Clenbuterol

Dylndob - Yes

Pete

Cheers pete, can start my cycle today

ORIGINAL: PartyBoy


Commonly employed dosing protocols

It is well known that Clenbuterol use results in rapid down-regulation of beta 2 receptors. This is due to the powerful stimulatory effect of the drug. It is therefore pointless to use Clen for long periods without a break. Some believe that a 2 day on, 2 day off dosing schedule will allow adequate potential for receptor up-regulation. However, I doubt this to be the case due to the relatively long half life of Clen, resulting in continued stimulation even throughout the ‘off’ days. A much better regime would be a 2 week on, 2 week off cycle.

I disagree, with all due respect.
In one study, horses given a semi-reasonable dose of clen (slightly over 1mcg/lb x2 a day) and excercised for 20mins, 3x a week ( I suppose they were Mentzer disciples) had significant decreases in %fat (-17.6%) and fat mass (-19.5%) at week 2, which was similar to Clen given to horses who didn’t excercise; in contrast, the excercised group had a different FFM response, which significantly increased (+4.4%) at week 6 (3). Week 6! (*Reference below)

So Let’s re-examine that first point I made: Clen vs. clen+excercise produce roughly the same results for the first 2 weeks! This means you are barely getting any additional results for the first 2 weeks over excercise alone! And then you reccomend going off the clen? Whats the point? I mean...all of tells me that the 2 weeks on and 2 weeks off schedule for clen dosing is far from optimal, and if you want the quasi-anabolic effect from the clen, it’ll take more than 2weeks on (6 weeks apparently)*. 2 weeks on and 2 weeks off will negate the possibility of the anabolic effect, since clearly it doesn't manifest itself until much later down the road. In addition, since clen alone is similar to clen+excercise for those first 2 weeks...why would you ever use a 2on/2off protocol?
Reference:
(*)J Appl Physiol 91: 2064-2070, 2001; 8750-7587/01
Chronic administration of therapeutic levels of clenbuterol acts as a repartitioning agent
Charles F. Kearns1, Kenneth H. McKeever1, Karyn Malinowski1, Maggie B. Struck1, and Takashi Abe2

ORIGINAL: PartyBoy
During the 2 ‘off’ weeks, an ECA stack can be used as required. ECA will not cause such a pronounced down regulation and desensitization of the receptors, certainly not to the extent of Clen. Ephedrine has a short half life in contrast to Clen which results in times throughout the day where the beta's will partially recover from stimulation by adrenaline and nor-adrenaline. Potency is also much weaker that that of Clen, as it is not a specific agonist...

How can you reccomend using ECA in the off weeks from clen? You won't upgrade your beta-2 receptors...you'll just further downgrade them. As you can see from the graph below(ephedrine is represented by the the solid circles), ephedrine reduced Beta-2-AndrenergicReceptor levels to 32% of the control level after 24 hours. Read this again:

Ephedrine, in this study, reduces Beta-2 receptor levels to 32% of control after 24 hours. How can you reccomend using it to upgrade your receptors at all? Ephedring sucks 2/3rds of your beta receptor levels away within 24 hours! And you think it will upgrade them when compared to clen? Do you have a study showing it doing this at all, or that clen sucks more then 68% of your receptor efficiency away in the same time period? Because from what I see, it absolutely bangs your beta-2's down to 32% effeciency after 24hours, and thats not going to upgrade anything!

Here's that chart, taken from a medical journal:



Chart taken from: ASPET Journals, Vol. 58, Issue 2, 421-430, August 2000
Kinetic Analysis of Agonist-Induced Down-Regulation of the 2-Adrenergic Receptor in BEAS-2B Cells Reveals High- and Low-Affinity Components
Bruce R. Williams, Roger Barber, and Richard B. Clark

I don't want to come off rude or anything, but you are reccomending the 2-week on/off thing, which really (as I've shown) isn't using clen maximally, and then you reccomend taking something to upgrade your beta-2's that absolutely destroys them...

Can you point me to any studies verifying your claims? I've referenced two studies that I think invalidates your claims, but if you have something supporting your claims, please post it...or e-mail it to me, because I am very interested in where your information is from.

Partyboy wuts up?? do u still think its bull ****???

How would the author defending his point of view mean there is "something up" with me??

Study suggesting strong down regulation of beta-2's in mice after 12 days:

Am J Physiol Regul Integr Comp Physiol. 2002 Jan;282(1):R317-22.

