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    Default Clenbuterol

    Clenbuterol

    (Clen)


    Clenbuterol (Clen) is a selective beta-2 agonist/antagonist and a bronchodilator. What this means, is that it stimulates your beta-2 receptors. Of great importance, is that Clenbuterol is a selective beta-2 agonist (because it works selectively on the beta-2-andrenergic-receptors), right? The thing is, Clenbuterol is selective...like hitting a tack (the tack being your beta-2 receptors) with a small hammer (the hammer being the Clen)...thus, it hits the beta-2 receptors selectively. Sorry if that seems repetitious, but it´s very important to understand that fact before we move on. Since clenbuterol has very little beta-1 stimulating ability, it has the ability to reduce certain kinds of airway obstruction without much in the way of cardiovascular effect (more about that later), and this is why it is used as an asthma medication.

    So what exactly dose a stimulant like Clen (or Ephedrine) do when it stimulates those Beta Receptors? Well, it serves to increase your body temperature a bit by increasing heat production in the Mitochondria, increase your basal metabolic rate, and decrease your appetite (1). This partly explains how Beta-2 agonists directly stimulate fat cells and increase lypolysis (fat-loss)(1)(13). And also, because it is a Beta-2 agent, clen can decrease insulin sensitivity (2), unfortunately.

    Clenbuterol Fat Loss

    Clenbuterol is a very effective repartitioning agent, and this is what it´s most often used for in athletic circles. It will increase your ratio of Fat Free Mass (FFM) to Fat Mass, by decreasing your Fat and possibly increasing your FFM (3). Lets quantify that a bit:

    In one study, horses given a semi-reasonable dose of clen (slightly over 1mcg/lb x2 a day) and exercised for 20mins, 3x a week ( I suppose they were Mentzer disciples) had significant decreases in %fat (-17.6%) and fat mass (-19.5%) at week 2, which was similar to Clen given to horses who didn´t exercise; in contrast, the exercised group had a different FFM response, which significantly increased (+4.4%) at week 6 (3). Week 6! Here´s a chart illustrating the changes in % of Body Fat experienced in the various test groups, followed by a chart showing the increase in Fat Free Mass experienced by the same groups:


    Changes in percent body fat (%fat) over time in clenbuterol and exercise (ClenEx; A), clenbuterol only (Clen; B), exercise only (Ex; C), and control (Con; D) groups. Means with different letters (A and B) are significantly different.


    Changes in fat free mass (FFM) over time in ClenEx (A), Clen (B), Ex (C), and Con (D). Means with different letters (a-c) are significantly different.

    I think those charts should clearly illustrate the repartitioning effects of Clen, even though it is known that it´s effects on animals are typically much more dramatic than in humans& .There´s still no doubt about it, in my mind Clen will help you lose fat and gain muscle.

    So Let´s re-examine that first point I made: Clen vs. clen+ exercise produce roughly the same results for the first 2 weeks! This tells me that the 2 weeks on and 2 weeks off schedule for clen dosing is far from optimal, and if you want the quasi-anabolic effect from the clen, it´ll take more than 2weeks on (6 weeks apparently). In addition, since clen alone is similar to clen+ exercise for those first 2 weeks...why would you ever use a 2on/2off protocol? Keep in mind that animal responses to beta-agonist/antagonists differ a bit from ours but I´m sure that you get the idea that 2on/2off is not a great dosing protocol. If I were using clen, I´d be using it for 6-12 weeks at a time, if I expected to get maximum results from it, but certainly, the most dramatic effects on fat loss appear to be in weeks 1-2. The reasons for the further increase in FFM around week 6 despite no changes in %fat or fat mass is not easily explained... It might be that clenbuterol can increases FFM through another nonreceptor-mediated pathway, which would be very good for us, since the anabolic effects would also be applicable in humans, despite the fact that animals often respond more dramatically to beta-agonist/antagonists, due to receptor properties.. However, clenbuterol is highly lipophylic and can also enter muscle tissue (12), so that could indicate a possible mechanism of work. Maybe that would explain the significant increase in FFM of 13 kg in at 8 wks in the study? Certainly, muscle protein synthesis (MPS) must be a part of it, since clen will increase MPS in your body (17)& But it has even been speculated that the growth-promoting effect of clenbuterol may be specific to muscle and that the drug may act in a not-yet-understood manner which circumvents (!) the physiological mechanisms responsible for the control of muscle growth (13). This may mean that clenbuterol can help blast you past "sticking points" in your training by circumventing the usual mechanisms by which anabolism is experienced! It is of note that both muscle composition and fiber size has been shown to increase with administration of clen (14).

