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Clenbuterol Handbook
CLENBUTERAL FAQ: EVERYTHING YOU NEEDED TO KNOW ABOUT CLENBUTEROL by BigAndy69 (Dosing/Cycle example by Scheizekopf) What is Clenbuterol? Clenbuterol is a beta-2 agonist and is used in many countries as a bronchodilator for the treatment of asthma. Because of its long half life, Clenbuterol is not FDA approved for medical use. It is a central nervous system stimulant and acts like adrenaline. It shares many of the same side effects as other CNS stimulants like ephedrine. Contrary to popular belief, Clenbuterol has a half life of 35 hours and not 48 hours. Dosing and Cycling Clenbuterol comes in 20mcg tablets, although it is also available in syrup, pump and injectable form. It's also available as a powder in some areas. Doses are very dependent on how well the user responds to the side effects, but somewhere in the range of 4-8 tablets per day for men and 2-4 tablets a day for women is most common. Clenbuterol loses its thermogenic effects after around 8 weeks when body temperature drops back to normal. Its anabolic/anti-catabolic properties fade away at around the 18 day mark. Taking the long half life into consideration, the most effective way of cycling clen is 2 weeks on/ 2 weeks off for no more than 12 weeks. Ephedrine or Yohimbine can be used in the off weeks. Clenbuterol vs. Ephedrine vs. DNP Ephedrine will raise metabolic levels by about 2-3 percent and 200mg of DNP raises metabolic levels by about 30 percent. Clenbuterol raises metabolic levels about 10 percent and it can raise body temperature several degrees. DNP is by far the most effective fat burner but many people will never use it because of the risks associated with it. It also offers no anti-catabolic benefit. Although it does have anti-catabolic effect, ephedrine's short half-life prevents it from being all that effective. As far as side effects, Clenbuterol's are certainly milder than DNP's, and some would even say milder than an ECA stack. There is no ECA-style crash on Clenbuterol and many users find it easier on the prostate and sex drive. This may in part be due to the fact that Clen is generally used for only 2 weeks at a time. Side effects NAUSEA NERVOUSNESS DIZZINESS DROWSINESS DRY MOUTH FACIAL FLUSHING HEADACHE HEARTBURN INCREASED BLOOD PRESSURE INCREASED SWEATING INSOMNIA LIGHTHEADEDNESS MUSCLE CRAMPS TREMORS VOMITING CHEST PAIN The most significant side effects are muscle cramps, nervousness, headaches, and increased blood pressure. Muscle cramps can be avoided by drinking 1.5-2 gallons of water and consuming bananas and oranges or supplementing with potassium tablets at 200-400mg a day taken before bed on an empty stomach. Taurine at 3-5grams is a necessity in minimizing cramps. Headaches can easily be avoided with Tylenol Extra Strength taking at the first signs of a headache. Common Uses 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 its 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 down regulates. 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. I would suggest taking benadryl during clen cycles at 50-75mg per night. It is much easier to obtain than Keto. 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: Clen - 100mcg/ml Day1: 20mcg = 1/5ml = 0.2ml Day2: 40mcg = 2/5ml = 0.4ml Day3: 60mcg = 3/5ml = 0.6ml Day4: 80mcg = 4/5ml = 0.8ml Day5: 80mcg = 4/5ml = 0.8ml Day6: 100mcg = 1/1ml = 1ml Day7: 100mcg = 1/1ml = 1ml Day8: 100mcg = 1/1ml = 1ml Day9: 100mcg = 1/1ml = 1ml Day10: 100mcg = 1/1ml = 1ml Day11: 100mcg = 1/1ml = 1ml Day12: 100mcg = 1/1ml = 1ml Day13: 80 mcg = 4/5ml = 0.8ml Day14: 60 mcgs = 3/5ml = 0.6ml Day15: off Day16: off Day 17-Day 28: EC Stack Example of a secondcycle: Day1: 60mcg = 3/5ml = 0.6ml Day2: 80mcg = 4/5ml = 0.8ml Day3: 80mcg = 4/5ml = 0.8ml Day4: 100mcg = 1/1ml = 1ml Day5: 100mcg = 1/1ml = 1ml Day6: 120mcg = 6/5ml = 1.2ml Day7: 120mcg = 6/5ml = 1.2ml Day8: 120mcg = 6/5ml = 1.2ml Day9: 120mcg = 6/5ml = 1.2ml Day10: 120mcg = 6/5ml = 1.2ml Day11: 120mcg = 6/5ml = 1.2ml Day12: 120mcg = 6/5ml = 1.2ml Day13: 100 mcg = 1/1ml = 1ml Day14: 80 mcgs = 4/5ml = 0.8ml Day15: off Day16: off Day 17-Day 28: EC 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 completely 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 I dont agree with this completely. You can dose Clen right before sleep to experience much less sides. ------------------------------------------------------------------------------------------------------------ Steroid.com Info Description: Is available in 10 - 20 mcg tablets or in the .016 mg/gram Ventapulmin Vet variety. Clenbuterol is known as a sympathomimetic. These hormones are taken to mimic adrenaline and noradrenalin in the human body. Clenbuterol is a selective beta-2 agonist that is used to stimulate the beta-receptors in fat and muscle tissue in the body. Clenbuterol exhibits most of its effects on the stimulation of both type 2 and 3 beta-receptors. Clenbuterol is really one of bodybuilding's most misunderstood performance enhancement drugs. It is true that it is effective in helping to burn body fat but it is often been stated that Clenbuterol is effective in causing anabolic gains and has in times even been compared to some of the weaker anabolic steroids. Books such as the World Anabolic Review, 1996, by P. Grunding and M. Bachmann state incorrectly that, "its effects, however, can by all means be compared to those of steroids. Similar to a combination of Winstrol Depot and Oxandrolone...." These statements are inaccurate