schedule will allow adequate potential for receptor up-regulation. However, I doubt this to be the case due to the relatively long half life of clen, resulting in continued stimulation even throughout the 'off' days. A much better regime would be a two week on, two week off cycle. Maximum plasma levels are reached around 2-3 hours after oral administration, and terminal half life at 34 hours (Zimmer, 1976).

A tapering up of dosages is recommended in an attempt to limit harsh side effects. Most commonly, a user will start by taking one 20mcg tablet on day 1, followed by an increase of one tablet on subsequent days. Subject to personal tolerance levels, a dosage of 140mcg (seven tabs) will be used by day 7, and this level should be maintained for the entire second week. It would be fruitless to exceed seven or eight tablets daily due to receptor over-saturation. There is no requirement to taper down.

For the next 'cycle' of clen (i.e. weeks 5 & 6), there is no requirement to taper up from one tablet as your tolerance level should now be known. As an example, if the user finished the first cycle of clen on 7 tabs, they could recommence at a slightly lower dose of 4 or 5, and taper up again from this level. Again though, the user should again limit their intake to 7 or 8 tabs daily.

During the two 'off' weeks, an ECA stack can be used as required. ECA will not cause such a pronounced down regulation and desensitization of the receptors, certainly not to the extent of clen. Ephedrine has a short half life in contrast to clen which results in times throughout the day where the betas will partially recover from stimulation by adrenaline and nor-adrenaline. Potency is also much weaker that that of clen, as it is not a specific agonist. Ephedrine is also thought to increase the conversion of endogenous/exogenous T4 to T3 through the activation of deiodinase enzymes responsible for this process. This is important as clen is known to slow the rate of T4 to T3 conversion. As a side note, some bodybuilders will use T3 concurrently with the Clenbuterol/ECA cutting cycle (together with certain anabolic/androgenic steroids no doubt!) in an attempt to at least maintain plasma T3 levels.

Cycles of Clen/ECA are normally limited to 12 weeks in total, though are often shorter.

Female dosages tend to be slightly lower than those of male users, with an upper limit of 80-120mcg (4-6 tabs).

Aside from its fat burning properties, Clen is often used as an anti-catabolic to maintain muscular gains following a steroid cycle. A dosage of 40mcg daily would be suited to this situation.

There is no particular requirement to split the dosage throughout the day due to the long half life. Most will take the full daily dose in the morning, though some prefer to take their dose just before bed in an attempt to avoid most of the side effects as they sleep.

Some user accounts suggest that splitting the dose may lessen side effects slightly. It is a trial and error process in essence, to ascertain which method suits you personally.

Muscular cramping

Cramping whilst using Clenbuterol is a fairly common side effect. This is most probably due to depletion of the amino acid taurine in the liver together with deficits in the electrolytes sodium and potassium, as well as inadequate hydration. Taurine helps stabilize cell membranes and prevent nerves from becoming over-excited. Some studies show that giving taurine supplements relieves painful muscle cramps. Japanese researchers found that the longer rats exercised, the more taurine they lost from their muscles (Matsuzaki et al, 2002).

Symptoms of cramping may be alleviated by:
Eating fruit particularly bananas
Ensuring adequate hydration
Taurine supplementation - 3-5g daily
Potassium supplementation - 200-400mg daily taken before bed on an empty stomach

Ketotifen

Ketotifen is an anti-histamine used medically to treat bronchial asthma and allergies. It has a sedative and depressant effect on the brain. It acts by decreasing the release of histamine which is a chemical released when an allergic reaction occurs. Ketotifen blocks the action of histamine on special histamine receptors and reduces the nerve response when an allergic reaction occurs.

Histamine is the chemical in the body that causes the symptoms of an allergic (hypersensitivity) reaction. These can include inflammation of the skin, airways or tissues, rashes, itching and of the skin, eyes or nose, nasal congestion and narrowing of the airways. By blocking the actions of histamine, ketotifen may prevent and relieve the narrowing of the airways that occurs in asthma due to allergies.

However, bodybuilders are interested in the drug as it has been shown to inhibit the down regulation of the beta receptors, including the beta 2s that clen stimulates. 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. A dose of 2-3mg daily 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 you can take about 30-40% less clen and it be equally effective.

No studies have been done to find the most effective dose though most users should find 3-4mg daily ideal, which can be split or taken in one sitting. Higher doses are likely to cause (sometimes severe) drowsiness and increase appetite.