faq on clen!!!!

.What is Clenbuterol and how does it work?

Simply put, Clenbuterol hydrochloride (the full chemical name for Clenbuterol)
is a beta-2-adrenergic agonist, and was initially used to treat asthma in
humans. Other such drugs in this class are albuterol (I believe this is brand
named as Ventolin, the blue inhaler commonly seen), pirbuterol, terbutaline and
salmeterol.

Clenbuterol has two secondary effects that are beneficial to athletes and
bodybuilders. The first is a strong anti-catabolic effect, which means it
decreases the rate at which protein is used up in the muscle cells, consequently
causing hypertrophy of muscle cells (with proper training, of course). Clen
accomplishes this by the stimulation of both type 2 and 3 beta-receptors.
3-beta receptors are more abundant in livestock than in humans. This explains
the pronounced anabolic effects on livestock as opposed to humans.

Secondly, Clen has a wonderful thermogenic effect. This is the main reason that
is included in nearly every cutting cycle in some form or fashion. This means
that it slightly raises the body temperature of the person taking it. When the
bodys temperature rises it burns fat more productively. When stacked with an
LT-3 hormone such as Cytomel, the body turns into the fiery pits of hell and
burns fat like a stripper scoops up dollar bills on a Friday night.

Clenbuterol is known by the following brand names:

Broncodil, Broncoterol, Cesbron, Clenasma, Clenbuter.Pharmachim, Contrasmina,
Contraspasmina, Monores, Novegam, Oxyflux, Prontovent, Spiropent, Ventolase, and
Ventapulmin It is generally available in 10 - 20 mcg tablets, although syrup,
injectables and "Super Clen" (x20 the normal dosage of normal tabs) are also
somewhat popular.

2. Will Clenbuterol help me if I am on AS?

Yes, particularly at the end of a cycle to keep gains. Bodybuilders use
Clenbuterol after steroid cycles to balance the resulting catabolic phase
following a cycle and to retain strength and muscle mass. Also, as a result of
the higher body temperatures, Clenbuterol magnifies the effect of
anabolic/androgenic steroids taken simultaneously, since the protein processing
is increased. ?2

***GEEKY MEDICAL TERMINOLOGY WARNING*******

(Taken from Clenbuterol.com) "When these agonists bind to beta-2 adrenoceptors,
they activate adenyl cyclase which leads to an increase in the intracellular
concentration of the second messenger cyclic adenosine monophosphate (cAMP) and
activation of protein kinase A (PKA). In the tracheobronchial tree, beta-2
agonists, cAMP and PKA inhibit smooth muscle contraction by opening K+ channels
and by down-regulation of myosin light chain kinase activity." ?1

In the airways, beta-2 adrenoceptors are not restricted to smooth muscle. They
also occur on epithelium, inflammatory cells, and the vasculature. When
epithelial beta adrenoceptors are activated, cilliary beat frequency increases.
The effect on mucus secretion is less consistent, but the weight of opinion
indicates that beta-2 agonists increase mucocillary clearance. Activation of
beta-2 adrenoceptors on inflammatory cells reduces the release of inflammatory
mediators, and activation of those in vasculature can inhibit the permeability
increase that occurs in inflammation. Thus making it easier to breath.

******* END GEEKY MEDICAL TERMINOLOGY*************

3. Will Clenbuterol help me burn fat?

Hell yes and no. The yes is stated above--Clen is a strong thermogenic. Diet
and cardio are most important in this process (of course), as is a good weight
training regimen. If one keeps a clean diet, does regular cardio (3-4+ times a
week) then Clenbuterol will greatly assist in fat loss. If one sits around the
couch all day, eats empty calories like sugars and simple carbs, Clenbuterol
will be as useful as a sugar pill.

4. What is the recommended dosage for Clenbuterol?

This has become a matter of controversy among the Bodybuilding community. Due
to erroneous assumptions based on livestock dosing based on the types of
receptors that humans and livestock have , 2 days on-2 days off was thought to
be the proper dosage. Given Clenbuterols half-life of about 10 hours, with a
2-days on/2-days off cycle you never have time to get enough of the clenbuterol
out of your system for this to be an effective cycle. In actuality, it probably
hasn even dropped to 50% of your peak concentration before one is taking the
drug again. With this all taken into account, there is no reason to think that
this cycling would significantly reduce the problem of receptor desensitization.
2-weeks on/2-weeks off is a better cycle, with ECA stacked in between.

