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Myth of ECA Cycling

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myth of eca cycling
Since I started writing most of the Industry Insider columns for Ironmag some 4 months ago after the departure of a previous writer, I've spent quite a bit of my spare time reviewing a lot of the literature currently available on the internet pertaining to bodybuilding. To be honest, during the time before I was approached by Ironmag to write for them, I didn't really think bodybuilders had much time for computers and internet surfing. While I still believe many real bodybuilders have better things to do than surf the 'net, I still believe they turn to the internet as a source of up to date information that isn't written for beginner bodybuilders who most often purchase printed magazines like Muscle & Fitness.

One of the most common questions I see on the world wide web's new bodybuilding population involves the ECA stack and fat burning. Most likely through printed magazines or mass market bodybuilding sites aimed at beginner bodybuilders like or Elite Fitness (two sites I now avoid completely) I find the theories of cycling ECA with some odd "cycling patterns". Some bodybuilders favor a two day on, two day off cycle; others say that receptor downgrade occurs after 2 weeks; and still other's quote longer times of 2 months. Well they're all wrong. Yes the notion that you have to cycle ECA or it's fat burning effects will dwindle to nothing are simply not true.

To understand why it's not necessary to design elaborate (and ineffective) cycles for ECA, one must look at it's primary ingredient, ephedrine (the herbal forms being ma huang or sida cordefolia) and how it works.

Ephedrine works by stimulating the release of 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. Previous thought was that catecholamines mobilize energy-rich lipids by stimulating lipolysis in fat cells and thermogenesis in brown adipose tissue and skeletal muscle. Originally, these effects were believed to be only mediated by (beta)1- and (beta)2-adrenergic receptors. However there is also an additional adrenergic receptor, (beta)3, that is involved as well. Pharmacologically, the (beta)3-adrenergic receptor differs from the (beta)1- and (beta)2-adrenergic receptors in two important ways (2): it has a lower affinity for catecholamines, and it resists desensitization (i.e., down-regulation).

In the past scientists screened drugs for their thermogenic potential, and during tests on non-selective adrenergic drugs like ephedrine, some studies showed that the thermogenic effect of ephedrine was maintained and even increased with long term use. It was found that agonists for post-synaptic adrenoceptors were found to be much less effective in chronically enhancing thermogenesis and fat losses than sympathetic stimulants capable of increasing the synaptic levels of noradrenaline. As we all know studies done have shown that that a combination of ephedrine (20 mg) and caffeine (200 mg) taken orally three times a day in combination with a low calorie diet improves weight loss for 24 weeks. However what is not noted in most articles or literature about ECA is that the combination can maintain or slightly improve weight loss during treatment from the time after 26 weeks.

This discovery led to further studies in the hopes of uncovering an undiscovered receptor involved in noradrenaline-induced thermogenesis. The scientists found that even after blocking all the known adrenergic receptors non-selective drugs like ephedrine still caused a significant thermogenic effect. Eventually, this led to the discovery of the beta 3 receptor that, as mentioned above is more resistant to downregulation than the other beta receptors. This is why the thermogenic effect of ECA is maintained so well during long term use. This discovery effectively shows that cycling of ECA is simply wrong.

Now I'm going to explain just why the thermogenic effects of ECA actually increase with long term use. I really only need two words. Brown Fat.

Brown fat (adipose) tissue is sometimes mistaken for a type of gland, which it resembles more than white adipose tissue. It varies in color from dark red to tan, reflecting lipid content. Its lipid reserves are depleted when the animal is exposed to a cold environment, and the color darkens. In contrast to white fat, brown fat is richly vascularized and has numerous unmyelinated nerves which provide sympathetic stimulation to the adipocytes. Brown fat is of particular importance in cold environments, and animals that hibernate, because it has the ability to dissipate stored energy as heat. In contrast to other cells, including white adipocytes, brown adipocytes express mitochondrial uncoupling protein, which gives the cell's mitochondria an ability to uncouple oxidative phosphorylation and utilize substrates to generate heat rather than ATP. Exposure to cold leads to sympathetic stimulation of brown adipocyte via norepinephrine binding to beta- adrenergic receptors. As in white fat, sympathetic stimulation promotes hydrolysis of triglyceride, with release of fatty acids and glycerol. However, within brown adipocytes, most fatty acids are immediately oxidized in mitochondria and, because of the uncoupling protein, a large amount of heat is produced. This process is part of what is called non-shivering thermogenesis.

Beta-3 receptor sites are found predominantly in brown adipose tissue. We know that rats and mice have large areas of fat that are exclusively made of brown fat to help them regulate their body temperature, in the interscapular region and the axillae, and minor amounts are found near the thymus and in the dorsal midline region of the thorax and abdomen. During maturation, in non-hibernating animals, brown adipose tissue is metabolically less active, although cold exposure can activate it. Newborn human babies have distinct areas of brown fat. Adult humans though don't have a lot of distinct brown fat. However the key with brown adipose tissue in adults, is that it is scattered about the more common white fat in a diffuse manner - especially around the viscera, and that each of these small deposits of brown fat actually adds up to a large amount. The beta-3 receptor found in brown fat is responsible for burning off fat in the midsection of the body.

Long term use of the ECA stack does lead to beta-2 downregulation. It does not cause rapid desensitization and/or down-regulation of adrenergic receptors, however after about 4 months it will cause the beta-2 receptors on muscle and fat cells will be drawn into the cell membrane to reduce their availability. This is the cause of the loss of stimulatory effects associated with the ECA stack. However, thermogenesis is actually increasing through beta-3 receptor stimulation.

I recommned adjusting your dosing schedule of ECA to every 2 hours during the first 4 months. This will enhance the duration and consistency of beta-adrenergic activity. Don't forget adjust the amount you take each time in order to maintain the total amount taken over the course of a day. It has been demonstrated, that when you infuse beta agonists with short half-lives, you can elicit the anabolic activity, that is similar to the anabolic activity of clenbuterol. Muscle preservation through the use of ephedrine is negigable over long term use. This is most likely the only valid reason for the cycling of ECA. As a fat loss catalyist though, there is no reason.

After four months switch back to your usual 3 times a day dosage. You can continue to burn fat for as long as you use ECA.

Astrup A, Lundsgaard C, Madsen J, Christensen NJ "Enhanced thermogenic responsiveness during chronic ephedrine treatment in man" Am J Clin Nutr 1985, Vol 42 (1), Pg 83-94, PMID: 0004014068.

Dulloo, AG "Ephedrine, xanthines and prostaglandin-inhibitors: actions and interactions in the stimulation of thermogenesis." Int J Obes 1993 Feb, Vol 17 (Suppl 1), Pg S35-40, PMID: 0008384178.

P. Marin, B. Anderson, M. Ottoson, et al, "The Morphology and Metabolism of Intraabdominal Fat in Men," Metabolism 41 (1992) : 1242-1248.

Rosenbaum M, Malbon CC, Hirsch J, Leibel RL. Lack of beta 3-adrenergic effect on lipolysis in human subcutaneous adipose tissue. J Clin Endocrinol Metab 1993 Aug;77(2):352-355

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great read!