    In any case, Clearly the results you want to reproduce for yourself are those to be gained by clen + exercise, for 6 weeks or more. This type of dramatic anabolic effect hasn´t been confirmed in human studies (8), but the anabolic effects of clen in animal (specifically equine and rodent) studies are clearly quite astounding.
    Now that I told you how great clen is; I´ll tell you how to take it.

    Clen 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.

    Clenbuterol Cycle

    Based on its 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-histamine 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 them as foreign, it breaks them down with phospholipase A2. This changes the structure of the outer membrane which results in desensitization 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.

    Ephedrine

    Since we´re speaking about beta-receptors and upregulation, here, let me address the claim that you can use ephedrine (or the ECA stack), alternating with clen, in order to avoid receptor downgrade. I´m not sure where this rumor came from, but it is totally incorrect.

    To dispel this myth, lets examine ephedrine for a second. Remember when I said that using clenbuterol to stimulate the beta-2 receptors is like hitting a tack with a hammer? Well, Ephedrine is like a sledge-hammer, it hits the beta-2´s and everything around them. That´s because it´s not selective, but rather it stimulates other receptors to a great degree as well.

    Anyway, one of those receptors that ephedrine hits is the Beta-2 (yeah...the same one as Clen). As you can see from the graph below (ephedrine is represented by the the solid circles), it reduced Beta-2-AndrenergicReceptor (what we call, in laymens terms, the "Beta-2 receptor") levels to 32% of the control level after 24 hours. Read this again:

    Ephedrine, in this study, reduces Beta-2 receptor levels to 32% of control after 24 hours.
    (see the solid circles in this graph represent ephedrine)


    Granted, it´s not perfect, it´s not in vivo, etc...But there´s no denying that ephedrine will downregulate beta-2 receptors....ergo you will not be able to use it on the weeks in between your clen to upgrade your receptors.

    Clenbuterol Side Effects

    Also, bear in mind that clenbuterol has some side effects. It isn´t great for your heart, and can cause some issues there (enlargement of ventricles, etc, ) but most studies showing clen to cause heart problems are with animals, and even though the dosing is almost similar to what humans take (in some studies it´s within the range of what would be double of a large human dose...) it´s important to remember that animals have more beta-2 receptors and they cause certain event chains that humans´ beta-2 receptors may not. Clen causes cardiac hypertrophy and cardiac necrosis (cell death) to some degree, in some cases. Again though, many studies showing the more significant, possibly irreversible, heart problems are with mg dosing. We humans take clen in mcg doses.

    If we want to duplicate those "theraputic" levels of clen seen in the more conservative studies, we´d still be taking just over 1mcg/lb of bodyweight, twice a day. I´d suggest a bit less than half of that dose, however.

    Performance issues with clen also vary. Some studies show reduced exercise (cardiovascular) performance with clen (9), while some show that clen can alleviate exercise induced asthma (10)!Clearly, this compound will have different effects on different people, and I suspect that a lot of it is sports specific. Many bodybuilders claim that clen makes it difficult for them to do cardio, yet I can play a full game of rugby on it. You need to figure out how it affects you, and tailor your dose personally.

    Finally, this brings me to the issue of cramps while on clen. I don´t get them. My friends don´t get them. Most of us are athletes who use clen during the season as well as the off season, and one of my friends even claims that it gives him more "wind" (cardiovascular stamina). Take on enough water every day and you should be fine. If you´re really concerned, you can take some extra minerals and taurine, since clen depletes taurine (11) as do most if not all beta-agonists. I don´t take anything more than my usual vitamins and minerals.