At a dosage of around 5-7 tablets or 100-140 mcg per day for men over a period
of 8-10 weeks. In females, dosages of 80-100 mcg/day are usually sufficient.
For fat loss, clenbuterol seems to stay effective for 3-6 weeks, then its
thermogenic properties seem to subside. This is noticed when the body
temperature drops back to normal. Its anabolic properties subside much quicker,
somewhere around 18 days. Also keep in mind that anything over 140 mcg a day is
useless since the beta receptors can only handle so much. ?

4. Should I taper Clenbuterol on and off?

Yes. With ANY thermogenic, the side effects can be pronounced and a shock to
the system. To lessen these, here is an optimal pill count for a two-week
cycle. (assuming standard Clen dosages of 20mcg such as Spriopent).

Week 1: 2, 3, 4, 5, 6, 6, 6
Week 2: 6, 6, 6, 5, 4, 3, 2

Weeks 3 and 4: ECA (Hydroxycut, Xenadrine, Stacker, etc.)

The ECA stacks in between will help prevent against the inevitable crash when
taking Clen.

5. What are some of Clenbuterols side effects?

Possible side effects of Clenbuterol include restlessness, palpitations, tremor
(involuntary trembling of fingers), headache, increased perspiration, insomnia,
possible muscle spasms, increased blood pres-sure, and nausea. Note that these
side effects are of a temporary nature and usually subside after 8-10 days,
despite continuation of the product.

COMMONLY ASKED QUESTIONS:

Q: Can I substiute Ventolase or another asthma medication for Clenbuterol since
they are the same category?

A: No. Remember that the only reason the FDA banned Clenbuterol was because of
the long half-life. Well approved asthma medications have very short
half-lives. Therefore, the effective dosage period is very low.

Q: Will Clenbuterol give me gyno, masculinization, shinkage of the boys or any
steroid-like side effect?

A: No. Clenbuterol has no steroid-like side-effects as the mechanisms are
totally different. This also means that you do not have to take Clomid or any
anti-estrogen during a Clenbuterol cycyle.

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. The NCAA is reputed not to, however this is
unknown. It is best to get a presciption from a doctor for asthma medication.
Ventolin, Albuterol and the like trigger the same tests as Clenbuterol. With a
doctors prescription for one of these similar products, the Clen will be seen
as a false positive.

Q: Ive read that the best way to gauge Clenbuterols effectiveness is to watch
for a rise in temperature. Is this true?

A: Although this will show when Clenbuterol is working, it is not the best way
to gauge effective dosage, as everyones body will react differently. This
reaction is sometimes independent of an effective dosage and is not a good way
to gauge if your current dose is effective. The above cycle is based on a
175-lb man. If you are below that, you may want to slightly decrease the dosage
if you find the shakes to be unbearable after 4-5 days.

Hi guys- here's some more scientific info on clen I just came across on AvantLabs- thanks Loki! (https://www.avantlabs.com/page.php?pageID=347)

************************************************** ******************

Pharmaceutical Phenotype Enhancement
by Loki

Clenbuterol Part I

First ‘The Man’ marginalized ephedra. Then we saw the realization of a second supplement ban—one which will effectively deprive the mainstream bodybuilding community of its most-preferred anti-catabolic ancillary: the pro-hormone or pro-steroid. So just how the hell is a dieter supposed to preserve lean body mass these days while languishing on laughably low calories? Well, aside from investing in our beloved LeptiGen and shipping out for real gear, it seems like a lot of would-be-chiseled chaps are taking a new interest in the age-old diet drug Clenbuterol (1-(4-Amino-3,5-dichlorophenyl)-2-tert-butyl-aminoethanol), a sympathomimetic beta2 adrenergic agonist most commonly used in veterinary therapeutics and livestock doping. But is this recent, glaringly rekindled curiosity in clen leading would-be and first-time users to the right drug? Or for that matter, is clen a safe drug? So, without further ado, I think it’s time M&M gave ephedra’s “wonder-cuz’” its full-on, discerning attention.

Clen in Context: Basic Pharmacology

I throw around the word sympathomimetic a lot to compensate for my chronically low self-esteem. In the forums, in my sleep, during sex—it’s just such a dazzlingly erudite sounding word. And using it makes me feel special. And while you yourself may not feel the inclination to use it colloquially any time soon, if phrases like “nutrient partitioning” or “fat loss while preserving muscle” pique your interest, you should care about how this class of compounds works and what those workings result in.

Chances are you wouldn’t be reading this article if you didn’t, so quickly: sympathomimetics (take “sympath” from ‘sympathetic nervous system,’ throw an ‘o’ on there, and add ‘mimetic’ [i.e. ‘to mimic’] and you’re in business) are a class of drugs that affect the sympathetic nervous system (SNS), either by prompting central catecholamine (NE/NA and E/A) release or by peripherally mimicking the effects of those same endogenous hormone/neurotransmitters. Most of a sympathomimetic’s pharmalogical interplay occurs via interaction with beta andrenoreceptors. Ephedrine is a sympathomimetic, norephedrine is a sympathomimetic, H.E.A.T. is a sympathomimetic, and boy is clenbuterol ever a sympathomimetic. There are also many others.

With clenbuterol specifically, what we see is both forms of sympathomimetic activity. Clen synthetic mimics some of norepinephrine’s and epinephrine’s effects in specific outreaches of the SNS, and centrally exerts these effects in skeletal muscle, adipose tissue, and in an often-overlooked third area: the brain. Yes, that’s right: clenbuterol crosses the blood brain barrier, and is able to readily activate certain central adrenoreceptors (1).

Virtually all of this peripheral mimicking occurs at the beta2 adrenergic receptor, which is the reason clenbuterol is characterized as a beta2 specific agonist. When it interacts with these receptors in muscle, clenbuterol is able to catalyze Cyclic Adenosine Monophosphate (cAMP) production, a second-messenger signal transducer which regulates rates of glycogen decomposition, protein synthesis, and lipolysis (among many other things). What distinguishes clenbuterol prominently from ephedrine is its specificity, potency, and duration of effect.

Ephedrine, whether you already knew it or not, has very little direct activity in muscle or fat. Rather, it stimulates central sympathetic nerve terminals, thereby inciting an indiscriminate release of NE/NA (and to a lesser extent, epinephrine/adrenalin), which then relays across the entirety of the SNS. This makes ephedrine a primarily indirect and non-specific sympathomimetic, as it effectively delivers a mild ‘catecholamine carpet-bombing’ to all your various beta receptors (beta1, beta2, atypical beta3, and putative, atypical beta4). It is also this mechanism that gives ephedrine its long-term pharmacological viability: although not very set-point friendly, it will nonetheless continue to indirectly agonize adrenergic receptors along your SNS, even after months of continual use.

Clenbuterol is somewhat of a different beast. As mentioned earlier, it is able to prompt a small degree of catecholamine release from central adrenoceptors, as well as interact directly with the beta2 receptor in a dose-dependent manner with a potency that far exceeds the resultant effects of ephedrine administration.

More Technical Stuff on Clen’s Workings than You Could Ever Possibly Want to Know: Lipolysis

Nutrient-partitioning junkies, your patience is about to be rewarded. Now that we’ve established some context, it’s time to move on and discuss ‘the goods.’ It’s time to discuss the bad-ass lipolytic and repartitioning effects of clenbuterol in vivo. And it goes a little something like this. Following administration, clenbuterol avoids first-pass metabolism (it’s oral bioavailability ranges between 89-98%) and doses typically reach peak plasma levels roughly two hours after a dosage is ingested. This peak will then stabilize and continue for four additional hours (2). Eventually, roughly 50% of ingested clenbuterol will undergo metabolization into its four primary metabolites; the remaining half will be excreted intact, without metabolic breakdown (3). This biphasic elimination lends clenbuterol a veritable half-life that clocks in at just under thirty six hours.

