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Possible reason for PE induced growth

Just a clarification on my last post. It could seem that I inverted things: with weigth-training, we want to make our muscle stronger, when with PE we want to make our penis weaker, so it can start a new grow-phase.

But, if I’m not confusing, what pudendum is exposing means that connective tissue become stronger while become bigger, because the only way it have to adapt to a stretching tension is producing new cells/fibers. So, saying “I have to take a decon break to weakening my penis and gaining again” makes no sense - if the penis get weaker, it get shorter/thiner.

It should be more logic that those who have no more results, despite the high tension, are experiencing an accumulation of tears in their penis that can’t no more heal/adapt; so, maybe, fibrotic tissue :it can’t grow, so the need of deconditioning. I.e., the phenomenon is similar to extreme overtraing, were we can have so much accumulation of trauma that a torn tendon or similar events could happen. The difference is that, fortunately, the tunica is so strong that is practically impossible that could be teared by longitudinal stretching, even with extreme hig tension.

I’ve read also, sometimes, that those who tried too aggressive PE (high tension) had a curved penis: here, the analogy with Peyronie’s Disease seem to be not casual.

A final note: I have some difficult to understand how the jelqs are so effective for PE; it’s hard to put jelqs on the two kind of stress that are discussed in the first post of this thread: they cause trauma via high tension like hanging/stretching? Jelq are short, and the force exerted is by far lower than with stretch. Maybe the enlarged -girth state weak the tunica, so it’s easily deformed longitudinally? If so, the “girth gains VS. length gain” theory should be a fallacie. And clamping before stretching should be the way to go.

Or maybe I’m tired and my mind is confused; it’s time to go bed :) .

Originally Posted by marinera
Just a clarification on my last post. It could seem that I inverted things: with weigth-training, we want to make our muscle stronger, when with PE we want to make our penis weaker, so it can start a new grow-phase.

But, if I’m not confusing, what pudendum is exposing means that connective tissue become stronger while become bigger, because the only way it have to adapt to a stretching tension is producing new cells/fibers. So, saying “I have to take a decon break to weakening my penis and gaining again” makes no sense - if the penis get weaker, it get shorter/thiner.

It should be more logic that those who have no more results, despite the high tension, are experiencing an accumulation of tears in their penis that can’t no more heal/adapt; so, maybe, fibrotic tissue :it can’t grow, so the need of deconditioning. I.e., the phenomenon is similar to extreme overtraing, were we can have so much accumulation of trauma that a torn tendon or similar events could happen. The difference is that, fortunately, the tunica is so strong that is practically impossible that could be teared by longitudinal stretching, even with extreme hig tension.

I’ve read also, sometimes, that those who tried too aggressive PE (high tension) had a curved penis: here, the analogy with Peyronie’s Disease seem to be not casual.

A final note: I have some difficult to understand how the jelqs are so effective for PE; it’s hard to put jelqs on the two kind of stress that are discussed in the first post of this thread: they cause trauma via high tension like hanging/stretching? Jelq are short, and the force exerted is by far lower than with stretch. Maybe the enlarged -girth state weak the tunica, so it’s easily deformed longitudinally? If so, the “girth gains VS. Length gain” theory should be a fallacie. And clamping before stretching should be the way to go.

Or maybe I’m tired and my mind is confused; it’s time to go bed :) .

Jelqing works by increasing the size of the cavernosa bodies. By pushing blood forward from one chamber to the next. Nighty night!


Speak softly carry a big dick, I'm mean stick!

Originally Posted by kingpole
Jelqing works by increasing the size of the cavernosa bodies. By pushing blood forward from one chamber to the next. Nighty night!

Yes, but how the longitudinal tunica deformation happens? Enlarging corpora cavernosa doesn’t give you more size if tunica has the same size, and enlarging tunica require high tension, as anybody who did stretching/hanging could tell. However, nighty night to you also, KP :) .

Originally Posted by marinera
Yes, but how the longitudinal tunica deformation happens? Enlarging corpora cavernosa doesn’t give you more size if tunica has the same size, and enlarging tunica require high tension, as anybody who did stretching/hanging could tell. However, nighty night to you also, KP :) .


My opinion on jelqing and girth increases comes from personal experience.

Before I started PE, I had firm but only rare rock hard erections. I was more than hard enough to have intercourse, but not hard enough to make me happy. I thought it was just the way things were.

In doing PE for over 8 months with manual pressure generating techniques (jelqing, squeezes and slinkies) without clamping or pumping, I have increased my girth by 1 inch and my erections are rock hard over 95% of the time. So how do I explain this?