A farnesyltransferase inhibitor attenuated beta-adrenergic receptor downregulation in rat skeletal muscle.

Lavoie JL, Calderone A, Beliveau L.

Departement de Kinesiologie, Universite de Montreal, Montreal, Quebec, Canada H3C 3J7.

Farnesylation represents an essential posttranslational modification of several well-defined proteins implicated in the homologous desensitization of the beta-adrenergic receptor (beta-ADR). The following study examined the effect of a novel farnesyltransferase inhibitor, BMS-191563, on agonist-mediated beta-ADR downregulation in skeletal muscle. Female Sprague-Dawley rats were treated for 12 days with the beta2-adrenergic agonist clenbuterol (4 mcg/kg) with or without the concurrent administration of BMS-191563 (2 mg x kg(-1) x day(-1)). Clenbuterol promoted gastrocnemius muscle hypertrophy, whereas the soleus muscle was unaffected. Total beta-ADR density was decreased by 45 and 40% in the soleus and medial gastrocnemius (MG), respectively, after clenbuterol treatment.

Extract taken from mindandmuscle.net (author "Loki")

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).

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


....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.

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

other "studies" - some more relative than others:

Brain Res Bull. 1996;41(2):93-6.

Down-regulation of rat beta-adrenoceptors by clenbuterol or desipramine does not require chronic treatment: [3H] CGP-12177 binding reveals rapid (24 hour) modulation.

Newman-Tancredi A, Verriele L, Chaput C, Millan MJ.

Department of Psychopharmacology, Institut de Recherches Servier, Paris, France.

Desipramine (DMI, 15 mg/kg, s.c.) decreased [3H]CGP-12177-labelled cortical beta-adrenoceptor density (Bmax) by 30% upon chronic (14 day) treatment. However, even a single dose (in mg/kg) of DMI (15) or the beta-adrenoceptor agonist, clenbuterol (20), induced a rapid (24 hour) and significant reduction of beta-adrenoceptor Bmax (-15%; p < 0.01). Acute treatment with amitryptiline (10), clorgyline (1), fluoxetine (10), nomifensine (10) or maprotiline (20) had no significant effect on [3H]CGP-12177-labelled beta-adrenoceptors, suggesting that rapid down-regulation may not be a general property of antidepressant drugs. None of the antidepressants altered the Bmax of [3H]ketanserin-labelled 5-HT2A receptors on acute treatment. These results show that beta-adrenoceptor down-regulation by clenbuterol and DMI is not dependent on chronic treatment and may, therefore, be a poor correlate of the gradual onset of therapeutic efficacy seen clinically with antidepressant drugs

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Equine Vet J. 2002 Sep;34(6):587-93

Regulation of equine lymphocyte beta-adrenoceptors under the influence of clenbuterol and dexamethasone.

Abraham G, Brodde OE, Ungemach FR.

Institute of Pharmacology, Pharmacy and Toxicology, Faculty of Veterinary Medicine, University of Leipzig, Germany.

In 12 healthy horses, the effects of the beta2-agonist clenbuterol and the glucocorticoid dexamethasone on the lymphocyte beta2-adrenoceptor density and affinity (determined by (-)-[125I]-iodocyanopindolol binding) as well as its responsiveness (assessed by lymphocyte cyclic AMP [cAMP] responses to 10 micromol/l (-)-isoprenaline) were studied. Clenbuterol treatment, 2 x 0.8 microg/kg/day i.v. for 12 days, decreased significantly ICYP binding sites by approximately 30-40%; concomitantly, lymphocyte cAMP response to (-)-isoprenaline was reduced. After withdrawal of clenbuterol, beta2-adrenoceptor density and responsiveness gradually increased, reaching predrug levels after 4 days. The effects of dexamethasone on clenbuterol-induced desensitisation were further investigated. Administration of dexamethasone (1 x 0.1 mg/kg/day, i.v. for 5 days) immediately after clenbuterol withdrawal accelerated beta2-adrenoceptor recovery: only 24 h after administration dexamethasone restored the number of binding sites and cAMP response to (-)-isoprenaline to levels statistically indistinguishable from values before clenbuterol treatment. Three days after dexamethasone administration, lymphocyte beta2-adrenoceptors were further increased about 2-fold the pretreatment values, and this increase declined gradually after dexamethasone withdrawal, reaching baseline values after 4 days. Furthermore, in groups exposed simultaneously to both drugs, dexamethasone completely prevented clenbuterol-induced decrease in lymphocyte beta2-adrenergic receptor density and responsiveness. No significant change was observed in the dissociation constant for ICYP in any of the situations. We conclude that dexamethasone (glucocorticoids) can reverse and prevent Clenbuterol-induced desensitisation (down-regulation) of the lymphocyte beta2-adrenoceptors and therefore, a combined therapy with clenbuterol and dexamethasone may be potentially beneficial in horses suffering from chronic obstructive pulmonary disease (COPD).