Once it gets to work clenbuterol, as I already mentioned, binds to cellular beta2 receptors. Intracellularly this will increase cAMP (4), which then binds to regulatory subunits of protein kinase A, causing the release of its catalytic subunit. This process activates the enzyme HSL (hormone sensitive lipase), which hydrolyzes triglycerides, breaking them down into glycerol and fatty acids to allow for beta oxidation.

Now, as you can probably guess, one of the facets to clenbuterol that makes it such a potent lipolytic drug is that it exerts its beta-agonism steadily and continuously. If ephedrine is ‘hit-it-and-quit-it,’ clenbuterol is a friggin’ marathon man when it comes to stimulation. Clen isn’t very cuddly though, so all you high-maintenance bodybuilders are just plum out of luck.

Clenbuterol is undeniably potent at its target receptor. However, clenbuterol cannot be said to own ephedrine (particularly when combined with caffeine) outright for fat loss. Remember, since clen is primarily direct-acting on a cellular level, it can’t prompt the same kind of NE-induced hypophagia (loss of appetite) as ephedrine, which has proved to be an essential pharmacological component in its ability to further weight loss (5). Individuals looking to use clenbuterol for weight loss need to keep this in mind: clenbuterol partitions energy intake, but it will not aide in regulating or helping to decrease it, hence my recommendation that those planning to cut on clen also look into ancillary appetite suppressants.

There is also the prevailing theory in a lot of bodybuilding circles that clenbuterol actually raises metabolic rate by increasing endogenous thermogenesis. So let’s explore the purported calorie-burning properties of clenbuterol. In animals, although clenbuterol increases thermogenesis in mutant rats (genetically obese Zucker rats), multiple studies have demonstrated that in normal rats—even those administered rather hefty dosages of the drug--- clenbuterol “did not affect energy intake [or] energy expenditure” (6,7).

In human studies, the direct infusion of the related beta2-specific agonists salbutamol and terbutaline in lean men caused a modest increase in whole body energy expenditure and respiratory exchange ratio—an increase of 0.6 kJ/min in terms EE adjusted for fat-free mass (8). In other words, the guys getting heavy-duty beta2 adrenergic stimulation would have ended up burning about 200 extra kcals over a twenty four hour period. So in other words, thermogenesis was enhanced, but not so much to suggest that clenbuterol has strong calorie-burning properties of its own. Interestingly enough, in the same study the researchers noted that:

during beta2-adrenergic stimulation, the increases in energy expenditure and plasma nonesterified fatty acids and glycerol concentrations were reduced in the obese group. Furthermore, lipid oxidation significantly increased in the normal weight group, but remained similar in the overweight group… [this] data suggests that beta2-adrenoceptor-mediated increases in thermogenesis and lipid utilization are impaired in the obese (8).

In other words, if you’re still in plus-size pants, you’re out of luck: clenbuterol isn’t going to help you lose a whole lot of weight, because your obesity-train-wrecked metabolism just ain’t havin’ that (9). Plus, given the effects of beta adrenergic agonists on heart rate contraction, the use of clenbuterol in significantly overweight individuals may pose significant danger to the user (10,11).

And again, the take home message is the same: when dieting, nutrient-partitioning definitely matters, but in the end it still comes down largely to energy expenditure vs. intake, and clen is a calorie re-distributor, not a burner.

Clenbuterol and its Interaction(s) With Your Mammoth Guns

If you get one sentence out of this section on clenbuterol and skeletal muscle, please let it be this: clen is never going to get you big, but it is extremely good at keeping you big once you get there. Yes, I know clenbuterol is wicked-anabolic in Dawley-Sprague hyperphagic wombats, but you are a human, and the amount of clenbuterol it would take for you to see a genuine anabolic effect would also put you in a coffin, so let’s just let that one go.

Now, I said clen’s not anabolic, but it certainly does have positive ramifications for protein synthesis, primarily through the beta2s, cAMP, and its ability to mitigate Ca2+-dependent proteolysis in skeletal muscle (12). A critical component to its full effect is its repartitioning properties. As stated earlier, clenbuterol is exceedingly good at liberating fatty acids from adipose tissue. But, more than that, clenbuterol exerts this effect in tandem with large scale, itself-induced skeletal muscular insulin resistance (13).

