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Preface: Part I Super Brief Quick Recap

Clenbuterol is a sympathomimetic drug. It is uber-lipolytic and potently anti-catabolic. It repartitions calories from fat deposits to skeletal muscle, and will initially kick more stimulation through your system than the sight of Jessica Alba in a two-or-less- piece, or for our female readers maybe Jude Law chopping wood or something (sorry, that’s as far as I can comfortably engage the latter half of the fantasy). It’s bad for your heart, and even worse taken with anabolic steroids, and is in general a drug that offers users significant cutting benefits, but at a very high potential cost to their health and well-being. In other words: if you choose to use it, realize you are doing so at your own risk.

Saying “Screw Loki, I’m Using This,” and Doing so at Your Own Risk

As mentioned in Part I, you get the good and the bad with clenbuterol. In particular, as athletes/bodybuilders, our three prime concerns are: 1. the potential for deleterious effects on cardiac function, 2. the impairment of exercise-performance capacity (see: a few sentences down), and 3. the eventual functional downregulation of your beta2 adrenergic receptors after continual exposure to clenbuterol, which is eventually going to downgrade the strength of clen’s lipolytic punch from “Early Mike Tyson” to “Late Mike Tyson”. So when using clenbuterol, obviously the informed and educated user should be looking to strike a balance to get as much of the benefits with as little ‘bad’ as possible.

Regarding clenbuterol’s potential to impair heart function and lead to cardiac complications, there’s really not too much you can do aside from keeping your clen dose as low and reasonable as possible, at a dosage where you’re still seeing effects. Obviously a beta-blocker would prevent the negative, but it is after all a beta-blocker, which isn’t exactly the kind of drug you want to stack with a beta adrenergic agonist if you want to see, well, anything positive.

Either a novel, selective beta1 antagonist or an angiotensin II type 1 blocker might make welcome contributions to the cellular well-being of your cardiac myocytes, but unless you saved the CEO of Merck from a recent bear attack or something, chances are you don’t have the kind of connections to acquire such drugs. Bottom line: dose in moderation. 40-80mcg/day should provide you all the clen you need to take advantage of its lipolytic and anti-catabolic effects without immediately giving your myocytes a Grade-A mauling.

Along similar lines, if work capacity—particularly aerobic—is a high priority for you, you’d do well to shop for a different diet drug (if not several). Clocking more cardio hours each week than strength training time? Consider your Spiropent privileges revoked if you aren’t stepping on stage for a contest a week from Tuesday. For starters, it stands to assume than any drug that can potentially exert significantly deleterious effects on the human heart isn’t prime weight-loss material for anybody needing iron aortas and slow, steady cardiac contractions to get them through that next triathlon or road-race.

Additionally, animal studies indicate that clenbuterol administration decreases muscle oxidative potential and expenditure efficiency, perhaps by preferentially increasing nonmitochondrial proteins &/or altering fiber-content (1,2). Reductions in cardiac capacity and structure, as well as VO2max, also seem to be implicated (3). And although in some studies consistent exercise training has been able to counteract some of clen’s performance-reducing effects, the general scientific consensus remains that chronic clenbuterol treatment is directly antagonistic to exercise performance in animals (4). In non-asthmatic humans, there is very little to indicate that beta-agonist drugs will improve anaerobic or aerobic work capacity (5,6,7).

So at low doses, you are at best breaking even. At high-doses, it is far more likely that your performance will be hampered and/or harmed through marked increases in systolic blood-pressure and impairment of the anaerobic expenditure process (8,9). This would hold particularly true in regards to activities like HIIT cardio and intensive, low-rest interval weight training.

Moreover, as previously noted in Part I, consistent clenbuterol use invariably leads to direct decreases in intracellular taurine and potassium concentrations (10) at higher doses. Taurine, as an important osmoregulator of cell-volume, is a very important asset to performance and plays a key role in signal transduction, muscle contraction, cardio-protection, protein synthesis, and cellular hydration in general (11,12,13,14). Thus, taurine supplementation in the 3-5g/day range should be considered an essential adjunct to clenbuterol use. Potassium supplementation, or a diet containing plenty of potassium-rich foods, would also likely help attenuate some of clenbuterol’s antagonistic effects towards exercise performance.

