T Nation

Comments on Clenbuterol


#1

What do you guys think of this article... seems like a bit of hype to me:

http://www.medpagetoday.com/PrimaryCare/WeightManagement/tb/2486


#2

No it is not over-hyped clenbutoral is dangerous, as I said before your body actually destroys it's beta-2 receptors to relieve itself from the drugs effects.


#3

I have always been taught the ECA stack is the way to go in terms of safety. But come to think of it, if ephedrine and clenbuterol are both beta 2 agonists, what makes ephedrine safer?


#4

from what i understand clen is beta-2 specific and ephedrine is a non-selective beta agonist. Beta 2 receptors are responsible for the function of your smooth muscles (muscles that control body functions but that you do not have control over). clen can also cause hardening of the heart tissue over time.


#5

I hate articles like this:
"Isn?t clenbuterol just a safe alternative to steroids??? they ask. ?The answer is ?no.??

Am I the only one who would like more information?

Or this:

A case report published in a September issue of Circulation, Journal of the American Heart Association, reported on a myocardial infarction suffered by a 17-year-old body builder who used only clenbuterol. Researchers at the Institute of Pediatrics at Medical University in Lodz, Poland, said the boy had been previously healthy.

One case. An amazing study to back up the article.... Im sure the boy had a prior ekg.....So, they know he was healthy. How many non-clen using athletes have died on the field of play from heart failor who were "previosly healthy"
Im not saying it does not pose any risk but, its been around how long and how many thousands of men and woman have used it? Freak


#6

Dade,
Why would you say ephedrine is safer? Our wonderful congress thought it was killing so many that a ban was put on it......which a federal judge overturned. Either way, there were a few deaths directly caused by ephedrine use. Im not sure I know of any caused by Clen...........Freak


#7

No I am sorry but if you do a search you will find the literature out there to support a link between clen use and cardiac damage. It is no safer then using ECA, as ECA has its risks as well.

Basically to debate whether Clen is safer than ECA or vise versa is like debating which substance is more poisonous? Cyanide or arsenic?


#8

I'm completely unejamucated in this stuff, so this may be the dumbest thing you've ever heard.

What does over time mean? 4-6 weeks? or 25, 4-6 week cycles over a 15 year period?

That, and since it causes hardening of the heart tissue would increased cardio (greater usage at a greater intensity, higher BPM's) lessen the effects of this?


#9

No debate. I just pointed out that ephedrine has lead to enough deaths to make the congress hold session. So, for a member to say its a safer way to go......is far from the truth.
As far as literature on clen, Ive seen a study on rats that were given SQ doses of clen between 2mg/kg-5mg/kg. Thats a MONSTER dose. Ill bet there is less literature on this drug and human use than any other drug profiled on a BB forum. Freak


#10

I never said ephedrine was safer. I said I had been taught it was and then questioned it since ephedrine and clenbuterol are similar drugs. It makes sense to me that they may both be equally dangerous. However, Freak, you seem to be defending clenbuterol in your previous post. Also, I could care less whether Congress has met to discuss the dangers of a substance. Congress is probably the last place I would look for information concerning any drug. Maybe next month they can ban alcohol, tobacco, tylenol and ibuprofen.


#11

Check these articles out... You will find them to be well researched with lots of scientific studies cited...

Pharmaceutical Phenotype Enhancement
by Chris Clancey aka Loki

Clenbuterol Part I

First ?The Man? marginalized ephedra. Then we saw the realization of a second supplement ban?one which will effectively deprive the mainstream bodybuilding community of its most-preferred anti-catabolic ancillary: the pro-hormone or pro-steroid. So just how the hell is a dieter supposed to preserve lean body mass these days while languishing on laughably low calories? Well, aside from investing in our beloved LeptiGen and shipping out for real gear, it seems like a lot of would-be-chiseled chaps are taking a new interest in the age-old diet drug Clenbuterol (1-(4-Amino-3,5-dichlorophenyl)-2-tert-butyl-aminoethanol), a sympathomimetic beta2 adrenergic agonist most commonly used in veterinary therapeutics and livestock doping. But is this recent, glaringly rekindled curiosity in clen leading would-be and first-time users to the right drug? Or for that matter, is clen a safe drug? So, without further ado, I think it?s time M&M gave ephedra?s ?wonder-cuz?? its full-on, discerning attention.

Clen in Context: Basic Pharmacology

I throw around the word sympathomimetic a lot to compensate for my chronically low self-esteem. In the forums, in my sleep, during sex?it?s just such a dazzlingly erudite sounding word. And using it makes me feel special. And while you yourself may not feel the inclination to use it colloquially any time soon, if phrases like ?nutrient partitioning? or ?fat loss while preserving muscle? pique your interest, you should care about how this class of compounds works and what those workings result in.