    1st Graph Reference:
    ASPET Journals, Vol. 58, Issue 2, 421-430, August 2000
    Kinetic Analysis of Agonist-Induced Down-Regulation of the 2-Adrenergic Receptor in BEAS-2B Cells Reveals High- and Low-Affinity Components
    Bruce R. Williams, Roger Barber, and Richard B. Clark
    2nd set of Graph references:
    J Appl Physiol 91: 2064-2070, 2001; 8750-7587/01
    Chronic administration of therapeutic levels of clenbuterol acts as a repartitioning agent
    Charles F. Kearns1, Kenneth H. McKeever1, Karyn Malinowski1, Maggie B. Struck1, and Takashi Abe2

    References:

    1. Int J Obes Relat Metab Disord. 1994 Jun;18(6):429-33.
    2. Am J Physiol Endocrinol Metab. 2002 Jul;283(1):E146-53
    3. J Appl Physiol. 2001 Nov;91(5):2064-70
    4. J Anal Toxicol. 2001 May-Jun;25(4):280-7.
    5. J Pharmacobiodyn. 1985 May;8(5):385-91.
    6. J Anim Physiol Anim Nutr (Berl). 2004 Apr;88(3-4):94-100
    7. Prog Clin Biol Res. 1981;63:383-8
    8. Ann Pharmacother. 1995 Jan;29(1):75-7
    9. Med Sci Sports Exerc. 2002 Dec;34(12):1976-85.
    10. Respiration. 1987;51(3):205-13.
    11. Adv Exp Med Biol. 1996;403:233-45
    12. Food Addit Contam 13: 259-274, 1996
    13. Biochem J. 1989 Jul 1;261(1):1-10.
    14. Biosci Rep. 1987 Feb;7(2):143-9.
    15. Z Erkr Atmungsorgane. 1990;175(3):141-6
    16. Comp Biochem Physiol C. 1989;92(1):143-8.
    17. Biosci Rep. 1984 Jan;4(1):83-91.
    All posts are for entertainment and may contain fiction. Consult a doctor before using any medication.


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    Fat Attack
    By Dan Gwartney, MD

    Clenbuterol Can Have Negative Effects On The Heart And Blood Vessels

    PQ: The late professional bodybuilder Andreas Munzer is reported to have used clenbuterol in what is termed the “death stack” believed to be responsible for his sudden and unexpected death.

    Most people live fairly simple lives, without regular access to many of the luxuries discussed on lifestyle shows or flaunted in series like NBC’s “Las Vegas” or CBS’s “Dallas” (for those of you old enough to remember life on the Ewing Ranch). Yet, events arise from time to time allowing one to expand his horizons and experience some of the fineries of the elite…perhaps a wedding or a business trip with an expense account. The formal surroundings that often accompany these events provide opportunities to dance the waltz, consume foie gras (duck liver) or stay at a five-star hotel. The great majority never develops a taste for waltzing or exotic hors d’oeuvres, but some find themselves budgeting to indulge in these pleasures regularly.

    A similar situation is seen in the culture of anabolic steroid (AAS) users. Most AAS users are “meat and potatoes” types who follow simple cycles of testosterone or Deca; some may dress up the cycle by stacking with an oral or adding an aromatase inhibitor, but nothing overly risky or cutting-edge. Yet, occasionally the opportunity comes along to try one of the drugs often mentioned in “elite”-level stacks. One such drug has long held an allure for those looking to define the physique…or female bodybuilders and the Hollywood/South Beach crowd seeking to lose weight. That drug is clenbuterol.

    Clenbuterol is a stimulant that activates some of the same receptors that are activated during an adrenaline rush, during the familiar caffeine buzz enjoyed after that third cup of coffee, or by ephedrine-containing products. However, clenbuterol is different from adrenaline, ephedrine and caffeine in that it is relatively specific about how it stimulates certain tissues of the body.1 Even more intriguing is the (highly disputed) possibility that clenbuterol may actually help build muscle as well.2,3 Clenbuterol’s welcome reception by male bodybuilders comes during precontest phases, as the drug is a potent addition to the fat-stripping effects of thyroid hormone; female bodybuilders may use the drug in the off-season, stacking the drug as a nonandrogen-based anabolic; the glamorati often use the drug year-round in pursuit of the fashionably (and questionably anorexic) ideal weight.

    Clenbuterol is often considered safe by its users because it is more specific in its actions than adrenaline. When adrenaline flushes the system during a period of fright or excitement, the heart speeds up; blood vessels relax in the heart, lungs and skeletal muscle; and the cellular furnace turns up the heat to provide immediate energy to face an impending threat. These and other metabolic responses take place because adrenalin (also called epinephrine) interacts with three different classes of receptors on the various organs and tissues of the body called b1, b2 and b3…b is for beta. [There is another class of adrenalin-responsive receptors called a-receptors, but they are not relevant to this discussion] B1 receptors cause the heart to race and drop blood pressure, whereas b2 is responsible for the fat-loss and calorie-burning effects; the role of b3 is not fully understood in humans, but it appears to be similar to b2.4 Clenbuterol is called a b2-agonist because it stimulates b2-receptors, pretty much ignoring b1-receptors.

