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oratropin and heart hypertrophy @IBE

french_muscle

Member
after all the research and studies I've read on the role of the GH / IGF-1 axis on the cardiac myocytes, that GH and IGF1 are critical in the regulation of cardiomyocyte growth, I was wondering, LR3 IGF-1 (non mediated) should in theory provoke enlargment of the heart right ? But what about OT ? as it's cell mediated, I suppose that (and I Hope) the lr3 IGF 1 only reach skeletal muscle, and when the receptors saturate, it stops delivering the IGF, the explanation is not very precise but you get my point .... In a study involving steroids using athletes and steroids + GH users, they had their heart examinated. In the steroids only group, left ventricular weight increased from 167g (control) to 257g ; ratio left ventricular weight: length increased from 93g/m (control) to 141g/m ; relative wall thickness from 0.37 (control) to 0.42. Now in the GH + steroids group it's even worse : left ventricular weight increased from 167g to 342g ; ratio left ventricular weight: length increased from 93g/m (control) to 191g/m ; relative wall thickness from 0.37 (control) to 0.53. Some abstract :

"Steroids and the combination of steroids and growth hormone change the structure of the heart, the table suggests. But that doesn’t have any consequences for the cardiovascular health of at least the steroid users. Their diastolic blood pressure – reported to rise phenomenally in some steroid related medical horror-stories – was fine, and more interestingly, their E/A ratio improved. Cardiologists use the E/A ratio to measure the hearts efficiency. According to the table, in the steroids only group deterioration of the heart muscle didn’t occur.

But growth hormone, well, that is another story. The table speaks for itself. The higher steroid doses that the GH-users took can only explain a small part of the serious ventricular hypertrophy, the Finnish stress. They suspect that the lowering effect of androgens on the IGF-1-binding protein 3 concentrations causes the ventricular growth "
 
So what if one is taking LR3 IGF-1 by itself, with no androgens? Will that evidence the same effect as that exhibited by AAS/HGH/IGF use?

This is a great question which I asked in another thread but it was never answered. I found anecdotal evidence (in rats) that IFG-1 standalone actually improved cardiac function. But that is in rats, with no real human data.
 
what ??! I downloaded it from a medical website and I just scanned it, no viruses were found. That's weird, what software you use ? (mine is norton and got the latest virus definitions upgrades)
 
This is one reason I have not used tany GH / IGF-1 product. I'm afraid of more growing then just muscles.
 
badbart said:
This is one reason I have not used tany GH / IGF-1 product. I'm afraid of more growing then just muscles.
Click to expand...

From what I understand, it is not going to limit itself to "skeletal" muscle. IGF-1 essentially, from what I understand, induces cells to divide (hyperplasia). Whether they become "muscle cells" or "Heart cells" or "intestine cells" I think is dependent upon alot of factors. If your muscles are stressed and torn, they may send out chemical signals indicating that they need some satellite cells to convert into muscle cells. I don't know what the rate of conversion is. Some parts of the body have a higher turnover rate in terms of cells and have faster rates of cell division. I imagine that your intestines, stomach, liver all have higher rates of cell division, and therefore, have a high affinity for these satellite cells. I do IM injects directly into chest, bicep, lats, etc. hoping that it will induce only localized growth. In another thread I believe Einstein or Bobo produced an article with some anecdotal evidence that locallized IM injections do indeed allow for more locallized hyperplasia.

Again, as with all things, there are individual sensitivities. But most effects I would imagine are governed by a dose-response relationship. High doses for an extended period of time may cause permanent changes. lower doses for a short period of time may allow for more "acute" negative side effects versus permanent long-lasting negative side effects.

Of course, these are just my own opinions. I could be completely wrong. I guess I'll know in about 20 days when my current "research project" is over, and I am able to better judge what negative effects occurred. Although blood work will not be performed so it will be hard to determine.
 
It's a big unknown as always. Cardiac hypertrophy is just a fact of life for any PL, BB or anyone using AAS. Now that people are finally studying this, hopefully we can get a better idea how bad or good it is, what the safe limits are et cetera.

It's been fairly well established that high level atheletes have shortened lifespans regardless of drug use.

He who burns twice as bright, burns half as long.
 
re: He who burns...

Watch Blade runner! Great movie loadsa quotes.

Hasn't OT-1 been developed to only released and be active when the receptor site is free and aren't the side effect you are mentioning in the heart linked more to abuse, than use????

Mr Tee (A wanna be user of OT-1)
1st post, not looking to piss anyone off... Yet ;-)
 
Mr_Tee said:
Watch Blade runner! Great movie loadsa quotes.

Hasn't OT-1 been developed to only released and be active when the receptor site is free and aren't the side effect you are mentioning in the heart linked more to abuse, than use????

Mr Tee (A wanna be user of OT-1)
1st post, not looking to piss anyone off... Yet ;-)
Click to expand...

Glad to see you made it over!
 
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