Chances are you wouldn?t be reading this article if you didn?t, so quickly: sympathomimetics (take ?sympath? from ?sympathetic nervous system,? throw an ?o? on there, and add ?mimetic? [i.e. ?to mimic?] and you?re in business) are a class of drugs that affect the sympathetic nervous system (SNS), either by prompting central catecholamine (NE/NA and E/A) release or by peripherally mimicking the effects of those same endogenous hormone/neurotransmitters. Most of a sympathomimetic?s pharmalogical interplay occurs via interaction with beta andrenoreceptors. Ephedrine is a sympathomimetic, norephedrine is a sympathomimetic, H.E.A.T. is a sympathomimetic, and boy is clenbuterol ever a sympathomimetic. There are also many others.

With clenbuterol specifically, what we see is both forms of sympathomimetic activity. Clen synthetic mimics some of norepinephrine?s and epinephrine?s effects in specific outreaches of the SNS, and centrally exerts these effects in skeletal muscle, adipose tissue, and in an often-overlooked third area: the brain. Yes, that?s right: clenbuterol crosses the blood brain barrier, and is able to readily activate certain central adrenoreceptors (1).

Virtually all of this peripheral mimicking occurs at the beta2 adrenergic receptor, which is the reason clenbuterol is characterized as a beta2 specific agonist. When it interacts with these receptors in muscle, clenbuterol is able to catalyze Cyclic Adenosine Monophosphate (cAMP) production, a second-messenger signal transducer which regulates rates of glycogen decomposition, protein synthesis, and lipolysis (among many other things). What distinguishes clenbuterol prominently from ephedrine is its specificity, potency, and duration of effect.

Ephedrine, whether you already knew it or not, has very little direct activity in muscle or fat. Rather, it stimulates central sympathetic nerve terminals, thereby inciting an indiscriminate release of NE/NA (and to a lesser extent, epinephrine/adrenalin), which then relays across the entirety of the SNS. This makes ephedrine a primarily indirect and non-specific sympathomimetic, as it effectively delivers a mild ?catecholamine carpet-bombing? to all your various beta receptors (beta1, beta2, atypical beta3, and putative, atypical beta4). It is also this mechanism that gives ephedrine its long-term pharmacological viability: although not very set-point friendly, it will nonetheless continue to indirectly agonize adrenergic receptors along your SNS, even after months of continual use.

Clenbuterol is somewhat of a different beast. As mentioned earlier, it is able to prompt a small degree of catecholamine release from central adrenoceptors, as well as interact directly with the beta2 receptor in a dose-dependent manner with a potency that far exceeds the resultant effects of ephedrine administration.

More Technical Stuff on Clen?s Workings than You Could Ever Possibly Want to Know: Lipolysis

Nutrient-partitioning junkies, your patience is about to be rewarded. Now that we?ve established some context, it?s time to move on and discuss ?the goods.? It?s time to discuss the bad-ass lipolytic and repartitioning effects of clenbuterol in vivo. And it goes a little something like this. Following administration, clenbuterol avoids first-pass metabolism (it?s oral bioavailability ranges between 89-98%) and doses typically reach peak plasma levels roughly two hours after a dosage is ingested. This peak will then stabilize and continue for four additional hours (2). Eventually, roughly 50% of ingested clenbuterol will undergo metabolization into its four primary metabolites; the remaining half will be excreted intact, without metabolic breakdown (3). This biphasic elimination lends clenbuterol a veritable half-life that clocks in at just under thirty six hours.

Once it gets to work clenbuterol, as I already mentioned, binds to cellular beta2 receptors. Intracellularly this will increase cAMP (4), which then binds to regulatory subunits of protein kinase A, causing the release of its catalytic subunit. This process activates the enzyme HSL (hormone sensitive lipase), which hydrolyzes triglycerides, breaking them down into glycerol and fatty acids to allow for beta oxidation.

Now, as you can probably guess, one of the facets to clenbuterol that makes it such a potent lipolytic drug is that it exerts its beta-agonism steadily and continuously. If ephedrine is ?hit-it-and-quit-it,? clenbuterol is a friggin? marathon man when it comes to stimulation. Clen isn?t very cuddly though, so all you high-maintenance bodybuilders are just plum out of luck.

Clenbuterol is undeniably potent at its target receptor. However, clenbuterol cannot be said to own ephedrine (particularly when combined with caffeine) outright for fat loss. Remember, since clen is primarily direct-acting on a cellular level, it can?t prompt the same kind of NE-induced hypophagia (loss of appetite) as ephedrine, which has proved to be an essential pharmacological component in its ability to further weight loss (5). Individuals looking to use clenbuterol for weight loss need to keep this in mind: clenbuterol partitions energy intake, but it will not aide in regulating or helping to decrease it, hence my recommendation that those planning to cut on clen also look into ancillary appetite suppressants.