and misleading to say the least. A lot of these claims as to the anabolic effects of Clenbuterol are derived from studying the effects of Clenbuterol on livestock. Clenbuterol is effective in increasing muscle mass and decreasing fat loss in animals. The problem with the variation in anabolic effects between humans and livestock is that livestock have an abundance of the type 3 beta receptors whereas humans have little if any of the type 3 beta receptors. These beta-3 receptors increases insulin secretion and sensitivity, causing more glucose and amino acids to be transported into skeletal muscle thus causing the anabolic effects that we, humans, just aren't seeing. As Dan Duchaine stated in his Muscle Media article on Clenbuterol, "In those animal research studies showing an anabolic effect from Clenbuterol, it's my guess the anabolism happens specifically when the beta2 receptor stops working. At that point, the beta3 increases and causes the anabolic effect through insulin mechanisms." Since humans, again, have either very little or no beta-3 receptors, there is no chance of this anabolic effect. Just another of the studies where everyone assumed that what works in animals must work in humans. This is just simply not the case with Clenbuterol. Clenbuterol does work effectively as a fat burner though. It does this by slight increases in the body temperature. With each degree that the temperature in your body is raised from the use of Clenbuterol, you will burn up approximately an extra 5% of maintenance calories. This makes it effective as a fat burner. Your body will fight this by cutting down on the amount of active thyroid in the body as well as through beta-receptor down regulation, which explains why you only have a limited effective period to take Clenbuterol. While I am on the subject of beta-receptor down regulation, I would like to dispose of another myth. This involves the two on/two off cycling theory that I believe was originated by Bill Phillips in the Anabolic Reference Guide and has somehow made it's was into every other steroid book since then including the WAR and Physical Enhancement with an Edge. The two on-two off theory simply will not work because of one main reason: the half life of Clenbuterol. This 2-on/2-off idea was a THEORY ONLY, not by a doctor or scientist, and not based on specific knowledge of Clenbuterol, but derived by imitation from other drugs with shorter half lives. Clenbuterol has been reported as having a half life of about 2 days, but that is not actually correct, since it has biphasic elimination, with the half-life of the rapid phase being about 10 hours, and the slower phase being several days. Supposedly, this is one of the reasons the FDA never approved Clenbuterol as an anti-asthmatic drug...the FDA frowns on drugs with long half-lives if drugs with more normal half-lives are available. So with a 2-on/2-off cycle you never have time to get enough of the Clenbuterol out of your system for this theory to be reasonable. In actuality, it probably hasn't even dropped to 50% of your peak concentration before you are 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. A more reasonable approach would be either one week on, one week off, or alternately, two weeks on two weeks off. The two week cycle has the disadvantage of a "crash" period afterwards. This crash period can be helped with the use of ephedrine to lessen the lethargy that you will experience. If you are interested in taking Clenbuterol for anything other than fat loss then you might as well stay away from this compound. There is a lot of talk as to how Clenbuterol compares to ephedrine as well. Most "experts" feel that clen gives a better bang for the buck than the ECA stack. It should be noted that clenbuterol’s results and effects are much shorter lived. They work through very similar mechanisms. Both products stimulate the beta-receptors but Clenbuterol seems to be a more refined version, called a second generation beta-agonist drug, than ephedrine. Clenbuterol targets the proper receptors, being the beta-2 and 3 receptors than ephedrine more specifically which should in theory make Clenbuterol more effective of a fat burner. Again, most of the so called "experts" say that Clenbuterol is more effective than ephedrine. I, personally, get worse results with clen vs. the good old ECA stack. Clenbuterol also didn't blunt my hunger either and I ate more while taking it as well. I also seem to get much better effects out of cytomel as a fat burner as well. Even better than the ECA stack or Clenbuterol. But, again, that is my personal opinion. Effective Dose: 80-140 mcgs. / Day in split doses throughout the day. Anything over 140 mcg a day is overkill since the beta receptors can only take so much of a product and then more is just wasteful. Street Price: $.50 - 1.00 / tab. fairly inexpensive in Mexico though. Spiropent is currently going for about $7.50/box, Novegam for $5.25/box, and Oxyflux for about $3.30/box. Effective Dose: A few drops under the tongue and not used for but a few weeks at a time. Street Price: Not a clue. Too hard to find. Even if I could find it I would not buy it. |
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anything copied from Steroid.com gets moved to the Newbie Info forum.....plus alot of that information in there is just plain WRONG. Clen doesnt have any anticatabolic or anabolic effects...its a myth. Also, DNP is anticatabolic. And they left out the most important fact that CLEN KILLS HEART MUSCLE CELLS.
