The Penis (smooth) Muscle Theory

I think I have failed to point out how important I think this discussion is. Thank you all for developing this thread because knowledge of the composition of the penis is paramount in importance when it comes to refining PIs, developing routines, avoiding injury etc.

Hey guys,

I am glad to see this thread is getting so much attention. I love these types of discussions!!! I haven’t been able to do more than skim the thread, but I will soon. There is one thing I noticed, and I feel obliged to point it out:

I believe there are only two documented scientific articles on megalophallus. Perhaps there is more — and if so, I’d love to read them. But here are the two I found:

and

The first one is the newest one (published in year 2000, I believe). Anyways, it is important to note that both of these articles published hypotheses for the priapism-induced-megalophallus. One of these reports (the first one, if my memory recalls correctly) stated that the penis might have enlarged because of a loss of tunica elasticity. The way I understand it, this was their best guess.

I’m pretty sure there was no evidence backing up these claims. Therefore, just because the doctors that published this article hypothesises a loss of tunica elasticity caused the megalophallus, this doesn’t necessarily mean they are right (or wrong, for that matter.) Just a thought. :)

OK fine, I’ll do it:

That’s my memory as well. Thanks for the clarification.

Hey remek,

I think that the evidence is actually pretty good.

"Comment

Megalophallus has been previously reported,[2] but it is not generally recognized as a sequela of priapism. In our patient, this complication developed immediately after a prolonged and intense episode of priapism 9 years before the patient presented to us. This sequela did not interfere with subsequent erections. Fibrosis of the corpora cavernosa, as previously hypothesized, [2] should result in low flow by Doppler imaging. The reverse was true in our patient.

We propose an alternative mechanism for this sequela. The increase in penile circumference follows a sudden and permanent loss of elasticity of the tunica albuginea, brought about by a particularly intense priapism and a very engorged organ. The loss of elasticity of the tunica albuginea releases constraints on the corpora cavernosa, which then expand like a sponge. This expansion, helped by some subtunical venous impairment that is secondary to the remaining elasticity of the stretched tunica, results in pooled, deoxygenated blood in the corpora cavernosa consistent with our BOLD-MRI findings. BOLD-MRI defines the presence of deoxygenated blood, eliminating the need for an invasive procedure.

The plausibility of this mechanism for megalophallus is supported by the lack of increase in the circumference of the glans in our patient and the one previously described. The glans penis sinusoids are larger and the tunica albuginea is absent, and thus do not provide the bases for the pathologic features observed. The decreased elastic compression of the tunica explains the lack of pain despite the enlargement of the penis. The residual elastic restraint to expansion produces moderate blood stasis, explaining our BOLD-MRI findings. Finally, conservation of the capacity for full erection is due to the intactness of the corpora cavernosa and the infratunica venule system."

1) Megaphallus developed immediately after a long and intense priapism.

2) The size of the glans didn’t increase.

3) The pooled blood strongly suggests that the tunica is permanently expanded.

If there was massive cell growth of the smooth muscle, it would take awhile to develop and the glans should have grown as well.

http://www.ncbi .nlm.nih.gov/en … l=pubmed_docsum

Nice work.

With risk of turning this thread into an ugly mess, I’d like to ask if anyone has an idea about smooth muscle and testosterone, as in steroids or similar. Beneficial, detrimental or no consequence?

It is important for penile smooth muscle function. The enothelial (thin layer of cells that line the interior of blood vessels) and smooth muscle cells of the rat penis require it.

T supplementation (in castrated rats) completely restored PDE5 expression, erectile response to ES (electro stimulation of erection) and responsiveness to PDE5 inhibitor.

Testosterone regulates PDE5 expression and in vivo responsiveness to tadalafil in rat corpus cavernosum.

Zhang XH, Morelli A, Luconi M, Vignozzi L, Filippi S, Marini M, Vannelli GB, Mancina R, Forti G, Maggi M.

Andrology Unit, Department of Clinical Physiopathology, University of Florence, V.le G. Pieraccini, 6, 50139 Florence, Italy.