There is also the prevailing theory in a lot of bodybuilding circles that clenbuterol actually raises metabolic rate by increasing endogenous thermogenesis. So let?s explore the purported calorie-burning properties of clenbuterol. In animals, although clenbuterol increases thermogenesis in mutant rats (genetically obese Zucker rats), multiple studies have demonstrated that in normal rats?even those administered rather hefty dosages of the drug--- clenbuterol ?did not affect energy intake [or] energy expenditure? (6,7).

In human studies, the direct infusion of the related beta2-specific agonists salbutamol and terbutaline in lean men caused a modest increase in whole body energy expenditure and respiratory exchange ratio?an increase of 0.6 kJ/min in terms EE adjusted for fat-free mass (8). In other words, the guys getting heavy-duty beta2 adrenergic stimulation would have ended up burning about 200 extra kcals over a twenty four hour period. So in other words, thermogenesis was enhanced, but not so much to suggest that clenbuterol has strong calorie-burning properties of its own. Interestingly enough, in the same study the researchers noted that:

during beta2-adrenergic stimulation, the increases in energy expenditure and plasma nonesterified fatty acids and glycerol concentrations were reduced in the obese group. Furthermore, lipid oxidation significantly increased in the normal weight group, but remained similar in the overweight group? [this] data suggests that beta2-adrenoceptor-mediated increases in thermogenesis and lipid utilization are impaired in the obese (8).

In other words, if you?re still in plus-size pants, you?re out of luck: clenbuterol isn?t going to help you lose a whole lot of weight, because your obesity-train-wrecked metabolism just ain?t havin? that (9). Plus, given the effects of beta adrenergic agonists on heart rate contraction, the use of clenbuterol in significantly overweight individuals may pose significant danger to the user (10,11).

And again, the take home message is the same: when dieting, nutrient-partitioning definitely matters, but in the end it still comes down largely to energy expenditure vs. intake, and clen is a calorie re-distributor, not a burner.

Clenbuterol and its Interaction(s) With Your Mammoth Guns

If you get one sentence out of this section on clenbuterol and skeletal muscle, please let it be this: clen is never going to get you big, but it is extremely good at keeping you big once you get there. Yes, I know clenbuterol is wicked-anabolic in Dawley-Sprague hyperphagic wombats, but you are a human, and the amount of clenbuterol it would take for you to see a genuine anabolic effect would also put you in a coffin, so let?s just let that one go.

Now, I said clen?s not anabolic, but it certainly does have positive ramifications for protein synthesis, primarily through the beta2s, cAMP, and its ability to mitigate Ca2+-dependent proteolysis in skeletal muscle (12). A critical component to its full effect is its repartitioning properties. As stated earlier, clenbuterol is exceedingly good at liberating fatty acids from adipose tissue. But, more than that, clenbuterol exerts this effect in tandem with large scale, itself-induced skeletal muscular insulin resistance (13).

Now, when you?re a type II diabetic, this isn?t so hot. However, in a healthy bodybuilder using a strong sympathomimetic you basically have the best of all worlds: plenty of free-fatty acids getting released for oxidation in muscle, plenty of insulin-resistant muscle to feast on them, and pretty much all consumed calories getting spared for muscle retention and protein synthesis. Granted, there?s very little good research on human skeletal muscle in the presence of clenbuterol (particularly when it comes to athletes), but reasoned inference and extrapolation certainly paints a pretty convincing picture that clenbuterol is significantly anti-catabolic.

For starters, human research with ephedrine and caffeine has demonstrated that indiscriminate, weaker beta-adrenergic agonism significantly improves protein deposition and preserves lean body mass during periods of caloric restriction (14). Also interesting was the researchers? discovery that the ephedrine and caffeine mixture wasn?t attenuating skeletal muscular breakdown, but was in fact accelerating protein synthesis. This was proved clinically by 3-methylhistidine examination, an index for skeletal muscle breakdown.

In the sympathomimetic group, an increase in nitrogen balance was demonstrated independent of 3-methylhistidine, which means the ephedrine was actually helping to synthesize lean tissue at a faster rate, and thereby counteracting the increase in diet-induced catabolism (15). See? I wasn?t lying when I said clenbuterol could be anabolic; you just can?t take a high enough dose to get an anabolic degree of protein synthesis augmentation without ending up in the ER long before you could get your shaky ass anywhere near a squat rack.

Nonetheless, because of its pharmacology, clenbuterol is currently recognized in the scientific community as a valid remedial treatment for muscle-wasting conditions (16,17). In rodents, clenbuterol also actively inhibits glucocorticoid-induced muscle atrophy, and one can speculate that it may also exert similar anti-glucocorticoid properties in humans as well (18). Clenbuterol, by virtue of its beta-agonism, may also even be more effective at reducing glucocorticoid activity than that though, as it has been demonstrated that beta-receptor antagonism increases the release of adrenocorticotrophin (ACTH) in humans subjected to stress (19). For those unaware, ACTH is a pituitary hormone that stimulates cortisol secretion, which means there is a possibility that beta-receptor agonism may in fact be able to prompt the opposite: a decrease in ACTH release in response to stress.