Now, when you’re a type II diabetic, this isn’t so hot. However, in a healthy bodybuilder using a strong sympathomimetic you basically have the best of all worlds: plenty of free-fatty acids getting released for oxidation in muscle, plenty of insulin-resistant muscle to feast on them, and pretty much all consumed calories getting spared for muscle retention and protein synthesis. Granted, there’s very little good research on human skeletal muscle in the presence of clenbuterol (particularly when it comes to athletes), but reasoned inference and extrapolation certainly paints a pretty convincing picture that clenbuterol is significantly anti-catabolic.

For starters, human research with ephedrine and caffeine has demonstrated that indiscriminate, weaker beta-adrenergic agonism significantly improves protein deposition and preserves lean body mass during periods of caloric restriction (14). Also interesting was the researchers’ discovery that the ephedrine and caffeine mixture wasn’t attenuating skeletal muscular breakdown, but was in fact accelerating protein synthesis. This was proved clinically by 3-methylhistidine examination, an index for skeletal muscle breakdown.

In the sympathomimetic group, an increase in nitrogen balance was demonstrated independent of 3-methylhistidine, which means the ephedrine was actually helping to synthesize lean tissue at a faster rate, and thereby counteracting the increase in diet-induced catabolism (15). See? I wasn’t lying when I said clenbuterol could be anabolic; you just can’t take a high enough dose to get an anabolic degree of protein synthesis augmentation without ending up in the ER long before you could get your shaky ass anywhere near a squat rack.

Nonetheless, because of its pharmacology, clenbuterol is currently recognized in the scientific community as a valid remedial treatment for muscle-wasting conditions (16,17). In rodents, clenbuterol also actively inhibits glucocorticoid-induced muscle atrophy, and one can speculate that it may also exert similar anti-glucocorticoid properties in humans as well (18). Clenbuterol, by virtue of its beta-agonism, may also even be more effective at reducing glucocorticoid activity than that though, as it has been demonstrated that beta-receptor antagonism increases the release of adrenocorticotrophin (ACTH) in humans subjected to stress (19). For those unaware, ACTH is a pituitary hormone that stimulates cortisol secretion, which means there is a possibility that beta-receptor agonism may in fact be able to prompt the opposite: a decrease in ACTH release in response to stress.

All told, clenbuterol is pretty much the bomb and the shiznit as far drugs go for preserving muscle during periods of energy restriction through a number of different pathways. Oh but there are just a few more things…

But I’m Too Sexy To Die… (Side Effects and Precautions Pt. I)

By now it should be clear that clenbuterol is a powerful drug. And with all powerful drugs, there are consequences, ‘cause life just sucks like that. So for those of you about to get all ‘clenbutaholic’ with your research chemicals, here’s a little info I counsel you to take to heart. In fact, speaking of hearts, let’s examine yours in relation to clenbuterol, because there definitely is some cause for concern.

For starters, there are more rodent studies under the sun that show clenbuterol use can cause significant cardiac hypertrophy—so many in fact that I’m not even going to bother citing them. Just type “clenbuterol” and “cardiac hypertrophy” into Google if you don’t believe me; no lie, it’s a little unsettling. However, clenbuterol also kills fat cells (adipocyte apoptosis) in rodents too, and it sure doesn’t in humans, so take that animal data for what it’s worth. Unfortunately though, things don’t look too much better when we move up the evolutionary chain and start looking at hearts in good-ole’ human beings either.

For example in 1998, the internal medicine outpatient clinic at the University of Alabama Birmingham received a walk-in from a previously healthy 26-year-old bodybuilder complaining of significant chest pains. The man, who had a history of moderate anabolic steroid use but who had not used any steroid preparations in the weeks leading up to his visit, revealed that he had continuously been using clenbuterol for nearly a month [Loki’s note: idiot]. During check-up, the man turned out to be completely fit and healthy with the only exception being a significant amount of left ventricle (heart) hypertrophy and cardiac dyskinesias (meaning distortion of muscle [in this case smooth muscle] activity)(20).

