Liquid Clen/T3/EC Cycle

[IronMax]

What do you guys think of the dosage of this cycle?

Weeks 1-2
Day 1-4 - 40mg Clen/12.5mg T3
Day 5-9 - 60mg Clen/25mg T3
Day 10-14 - 80mg Clen/50mg T3

Weeks 3-4
75mg T3/75mg Ephedrine

Weeks 5-6
Day 1-4 - 40 or 60mg Clen/50mg T3
Day 5-9 - 60 or 80mg Clen/25mg T3
Day 10-14 - 80 or 100mg Clen/12.5 mg T3

Weeks 7-8
75mg Ephedrine

[bjunior]

man I am not that knowledgeable about gear, but I am 99% sure you need to pyramid the T3...up and then down. Personally I would stay away from that ****. You blow out your thyroid, you are fuked??

[IronMax]

the t3 is in a pyramid.. im pretty sure the formula is 5%/40%/55% for T3.. which is 5% of the time on spent ramping up to maximum, 40% of the time is at max dose, and the other 55% is spent ramping down.. i split it up into a 33/33/33 split and im wondering if that would be a legit split and if i should change it.. my time on t3 longer or shorter.. pretty much any knowledgeable input.. im not worried about my dosage of clen or ephedrine..

[IronMax]

anyone??

[jlozan84]

Did you end up starting this IronMax?

How did it pan out?

[vassille]

Hey man, this schedule looks pretty weak. First off, you starting clen/t3 which is more potent than clen/t4. I would say clen/t4 is more for starters and that's what you should use. Secondly, where is the gear? This combo will burn the crap out of your muscle. Thirdly, you do not cycle T3/t4 but use it in a pyramid. If I saw your schedule correctly, you stop T3 for 2 weeks then taper? Not a good idea, take T3 or T4 in your case for 5-6 weeks max in a pyramid.
T4
Ex. 25/25/25/50/50/50/75/75/75/100/100/100/75/75/75/50/50/50/25/25/25 mcg/day.THis is a 21 day schedule. If you take it longer than this then stretch it out.
Clen you take 2 weeks on and 2 weeks off which is fine. Research it more for your own good bro,
hope this helps

[IronMax]

ok.. well i guess when i wrote that i didnt really explain myself.. i'm running a clen/t3 cycle because ive been using ephedrine for nearly 4 years now and the onyl step up is clen.. and as far as t4 for t3.. i didnt have the choice.. t3 is what i could get.. but this is what im running right now.. (no gear.. because the dosing isnt high enough for me to fear catabolism by use of t3, catabolism with t3 starts at 100mg ED and higher.. and clen is ephedrine with a longer halflife and i always am on and off ephedrine and still can put on muscle.. have no fear i read lol)

Weeks 1-3 - T3
12.5/25/50/75/75/75/75/75/75/75/75/75/75/75/75/75/75/75/75/75/75
Weeks 4-6 - T3
65/65/65/65/55/55/55/55/45/45/45/45/35/35/35/25/25/25/12.5/12.5/12.5

Clen
Week 1 - 50mcg CLen
Week 2 - 100mcg Clen/50mg Benadryl
Week 3 - OFF Clen/75mg Ephedrine/75mg Benadryl
Week 4 - OFF Clen/75mg Ephedrine/100mg Benadryl
Week 5 - 75mcg Clen
Week 6 - 100 mcg CLen/50mg Benadryl
Week 7 - Off Clen/100mg Ephedrine/75 Benadryl
Week 8 - Off Clen/100mg Ephedrine/100mg Benadryl
Week 9 & on - 100mg Bendryl tapered

[ResearchChemsOnline]

I would certainly be fearing catabolism with a regimen like that, but if you don't more power to you.

I recommend anyone ditch clenbuterol from their arsenal. There's too much negative information surrounding its use.
T3 and ephedrine should be more than efficient when coupled with proper diet.