Lastly, we arrive at the issue of functional downregulation with the beta2 receptor. Given clen’s agonistic potency, and the differing molecular structure of the beta2 receptor as opposed to its beta1 and beta3 counterparts, it is only a matter of time in all chronic clenbuterol users before almost complete, system-wide desensitization of the beta2 receptor-class sets in (15,16). More specifically, in rats undergoing high-dose (4 mg/kg) clenbuterol treatment, soleus and medial gastrocnemius tests showed a 40-45% decrease in total beta-adrenergic receptor density, with the entirety of the decrease coming from beta2 desensitization (17;18).

Brotologists Run for Your Lives… It’s Science!!!

The specific mechanisms responsible for adrenergic downregulation of the beta2 seem to be heavily G-protein implicated (18). More specifically, researchers speculate that the process begins with the uncoupling of the receptor’s heterotrimeric G after acute exposure to the agonist (19). Eventually, with enough chronic stimulation, the receptor/arrestin [note: arrestins are proteins which can bind or uncouple heterotrimeric G proteins from G protein-coupled receptors] complex, which would normally be recycled to the cellular membrane after exposure to the agonist is halted, is instead translocated to the lysosomes (20).

Lysosomes, for those not aware, are essentially the unheralded cousins of the peroxisomes. While the peroxisomes tend to get all the shine because the PPARs are so pivotal in regulating metabolic substrate oxidation and adipocyte differentiation, the lysosomes are the guys who tend to handle the cellular ‘grunt work’—eating up bacteria, decaying organelles, and other byproducts your cell doesn’t really want hanging around in there. In this case, with chronic clenbuterol exposure, your cell doesn’t want your beta2 receptors hanging around anymore, and the lysosomes eventually just start taking them out, Mafioso-style, in a process known in “Whachu’ talkin’ bout Willis?” terms as ‘homologous desensitization.’ And, just like that, beta2-mediated lipolysis is suddenly closed for business. My. How the tables have turned.

Synthesizing Our Savvy and Dialing it All In

At this point, you should have a pretty good understanding of clenbuterol, in terms of its effects and mechanisms. So let’s put principle into practice and discuss how to take the plunge without going off the deep end.


40-80mcg/day. If you are a newcomer to clenbuterol, start with an even lower dosage (10-20mcg) and assess your tolerance. Titration of dosing need be utilized only in regards to tolerance: if you know you can handle 60mcg of clenbuterol per day, and that’s your target, then get to that dosage as fast as possible and keep it there. There is no pragmatic need to ‘pyramid’ or ‘taper’ clenbuterol use above and beyond the stimulation factor, once you know the dosage you can tolerate and have selected an amount to run. And remember: because of the long, biphasic half-life, clenbuterol builds up in your system, a la DNP. A 40mcg dose on Monday noon and a second 40mcg dose the very next day means you’re already going to have circa ~60mcg active in your system after just two days, so bear that in mind.


In my personal opinion, clenbuterol cycles are best kept to about 7 days in duration before cycling off for at least an equal period of time. Granted, based on the literature, you’ll still have significant catecholamine-mediated lipolysis kicking around in that second week, but—and again, taking half-life into consideration—your beta2s are going to definitely be cashed out by the end of week 2. Thus, rather than exposing yourself to significant temporary down-regulation at all (as well as the negative systemic effects, which will only be aggravated as the drug continues to build up in your system), why not use clenbuterol in more of a precise manner and get big-time bang for your buck?

Anecdotally, 99% of clenbuterol users say their first cycle was the ill na na, and subsequent cycles were far less effective at drastically influencing body-composition. Whether there is any merit to this notion or not, the fact of the matter remains that some fraction of the first, full-fledged receptor-desensitization that clenbuterol elicits may be irreversible, a supposition which lends even more credence to the idea of shorter and/or lower-dosed cycles. And remember, always take at least as much off time from clenbuterol as you spend on it.