In fact, between 1988 and 1998, eight cases of medically-diagnosed cardiac hypertrophy have been reported in drug-using bodybuilders within the United States (21,22). We can assume many more went overlooked or unreported. Still, because of the steroid outlier (which could also be a potential factor in the pathology—or perhaps even the outright cause), the medical community has been unable to isolate clenbuterol’s true role in contributing to these instances of myocardial infarcation (20). Still, the researchers who have examined this phenomenon arrived at a conclusion that should give most clen user’s pause of thought. Namely that:

We suspect there may have been a synergistic role between the anabolic

steroid and clenbuterol. Hypothetically, the anabolic steroid may have caused cardiac hypertrophy, coronary artery spasm, or thrombosis. The clenbuterol

may have precipitated ischemia by producing intermittent tachycardia. Alternately, clenbuterol may have contributed primarily to the cardiac hypertrophy...(20)

Furthermore, clenbuterol ingestion (particularly excessive ingestion) has also been documented to cause tachycardia (sudden, rapid racing of the heart)(20,23,24), hypokalemia (23), hypophosphatemia (23), potassium depletion (24), taurine depletion (25), headaches (24), tremors (24), and vertigo (24). Now, it should be noted that the more severe of the aforementioned conditions have only been demonstrated in instances of clenbuterol overdose and are thus not directly applicable to carefully monitored doses within the 20-100mcg range. Nonetheless, clenbuterol is definitively a “big kid sympathomimetic,” and not a drug that lends itself to immoderation, recklessness, or just outright stupidity.

And for now, I’m afraid that’s just going to have to do it for Part I of our comprehensive look at Clenbuterol. Next issue we’ll get into receptor down-regulation, clenbuterol, the brain, and neuroprotection (for all my Chemically Correct homies), cycling, stacking recommendations, and potential novel uses for clenbuterol in the treatment of injuries and various diseases and conditions.

Questions or comments on this article? Post them in the Avant Labs Forums for live feedback from the author, as well as the Mind and Muscle staff and fellow readers!

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12. Luiz Carlos C. Navegantes, Neusa M.*Z. Resano, Renato H. Migliorini, and Ísis C. Kettelhut Catecholamines inhibit Ca2+-dependent proteolysis in rat skeletal muscle through beta2-adrenoceptors and cAMP. Am J Physiol Endocrinol Metab 281: E449-E454, 2001

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13. Kim J, Shigetomi S, Tanaka K, Yamada ZO, Hashimoto S, Fukuchi S. The role of beta 2-adrenoceptor on the pathogenesis of insulin resistance in essential hypertension. Nippon Naibunpi Gakkai Zasshi. 1994 Jun 20;70(5):521-8

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14. Astrup A, Buemann B, Christensen NJ, Toubro S, et al. The effect of ephedrine/caffeine mixture on energy expenditure and body composition in obese women. Metabolism 1992 Jul;41(7):686-688

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15. Pasquali R, Casimirri F Clinical aspects of ephedrine in the treatment of obesity. Int J Obes Relat Metab Disord;17 Suppl 1:S65-S68 1993

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17. Oya Y, Ogawa M, Kawai M. Therapeutic trial of beta 2-adrenergic agonist clenbuterol in muscular dystrophies. Rinsho Shinkeigaku. 2001 Oct;41(10):698-700

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19. Oberbeck R, Schurmeyer T, Jacobs R, Benschop RJ, Sommer B, Schmidt RE, Schedlowski M. Effects of beta-adrenoceptor-blockade on stress-induced adrenocorticotrophin release in humans. Eur J Appl Physiol Occup Physiol 1998 May;77(6):523-6

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21. McNutt et al. Acute myocardial farcation in a 22-year-old world class athlete using anabolic steroids. Am. Journal of Cardiology. 1988:62-164.

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22. Fisher et al. Myocardial infarcation with extensive intracoronary thrombus induced by anabolic steroids. Br. J. of Clin. Prac. 1996:50:222-223.

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24. Chodorowski Z, Sein Anand J. Acute poisoning with clenbuterol--a case report. Przegl Lek. 1997;54(10):763-4.

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25. Waterfield CJ, Jairath M, Asker DS, Timbrell JA. The biochemical effects of clenbuterol: with particular reference to taurine and muscle damage. Eur J Pharmacol. 1995 Jul 1;293(2):141-9