OK, enough of this foolishness, why is cycling ECA not recommended (or even mentioned) by research scientists? Simple, because the mode of action of ECA is different. Clenbuterol is a highly selective drug that becomes less effective after a short period of time because it selectively stimulates the beta 2 receptors, which downregulate. ECA, on the other hand, non-selectively stimulates all the beta receptors.
Remember how we learned that, in the 1980s, scientists screened drugs for their thermogenic potential? Well, when they tested non-selective adrenergic drugs like ephedrine, the scientists were surprised to find that the thermogenic effect was maintained and even increased with chronic use (26). Dulloo found that "agonists for the classical post-synaptic adrenoceptors [selective drugs] were found to be much less effective in chronically enhancing thermogenesis and fat losses than sympathetic stimulants [non-selective drugs] capable of increasing the synaptic levels of NA [noradrenaline] e.g. ephedrine, yohimbine, tranylcypromine" (8) [emphasis added].
Anecdotally, this persistent thermogenic effect has been experienced by people who have taken ECA non-stop for many years. Personally, I have taken ECA for over a decade and it still works for me. Furthermore, Toubro et al. found that ECA kept working throughout a 50-week clinical trial: "The major finding of this drug study indicates that a combination of ephedrine (20 mg) and caffeine (200 mg) taken orally three times a day as an adjuvant to a low calorie diet improves weight loss for 24 weeks. Furthermore, the combination can maintain or slightly improve weight loss during treatment from weeks 26-50" (10). When taken chronically, ECA lowers your set point by normalizing an important part of your biochemistry.
Here is how it works: Ephedrine works by stimulating the release of the bodies own noradrenaline, which stimulates ALL the adrenergic receptors. The stimulant side effects subside because they are primarily mediated by the beta-1 and beta-2 receptors, which downregulate during chronic use. Thus, the scientists were startled when they found that the thermogenic effect actually INCREASED with chronic use.
This phenomena led scientists to believe that there must be an undiscovered receptor involved in noradrenaline-induced thermogenesis. Then the scientists found that -- even after blocking all the known adrenergic receptors -- non-selective drugs like ephedrine still caused a significant thermogenic effect. The evidence supporting the existence of an undiscovered receptor that is stimulated by noradrenaline continued to increase.
Eventually, this led to the discovery of the beta 3 receptor, which is more resistant to desensitization (20, 21, 22, 23) than the other beta receptors -- and that is why the thermogenic effect of ECA is maintained so well during chronic use. Now you know why it is not necessary to "cycle" ECA. Indeed, why would you want to maintain the side effects when you can enjoy increased fat burning without ANY stimulation?
Cycling clenbuterol to try to prevent desensitization of the beta 2 receptors makes sense, but ECA is an entirely different story. ECA involves noradrenaline and the beta-3 receptors. The two drugs are similar in some ways, but in this extremely important way, it is like comparing apples and oranges.
OK, but why does the thermogenic effect INCREASE when you take ECA regularly? Because a thermogenic tissue called brown fat has a lot of beta-3 receptors that are stimulated by noradrenaline, which is released when you take non-selective sympathomimetic drugs like ephedrine. This stimulation of beta-3 receptors actually causes the brown fat to grow -- and more brown fat equals more thermogenesis. Fascinating stuff, this ephedrine. Like I said, apples and oranges.
Liu et al. (9) investigated this thermogenic mechanism:
"Ephedrine is believed to have some direct effect on both alpha adrenoceptors and beta adrenoceptors, but AT THERAPEUTIC DOSES, ephedrine exerts its thermogenic effect almost entirely via stimulating noradrenaline release from the sympathetic nerve terminals [endings] . . . at least 40% of the [thermogenic] response is mediated by an atypical receptor, which is presumed to be the beta 3-adrenoceptor."