OBJECTIVES: To investigate the effect of testosterone on PDE5 expression and PDE5 inhibitor tadalafil in vivo responsiveness in a rat model. METHODS: PDE5 expression was localized by immunohistochemistry in the rat corpus cavernosum (CC) and quantified by both real-time RT-PCR and Western blot analysis in several tissues. In the in vivo study, control, castrated and testosterone (T) supplemented castrated rats were treated with acute or chronic oral tadalafil. Erectile function was evaluated by monitoring intracavernous pressure (ICP) following electro-stimulation (ES) of the cavernous nerve and intracavernous injection of NO donor, sodium nitroprusside (SNP). RESULTS: Rat CC expressed the highest PDE5 mRNA level. PDE5 was specifically immunolocalized in endothelial and smooth muscle cells. Surgical castration induced a significant reduction of PDE5 gene and protein expression (p<0.05), and ES response at all stimulation frequencies (p<0.001). T supplementation completely restored PDE5 expression, erectile response to ES and responsiveness to PDE5 inhibitor. Both acute and chronic tadalafil treatment were ineffective in ameliorating the ES response in castrated rats. Injection of increasing concentrations of SNP in castrated rats resulted in a statistically significant increase in ICP/MAP ratio as that observed in intact rats. In addition, tadalafil did not amplify the SNP effect in castrated rats at all the doses tested (0.06-6 nmoles). CONCLUSIONS: Our findings demonstrate that testosterone positively regulates PDE5 expression and in vivo responsiveness to PDE5 inhibitor, tadalafil, in the rat CC.

http://www.ncbi .nlm.nih.gov/en … l=pubmed_docsum

Getting back to the megalophallus business, I see an inconsistency in the idea that it is caused by a loss of tunica “elasticity.” As far as I understand it, the tunica isn’t supposed to be “elastic,” at least not once it’s unfurled to it’s erect dimensions. It’s supposed to be tough and inelastic. If anything, it seems that megalophallus may be caused by tunica elasticity, not lack of elasticity.

Anatomy of the Human Penis: The Relationship of the Architecture Between Skeletal and Smooth Muscles

Full article:

http://www.andr ologyjournal.or … t/full/25/3/426

and attached.

Interesting, it looks like base thickening due to hanging, etc, might result from skeletal muscle development.

In trying to answer your question I dug this old thing up again:

http://www.ncbi .nlm.nih.gov/en … l=pubmed_docsum

I don’t have online access to articles dating this far back from this journal but someone else might. It might contain the answer.

I think you might be right. There are a fair number of prostaglandin E2 receptors in the human corpus cavernosum:

http://www.ncbi .nlm.nih.gov/en … l=pubmed_docsum

and prostaglandin E2 has a crazy "ripening effect" on the cervix during birth which Shiver pointed out and is well described here:

Online-Ambulance.com is for sale | HugeDomains

When I think about that and the use of PGE1 in the patent I can’t help but to wonder if the presence of it during long duration erections somehow changes the elastic properties of the tunica.

But I do feel confident that the tunica has a fair amount of elasticity because I do some extreme exercises to get my 5.5 inch girth up to 6.25 inches over several hours for sex and I don’t get much fluid build up in the process.

>>>But I do feel confident that the tunica has a fair amount of elasticity because I do some extreme exercises to get my 5.5 inch girth up to 6.25 inches over several hours for sex

And if your tunica were sufficiently inelastic, its capacity would remain at that bloated 6.25” forever thereafter (after the deformation from its initial state, that is).

Along the subject of tunica elasticity, are we talking only about girth? I think length and girth need to be looked at separately. Girth gets kind of complicated, because the “tunica” surrounding the CS is very thin compared with the one around the CCs. I wonder whether some or perhaps most of the girth expansion you (PS) see is due to CS expansion.

The only mechanism I know of that might explain why long duration clamping can immediately increase girth is visco-elastic creep. PGE2 might be another factor. Frankly, that might be the most interesting one. If PGE2 can “rip” the cervix (haven’t read the link but I assume it’s referring to dilation and effacement), it seems to have an ability to “unglue” cross-linkages between collagen fibers.

I don’t see that effect as relating to elasticity, at least in the short-term sense, but to reorganization of existing tissues.

Very interesting stuff. I’ll come back and read your links after my meeting :) .

MM and PG

Yes. In all of my years of PE I have only gained about a half inch of permanent girth. If I go a few months without PE I loose a little of that half inch but it comes back within a week when I resume so that loss might be due to erection quality.

When I do this:

Extreme Extreme Ulis

which I haven’t actually done in awhile, I can get up to about 6.25 inches and it is hard to know but I think that about a quarter inch at most is fluid build up. When doing this, my girth is bigger for awhile but when I quit, my gains are lost. I suspect that this 6.25 inch girth is the elastic limit of my tunica. Maybe, if I were to maintain the 6.25 inch girth for several hours straight, I would destroy the elasticity of my tunica and have a girth of 6.25 inches forever after. I don’t know and I never intend to find out because I think that I have already moved way past the limits of safety (the dick becomes covered in scabs due to skin tearing) with what I have done and I should thank my lucky stars that my penis still works properly.

So, I guess I am saying that a rock hard erection in the absence of PE is not the elastic limit of the tunica, although the rigidity of such an erections leads one to believe so. Those who have clamped know that they can exceed this volumetric limit after a period of work but the question then becomes, where does the limit lie I suppose it lies at the point where the longitudinal and lateral bundles are all straightened out and for me, I think this happens, perhaps, at a little over 6 inches.

Hmm, now I am starting to think that I might be wrong about the smooth muscle. Our penises retract in the cold because the smooth muscle contracts and when we are ererect the smooth muscle is relaxed. We know that we can have a partial erection that is somehow girthier than a rock hard erection and softer at the same time. This has been attributed to the "penis is a volume limited bag" theory but that is probably wrong. My erections after Uli work are of a greater volume than my normal erections.

Where am I going with this. Oh, yea. Perhaps you guys are right. Priapism induced megaphalus might result from a disruption of the ability of smooth muscle to contract and thus allow for the collagen bundles to fully align. Forgive me if I ramble, I only slept a few hours. An extended priapism could lead to a sudden loss of smooth muscle tone and there by lead to a sudden gain in size.

The stiffness of a rock hard erections suggests that the tunica is at its elastic limit but we can get partial erections of greater girth so perhaps the high degree of rigidity is more the result of an interplay between smooth and perhaps skeletal muscle (see the paper I linked yesterday). Extreme uli work, or clamping for that matter might result in a tiring of the smooth (and maybe skeletal) muscle in the short term and maybe smooth muscle growth or loss of function due to damage in the long term.

Does this mean that we cant stretch the tunica? Body builders stretch the tunica surrounding muscle. But the penis is a very unique structure and I really don’t know if we can or not.

I am finally getting some time to divulge myself into this thread a little bit more. I’m starting on page 3:

I remember reading this article some time ago. The procedure looked… well.. very painful! I am having a hard time putting two and two together, though. I can’t see how this article demonstrated how PE would be much easier without the tunica. In fact, the way I see it, I think it shows the opposite.

From what I understand,the doctors grafted the tunica. Meaning, they "surgically transplanted tissue" into the tunica. I briefly re-skimmed the article, but I believe this means they enlarged the tunica. Thus, making it thicker. And according to the tunica rule (the way I understand it), this make growth harder.

Exactly! When I started reading on smooth muscle, I started thinking the same thing. We all know that gains are much easier to re-obtain, then they were to initially obtain. This is especially apparent with older men who lose some of their penis size (and hardness) due to aging. Perhaps its because of the smooth muscle memory?

This is in absolute unison with my belief. The penis adapts to exercise, so we must up the intensity (and over a period of time, take a break). This is analogous to exercising the skeletal muscles (which are also surrounded by collagen).

I think once we find the cause of enlargement due to exercising (e.g. the smooth muscle, or the tunica, or maybe both), we can look at the chemicals that can help gains. Perhaps supplements like protein poweder, and NOX2 (the stuff BG uses) really do help increase growth potential, as they do in skeletal muscles.