![]() ![]() ![]() You must have periods of complete cessation of ECA, clen, and ehem, CAFFEINE, if you want to recover properly. THat is assuming that one doesn't use ECA during the off weeks. At least that way there will be little desensitization, and the sympathetic nervous system will not be in constant fight or flight. Not very specific, but I have no hard data to support that, only hearsay.įor fatloss, the best protocol, IMO, would be 1 weekon/1 off. There are no human studies looking at this phenomenon (primarily because extended studies would be required with constant stimulation and such would be extremely hazardous, and hence would not get NIH approval), but my guess is that significant desensitization will occur anywhere from 1-4 weeks. Densenstization is the problem, and this occurs very rapidly. I just don't think the turnover rate is fast enough for it to be a problem in short cycles. The actual receptor population has not been shown to decrease, although it would certainly happen over time. ![]() Downregulation has only been shown to occur primarily with expression of receptor mRNAs. This is unexcapable, even with regards to the beta3, only present in fat. Desensitization occurs very rapidly via lowered expression of adenylate cyclase and cAMP within the cell. The problem is that the beta adrenergic receptors quickly adapt to stimulation by densensitization and downregulation. Whatever fat loss benefit this drug offers is far less than ephedrine or other beta1+beta3 specific compounds.Īs far as practical use is concerned, there are obviously many variations. The anabolic properties of clen are EXTREMELY interesting, occuring from an entirely different mechanism than androgens. The jitteryness, increased heartrate,and increased bloodpressure (regardless of the vasodilatory effects) from clen and ephedrine result from their stimulation of receptor in the sympathetic neurons. The result is a much stronger thermogenic and neurotransmission effect. The reason why caffeine is so often combined with ephedrine is most preparations is that the increased intracellular calcium, and uncoupling of calcium with membrane hyperpolarization, is synergistic with the neurotropic effects of ephedrine. It works not via adrenergic receptors, but it has heavy influence of calcium and cAMP levels within cells, which is very significant, especially with regards to smooth muscle, like that in blood vessels and intestines. ![]() While caffeine is a totally different class of compound, a methylxanthine, it still has potent affects on the CNS. Clenbuterol is very specific for beta2, while ephedrine is relatively non selective, and therefore a better lipolytic agent. Beta3, so far only isolated in adipocytes (fat cells), increases lipolysis. Beta2 also mediates clenbuterol stimulated anabolic effects in muscle, but that is another VERY complicated issue. Beta2 increases muscle and liver glycogenolysis, increase glucagon (opposite of insulin) increase blood glucose, and major vascular dilation/relaxation. Beta1 stimulation results in increased heart rate, increased cardiac contractility, and increased lipolysis. There are three known subtypes of the beta receptor 1,2, and 3. These are very complex drugs, clen especially, so this is just a sort of quick overview of there mechanism of action and how they should be used, in my humble opinion of course.Ĭlenbuterol and ephedrine are agonists (activator) of adrenergic receptors, specifically the beta adrenergic receptor, which are widely distributed throughout the body. There is quite a bit of techie-talk in here, but I thought is necessary to get my point across. ![]()
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