    Fat cells have b2-receptors; under the influence of clenbuterol, stored fat is broken down and released.5 Muscle cells also have b2-receptors. When chronically exposed to clenbuterol, skeletal muscle cells turn on their genetic machinery and anabolic processes are enhanced.2 However, there is controversy as to whether this happens in humans at a tolerable dose, as the effect, when seen in animals, occurs at doses that would cause significant side effects.

    Indeed, as with most other drugs used in building muscle, clenbuterol’s benefits seem to be dose-related but are often capped by negative side effects. Additionally, some of the thermogenic effect of the drug rapidly wears off as the receptors are downregulated (fewer receptors or less of a biologic response) within a matter of hours to days.7 This is why many sources speak of cycling clenbuterol every few days and often suggest using the drug in conjunction with thyroid hormones.8 Be aware that several fitness and bodybuilding professionals have impaired their natural thyroid regulation and have become dependent on thyroid medications following this practice.

    In addition to being selective and potent (strong), clenbuterol is handled differently by the body in comparison to other adrenalin-like drugs. The body uses adrenalin to signal rapid changes and has enzymes that metabolize (clear out) adrenalin and related compounds quickly to prepare the body for another signal. However, the chemical structure of clenbuterol includes changes that make it difficult for the body to clear the drug, allowing it to stay active in the system for more than a day.9 Clenbuterol is also able to be administered orally, whereas most other drugs in the class need to be administered by inhaler or injection. While this makes it a very convenient drug for treating asthma (or aiding in weight loss, though that is not an approved use), it also makes it very easy to overdose on the drug.

    Several reports of clenbuterol overdose are present in the medical literature, including a recent report that demonstrates the immediate risks involved in using the drug.10-13 In this case, a 31-year-old bodybuilder was admitted into the emergency room complaining of heart palpitations (irregular or forceful heartbeat) and shortness of breath; he was also quite anxious.14 Surprisingly, his body temperature was not elevated (97.1º; normal body temperature is 98.6º). The doctors discovered that his heart rate was alarmingly high— 254 beats per minute. The formula for maximum heart rate commonly referenced is 220 minus your age (189 beats per minute in this case), so this person was clearly overly stimulated. In fact, the electrical process involved in heart contractions (remember, the heart is a specialized muscle) has a theoretical limit of 300 beats per minute and this cannot be maintained. This condition, called supraventricular tachycardia, is often seen in stimulant drug overdoses (cocaine, methamphetamine, etc).15,16

    Even after initial drug treatment, the patient’s heart rate remained elevated. A toxicology specialist was called in and further treatment with a beta-blocker (to reverse clenbuterol’s stimulation of the b1-receptors on the heart) managed to lower the heart rate to a safe range. However, as the heart rate dropped into normal range, a second and more dangerous abnormal heart rhythm emerged called atrial fibrillation. Fibrillation is a term that describes a type of shivering motion of the heart muscle that does not pump blood. Instead, the blood pools and quivers. This is dangerous not only because it provides poor circulation, but also because blood will clot if it is not in motion. Atrial fibrillation is one of the main causes of embolic strokes and pulmonary embolism (clots in the lung), both which can be fatal.17 After two days, the condition did not change and the patient was cardioverted (shocked using paddles) to shock the heart back into a normal rhythm.

    This was a healthy 31-year-old man, yet by taking less than 1/4mg of clenbuterol, he ended up in the hospital for four days and had to be shocked to restore a normal heartbeat. His is certainly not the only case of this drug affecting healthy young men in such a manner.10,13 In fact, this gentleman should consider himself fortunate, as others in similar situations died. The stimulatory effect of clenbuterol, said to be b2-specific, can affect the b1-receptors which control heart rate.18,19 B2-receptors also control heart rate, though this effect is minor in normal people. It is possible that b2-stimulation in a case of clenbuterol overdose contributes to tachycardia, though a recent study investigating the use of clenbuterol in acute heart failure challenges this position.20 This is particularly evident at high doses, as seen in this case. Yet, the greatest danger from clenbuterol overdose may not be the b1-stimulatory effect on the heart rate, but rather on the drug’s effect on the electrolyte balance.12,21 Electrolytes include familiar names, such as sodium, potassium, magnesium and calcium. Normally, the body maintains these electrolytes in a controlled range because they are involved in the conduction of electrical signals in the brain, nerves and heart muscle. In clenbuterol overdose, the electrolyte balance can be disturbed and electrical signals throughout the body may become abnormal. In extreme cases, this can lead to heart attacks, acute heart failure or even death.