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Am J Physiol Regul Integr Comp Physiol. 2002 Jan;282(1):R317-22.

Implications of feedback regulation of beta-adrenergic signaling
S. E. Mills
Department of Animal Science, Purdue University, West Lafayette, IN 47907

Pigs fed βAR ligands show a rapid response in growth and feed efficiency that tends to peak during the first 7 to 10 d but declines thereafter toward zero by approximately 6 wk. A similar pattern was reported in rats fed clenbuterol and was accompanied by a 50% reduction in βAR in skeletal muscle. Compensatory desensitization is a well-characterized response to chronically elevated agonist concentration that results in a net loss of beta-adrenergic receptors (βAR) from the plasma membrane and reduced tissue response. The ability of βAR agonists to affect pig growth and alter body composition may well be limited by βAR desensitization.

Regarding the possibility of muscle anabolism from Clen, there are many studies to suggest that anaerobic and aerobic capacity are diminished following clenbuterol, which to me would indicate direct muscle/strength loss, or indirectly - possibly as a result of decreased cardiac function. However, as you'd expect, the results are often contratictory from such "studies".


It has proved beneficial to mice with muscular dystrophy, yet deleterious to excercise performance in rats and mice:

Dupont-Versteegen, E. et al. 1995. Muscle and Nerve. 18:1447-1459.
Duncan, N.D. et al. 2000. Clinical Science. 98:339-347.
Zeman, R.J. et al. 1994. Am. J. Physiol. 267:C865-C868.
Ingalls, C.P. et al. 1996. J. Appl. Physiol. 80:795-801.

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Again, courtesy of mind and muscle, with references:

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).

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

imo it would be foolish to hail an opinion as gospel on the basis of the odd animal study here and there. Sure, they are useful to provide us with indications of what could be expected if replicated in humans, but as I'm sure you're all aware, you'll be hard pressed to not find a "study" to suggest that whatever you might be saying is actually true. Indeed, supplement manufacturers have been taking advantage of this fact for years!

As is the case when discussing steroid usage, it is rare to find an area that is truly black and white. Unfortunately, there are no rights or wrongs, merely suggestions based on a myriad of factors ranging from empirical data to experimental animal studies, and if we're very lucky, data derived from epidemiological studies.

There may indeed be some who respond more favourably to periods of longer duration, others may not. Personally, due to the nature of the drug (its potential for cardiac harm) and imo the inconclusive evidence to prove catagorically that longer cycles are "better", I will continue to advise that a 2 week on, 2 off protocol be used.

found it. this is what i was looking for. i remember this was posted on the first page awhile back. do you think it's still valid?

Example of a first cycle:

* Day 1: 20mcg
* Day 2: 40mcg
* Day 3: 60mcg
* Day 4: 80mcg
* Day 5: 80mcg(Note: Increase the dose only when the side effects are tolerable)
* Day 6 - Day 12: 100mcg
* Day 13: 80 mcg (Tapering is not necessary, but it helps some users get back to normal gradually)
* Day 14: 60 mcgs
* Day 15: off
* Day 16: off
* Day 17: ECA/ NYC stack

Example of a second cycle:

* Day 1: 60mcg
* Day 2: 80mcg
* Day 3: 80mcg
* Day 4: 100mcg
* Day 5: 100mcg
* Day 6 - Day 12: 120mcg
* Day 13: 100 mcg
* Day 14: 80 mcgs
* Day 15: off
* Day 16: off
* Day 17: ECA/ NYC stack

Looks reasonable bro but there's really no need for the taper down. The long half life acts as a natural taper.

after 2wks on clen is there much of a 'crash'? If using 2wk clen 2 wk eca for 12 weeks then stop using eitehr after that period whats the effect likely to be?

No not really mate, due in part to the long half life of clen.