All told, clenbuterol is pretty much the bomb and the shiznit as far drugs go for preserving muscle during periods of energy restriction through a number of different pathways. Oh but there are just a few more things?

But I?m Too Sexy To Die? (Side Effects and Precautions Pt. I)

By now it should be clear that clenbuterol is a powerful drug. And with all powerful drugs, there are consequences, ?cause life just sucks like that. So for those of you about to get all ?clenbutaholic? with your research chemicals, here?s a little info I counsel you to take to heart. In fact, speaking of hearts, let?s examine yours in relation to clenbuterol, because there definitely is some cause for concern.

For starters, there are more rodent studies under the sun that show clenbuterol use can cause significant cardiac hypertrophy?so many in fact that I?m not even going to bother citing them. Just type ?clenbuterol? and ?cardiac hypertrophy? into Google if you don?t believe me; no lie, it?s a little unsettling. However, clenbuterol also kills fat cells (adipocyte apoptosis) in rodents too, and it sure doesn?t in humans, so take that animal data for what it?s worth. Unfortunately though, things don?t look too much better when we move up the evolutionary chain and start looking at hearts in good-ole? human beings either.

For example in 1998, the internal medicine outpatient clinic at the University of Alabama Birmingham received a walk-in from a previously healthy 26-year-old bodybuilder complaining of significant chest pains. The man, who had a history of moderate anabolic steroid use but who had not used any steroid preparations in the weeks leading up to his visit, revealed that he had continuously been using clenbuterol for nearly a month [Loki?s note: idiot]. During check-up, the man turned out to be completely fit and healthy with the only exception being a significant amount of left ventricle (heart) hypertrophy and cardiac dyskinesias (meaning distortion of muscle [in this case smooth muscle] activity)(20).

In fact, between 1988 and 1998, eight cases of medically-diagnosed cardiac hypertrophy have been reported in drug-using bodybuilders within the United States (21,22). We can assume many more went overlooked or unreported. Still, because of the steroid outlier (which could also be a potential factor in the pathology?or perhaps even the outright cause), the medical community has been unable to isolate clenbuterol?s true role in contributing to these instances of myocardial infarcation (20). Still, the researchers who have examined this phenomenon arrived at a conclusion that should give most clen user?s pause of thought. Namely that:

We suspect there may have been a synergistic role between the anabolic

steroid and clenbuterol. Hypothetically, the anabolic steroid may have caused cardiac hypertrophy, coronary artery spasm, or thrombosis. The clenbuterol

may have precipitated ischemia by producing intermittent tachycardia. Alternately, clenbuterol may have contributed primarily to the cardiac hypertrophy...(20)

Furthermore, clenbuterol ingestion (particularly excessive ingestion) has also been documented to cause tachycardia (sudden, rapid racing of the heart)(20,23,24), hypokalemia (23), hypophosphatemia (23), potassium depletion (24), taurine depletion (25), headaches (24), tremors (24), and vertigo (24). Now, it should be noted that the more severe of the aforementioned conditions have only been demonstrated in instances of clenbuterol overdose and are thus not directly applicable to carefully monitored doses within the 20-100mcg range. Nonetheless, clenbuterol is definitively a ?big kid sympathomimetic,? and not a drug that lends itself to immoderation, recklessness, or just outright stupidity.

And for now, I?m afraid that?s just going to have to do it for Part I of our comprehensive look at Clenbuterol. Next issue we?ll get into receptor down-regulation, clenbuterol, the brain, and neuroprotection (for all my Chemically Correct homies), cycling, stacking recommendations, and potential novel uses for clenbuterol in the treatment of injuries and various diseases and conditions.

Questions or comments on this article? Post them in the Avant Labs Forums for live feedback from the author, as well as the Mind and Muscle staff and fellow readers!

References

  1. O'Donnell JM. Pharmacological characterization of the discriminative stimulus effects of clenbuterol in rats.

  2. Yamamoto I, Iwata K, Nakashima M. Pharmacokinetics of plasma and urine clenbuterol in man, rat, and rabbit. J Pharmacobiodyn. 1985 May;8(5):385-91

  3. Zimmer A. Administration of Clenbuterol in man. Single doses, multiple doses, and metabolite samples. Vetmedica GmbH; Ingelheim, Germany

  4. Tsuji T, Kato T, Kimata M, Miura T, Serizawa I, Inagaki N, Nagai H. Differential effects of beta2-adrenoceptor desensitization on the IgE-dependent release of chemical mediators from cultured human mast cells. Biol Pharm Bull. 2004 Oct;27(10):1549-54.