    Perhaps many will scoff at this, considering the many, many people who use clenbuterol with no problems. Certainly, the drug is effective at fat loss and when used by a healthy adult in a controlled fashion, is reasonably safe. In fact, clenbuterol is used in some countries to treat asthma and is even being studied in the United States for treating patients with heart failure.20,22 Interestingly, the heart failure patients received increasingly higher clenbuterol doses, being maintained on 700mcg three times a day. This is a dose nearly 20 times higher than the amount consumed by the healthy 31-year-old who sent him into the emergency room. The heart failure patients tolerate the excessively high clenbuterol concentrations because they are treated at the same time with a potent b1-blocking drug.

    However, clenbuterol is not currently approved for use by humans in the United States. It is allowed for use in veterinary preparations, which is a form commonly encountered in the bodybuilding world. Clenbuterol-containing syrups (e.g., Ventipulmin) are diverted from animal supply stores or brought across the border. Ventipulmin contains 72.5mcg/ml; note that the dose unit is mcg (microgram) as opposed to the more common mg (milligram). To give an idea of scale, a milligram contains 1,000 micrograms; a gram contains 1,000mg or 1,000,000 micrograms. Of course, most people prefer the convenience of tablets, which are also readily available via the Internet and other sources, usually in 20mcg units.

    According to author Bill Llewellyn in Anabolics 2005, common daily dosing of clenbuterol for male bodybuilders is in the range of 40mcg-160mcg/day.8 The man in the case report consumed approximately 100mcg-120mcg prior to being admitted to the emergency room, so it is somewhat surprising to see the extent of problems he occurred; the other drugs he reported using are not known to increase the risk of cardiotoxicity (tamoxifen, citrate, flaxseed oil, taurine and a multivitamin), though taurine is known to affect cardiac function in combination with caffeine.23,24

    However, when one considers that clenbuterol is a long-acting drug, it is possible that users may face a buildup in blood concentrations over time, especially if the drug is not cycled in the common two-on, two-off pattern. Though the half-life is reported to be 25-30 hours, this can vary among individuals considerably. Unfortunately, the treating physicians did not draw for clenbuterol levels, so it is impossible to state absolutely whether this emergency was precipitated by a single dose, or represents long-term or chronic-use toxicity.

    Given the emergence of clenbuterol into the fashion and entertainment world for weight loss and its long-term use in bodybuilding, there is an unjustified level of comfort for many with the drug. True, most people will not use the drug, as it is one of those luxuries that a “meat-and-potatoes” bodybuilder typically won’t indulge. However, with demand comes increased availability, so it is possible that the increasing awareness among desperate housewives and women with an obsessive desire to fit a size zero may introduce this drug to a more mainstream level.

    Though the number of reported overdoses are few and healthy and young adults can generally tolerate sympathetic overload (cocaine, methamphetamine, etc.), users should be aware of the risk of heart rhythm abnormalities that can occur with clenbuterol use, even in the typical dose range. The late professional bodybuilder Andreas Munzer is reported to have used clenbuterol in what is termed the “death stack” believed to be responsible for his sudden and unexpected death. Given the known reports of medical emergencies and even deaths caused by this drug, it needs to be viewed with a greater level of caution. Further, when one considers that many drugs used concurrently by those seeking to lose weight or fat (i.e., ephedrine, caffeine, Adderall, diuretics) may increase the risk of overstimulation or electrolyte abnormalities, it raises the level of concern even higher.

    References:

    1. O’Donnell SR. Selectivity of clenbuterol (NAB 365) in guinea-pig isolated tissues containing beta-adrenoceptors. Arch Int Pharmacodyn Ther, 1976;224:190-8.

    2. Spurlock DM, McDaneld TG, et al. Changes in skeletal muscle gene expression following clenbuterol administration. BMC Genomics, 2006;7:320-34.

    3. Burniston JG, McLean L, et al. Anabolic effects of a non-myotoxic dose of the beta2-adrenergic receptor agonist clenbuterol on rat plantaris muscle. Muscle Nerve, 2007;35:217-23.

