I have been dosing clen off and on for cycles for the past couple of years. Maybe three or four 1 month cycles in the last 2 years, as well as peptides here and there.
My recent ECG showed that I have an enlarged right atrium and an enlarged left ventricle. I now have to see a cardiologist to determine the severity of these issues but I fully attribute them to peptides and clen use.
Just an FYI y'all.
LOT of Bro Science going on in this thread. First off, anyone who lifts heavy weight often or trains intensely in other forms (does a lot of sprinting, etc.) will have an enlarged left ventricle (aka athlete's heart). Second, It's unlikely that peptides enlarged the heart as they do NOT substantially raise IGF levels for prolonged periods of time like GH does (thus why they dont work as well for fat loss, etc.) Comparing IGF levels from peptide use (or even direct IGF use) to that of someone running 4-5iu of GH for 4-6 months would be laughable. Third, the type of heart damage caused by Clen is not an enlargement, but rather apoptosis or heart muscle cell damage/death (see study below). Finally, high dose GH/AAS (especially in combination) can cause enlarged heart. Several studies show the two in unison seem to have a synergy for this. But it is unlikely that the Clen itself and peptides caused this enlargement. Clen simply is not noted for causing heart enlargment - just trying to separate fact from fiction. However,
Clen is NOT good for the heart when used in high doses and often. Enlarged hearts run in my family so I have done some reading on this. You, like me, could just have a genetic propensity to have a slightly enlarged heart. AAS/GH and weight training itself further enhances this.
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 - a common high end dose.
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.
One could speculate that the apoptosis, if extensive enough, could cause a thickening of the heart walls and a reduction in output/volume (i.e. heart failure) but I do not believe a literal ENLARGEMENT phenomenon is going on, at least not that I have read about.
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