Some food for thought:

J Appl Physiol. 2002 Nov;93(5):1824-32. Related Articles, Links

Myotoxic effects of clenbuterol in the rat heart and soleus muscle.

Burniston JG, Ng Y, Clark WA, Colyer J, Tan LB, Goldspink DF.

Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool L3 2ET, United Kingdom. hhsjburn@livjm.ac.jp

Myocyte-specific necrosis in the heart and soleus muscle of adult male Wistar rats was investigated in response to a single subcutaneous injection of the anabolic beta(2)-adrenergic receptor agonist clenbuterol. Necrosis was immunohistochemically detected by administration of a myosin antibody 1 h before the clenbuterol challenge and quantified by using image analysis. clenbuterol-induced myocyte necrosis occurred against a background of zero damage in control muscles. In the heart, the clenbuterol-induced necrosis was not uniform, being more abundant in the left subendocardium and peaking 2.4 mm from the apex. After position (2.4 mm from the apex), dose (5 mg clenbuterol/kg), and sampling time (12 h) were optimized, maximum cardiomyocyte necrosis was found to be 1.0 +/- 0.2%. In response to the same parameters (i.e., 5 mg of clenbuterol and sampled at 12 h), skeletal myocyte necrosis was 4.4 +/- 0.8% in the soleus. These data show significant myocyte-specific necrosis in the heart and skeletal muscle of the rat. Such irreversible damage in the heart suggests that clenbuterol may be damaging to long-term health.


Med Sci Sports Exerc. 2002 Apr;34(4):643-50. Related Articles, Links


Chronic clenbuterol administration negatively alters cardiac function.

Sleeper MM, Kearns CF, McKeever KH.

University of Pennsylvania, School of Veterinary Medicine, Philadelphia, PA, USA.

PURPOSE: Chronic administration of pharmacological levels of beta2-agonists have been shown to have toxic effects on the heart; however, no data exist on cardiac function after chronic clenbuterol administration. The purpose of this study was to examine the effect of therapeutic levels of clenbuterol on cardiac performance. METHODS: Twenty unfit Standardbred mares were divided into four experimental groups: clenbuterol (2.4 microg.kg(-1) twice daily 5 d.wk(-1)) plus exercise (20 min at 50% .VO(2max)) (clenEX; N = 6), clenbuterol (clen; N = 6), exercise (EX; N = 4), and control (CON; N = 4). M-mode and two-dimensional echocardiography (2.5-MHz sector scanner transducer) were used to measure cardiac size and function before and immediately after an incremental exercise test, before and after 8 wk of drug and/or exercise treatments. RESULTS: After treatment, clenEX and clen demonstrated significantly higher left ventricular internal dimension (LVD) at end diastole (+23.7 +/- 4.8%; +25.6 +/- 4.1%), LVD at end systole (+29.2 +/- 8.7%; +40.1 +/- 7.9%), interventricular septal wall thickness (IVS) at end diastole (+28.9 +/- 11.0%; +30.7 +/- 7.0%), IVS at end systole (+29.2 +/- 8.7%; +40.1 +/- 7.9%), and left ventricular posterior wall systolic thickness (+43.1 +/- 14.%; +45.8 +/- 14.1%). clenEX and clen had significantly increased aortic root dimensions (+29.9 +/- 6.1%; +24.0 +/- 1.7%), suggesting increased risk of aortic rupture. CONCLUSION: Taken together, these data indicate that chronic clenbuterol administration may negatively alter cardiac function.

Originally Posted by Nandi (R.I.P.)

Low Dose Clen Induces Cardiac Apoptosis

It's been known for some time that clenbuterol at high doses causes cardiac necrosis. This study in animals shows that doses of 1 mcg/kg BW induce apoptosis (programmed cell death) in heart tissue. Humans not uncommonly ingest this much clen. For instance, in a 220 lb (100 kg) bodybuilder this translates to 100 mcg. The CEM store sells clen at a concentration of 200 mcg/ml! Other UG labs sell it at similar concentrations, ranging from 100 to 200 mcg per ml.


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.