I believe, at least in my case (and I’ll bet many others), that before PE, the limits to larger erections was cavernosa volume and not low tunica compliance. What I’m trying to say is that the tunica was still compliant and had further distensibility. High (instantaneous) pressure jelqing increases cavernosa volume capacity by inducing remodeling the walls of the venous sinusoids that expand and hold blood during erection. The pressure induces deformation injury to the connective tissue/smooth muscle walls (trabeculae) which increases capacity.

The overall increase in cavernosa volume against a stretching tunica with decreasing compliance makes jelqing strokes at high pressures (when done at high degrees of erection) a significant tension stress to the tunica. This stress is much greater circumferential tension than longitudinal and causes tension-induced remodeling with girth gains.

As I mentioned in the initial post, the tunica experiences biaxial stretch. It has to to become long and beefy.

At the end of a mid-erection (50 - 70%) jelqing stroke, the pressure is at its highest. That’s why some of us have experience larger diameter towards the end vs. the base; baseball bat-like. (I reverse jelq against kegels to try to increase the base as well.) However, even at the end stroke, the stress will still be circumferential > longitudinal. If you want to attain longitudinal gains, you will have to do longitudinal tunica stretches.

I mentioned in another thread that increased flexibility can be experience with tendon and ligament stretch (legs, arms, back). In my mind this represents increased fiber length, not just fiber diameter. Yes these stretched ligaments are stronger, but they’re longer as well. I think the same is true in the tunica.

If you believe the clamping can generate a significant circumferential tunica wall stress (as I do as well), then why don’t you believe that high intensity, high erection jelqing can do the same thing?

Originally Posted by marinera
But, if I’m not confusing, what pudendum is exposing means that connective tissue become stronger while become bigger, because the only way it have to adapt to a stretching tension is producing new cells/fibers. So, saying “I have to take a decon break to weakening my penis and gaining again” makes no sense - if the penis get weaker, it get shorter/thinner.


Increases in length in collagen fibers requires inserting additional subunits within the fiber to make it longer. This is while at the same time fiber diameter is increase as more more collagen subunits are added to make the collagen fibers thicker.

During disuse, it would seem logical to me that it would be easier for collagen fibrils (links of individual lengths of collagen subunits; millions of these make up a single collagen fiber) to be removed off the collagen fibers, than it would be to remove length across an entire fiber. This would make the collagen fibers thinner but still longer. The study I presented earlier showed a decrease in surface are of the Achilles tendon with disuse, without changing length, meaning diameter decreased but at least to that period of disuse, collagen length had not decreased. Only after prolonged disuse (as after injury, bed rest or age) does length decrease as well. This takes time.

In my mind this means that decon breaks will make the suspensory ligaments and tunica “weaker” but still longer (as long as the break is not too long). Evidence from guys on this forum about decon experiences would favor this explanation.

Originally Posted by pudendum
My opinion on jelqing and girth increases comes from personal experience.
………………..
…………………..

Thanks for your explanation. I’m affording to digest all the information you putted here, and maybe this require some more time and/or more attention focus.

I had experience similar to yours with jelqs -even more impressive, because I credit jelqs (and especially dry-jelqs) to have been a cure for a beginning of ED.

This make me think that a more appropriate name for PE should be Penis Healthing - or something like that.

I had lenght and girth gains from jelqs; more lenght than girth, if you ask me. This originate my doubt, because
the strength we exert while jelqing is lower than strength-pulls force, and is diminished by the contemporary longitudinally and laterally resistence of the whole penis.
I wanted to put this suspect it in maths terms, to see if my reasoning is incorrect, but don’t think there is a real need, now (ok..just laziness ;) ).

About the effects of rest on size, could you explicate, if don’t mind, if the below statement is a correct inference, at the state of our knowledge: during decon-breaks, girth is, likelihood, lessen faster than lenght .

Thanks in advance.

Originally Posted by marinera
About the effects of rest on size, could you explicate, if don’t mind, if the below statement is a correct inference, at the state of our knowledge: during decon-breaks, girth is, likelihood, lessen faster than lenght .


Girth is basically circumferential length, if that makes any sense. There are a significant number of the tunica fibers that are arranged circumferentially. So a decrease in tunica girth is a decrease in tunica circumferential length. In my mind, the same processes would apply for decon regarding fiber size reduction vs. fiber length reduction here as for longitudinally arranged fiber length.

I hope this makes some sense.

Originally Posted by pudendum
Girth is .. Circumferential length

Yes: it is THAT simple.

Pudendum - you are a genius. