Why gains slow!

http://www.ncbi .nlm.nih.gov/en … t_uids=11479135

This is a very good read. Hit the "JOE" link to read the paper in full. The types of exercises that stop blood flow, even for a short amount of time might lead to fibrosis and a drastic slowing of gains. We all know that gains slow with time and this just might be why.
What do you guys think?

This is talk of the dangers of Priapism in the discussion as well so those who are considering it as a form of PE should read this as well.

Cheers,
PS

PDGF is the culprit in the last article but it may also up regulate the penile androgen receptors:

http://www.ncbi .nlm.nih.gov/en … st_uids=8499343

This may be why we gain when we clamp. It may also be why gains slow.

It is not easy to read but it may change the way we think about PE.

I read the first one, but don’t have enough time to absorb the second one just now (though I read the abstract).

I think it’s interesting that it says estradiol downregulates the AR. It also sounds like another reason why finasteride might not be good for PE (as well as the findings by Cya at 8 of the structural irregularities in the CC that it caused).

Do you think that a mild aromatase inhibitor might have a positive role to play?

It also makes me wonder about Supras experiment with creating a priapism like environment while administering DHT + IGF-LR3: Was he was inadvertantly upregulating the AR and PDGF expression?

I think I read that Stinging Nettle is supposed to be an aromatase inhibitor.

I didn’t know rats had penis’ like people, I seen a show on Discovery or TLC about animal penis’, and they showed that most animals had penis’ that were made erect with an actual bone, and they showed a few of the different penis bones of different animals like a hamster and horse etc.

Though I didn’t read it, can someone possible posts the results/analysis of this test in plain english. So I should know what not to do or what to do? Forgive me for not searching, what is priapism?

Well, I am not sure yet. There is evidence here that exercises that retard the flow of blood might result in a toughened and therefore less pliable and less easily enlarged penis. There is also evidence that retarding blood flow might trigger a cascade of events leading to a larger penis.

Be careful with these terms though. If ones penis goes without fresh blood for too long, as we all know, the tissue will die and one will have no penis.

I am hoping more people will read the links and offer input.

Shiver,

“I read the first one, but don’t have enough time to absorb the second one just now (though I read the abstract).

I think it’s interesting that it says estradiol downregulates the AR. It also sounds like another reason why finasteride might not be good for PE (as well as the findings by Cya at 8 of the structural irregularities in the CC that it caused).

Do you think that a mild aromatase inhibitor might have a positive role to play?

It also makes me wonder about Supras experiment with creating a priapism like environment while administering DHT + IGF-LR3: Was he was inadvertantly upregulating the AR and PDGF expression?”

I am still thinking about all of this. Whenever I start to respond to these question I start thinking, “well, what about this or that paper”, this is all very complicated for me. I just don’t know at this point.

Redwood,
Bones in their penis. Wow, that is new to me. I should have known that but didn’t. I don’t know about rodents.
Cheers,
PS

Good food for thought, Penismith.

Nevadathomas,

In a nutshell, the first study indicates reducing blood flow to your dick raises PDGF. But excessive PDGF may cause problems.

The second abstract is a study where the researchers squirted various things on bits of rat dicks. “With the exception of PDGF none of the treatments affected significantly cell growth, as measured by DNA synthesis and content.” This doesn’t tell us much. PDGF apparently affected cell growth, but by how much? And what was it growing, the fibrous crap we don’t want?

Given the possible implications of the first study, deliberately strangling a penis to raise PDGF strikes me as foolish.

Sensible PE routines seem to help maintain or increase circulation to and within the penis. The study provides one possible mechanism by which maintaining a healthy blood flow preserves penis health.

Perhaps I should make clear that when I’m talking about increasing collagen deposition, it is with the ideas in mind from the thread of Bud_do and papaya/bromelain (Papain from papaya latex).

The angle I have not figured out is that in one way we want new growth because, well, we want new growth. On the other hand we don’t want growth that contains our existing dimensions (crosslinking fibres, thickening of fibres or scar tissue).

The muddled idea that I would like to see clarified is "can we encourage new collagen growth while minimising crosslinking that would limit increases in size?". Hope that makes sense.

>Do you think that a mild aromatase inhibitor might have a positive role to play?

Personally, I doubt it would do anything to help PE gains. We had a lengthy discussion a while back about the futility of using androgens as a PE aid. Decreasing estrogen shouldn’t make any difference either.

Yea, I agree with this. Although the mechanism is unknown, I have read that our ARs decrease anywhere from 3 to 8 fold at the end of puberty. Based on anecdotal evidence, it does not seem likely that one can cause growth by saturating the remaining ARs with testosterone or similar molecules. It is also not clear that the remaining AR receptors are functioning in an identical way to those during puberty or that the distribution throughout the tissues is the same.

What I want to know is, what happens at the end of puberty that leads to the decrease. To answer this question I have been reading these articles:

/forum/newreply … wreply&p=291067

and requested the help of a very competent individual here at thunders.

Cheers,
PS

Yea, the second study is not as good but we do know that they are working with rat smooth muscle cells that are growing in vitro (or out of body, probably in a petri dish). I think the measuring of DNA content is a good way to measure cell number because each cell, no matter the size has the same amount of DNA, unless it is in the process of dividing. The fibrous crap is the scaffolding made of protein which is located out side of the cell. I am not even sure how much of a “limiting factor” this stuff is, I mean, does it give easily after the other tissues gives or is this stuff making girth gains darn near impossible for some of us?

It is also not clear how much of a blood flow restriction is required to produce the fibrous crap. We might be building it each time we do a Uli, or maybe none of us are making it.

It is quite attractive to consider that this might be the “conditioning” that takes place and that we can work around this somehow.

Cheers,
PS

Are you sure you pasted the correct url there? I get the reply screen to this current thread when I click that.

http://www.ncbi .nlm.nih.gov/en … rom_uid=9537291

Sorry

I’ve read quite a few of those now, and it’s becoming clear that TFG-beta1 at least (and possibly beta2, 3) is involved in the regulation of cell growth. By that I mean it’s purpose seems to be to keep things in check and prevent out of control growth. Fibrosis seems to be one of those results.

It also seems that AR downregulation alone will not prevent growth (though it may limit rate).

My main concern is that if you negate the ‘cell police’ in order to encourage growth, and there is damaged DNA, tumors or other undersirable states, then because we cannot precision administer we could be asking for trouble.