I cut and pasted from another site.
The Rise and Fall of Clenbuterol
by Jerry Brainium
Clenbuterol is a beta-2 adrenal agonist drug, which means it has a structure similar to the natural catecholamine hormones in the body, such as epinephrine. The primary medical uses for clenbuterol are for treatment of asthma and other respiratory diseases. Clenbuterol assists in respiration because, like epinephrine, it promotes dilation of the bronchial tubes in the lungs. Asthma is characterized by constriction and inflammation of the bronchial tubes.
Clenbuterol, however, has never been approved for sale in the United States for use by people. Drug companies are most interested in profit, and clenbuterol offers no particular medical advantages over existing beta-2 asthma drugs. Clenbuterol does have notable disadvantages, however. It has a long half-life, remaining active in the body for up to 36 hours. While that sounds good, it also increases the likelihood of serious side effects, thus making it less attractive to litigation-wary pharmaceutical companies. In contrast, the body degrades and eliminates the current leading beta-2 agonist drug sold in the U.S. after only about six hours.
Clenbuterol is sold in other countries, chiefly by Mexican pharmacies, under various trade names, such as Clenasma, Spiropent and the veterinary injectable Ventipulmin. It first attracted the attention of bodybuilders years ago after animal research showed that it offered potent repartitioning effects—it appeared to decrease bodyfat while simultaneously fostering increased muscle size, particularly in the type 2 fast-twitch fibers, the fibers most amenable to hypertrophy from weight training.
Those animal studies, however, typically used dosages in the one-to-five-milligram-per-kilogram-of-bodyweight range. That amounts to a daily dose of 450 milligrams of clenbuterol in a 200-pound athlete. For human use clenbuterol comes in microgram amounts. One thousand micrograms equal one milligram.
Despite those discrepancies, clenbuterol quickly earned a reputation as an anabolic and “cutting” drug, favored in precontest cycles, and athletes who tried it soon discovered two things: 1) Its effects didn’t last more than three to four weeks, since beta-adrenergic receptors are extremely sensitive and turn off, or downregulate, rapidly; and 2) it provided no discernible anabolic effect. It did, however, provide a potent thermogenic effect conducive to fat oxidation. You could tell the thermogenic properties were working by the perception of increased body heat.
The most common suggested clenbuterol dosage was one to two tablets a day, gradually increasing to eight to 10 per day. To extend its therapeutic potency and blunt down-regulation of beta-adrenergic receptors, users were advised to take the drug on a two-days-on/one-day-off cycle; however, it was never proven scientifically that the off-and-on cycle offered any real advantages.
The same holds true for another drug, ketotifen, said to help maintain the potency of beta receptors. Whatever benefits ketotifen confer on open beta receptors come at a price. Ketotifen is an antihistamine, which can cause acute drowsiness—not exactly conducive to intense training. What of side effects? Taking too much clenbuterol has the same effect as a flood of epinephrine in your body. Symptoms include increased blood pressure, possible heart-rhythm disturbances, muscle tremor and insomnia. In Europe clenbuterol was used in meat processing, and some who ate the drug-laden beef experienced the same side effects.
More recent animal studies—again using far higher doses than would ever be ingested by humans—showed that clenbuterol decreases endurance by degrading the heart structure. Indeed, some of the research animals died from heart failure. A recent study that examined the heart and skeletal muscles of rats given clenbuterol identified direct toxic effects from the drug.1 What’s particularly interesting about that study is that the bad effects resulted from just a single dose of injectable clenbuterol—a form favored by some bodybuilders and other athletes.
The results showed that clenbuterol didn’t just harm heart-muscle cells but actually killed them. Heart-muscle-cell loss led to increased collagen deposition. In effect, active heart cells were replaced by scar tissue, setting the stage for sudden heart failure.
Several theories explain clenbuterol’s adverse effects. The first involves the fact that clenbuterol depletes the amino acid taurine in the heart; taurine has protective properties, such as modulating the calcium levels that keep heart rhythm stable. Clenbuterol may also increase norepinephrine-induced stimulation of the heart, which can damage the heart if excessive.
You may reason that the research animals got megadoses of clenbuterol and that the lesser doses athletes use wouldn’t have the same effects—but that’s just wishful thinking. According to something called Kleiber’s law, the animal dose of clenbuterol is equal to a human dose of five to six tablets. So the same side effects could be expected. In addition, because of the extended time that clenbuterol takes to degrade in the body, it could build up and have cumulative effects.
The findings of heart damage from clenbuterol could partly explain the mysterious deaths of a few bodybuilders who combined clen with anabolic steroids. That is, of course, pure speculation. Athletes who use clenbuterol should ensure that they also supplement taurine, which may offer some heart protection.
Other studies send further grim news about clenbuterol.2,3 When it was given to pigs, the portion of the testes that synthesizes testosterone (Leydig cells) increased in size, suggesting increased testosterone production. But the testes cells where sperm is manufactured (Sertoli cells) were permanently damaged. That implies that clenbuterol may adversely affect fertility.
The increase in the cells that secrete testosterone isn’t that surprising. Natural catecholamines like epinephrine, for which clenbuterol serves as a synthetic substitute to some degree, are known to promote testosterone synthesis. Short-term stress, characterized by increased catecholamine release into the blood, leads to upgraded testosterone. But if the stress persists, other stress hormones, such as cortisol, are released and reverse that effect—that is, decrease testosterone synthesis and release.
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Originally Posted by perfectbeast2001