  5. Astrup A, Toubro S. Thermogenic, metabolic, and cardiovascular responses to ephedrine and caffeine in man. Int J Obes Relat Metab Disord 1993 Feb;17 Suppl 1:S41-3

  6. Reichel K, Rehfeldt C, Weikard R, Schadereit R, Krawielitzki K. Effect of a beta-agonist and a beta-agonist/beta-antagonist combination on muscle growth, body composition and protein metabolism in rats. Arch Tierernahr. 1993;45(3):211-25.

  7. Rothwell NJ, Stock MJ. Effect of a selective beta 2-adrenergic agonist (clenbuterol) on energy balance and body composition in normal and protein deficient rats. Biosci Rep. 1987 Dec;7(12):933-40.

  8. S. L. H. Schiffelers, W. H. M. Saris, F. Boomsma and M. A. van Baak Beta1- and Beta2-Adrenoceptor-Mediated Thermogenesis and Lipid Utilization in Obese and Lean Men. The Journal of Clinical Endocrinology & Metabolism Vol. 86, No. 5 2191-2199

  9. Jung RT, Shetty PS, James WP, Barrand MA, Callingham BA. Reduced thermogenesis in obesity. Nature. 1979 May 24;279(5711):322-3.

  10. Abramson MJ, Walters J, Walters EH. Adverse effects of beta-agonists: are they clinically relevant? Am J Respir Med. 2003;2(4):287-97.

  11. O de Divitiis, S Fazio, M Petitto, G Maddalena, F Contaldo and M Mancini. Obesity and cardiac function. Circulation, Vol 64, 477-482

  12. Luiz Carlos C. Navegantes, Neusa M. Z. Resano, Renato H. Migliorini, and ?sis C. Kettelhut Catecholamines inhibit Ca2+-dependent proteolysis in rat skeletal muscle through beta2-adrenoceptors and cAMP. Am J Physiol Endocrinol Metab 281: E449-E454, 2001

  13. Kim J, Shigetomi S, Tanaka K, Yamada ZO, Hashimoto S, Fukuchi S. The role of beta 2-adrenoceptor on the pathogenesis of insulin resistance in essential hypertension. Nippon Naibunpi Gakkai Zasshi. 1994 Jun 20;70(5):521-8

  14. Astrup A, Buemann B, Christensen NJ, Toubro S, et al. The effect of ephedrine/caffeine mixture on energy expenditure and body composition in obese women. Metabolism 1992 Jul;41(7):686-688

  15. Pasquali R, Casimirri F Clinical aspects of ephedrine in the treatment of obesity. Int J Obes Relat Metab Disord;17 Suppl 1:S65-S68 1993

  16. Maltin CA, Delday MI, Watson JS, Heys SD, Nevison IM, Ritchie IK, Gibson PH. Clenbuterol, a beta-adrenoceptor agonist, increases relative muscle strength in orthopaedic patients. Clin Sci (Lond). 1993 Jun;84(6):651-4.

  17. Oya Y, Ogawa M, Kawai M. Therapeutic trial of beta 2-adrenergic agonist clenbuterol in muscular dystrophies. Rinsho Shinkeigaku. 2001 Oct;41(10):698-700

  18. Pellegrino MA, D'Antona G, Bortolotto S, Boschi F, Pastoris O, Bottinelli R, Polla B, Reggiani C. Clenbuterol antagonizes glucocorticoid-induced atrophy and fibre type transformation in mice. Exp Physiol 89.1 pp 89-100

  19. Oberbeck R, Schurmeyer T, Jacobs R, Benschop RJ, Sommer B, Schmidt RE, Schedlowski M. Effects of beta-adrenoceptor-blockade on stress-induced adrenocorticotrophin release in humans. Eur J Appl Physiol Occup Physiol 1998 May;77(6):523-6

  20. Goldstein et al. Clenbuterol and anabolic steroids: a previously unreported case of myocardial infarcation with normal coronary arteriograms. Southern Medical Journal. 1998:780-784.

  21. McNutt et al. Acute myocardial farcation in a 22-year-old world class athlete using anabolic steroids. Am. Journal of Cardiology. 1988:62-164.

  22. Fisher et al. Myocardial infarcation with extensive intracoronary thrombus induced by anabolic steroids. Br. J. of Clin. Prac. 1996:50:222-223.

  23. Hoffman RJ, Hoffman RS, Freyberg CL, Poppenga RH, Nelson LS. Clenbuterol ingestion causing prolonged tachycardia, hypokalemia, and hypophosphatemia with confirmation by quantitative levels. J Toxicol Clin Toxicol. 2001;39(4):339-44

  24. Chodorowski Z, Sein Anand J. Acute poisoning with clenbuterol--a case report. Przegl Lek. 1997;54(10):763-4.

  25. 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

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Pharmaceutical Phenotype Enhancement: Clenbuterol Part II
by Chris Clancey aka Loki

Clenbuterol Part II

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.

Dosage

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.

Cycling

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.

Stacking

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.

PhenoGen: 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.

