A large number of scientific works have been devoted to studying the role of the beta-agonist system in the control of fat deposition, muscle hypertrophy, and the body’s response to physical activity over the past 10 years. To begin with, it must be said that the beta-agonist system in the body is one of the most important signaling systems. To understand how the beta-agonist system works and what role caffeine, ephedrine and aspirin play in this work, you must first understand what beta-agonists are and what they do.
Beta receptors are located on the surface of many cells in the body (in this case we are considering muscle and fat tissue). These beta receptors pick up and hold substances called beta agonists (epinephrine and norepinephrine). When a beta agonist is captured by a beta receptor, the latter initiates a series of chemical reactions that lead to the production of an active substance that carries information, C-AMP (CAMP). C-AMP in turn activates enzymes that saturate proteins with phosphorus . Why is this interesting? Many of these proteins are enzymes, and phosphorus saturation activates some of these enzymes and deactivates others. Enzymes that initiate lipolysis (the breakdown of fat) are activated in fat cells. Enzymes are activated in muscle tissue cells, accelerating metabolism and causing a chain of other important reactions that control the growth of muscle tissue, the type of tissue and the overall concentration of enzymes. How do ephedrine, caffeine and aspirin wedge themselves into this system? Ephedrine enhances the production of beta-agonists and even acts as a beta-agonist itself. Caffeine inhibits the breakdown of C-AMP. Aspirin inhibits negative feedback, which can reduce the production of beta-agonists. Thus, these three substances, taken together, improve the functioning of the beta-agonist system in three or four stages.
The role of ephedrine as a lipolysis agent has been known for some time. It has been shown that taking therapeutic doses of ephedrine may be moderately effective in treating obesity. The problem is that the initial effect of lipolysis when using ephedrine very soon disappears due to the negative effect of the feedback mechanism. To solve this problem, various additional components, including caffeine and aspirin, were added to the prescribed set of drugs. The result was a very effective combination for combating obesity (the prescribed doses were 20 mg ephedrine, 30 mg caffeine and 80 mg aspirin, which roughly compares to taking one standard ephedrine tablet, a cup of coffee and an aspirin tablet). In fact, over time, the effect of using the E-C-A (lipolysis) combination not only did not decrease, as is the case with most medications, but even increased. The effect of E-K-A was assessed in terms of positive and negative effects. Positive effects included lipolysis and increased protein synthesis (people taking E-K-A gained more muscle mass than those taking placebo).
Interestingly, the positive effect did not disappear over time. Undesirable effects, rapid heartbeat and tremors, lasted several days and disappeared without a trace. In fact, after a year’s course, users experienced no unwanted side effects, but continued to experience positive effects in the form of lipolysis and protein synthesis. To date, it remains unclear how E-K-A works in healthy adults who exercise. However, based on what we know about how the beta-agonist system works, a positive effect is possible. It is also important to note that during testing, from a large number of people, a certain part was eliminated who were found to be incompatible with some of the drugs or with E-K-A in general. Thus, we can conclude that for most people the course of E-K-A is quite possible, but for some people there may be incompatibility. Before starting the course, it is recommended to consult a doctor.
The beta-agonist system can cause processes other than lipolysis and muscle gain. For example, in experiments with chickens, beta-agonists turned out to be much more powerful growth stimulants than steroids. (Believe it or not, poultry farmers are doing the same thing we are doing – raising increasingly muscular chickens). In fact, it appears that beta-agonists cause muscle growth without the external influence of exercise, something that not every steroid achieves. However, in experiments on rats, beta-agonists were not so effective and their effect on humans can only be guessed at. For example, such a well-known beta-agonist as Clenbuterol can cause the transformation of so-called “slow” muscle tissue into “fast” muscle tissue. It also prevents muscle tissue atrophy due to forced inactivity.
Other studies show that beta antagonists (active substances that block beta receptors and keep them from working) cause muscle wasting by converting “fast” muscle tissue into “slow” muscle tissue. These studies suggest that beta-agonists may play an important role in the formation of fast-twitch muscle fibers and in building and possibly increasing muscle mass. There is no doubt that large amounts of beta-agonists (epinephrine and norepinephrine) are released during high-intensity exercise. Perhaps these beta-agonists are necessary to stimulate the growth of muscle tissue.
It should be noted that some beta-agonists may be dangerous (eg, clenbuterol and cocaine) and are not approved for use. Again, as noted above, although the E-C-A combination has proven to be harmless for most people (and not prohibited for use!), it may have an inadequate effect on some, so consultation with a doctor is strongly recommended before starting the course.
Author: Mike Prevost Ph.D.
