Tweetfor me 2 days on 2 days off at 120mcg is perfect

TweetMake him read this before he starts Clen:
Basically he should ramp up slow starting at 20mcg and go up to 80 or so, run it for 2 weeks on 2 weeks off, get in 4g Taurine ED, eat banannas, and supplement with extra magnesium and potassium. Also he can take bebnedryl or ketotifen to help the receptors from downregulating.
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Clenbuterol FAQ
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. ?


***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 hasnt 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.

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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 downregulates. 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


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!



References

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2. Yamamoto I, Iwata K, Nakashima M. Pharmacokinetics of plasma and urine clenbuterol in man, rat, and rabbit. J Pharmacobiodyn. 1985 May;8(5):385-91

3. Zimmer A. Administration of Clenbuterol in man. Single doses, multiple doses, and metabolite samples.* Vetmedica GmbH; Ingelheim, Germany

4. Tsuji T, Kato T, Kimata M, Miura T, Serizawa I, Inagaki N, Nagai H. Differential effects of beta2-adrenoceptor desensitization on the IgE-dependent release of chemical mediators from cultured human mast cells. Biol Pharm Bull. 2004 Oct;27(10):1549-54.

5. Astrup A, Toubro S. Thermogenic, metabolic, and cardiovascular responses to ephedrine and caffeine in man. Int J Obes Relat Metab Disord 1993 Feb;17 Suppl 1:S41-3

6. Reichel K, Rehfeldt C, Weikard R, Schadereit R, Krawielitzki K. Effect of a beta-agonist and a beta-agonist/beta-antagonist combination on muscle growth, body composition and protein metabolism in rats. Arch Tierernahr. 1993;45(3):211-25.

7. Rothwell NJ, Stock MJ. Effect of a selective beta 2-adrenergic agonist (clenbuterol) on energy balance and body composition in normal and protein deficient rats. Biosci Rep. 1987 Dec;7(12):933-40.

8. S. L. H. Schiffelers, W. H. M. Saris, F. Boomsma and M. A. van Baak Beta1- and Beta2-Adrenoceptor-Mediated Thermogenesis and Lipid Utilization in Obese and Lean Men. The Journal of Clinical Endocrinology & Metabolism Vol. 86, No. 5 2191-2199

9. Jung RT, Shetty PS, James WP, Barrand MA, Callingham BA. Reduced thermogenesis in obesity. Nature. 1979 May 24;279(5711):322-3.

10. Abramson MJ, Walters J, Walters EH. Adverse effects of beta-agonists: are they clinically relevant? Am J Respir Med. 2003;2(4):287-97.

11. O de Divitiis, S Fazio, M Petitto, G Maddalena, F Contaldo and M Mancini. Obesity and cardiac function.* Circulation, Vol 64, 477-482

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

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

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

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

16. Maltin CA, Delday MI, Watson JS, Heys SD, Nevison IM, Ritchie IK, Gibson PH. Clenbuterol, a beta-adrenoceptor agonist, increases relative muscle strength in orthopaedic patients. Clin Sci (Lond). 1993 Jun;84(6):651-4.

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

18. Pellegrino MA, D'Antona G, Bortolotto S, Boschi F, Pastoris O, Bottinelli R, Polla B, Reggiani C. Clenbuterol antagonizes glucocorticoid-induced atrophy and fibre type transformation in mice. Exp Physiol 89.1 pp 89-100

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

20. Goldstein et al. Clenbuterol and anabolic steroids: a previously unreported case of myocardial infarcation with normal coronary arteriograms. Southern Medical Journal. 1998:780-784.

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.

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

23. Hoffman RJ, Hoffman RS, Freyberg CL, Poppenga RH, Nelson LS. Clenbuterol ingestion causing prolonged tachycardia, hypokalemia, and hypophosphatemia with confirmation by quantitative levels. J Toxicol Clin Toxicol. 2001;39(4):339-44

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

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


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TweetClen has a biphastic elimination, which means that it is technically reduced in your body in 2 different stages. This isn’t particularly important, as a recent study has shown that for most intents and purposes, clen concentrations in the body decline with a ½ life (approximately) equivalent to 7-9.2hours and again up to as much as 35 hours later(4)(5). If you’re really interested, though, clen technically declines biphastically at 10 and then 36 hours. But really, in our little world, where we use ½ life to tell us when to take our next dose, who the hell is going to take clen, then a dose 10 hours later, then a dose 36 hours later? We’ll stick with the earlier 7-9 hour ½ life for dosing purposes, and take our clen every 3.5-4.5 hours that we’re awake, stopping early enough to still be able to get to bed. Clen can, in some people, cause insomnia (and as with all stimulants, can cause anxiety in some). Recently, it’s become popular to take a whopping dose of clen in the morning, and that’s it for the day. There’s nothing wrong with this, I guess, but I’d rather not go through that kind of roller-coaster of sweating and shaking until it wore off.