T3/Trimax/Triac/etc: 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.

Ketotifen: 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?

PSYCHE!!!!

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.

References

  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 b?ta-adr?nergiques. M?canismes d'action: lipomobilisation et anabolisme. Reprod Nutr D?velop 1988;28:61-84.

  1. 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

  2. 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

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

  4. 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.

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

  6. 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.

  7. 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

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

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

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

  11. 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

  12. 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

Mind and Muscle Magazine is a division of Par Deus, Inc.
? 2001 ? 2006 Par Deus Inc. All Rights Reserved.


#12

You'll find all of the articles there to be well researched and with alot of scientific references cited. I should know, as I assist in editing that particular online magazine...


#13

another:

J Appl Physiol. 2004 Dec 10; [Epub ahead of print] Related Articles, Links

{beta}2-Adrenergic receptor stimulation in vivo induces apoptosis in the rat heart and soleus muscle.

Burniston JG, Tan LB, Goldspink DF.

Research Institute for Sports and Exercise Sciences, Liverpool John Moores University, Liverpool, United Kingdom.

High doses of the beta2-adrenergic receptor (AR) agonist, clenbuterol, can induce necrotic myocyte death in the heart and slow-twitch skeletal muscle of the rat. However, it is not known if this agent can also induce myocyte apoptosis and whether this would occur at a lower dose than previously reported for myocyte necrosis. Male Wistar rats were given single subcutaneous injections of clenbuterol. Immunohistochemistry was used to detect myocyte specific apoptosis (detected on cryosections using a caspase 3 antibody and confirmed using annexin V, single-strand DNA labelling and TUNEL). Myocyte apoptosis was first detected at 2 h, and peaked 4 h after clenbuterol administration. The lowest dose of clenbuterol to induce cardiomyocyte apoptosis was 1 microg kg(-1), with peak apoptosis (0.35 +/- 0.005 %; P<0.05) occurring in response to 5 mg kg(-1) . In the soleus, peak apoptosis (5.8 +/- 2 %; P<0.05) was induced by the lower dose of 10 microg kg(-1). Cardiomyocyte apoptosis occurred throughout the ventricles, atria and papillary muscles. However, this damage was most abundant in the left ventricular subendocardium at a point 1.6 mm, that is, approximately one-quarter of the way from the apex towards the base. beta-AR antagonism (involving propranolol, bisoprolol or ICI 118,551) or reserpine was used to show that clenbuterol-induced myocardial apoptosis was mediated through neuromodulation of the sympathetic system and the cardiomyocyte beta1-AR, whereas in the soleus direct stimulation of the myocyte beta2-AR was involved. These data show that when administered in vivo, beta2-AR stimulation by clenbuterol is detrimental to cardiac and skeletal muscles even at low doses, by inducing apoptosis through beta1- and beta2-AR, respectively.


#14

Dont get me wrong, I have no problem with Clen or Ephendrine. Ill use both in moderation. However, when I mention liturature.....Im not talking about an article by bodybuilders.....for BB's. I was refering to clinical studies......which just wont happen since its a vet compound. However, since LV thickening was braught up in the article posted, I thought the following study might be of interest:
Cardiomyopathy and Athletics

Gary Stephen Ferenchick
Department of Medicine
Michigan State University
East Lansing, Michigan
USA