Much to my chagrin, chances are if you’re using clenbuterol in the first place you pretty much have no reservations about what you do to your body to achieve your fat-loss results. And by that same token, chances are you have no qualms with stacking a 1Fast400’s inventory-shelf worth of supplements alongside it just for the sake of expediting things a tad. So, for the sake of getting you conveniently cut ASAP so you can get the hell off the drug, here’s the stuff you want to look into:

Green Tea Extract:

EGCG, the principal active ‘weight-loss catechin’ in green tea is a catecholamine-O-methyltransferase (COMT) inhibitor. COMT is an enzyme which metabolizes catecholamines peripherally. Inhibiting COMT potentiates catecholamine-induced thermogenesis.


GPA, one of the three actives in PhenoGen, when administered concurrently with clenbuterol decreases clenbuterol-treatment-only impairments in response to exercise-induced increases in GLUT4 protein concentrations. GPA also increases beta-adrenergic receptor density in skeletal muscle, giving you more adrenergic receptors for clenbuterol to agonize, thereby accelerating its fat-burning properties.


While the author of this article loathes synthetic thyroid modulation with a passion, he does admit that it makes for a pretty ridiculous one-two fat-burning punch when combined with clenbuterol. T3, like GPA, upregulates beta-adrenergic receptor density in skeletal muscle. Additionally, T3 also increases uncoupling protein (UCP) expression in the mitochondria (thereby increasing metabolic rate and cellular respiration) and accelerates substrate-cycling/reformation in stored TAGs. Thirdly, as a potent anti-catabolic agent, clenbuterol also makes a good adjunct to the immensely catabolic T3, given its abilities to attenuate proteolysis, particularly that which takes place in the ubiquitin-proteasome pathway.

H.E.A.T. Stack:

This one, while it might not occur too many, makes significant practical sense assuming one is knowledgeable about his or her stimulant tolerance and is aware of the potential risks. The simple gist is that clenbuterol’s lipolytic effects are predominately beta2-mediated. Adding H.E.A.T. Stack in conjunction will allow the user to markedly increase beta1 and beta3 mediated lipolysis simultaneously, thereby creating a bonafide peripheral lipolytic jamboree, in addition to providing some much-needed appetite suppression—one of clenbuterol’s significant pharmacological shortcomings when it comes to dieting.

Miserly, risk-prone bastards could also use E/C in place of H.E.A.T. Stack, assuming they have no problems knowing that they are antagonizing the fed state and putting themselves at a much higher risk of negative cardiac and/or blood-pressure related interactions, both of which would be well above and beyond what one would be dealing with when using the much more benign and—dare I say—“classy” *wink* H.E.A.T. Stack.


A pharma anti-histamine that attenuates clenbuterol-induced beta2 receptor desensitization, allowing you to stay on longer and keep the ball rolling on lipolysis. Note: hopefully you will realize this is not necessarily an entirely a good thing. Also, please actually research this drug before just going out and getting all polypharmacological in the name of a never-ending clen cycle.

And That’s Almost All She Wrote

And thus we arrive at the end of our M&M examination of clenbuterol…


No, but with all seriousness, for the sake of this article meeting its deadline, this will conclude Pharmaceutical Phenotype Enhancement’s general installment on the diet drug clenbuterol. However, because I said at the end of Part I that I planned on discussing clen’s neurological effects, as well as its potential role as a curative for certain pathologies, and because I’m not a pathological liar, look for a “Clenbuterol Addendum” to pop up in good old Issue #30. Yes, I know. I live to give; I love my fans and puppy dogs very much; I am a Leo; I find Sprite’s cool, crisp, lemon-limey flavor very refreshing; and please direct all fan male to my secretary and Avant eunuch, Robboe. Cheers all.