    4. Lohmann FW, Loesment WA, et al. Beta-receptor blockade, physical activity, and metabolism. J Cardiovasc Pharmacol 1990;16 Suppl, 5:S45-52.

    5. Arner P. Catecholamine-induced lipolysis in obesity. Int J Obes Relat Metab Disord, 1999;23 Suppl 1:10-3.

    6. Reeds PJ, Hay SM, et al. Stimulation of muscle growth by clenbuterol: Lack of effect on muscle protein biosynthesis. Br J Nutr, 1986;56:249-58.

    7. Newman-Tancredi A, Verriele L, et al. Down-regulation of rat beta-adrenoceptors by clenbuterol or desipramine does not require chronic treatment: [3H] CGP-12177 binding reveals rapid (24 hour) modulation. Brain Res Bull, 1996;41:93-6.

    8. Llewellyn W. Clenbuterol. Anabolics 2005. Body of Science Press, Jupiter, FL;2005:267-8.

    9. Yamamoto I, Iwata K, et al. Pharmacokinetics of plasma and urine clenbuterol in man, rat, and rabbit. J Pharmacobiodyn, 1985;8:385-91.

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

    11. Goldstein DR, Dobbs T, et al. Clenbuterol and anabolic steroids: a previously unreported case of myocardial infarction with normal coronary arteriograms. Southern Med J, 1998;91:780-4.

    12. Hoffman RJ, Hoffman RS, et al. Clenbuterol ingestion causing prolonged tachycardia, hypokalemia, and hypophosphatemia with confirmation by quantitative levels. J Toxicol Clin Toxicol, 2001;39:339-44.

    13. van der Kuy PH, Stegeman A, et al. Falsification of Thai dianabol. Pharm World Sci, 1997;19:208-9.

    14. Daubert GP, Mabasa VH, et al. Acute clenbuterol overdose resulting in supraventricular tachycardia and atrial fibrillation. J Med Toxicol, 2007;3:56-60.

    15. Isner JM, Estes NA 3rd, et al. Acute cardiac events temporally related to cocaine abuse. N Engl J Med, 1986;315:1438-43.

    16. Chan P, Chen JH, et al. Fatal and nonfatal methamphetamine intoxication in the intensive care unit. J Toxicol Clin Toxicol, 1994;32:147-55.

    17. Murtagh B, Smalling RW. Cardioembolic stroke. Curr Atheroscler Rep, 2006;8:310-6.

    18. Mazzanti G, Di Sotto A, et al. A pharmacodynamic study on clenbuterol-induced toxicity: beta1- and beta2-adrenoceptors involvement in guinea-pig tachycardia in an in vitro model. Food Chem Toxicol, 2007;45:1694-9.

    19. Santos IN, Spadari-Bratfisch RC. Stress and cardiac beta adrenoceptors. Stress, 2006;9:69-84.

    20. Birks EJ, Tansley PD, et al. Left ventricular assist device and drug therapy for the reversal of heart failure. N Engl J Med, 2006;355:1873-84.

    21. Bilkoo P, Thomas J, et al. Clenbuterol toxicity: an emerging epidemic. A case report and review. Conn Med, 2007;71:89-91.

    22. Wheatley D. Clenbuterol ("Spiropent”): a long-acting bronchodilator. Curr Med Res Opin, 1982;8:113-9.

    23. Steele DS, Smith GL, et al. The effects of taurine on Ca2+ uptake by the sarcoplasmic reticulum and Ca2+ sensitivity of chemically skinned rat heart. J Physiol, 1990;422:499-511.

    24. Baum M, Weiss M. The influence of a taurine containing drink on cardiac parameters before and after exercise measured by echocardiography. Amino Acids, 2001;20:75-82.
    All posts are for entertainment and may contain fiction. Consult a doctor before using any medication.


  3. #3
    Super Moderator heavyiron's Avatar
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    Clenbuterol is anabolic in humans

    by Anthony Roberts

    Back in 2004 I wrote the first heavily researched article of my career. It was about Clenbuterol, and you can still find it in article forums and profile sections on most major sites. One of the most controversial points I made was that Clenbuterol is anabolic. At the time there was a pretty reasonable amount of animal data (rodents, horses, etc…) and I was fairly confidant saying that Clen has anabolic – or at least strongly anti-cabtabolic – effects in humans. Back when I wrote that article, and my subsequent book(s), there was no published medical data on the accrual of fat free mass in humans using Clenbuterol. And frankly, most bodybuilders who used the stuff were also using a lot of other stuff too.