you want to use clen its your business, but you'll probably have a heart attack one day. good luck.
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Only the bottom portion is from Steroid.com.
Do you have a link to a study where CLEN KILLS HEART MUSCLE CELLS? I've read studies that use clen to help with heart problems. |
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I am not going to get into a pissing match here but ahve you read the doses that the rats received...the ones that shown heart damage? Its something like 5mg/kg......crazy amounts. I will find one said study and post it here.
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Here read this:
Myotoxic effects of clenbuterol in the rat heart and soleus muscle. Burniston JG, Ng Y, Clark WA, Colyer J, Tan LB, Goldspink DF. Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool L3 2ET, United Kingdom. hhsjburn@livjm.ac.jp Myocyte-specific necrosis in the heart and soleus muscle of adult male Wistar rats was investigated in response to a single subcutaneous injection of the anabolic beta(2)-adrenergic receptor agonist clenbuterol. Necrosis was immunohistochemically detected by administration of a myosin antibody 1 h before the clenbuterol challenge and quantified by using image analysis. clenbuterol-induced myocyte necrosis occurred against a background of zero damage in control muscles. In the heart, the clenbuterol-induced necrosis was not uniform, being more abundant in the left subendocardium and peaking 2.4 mm from the apex. After position (2.4 mm from the apex), dose (5 mg clenbuterol/kg), and sampling time (12 h) were optimized, maximum cardiomyocyte necrosis was found to be 1.0 +/- 0.2%. In response to the same parameters (i.e., 5 mg of clenbuterol and sampled at 12 h), skeletal myocyte necrosis was 4.4 +/- 0.8% in the soleus. These data show significant myocyte-specific necrosis in the heart and skeletal muscle of the rat. Such irreversible damage in the heart suggests that clenbuterol may be damaging to long-term health. PMID: 12381771 [PubMed - indexed for MEDLINE] ================================== Characterization of adrenoceptor involvement in skeletal and cardiac myotoxicity Induced by sympathomimetic agents: toward a new bioassay for beta-blockers. Tan LB, Burniston JG, Clark WA, Ng Y, Goldspink DF. Academic Unit of Molecular Vascular Medicine, University of Leeds, England. Excessive levels of catecholamines have long been known to be cardiotoxic, but less well known are their toxic effects on skeletal muscle. By using an antimyosin monoclonal antibody and quantitative methods to measure the extent of myocyte necrosis, and by employing modulators of adrenoceptors (ARs), including clenbuterol, bupranolol, propranolol, bisoprolol, atenolol, ICI-118551, phenoxybenzamine, prazosin, and yohimbine, the involvement of ARs in isoproterenol-induced myotoxicity was characterized. In the myocardium, the toxic effects were predominantly mediated via the beta(1)-ARs. In the soleus muscle, it was almost solely via the beta(2)-ARs. Myotoxicity was also observed in the myocardium when challenged with the beta(2)-AR agonist clenbuterol. This was found to be mediated via sympathetic presynaptic beta(2)-ARs, leading to enhanced release of norepinephrine. This effect was abolished by prior treatment with reserpine. The skeletal muscle was found to be more sensitive to the myotoxic effects than cardiac muscle at lower doses of beta-AR agonists. These experiments introduce a new way of assaying beta-AR antagonists by classifying them according to their ability to prevent catecholamine-induced myotoxicity. Further research along these lines may deepen understanding of which beta-blockers work best in heart failure therapy. PMID: 12658052 [PubMed - indexed for MEDLINE] ===================================== Dose-dependent separation of the hypertrophic and myotoxic effects of the beta(2)-adrenergic receptor agonist clenbuterol in rat striated muscles. Burniston JG, Clark WA, Tan LB, Goldspink DF. Research Institute for Sport & Exercise Sciences, Liverpool John Moores University, Webster Street, Liverpool L3 2ET, UK. Muscle growth in response to large doses (milligrams per kilogram) of beta(2)-adrenergic receptor agonists has been reported consistently. However, such doses may also induce myocyte death in the heart and skeletal muscles and hence may not be safe doses for humans. We report the hypertrophic