Clenbuterol and ECA, and Overview
There is quite a bit of techie-talk in here, but I thought is necessary to get my point across. 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.
Clenbuterol and ephedrine are agonists (activator) of adrenergic receptors, specifically the beta adrenergic receptor, which are widely distributed throughout the body. There are three known subtypes of the beta receptor; 1,2, and 3. Beta1 stimulation results in increased heart rate, increased cardiac contractility, and increased lipolysis. Beta2 increases muscle and liver glycogenolysis, increase glucagon (opposite of insulin) increase blood glucose, and major vascular dilation/relaxation. Beta2 also mediates clenbuterol stimulated anabolic effects in muscle, but that is another VERY complicated issue. Beta3, so far only isolated in adipocytes (fat cells), increases lipolysis. Clenbuterol is very specific for beta2, while ephedrine is relatively non selective, and therefore a better lipolytic agent. While caffeine is a totally different class of compound, a methylxanthine, it still has potent affects on the CNS. 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. 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. The result is a much stronger thermogenic and neurotransmission effect.
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 anabolic properties of clen are EXTREMELY interesting, occuring from an entirely different mechanism than androgens. Whatever fat loss benefit this drug offers is far less than ephedrine or other beta1+beta3 specific compounds.
As far as practical use is concerned, there are obviously many variations. The problem is that the beta adrenergic receptors quickly adapt to stimulation by densensitization and downregulation. Desensitization occurs very rapidly via lowered expression of adenylate cyclase and cAMP within the cell. This is unexcapable, even with regards to the beta3, only present in fat. Downregulation has only been shown to occur primarily with expression of receptor mRNAs. The actual receptor population has not been shown to decrease, although it would certainly happen over time. I just don't think the turnover rate is fast enough for it to be a problem in short cycles. Densenstization is the problem, and this occurs very rapidly. 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. Not very specific, but I have no hard data to support that, only hearsay.
For fatloss, the best protocol, IMO, would be 1 weekon/1 off. At least that way there will be little desensitization, and the sympathetic nervous system will not be in constant fight or flight. THat is assuming that one doesn't use ECA during the off weeks. That would be the worst thing to do. You must have periods of complete cessation of ECA, clen, and ehem, CAFFEINE, if you want to recover properly. Ephedrine and caffeine both have halflife of 3-7 hours, while clenbuterol is considerably longer, 10-12 if I rememeber correctly. Using caffeine during ones off period of clen/ECA will not affect the adrenergic receptors, but is will lead to problems with neuronal desensitization. My advice, when not using clen or ECA, don't use any form of CNS stimulant. Simply upping the dosage will not serve any purpose as the receptors have been maximally stimulated and the intracellular machinery has been in effect shut off. A total break from use is required. However, as long as the desensitization is reversed periodically there should not be a reduction in effectiveness of these compounds over the long term. Clen especiall could be used post androgen use if so desired as a way to circumvent the loss of muscle that will inevitably occur after steroid cycles. Clens neurotropic and myotropic effects could be of great use, but I still recommend coming off everything when stopping androgen use.
Since ever individual seems to have a variable tolerance for clen, I would suggest starting at 50 mcg day for men, and 25mcg day for women. If you feel okay up the dose slowly in 20mcg increments every 2-3 days. You will most likely be jittery, but you should not feel sick on excessively trembly. Increase the dose to that point, and hold it there. THere next on period can begin at that dose. THere is no need to pyramid up or down once you know your maximal tolerable and effective dose. Ephedrine should be used in same manner. Find the set point and stick with that dose. By all means though, step up gradually if you have never used these compounds before. They are not like androgens in that an accute excessive dose can kill you. IMO, they are the most deadly of the commonly used bodybuilding drugs, except for diuretics.
Now, while neither ephedrine, nor any of the other beta agonists, have any noticeable anabolic effects, clenbuterol does. It does stimulate muscle-specific protein anabolism that is in part due to beta-2 adrenergic receptor agonism. Rats that have the beta2 receptor knocked out do not show any of the anabolic or innervation effects of clen. So the beta2 receptor is required, but probably not sufficient, since other beta agonists do not have clens anabolic effects.
Clenbuterol is able to produce effects similar to innervation in muscle fibers that have been denervated. It effects expression of neurotropic (compounds normally stimulated or released by neurons) compounds such as IGF-II and an entire host of other signaling proteins, and greatly inhances local muscle expression of IGF-1 and the various binding proteins involved. It is used clinically in patients with neuronal damage, which is normally associated with extreme muscle wasting. The innervation effects are totally unique to clen, as far as I know. This innervation is the most important feature of clen anabolism. It would in effect make ones muscles much more effecient. This is readily apparent as the rapid increases in strength seen with initiation of clen usage. It could potential be dangerous however. Depending on the severity, the increase in muscle contractility combined with greater motor unit activation could override the inherent protective effects the muscle has in place and injuries could result. This is only for very extreme cases, but still worth mentioning. THe more and more I look into clen, the more and more I think it has the potential to be very useful for bodybuilders and other strength athletes.
Another very interesting and unique effect it that when clen is combined with triodothyronine (T3), there is a change of phenotype of slow twitch muscle fibers to fast twitch. This could have major implications to bodybuilders, since the fast twitch fibers have a much greater capacity for growth. The activity of several ribosomal proteins involved in protein synthesis is also heavily increased. How important this is to muscle hypertrophy I don't know. The studies I have seen are all in rats however, and they do not say the dosing used, so I can't say what doses caused these effects. THat being said, rats physiology and metabolism is highly analogus to humans, so the data seen with rat studies is probably applicable to humans.