Based on it’s rate of elimination from the body, and how much is usually needed to be effective for athletes, my recommendations are the same for both men and women. You’ll need to take 20mcgs upon rising, and then repeat that same dose again later in the day, and then once again in that day (if you find you can tolerate the effects). So you’ll start with 20mcgs, and then repeat that dose 2 more times that same day if you can tolerate it (side effects will determine this…hand shaking, sweating, etc…classic stimulant sides). Then you can start increasing the dose gradually. Personally, I wouldn’t work my way up to more than 200mcg/day. 60-120mcg/day is an average dose. And keep your Blood Pressure at (or under) 140/90, while on clen, just to be safe. If you go over that, lower the dose. You’ll also want to know your body temperature, upon rising, for the week before you start taking your clen, and then monitor it (again, as soon as you wake up) throughout your clen regimen. When it returns to the level it was at before you began taking the clen, you’ll need to start taking your Benadryl or Ketotifen, as the decrease in Body Temperature back to original levels indicates the thermogenic effect is beginning to decline.

Clenbuterol can also cause a downregulation in testicular androgen receptors and in pulmonary, cardiac and central nervous system beta-adrenergic receptors(6.)…possibly making steroids less effective (if there is androgen receptor downregulation elsewhere as well, then it's highly probable) while you are on clen; but definitely making clen less effective as time goes on and you keep taking it. To counteract this, you can take some ketotifen every 3rd or 4th week that you remain on clen. It’s a prescription anti-histimines, so it’ll make you drowsy (take before bedtime). Basically, the way this works is to reduce beta-2 receptor activity, and restore receptor function (15).

Another option, if you are worried about receptor downgrade, is taking Benadryl, at around 50-100mgs/night before bed (every 3rd week or so, for that week). Benadryl is sold as an anti-histimine in the United States, and/or a sleep aid elsewhere in the world. However, Beta receptors are embedded in the cell's outer phospholipid membrane. The stability of the membrane has a lot to do with the proper function of the receptors. Methylation of the phospholipids is stimulated by the binding of beta agonists to their receptors. Methylated phospholipids are foreign to the body, and when the body recognizes tham as foreign, it breaks them down with phospholipase A2. This changes the structure of the outer membrane which results in desensitizaton of the beta receptors. On the other hand, agents that inhibit phospholipase A2 slow desensitization.

Cationic ampiphylic drugs are known for their ability to inhibit phospholipase A2. Benadryl (diphenhydramine) is a cationic ampiphylic drug.

Ergo, Benadryl slows desensitization of Beta receptors (i.e. Upgrades them) by inhibiting phospholipase A2, which is the enzyme that breaks down methylated phospholipids, and this action in turn keeps the phospholipid membrane stable, and thus keeps the receptors functioning properly. (7). This will allow you to use clen for much longer and it'll still have the same effects. Also, since Benadryl is an anti-histamine, and histamines have a direct effect on beta-adrenoreceptors (not just Beta-2’s but all of them), using an anti-histamine will have a direct effect on reducing beta-receptor stimulation (16), and thus upregulating your beta-receptors.

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Originally Posted by rckpytn

for me 2 days on 2 days off at 120mcg is perfect

For me, jumping on at 120mcg right away would give me a heart attack. I prefer the 2 week on 2 week off method. Start with 60mcg for 2 days, then 80mcg for 2 days, then 100mcg for 2 days, then 120 or 140mcg for the remainder of the cycle.

TweetDay1: 60mcg
Day2: 80mcg
Day3: 80mcg
Day4: 100mcg
Day5: 100mcg
Day6-Day12: 120mcg
Day13: 100 mcg
Day14: 80 mcgs


i ramp up and down.
if i start too high i shake bad and if i come off to fast i get headaches.

TweetYou must spread some Reputation around before giving it to geesler again.

great posts gees... i think the key here is to ramp up nice and slow, just like the articles state. the side effects of using too much too fast are very unpleasant (to me at least)

TweetCLEN, not CLEM! sheesh. its not the magic weight loss drug, DNP is

Tweetclembutteroil?

Tweeti think a good ECA stack is just as effective without the jitters. Also the anabolic effects of clenbuterol is usually only seen in animals, ive never heard of one person gaining muscle on clen and ive used it along with alot of guys I know have used so dont buy into that.

Tweetyeah Clen works by the stimulation of both type 2 and 3 beta-receptors.
3-beta receptors are more abundant in livestock than in humans, so it works like that for cows but not for us.

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