and myotoxic effects of different doses of clenbuterol. Rats were infused with clenbuterol (range, 1 mug to 1 mg.kg(-1)) for 14 days. Muscle protein content, myofiber cross-sectional area, and myocyte death were then investigated. Infusions of >/=10 mug.kg(-1).d(-1) of clenbuterol significantly (P < 0.05) increased the protein content of the heart (12%-15%), soleus (12%), plantaris (18%-29%), and tibialis anterior (11%-22%) muscles, with concomitant myofiber hypertrophy. Larger doses (100 mug or 1 mg) induced significant (P < 0.05) myocyte death in the soleus (peak 0.2 +/- 0.1% apoptosis), diaphragm (peak 0.15 +/- 0.1% apoptosis), and plantaris (peak 0.3 +/- 0.05% necrosis), and significantly increased the area fraction of collagen in the myocardium. These data show that the low dose of 10 mug.kg(-1).d(-1) can be used in rats to investigate the anabolic effects of clenbuterol in the absence of myocyte death. Muscle Nerve, 2006. PMID: 16411205 [PubMed - in process] ================================ J Appl Physiol. 2004 Dec 10; [Epub ahead of print] Related Articles, Links {beta}2-Adrenergic receptor stimulation in vivo induces apoptosis in the rat heart and soleus muscle. Burniston JG, Tan LB, Goldspink DF. Research Institute for Sports and Exercise Sciences, Liverpool John Moores University, Liverpool, United Kingdom. High doses of the beta2-adrenergic receptor (AR) agonist, clenbuterol, can induce necrotic myocyte death in the heart and slow-twitch skeletal muscle of the rat. However, it is not known if this agent can also induce myocyte apoptosis and whether this would occur at a lower dose than previously reported for myocyte necrosis. Male Wistar rats were given single subcutaneous injections of clenbuterol. Immunohistochemistry was used to detect myocyte specific apoptosis (detected on cryosections using a caspase 3 antibody and confirmed using annexin V, single-strand DNA labelling and TUNEL). Myocyte apoptosis was first detected at 2 h, and peaked 4 h after clenbuterol administration. The lowest dose of clenbuterol to induce cardiomyocyte apoptosis was 1 microg kg(-1), with peak apoptosis (0.35 +/- 0.005 %; P<0.05) occurring in response to 5 mg kg(-1) . In the soleus, peak apoptosis (5.8 +/- 2 %; P<0.05) was induced by the lower dose of 10 microg kg(-1). Cardiomyocyte apoptosis occurred throughout the ventricles, atria and papillary muscles. However, this damage was most abundant in the left ventricular subendocardium at a point 1.6 mm, that is, approximately one-quarter of the way from the apex towards the base. beta-AR antagonism (involving propranolol, bisoprolol or ICI 118,551) or reserpine was used to show that clenbuterol-induced myocardial apoptosis was mediated through neuromodulation of the sympathetic system and the cardiomyocyte beta1-AR, whereas in the soleus direct stimulation of the myocyte beta2-AR was involved. These data show that when administered in vivo, beta2-AR stimulation by clenbuterol is detrimental to cardiac and skeletal muscles even at low doses, by inducing apoptosis through beta1- and beta2-AR, respectively. Don't you all understand WTF kind of doese that would mean a 220lb man would need to take? Lets just talk about a 100kg man..that would be 500G read 500GRAMS of Clen. Hell I am not sure about yall but I take between 40-180 MCG ED
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My max dose was 160mcg.
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i'm sure the rats dont eat a steady diet of beef and eggs and other cholesterol causing foods also.
you know how everyone says you should take alot of taurine while on clen to prevent muscle cramps? thats because clen depletes your muscles of taurine. guess what else taurine does thats so important? it is the amino acid that regulates heart rhythm. put two and two together. not worth the long term risk IMO just for a short term benefit of some fat loss from clen.
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Welcome to the most secure board on the web. No hidden agendas. No Mods I don't know personally. No sources with multiple handles. No mysterious post deletions. No selling or post-whoring to VIP status. PGP use encouraged. ...oh yeah, and no VinDiesel or "alliance" with homo boards. Check out the AnonBB Supersite at www.anonymousbodybuilding.com and our new sister sites: www.steroid-sources.com www.sub-q.com |
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