Cardiomyopathy is defined as a disease of the heart muscle that results in loss of function.  Although most heart diseases ultimately cause dysfunction of the heart muscle, cardiomyopathy typically refers to disease originating in the cardiac muscle itself, as opposed to the cardiac valves or coronary arteries.  An identifiable specific cause of cardiomyopathy is frequently absent.
The three basic subtypes of cardiomyopathy include dilated, hypertrophic and restrictive.  Dilated cardiomyopathy is the most common subtype.  The hallmark of dilated cardiomyopathy is an enlargement in the size of the heart's pumping chambers or ventricles.  As a result of this dilation, the forward pumping action of the heart is impaired and blood flow through the circulation is decreased, leading to fluid congestion in body tissues and the lungs.  Symptoms such as swelling in the ankles and shortness of breath are commonly encountered.  
Inflammation of the heart muscle due to a viral infection, or possibly autoimmune process (an antibody response against heart muscle cells) can predispose to dilated cardiomyopathy.  Toxic agents such as alcohol can also damage heart muscle cells and cause dilated cardiomyopathy.    
Hypertrophic cardiomyopathy can be an inherited condition.  In contrast to dilated cardiomyopathy the size of the ventricular chamber in hypertrophic cardiomyopathy is either normal or decreased.  The primary abnormality in hypertrophic cardiomyopathy is an abnormal increase in the size of the heart muscle.  This increase may affect the entire heart and therefore produce symmetric enlargement of heart muscle, but can also be asymmetric with the most obvious enlargement in the ventricular septum which is the muscular wall that separates the right and left ventricles.  As the septum increases in size it becomes more difficult for the heart to pump blood out of the left ventricle, this can produce symptoms of light-headedness or passing out. 
With symmetric enlargement of the heart muscle, the "forward" pumping action of the heart is not impaired and symptoms such as swelling in the ankles are rarely encountered.  The abnormal increase in muscle mass seen in hypertrophic cardiomyopathy can increases the "stiffness" of the heart which in turn produces high pressures inside the heart's chambers.  This high pressure can produce fluid backup in the lungs leading to difficulty in breathing.  
In addition to muscle thickness, an abnormality in the "organization" of the heart's muscle cells has also been described in the inherited form of hypertrophic cardiomyopathy.  In normal hearts the muscle cells lie parallel to one another, however non-parallel or "chaotic" arrangement is common in inherited hypertrophic cardiomyopathy.  This chaotic arrangement can make the electrical impulses in the heart unstable producing significant abnormalities in the rhythm of the heart, sometimes leading to death.  Sudden death in seemingly healthy athletes frequently have the inherited form of hypertrophic cardiomyopathy as the underlying reason.  Commonly, death occurs during or shortly after  exertion.
Restrictive cardiomyopathy represents the least common form of cardiomyopathy.  In this type the ventricles are "restricted" in their ability to fill up with blood by an abnormal accumulation of substances or scars within the heart muscle.  This type of cardiomyopathy has been termed nondilated, nonhypertrophic cardiomyopathy.  Like hypertrophic cardiomyopathy, pressures inside the ventricles increase in restrictive cardiomyopathy which can ultimately produce fluid congestion inside the lungs. 
When assessed by chest X-rays, electrocardiograms (EKG's) or other means, athletes' hearts frequently differ from the hearts of normal sedentary persons.  The "athlete's heart" refers to changes in the structure and function of the heart brought about by intense physical exercise.  Increases in heart muscle mass as well as in the size of the ventricular chambers are commonly seen in endurance athletes.  These changes result in a more efficient heart with an increase in the amount of blood pumped per heartbeat.  The "athlete's heart" therefore represents a normal adaptation to intense physical activity and is not, in and of itself, a disease.
Sudden death as a result of heart disease in amateur and professional athletes remains a rare event.  However, as with all people, a certain percentage of athletes have heart disease and some can be expected to die during competition as a result.  A variety of heart diseases have been associated with sudden death in athletes including congenital abnormalities, diseases of the valves and blood vessels of the heart as well as Cardiomyopathies.  Coronary artery disease likely represents the leading cause of death in athletes over 30 years of age.  In coronary artery disease the inside of the blood vessels become narrowed with "plaques" which represent the accumulation of cholesterol and other substances.  As the plaque "grows" the blood vessel becomes narrower.  Eventually complete blockage occurs usually as a result of a blood clot forming on top of the plaque.  In a "heart attack," the heart tissue which was dependent upon the blood flow in that vessel dies and the pumping action of the heart can become chaotic leading to sudden death.
The inherited form of hypertrophic cardiomyopathy represents the most common heart abnormality associated with sudden death in athletes under the age of 30.  It has a prevalence of about 0.1% in the general population and probably a similar prevalence in the athletic population.  Several well publicized cases of sudden death associated with hypertrophic cardiomyopathy have occurred in the past several years.  
The use of anabolic steroids to enhance athletic performance is a well-known practice among some amateur and professional athletes.  The effect of these drugs on the heart is becoming increasingly known.  For example, animal studies have demonstrated a direct effect of anabolic steroids on the heart, possibly through specific steroid receptors on the heart.  Among the effects seen in animals include greater heart weights and cardiac hypertrophy.  Microscopic studies of heart cells from steroid-treated rats demonstrate microscopic changes similar to those seen in early heart failure in humans.  Such changes are possibly the result of steroid-induced changes in the function of lysosomes, which contain enzymes capable of destroying cellular proteins. 
Case reports have linked anabolic steroids with increased left ventricular mass, cardiomyopathy, and sudden death in weightlifters and other athletes.  Furthermore, two small studies of steroid-using athletes demonstrated a relationship between steroid use and impaired function and an increased size of the heart's chambers.  However, in two other studies utilizing a sound wave assessment of left ventricular size and function in weightlifters, steroid use was not associated with myocardial hypertrophy.
The evaluation of persons with suspected cardiomyopathy includes obtaining a good history.  Symptoms such as decreased exercise tolerance, shortness-of-breath (especially shortness-of-breath after lying flat), dizziness or passing out should be investigated.  However, in the athletic population no symptoms may be present.  One should ask about the presence of congenital heart disease or sudden death in the family history.  The physical examination may reveal a low blood pressure, dilated veins in the neck, lung sounds of pulmonary congestion, evidence of an enlarged heart along with abnormal heart sounds, including extra sounds and murmurs.  In particular, patients with the inherited form of hypertrophic cardiomyopathy may have a loud murmur heard during the contraction of the heart.  Basic diagnostic evaluation may include a chest X-ray and electrocardiogram (EKG) which could reveal an enlarged heart, fluid in the lungs, and findings of abnormal electrical impulses in the heart.  A sound wave test of the heart (echocardiogram or ECHO) represents one of the most important early diagnostic tests for cardiomyopathy.  In the course of this test a series of sound waves are "bounced" off the heart and pictures of the heart are obtained.  The ECHO is helpful in determining the thickness of the heart muscle, the size of the heart's chambers, the anatomy and function of the heart's valves as well as estimating the pumping action of the heart.  	
Other tests which may be helpful in the assessment of cardiomyopathy include cardiac catheterization.  A catheter (tube) is placed directly into the chambers of the heart and a type of "dye" is directly injected into the heart.  During this process X-rays are able to assess the structure of the heart and pressure monitors are able to assess for function of the heart.
Treatment of cardiomyopathy largely depends on the type (dilated vs. hypertrophic vs. restrictive) and the presence of symptoms.  For the inherited form of hypertrophic cardiomyopathy, medications may improve the pumping action of the heart and help regulate the heart's rhythm.  Unfortunately the various medications required to attain these outcomes may be toxic.  Surgery of the heart may also be indicated in patients who continue to have symptoms in spite of medical treatment.  However, in spite of potentially useful treatment, it is generally recommended that individuals who have the inherited form of hypertrophic cardiomyopathy be discouraged from participating in competitive sports or strenuous exercise due to the risks of sudden death.