    Naturally, because there was no human data to support this notion, online steroid”experts” rallied behind the notion that because there was no human data proving otherwise, Clen must not have that effect outside of animals. Anyway, a couple of studies have recently popped up in the US National Library of Medicine, that are new or were previously unavailable or unpublished. One is from all the way back in 1993, and was conducted in the UK, and seems to indicate that Clen helped patients regain muscle strength more quickly after orthopedic surgery:

    Clin Sci (Lond). 1993 Jun;84(6):651-4.

    Clenbuterol, a beta-adrenoceptor agonist, increases relative muscle strength in orthopaedic patients.

    Maltin CA, Delday MI, Watson JS, Heys SD, Nevison IM, Ritchie IK, Gibson PH.

    Rowett Research Institute, Bucksburn, Aberdeen, U.K.

    Abstract

    1. The sympathomimetic agent clenbuterol has a muscle-specific anabolic effect in normal and wasted muscles from animals. This trial was designed to examine the effect of the drug on the recovery of muscle strength and area after open medial meniscectomy. 2. A double-blind, completely randomized, placebo-controlled study was carried out on 20 healthy male patients. Muscle strength and cross-sectional area were determined before and after surgery. Patients were treated with drug or placebo for 4 weeks postoperatively and there was a 2 week washout period. 3. The results suggest that, in the operated leg, clenbuterol treatment is associated with a more rapid rehabilitation of strength in knee extensor muscles; in the unoperated leg, knee extensor strength increased above the initial values after 6 weeks (P = 0.01). However, in terms of absolute strength the differences were not significant between the two groups. 4. It is concluded that the data lend support to the proposition that clenbuterol has therapeutic potential in the treatment of muscle-wasting conditions.

    In this next study, patients with chronic heart failure were given Clenbuterol, and made some decent gains in muscle size & strength, as well as their lean mass to fat mass ratio:

    J Heart Lung Transplant. 2008 Apr;27(4):457-61.

    Clenbuterol increases lean muscle mass but not endurance in patients with chronic heart failure.

    Kamalakkannan G, Petrilli CM, George I, LaManca J, McLaughlin BT, Shane E, Mancini DM, Maybaum S.

    Division of Cardiology, Department of Medicine, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, New York, USA.

    Abstract

    Clenbuterol, a beta(2)-agonist with potent anabolic properties, has been shown to improve skeletal muscle function in healthy subjects, and in high doses, promotes cardiac recovery in patients with left ventricular assist devices. In a small, randomized controlled study, we investigated the effect of clenbuterol on skeletal muscle function, cardiac function, and exercise capacity in patients with chronic heart failure. Clenbuterol was well tolerated and led to a significant increase in both lean mass and the lean/fat ratio. Maximal strength increased significantly with both clenbuterol (27%) and placebo (14%); however, endurance and exercise duration decreased after clenbuterol. Prior data support combining exercise training with clenbuterol to maximize performance, and on-going studies will evaluate this approach.

    Anyway, the point here is that human data is beginning to filter in, albeit in a rehab/post-operative scenario, showing that Clenbuterol does in fact have an anabolic effect in humans.
    All posts are for entertainment and may contain fiction. Consult a doctor before using any medication.


  4. #4
    Iron Addict brundel's Avatar
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    Awesome.

  5. #5

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    As always Heavy, thanx for the great info

  6. #6

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    so then theoreticaly, if one were using benadryl as a sleep aid nightly wile on AAS, there wouldn't be a need to worry about down regulation every 3-4 weeks and could just stay on clen for a 12 week pre-contest cycle?

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    Great info, thanks.

  8. #8
    Informant
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    Great read

  9. #9
    Dedicated Noob
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    Do bodybuilders use beta agonists to combat high progesterone induced fatigue?

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    Clenbuterol, marketed as Spiropent and Ventipulmin, is a sympathomimetic amine used by sufferers of breathing disorders as a decongestant and bronchodilator. People with chronic breathing disorders such as asthma use this as a bronchodilator to make breathing easier. It is most commonly available as the hydrochloride salt, clenbuterol hydrochloride.

  11. #11
    Barbarian Ajthemeso's Avatar
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    informative thread heavy. thanks.

  12. #12

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    Never really liked it. ECA better.

  13. #13

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    eca is my fav too.

    And damn OP is that u in ur pic? Fuckin ripped

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