There is quite a bit of techie-talk in here, but I thought is necessary to get my point across. 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.
Clenbuterol and ephedrine are agonists (activator) of adrenergic receptors, specifically the beta adrenergic receptor, which are widely distributed throughout the body. There are three known subtypes of the beta receptor; 1,2, and 3. Beta1 stimulation results in increased heart rate, increased cardiac contractility, and increased lipolysis. Beta2 increases muscle and liver glycogenolysis, increase glucagon (opposite of insulin) increase blood glucose, and major vascular dilation/relaxation. Beta2 also mediates clenbuterol stimulated anabolic effects in muscle, but that is another VERY complicated issue. Beta3, so far only isolated in adipocytes (fat cells), increases lipolysis. Clenbuterol is very specific for beta2, while ephedrine is relatively non selective, and therefore a better lipolytic agent. While caffeine is a totally different class of compound, a methylxanthine, it still has potent affects on the CNS. 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. 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. The result is a much stronger thermogenic and neurotransmission effect.
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 anabolic properties of clen are EXTREMELY interesting, occuring from an entirely different mechanism than androgens. Whatever fat loss benefit this drug offers is far less than ephedrine or other beta1+beta3 specific compounds.
As far as practical use is concerned, there are obviously many variations. The problem is that the beta adrenergic receptors quickly adapt to stimulation by densensitization and downregulation. Desensitization occurs very rapidly via lowered expression of adenylate cyclase and cAMP within the cell. This is unexcapable, even with regards to the beta3, only present in fat. Downregulation has only been shown to occur primarily with expression of receptor mRNAs. The actual receptor population has not been shown to decrease, although it would certainly happen over time. I just don't think the turnover rate is fast enough for it to be a problem in short cycles. Densenstization is the problem, and this occurs very rapidly. 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. Not very specific, but I have no hard data to support that, only hearsay.
For fatloss, the best protocol, IMO, would be 1 weekon/1 off. At least that way there will be little desensitization, and the sympathetic nervous system will not be in constant fight or flight. THat is assuming that one doesn't use ECA during the off weeks. That would be the worst thing to do. You must have periods of complete cessation of ECA, clen, and ehem, CAFFEINE, if you want to recover properly. Ephedrine and caffeine both have halflife of 3-7 hours, while clenbuterol is considerably longer, 10-12 if I rememeber correctly. Using caffeine during ones off period of clen/ECA will not affect the adrenergic receptors, but is will lead to problems with neuronal desensitization. My advice, when not using clen or ECA, don't use any form of CNS stimulant. Simply upping the dosage will not serve any purpose as the receptors have been maximally stimulated and the intracellular machinery has been in effect shut off. A total break from use is required. However, as long as the desensitization is reversed periodically there should not be a reduction in effectiveness of these compounds over the long term. Clen especiall could be used post androgen use if so desired as a way to circumvent the loss of muscle that will inevitably occur after steroid cycles. Clens neurotropic and myotropic effects could be of great use, but I still recommend coming off everything when stopping androgen use.
Since ever individual seems to have a variable tolerance for clen, I would suggest starting at 50 mcg day for men, and 25mcg day for women. If you feel okay up the dose slowly in 20mcg increments every 2-3 days. You will most likely be jittery, but you should not feel sick on excessively trembly. Increase the dose to that point, and hold it there. THere next on period can begin at that dose. THere is no need to pyramid up or down once you know your maximal tolerable and effective dose. Ephedrine should be used in same manner. Find the set point and stick with that dose. By all means though, step up gradually if you have never used these compounds before. They are not like androgens in that an accute excessive dose can kill you. IMO, they are the most deadly of the commonly used bodybuilding drugs, except for diuretics.
Now, while neither ephedrine, nor any of the other beta agonists, have any noticeable anabolic effects, clenbuterol does. It does stimulate muscle-specific protein anabolism that is in part due to beta-2 adrenergic receptor agonism. Rats that have the beta2 receptor knocked out do not show any of the anabolic or innervation effects of clen. So the beta2 receptor is required, but probably not sufficient, since other beta agonists do not have clens anabolic effects.
Clenbuterol is able to produce effects similar to innervation in muscle fibers that have been denervated. It effects expression of neurotropic (compounds normally stimulated or released by neurons) compounds such as IGF-II and an entire host of other signaling proteins, and greatly inhances local muscle expression of IGF-1 and the various binding proteins involved. It is used clinically in patients with neuronal damage, which is normally associated with extreme muscle wasting. The innervation effects are totally unique to clen, as far as I know. This innervation is the most important feature of clen anabolism. It would in effect make ones muscles much more effecient. This is readily apparent as the rapid increases in strength seen with initiation of clen usage. It could potential be dangerous however. Depending on the severity, the increase in muscle contractility combined with greater motor unit activation could override the inherent protective effects the muscle has in place and injuries could result. This is only for very extreme cases, but still worth mentioning. THe more and more I look into clen, the more and more I think it has the potential to be very useful for bodybuilders and other strength athletes.
Another very interesting and unique effect it that when clen is combined with triodothyronine (T3), there is a change of phenotype of slow twitch muscle fibers to fast twitch. This could have major implications to bodybuilders, since the fast twitch fibers have a much greater capacity for growth. The activity of several ribosomal proteins involved in protein synthesis is also heavily increased. How important this is to muscle hypertrophy I don't know. The studies I have seen are all in rats however, and they do not say the dosing used, so I can't say what doses caused these effects. THat being said, rats physiology and metabolism is highly analogus to humans, so the data seen with rat studies is probably applicable to humans.