References
1. Baughman, K.L. Hypertrophic cardiomyopathy. J. Am. Med. Assoc. 267:846-849, 1992.
2. Ferenchick, G.S., et al. Steroids and cardiomyopathy: How strong the connection? Physician Sportsmed 19:107-110, 1991
3. Kelley, W.N. (ed) Myocardial Diseases, in Essentials of Internal Medicine, Philadelphia: JB Lippincott Co., 1994, , pp 14-19.
4. Maron, B.J. Hypertrophic cardiomyopathy in athletes: Catching a killer. Physician Sportsmed ;21:83-91, 1993
5. Thompson, P.D. Athletes, athletics and sudden cardiac death. Med Sci Sports Med ;25:981-984, 1993.


#15

A freind of mine has recently shown some interest in clenbuterol. I personally dont' like it much (makes my face red, made me sleepy then all sped up in a matter of minutes, made me sweat like a whore in church then have the chills seconds later, I just didn't care for it). I told him all of these things and said if he's serious then I'll make him a diet to follow, give him some otc supps to take, put together a routine ect.ect. be his personal trainer.

He's shy so he doesnt'want to go to the gym to get his bf tested (he can only go when it's busy and he's self concsious, real nice guy though). Anyway, I've always wanted a bdyft testing caliper so guess who just helped pay for most of one? :slight_smile: He's somewhere around 22%, I tested him several times and I also did myself, which was real close to the same as what a trainer friend of mine said I was about 1 month ago, so I'm pretty confident with the measure.

He's making steady progress as is but he's still set on it and I told him if he is still serious when he's at 18-15% then I'll pick him up some along with some t3 and var.I'm going to get clen with ketotifen (mixed). I understand the idea would be that with the ketotifen you can take clen for a longer period of time, however I'm kinda hesitant to reccomend that a freind go over 2-3 weeks with clen.

Imo,it seems like keeping him at say 2 weeks or maybe even 10 days on and 10 days off would be just fine, and running something like HOT-ROX or scorch in the off time. Does this sound reasonable, safe, and effective to all of you?


#16

Cy, you out there?? Help cut through the BS and scientific muddle on this...this stuff sounds dangerous.

MB


#17

This is enough to keep me off clen. Wow. Just wow.

200kcal/day is NOT worth, let me repeat, NOT worth cardiac damage, reduced exercise capacity, or the discomfort of high blood pressure.

I'd rather just go running.


#18

Bumping a 2 year-old thread? Thanks for the advice, we will all take this to heart.

Priceless.


#19

how long would It take of use,to cause probs ?
my cousin did a few cycles of clen with T3 stopped..seem to be know sides..I felt fine..I go to dr. and now T4 is realy high TSH is realy low,did not test T3 im going for T3,T4,TSI,ANTIBODIES TEST THIS WEEK..

he said he used 200mcgs a day of clen and 100mcgs of T3, DID 3-4 WEEK CYCLE..TOOK A 2 WEEKS OFF DID IT AGAIN..I THINK A RD TIME ALSO...?? does not seem to smart..any idea what happen ? or what hes in for..
ps he went to dr. cause of his heart rate..its 100BPM 24/7 even at rest...thanks guys


#20

I prefer taking Cyanide over Arsenic. Cyanide has that kick that everyone should experience at least once.