1. Ingalls CP, Barnes WS, Smith SB: Interaction between clenbuterol and run training: effects on exercise performance and MLC isoform content. J Appl Physiol 1996;80(3):795-801

2. Stevens L, Firinga C, Gohlsch B, Bastide B, Mounier Y, Pette D. Effects of unweighting and clenbuterol on myosin light and heavy chains in fast and slow muscles of rat. Am J Physiol Cell Physiol. 2000 Nov;279(5):C1558-63.

3. Kearns CF, McKeever KH. Clenbuterol diminishes aerobic performance in horses. Med Sci Sports Exerc. 2002 Dec;34(12):1976-85.

4. Duncan ND, Williams DA, Lynch GS. Deleterious effects of chronic clenbuterol treatment on endurance and sprint exercise performance in rats. Clin Sci (Lond). 2000 Mar;98(3):339-47.

5. Meeuwisse WH, Mckenzie DC, Hopkins SR, et al: The effect of salbutamol on performance in elite non-asthmatic athletes. Med Sci Sports Exerc 1992;24(10):1161-1166

6. Morton AR, Joyce K, Papalia SM, et al: Is salmeterol ergogenic? Clin J Sports Med 1996;6(4):220-225

7. Robertson W, Simkins J, O’Hickey SP, et al: Does single dose salmeterol affect exercise capacity in asthmatic men? Eur Respir J 1994;7(11):1978-1984

8 . Lafontan M, Berlan M, Prud’hon M. Les agonistes bêta-adrénergiques. Mécanismes d’action: lipomobilisation et anabolisme. Reprod Nutr Dévelop 1988;28:61-84.

9. Morton AR, Papalia SM, Fitch KD: Changes in anaerobic power and strength performance after inhalation of salbutamol in non-asthmatic athletes. Clin J Sports Med 1993;3(1):14-19

10. Waterfield CJ, Jairath M, Asker DS, Timbrell JA. The biochemical effects of clenbuterol: with particular reference to taurine and muscle damage. Eur J Pharmacol. 1995 Jul 1;293(2):141-9

11. Huxtable RJ, et al. Effects of taurine on a muscle intracellular membrane. Biochim Biophys Acta 1973 323: 573-583,

12. Kim RD, Stein GS, Chari RS. Impact of cell swelling on proliferative signal transduction in the liver. J Cell Biochem. 2001 Jun 26-Jul 25;83(1):56-69.

13. Oja SS & Kontro P: Taurine. In: Laijtha A, ed: Handbook of Neurochemistry. New York: Plenum Publ .Corp, 501-533, 1983

14. Cuisinier C, Michotte De Welle J, Verbeeck RK, Poortmans JR, Ward R, Sturbois X, Francaux M. Role of taurine in osmoregulation during endurance exercise. Eur J Appl Physiol. 2002 Oct;87(6):489-95. Epub 2002 Aug 10.

15. M Zhao and KH Muntz Differential downregulation of beta 2-adrenergic receptors in tissue compartments of rat heart is not altered by sympathetic denervation Circulation Research, Vol 73, 943-951

16. Boldt Perioperative management of patients with impaired left ventricular function. Current Opinion in Anaesthesiology. 11(3):315-319, June 1998

17. Julie Lavoie, Angelino Calderone, and Louise Béliveau A farnesyltransferase inhibitor attenuated beta-adrenergic receptor downregulation in rat skeletal muscle. Am J Physiol Regul Integr Comp Physiol 282: R317-R322, 2002

18. Bouvier, M, and Rousseau G. Subtype-specific regulation of the -adrenergic receptors. Adv Pharmacol 42: 433-438, 1998

19. Fergurson, SSG, Zhang J, Barak LS, and Caron MG. G-protein-coupled receptor kinases and arrestins: regulators of G-protein-coupled receptor sequestration. Biochem Soc Trans 24: 953-959, 1996

20. Zhang, J, Barak LS, Anborgh PH, Laporte SA, Caron MG, and Ferguson SSG Cellular trafficking of G protein-coupled receptor/ -arrestin endocytic complexes. J Biol Chem 274: 10999-11006, 1999

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