2 weeks isn't long enough to risk any dependancy on eph either.

i started a course of clen last wednesday (18/05/05) on top of my juice cycle (test cyp, eq, d bol) which was started on the monday before(16/05/05). began with one tab of clen to see if i reacted ok to it and i felt fine(no shakes), then the next day two tabs then three the next, still had no shakes but on the thursday(19/05/05) i woke up with pains in my stomach, a dull ache like i've been winded, didn't think much of it as i trained legs the day before and thought i had just strained a bit to hard. but it is now 5 days since (24/05/05) and i still have the pain! could this have anything to do with the clen? you said about it can cause muscle cramp but i stopped taking it after three days and yet as i say the ache is still there?!

Possible as clen's half life is long, so it sticks around for a while. I would be more inclined to suspect some kind of gastro-intestinal upset possibly caused by the d-bol though.

btw, why are/were you running clen whilst running what looks like a bulking cycle? (And please don't say to keep the fat off lol)

i read that cyp and eq would give you good lean gains without making you to puffy, i only threw the d bol in as i have a load lying about, should i leave the d bol out? also the clen i'm told is good at stimulating muscle growth aswell as burning fat.

Yes cyp & Eq is fine for cutting. D-bol will bloat you make cardio very difficult - not ideal when you're cutting as I'd assume cardio features strongly in your regime.

Clen won't put any muscle on you. It has been shown to be mildly anabolic in animal, but not human studies, as mentioned here:


http://www.muscletalk.co.uk/article-clenbuterol.asp

hey PB, doing some research on clen , and was just wondering what would be ideal for me? im like 190, 5'8, really overweight 18 yrs old. Im not really into takin ECA stack ( this is ephadrine/caffeine right ?) I want to lose about 35-40 lbs. getting pretty cut. So would taking winstrol help in this process ? So would i do clen/wintrol for 2 weeks then just winstrol for the other two, repeating for about several weeks ? If not winstrol, what other steroid would help me get nice and defined ? What procedure would be necessary with a clen/steroid cycle? Again, i want to lose alot of fat, but yet be pretty cut up. Obviously will maintain good cardio/weight/diet training. A multivitamin would be good to everyday ? Thanks in advance

ORIGINAL: MuscleStyLez

hey PB, doing some research on clen , and was just wondering what would be ideal for me? im like 190, 5'8, really overweight 18 yrs old.

Welcome to the board. The first thing you must realise is that drugs are no subsitute for hard work. By hard work I refer to hard regular training, a good scheduled cardio routine, and your diet nailed. Without these basics in place you will not lose weight - drugs or no drugs.

Im not really into takin ECA stack ( this is ephadrine/caffeine right ?)

Out of interest, what are your reasons for this avoidance?

I want to lose about 35-40 lbs. getting pretty cut. So would taking winstrol help in this process ?

No it wouldn't. Of this I have no doubt. Steroids do not shift fat and will not cut you up. The only reason bbers use steroids whilst they are cutting is to minimise/avoid any muscle losses whilst they are generally in a catabolic state from calorie restriction. That said, using steroids for this reason isn't particularly necessary imo unless you are either above or very close to your genetic muscular limit (highly unlikely for 90% of us on here), and/or whilst trying to shed the last few lbs to attain a %BF of sub 10% where the individual may need to drop cals/increase cardio quite harshly to achieve the goal.

So, from the information you have supplied, there is no need whatsoever to use any form of steroid. Aside from the reasons already supplied, there is also the major issues associated with teenagers using steroids and the complications that can follow.

what other steroid would help me get nice and defined ?

As said, NONE. If just doesn't happen I'm afraid. There is no easy, quick fix for fat loss. It's all down to your efforts implementing the basics as outlined above.


From your current situation, I feel there is no need for you to use any fat loss aids (Eph, Clen etc etc) at this stage as merely manipulating your diet/cardio/training should literally see the fat dropping off you. Don't look for a quick solution - its not a good idea. The fat didn't get deposited quickly and it won't be lost quickly. It is a gradual process of physique adjustment. Aim to lose around 2lb per week consistently.

After 3 months, you should be very near your target and you will probably notice that weight loss may become more difficult as the body tries to hold on to remaining fat stores and metabolism is reduced. This is the time where you should be considering cranking up the fat loss again through aids such as clen, not anytime before.

Hope this helps.

is 20mcg the same dose as .02mg?

Yes

Has anyone come across 40mcg tabs of clen produced by Generic Labs??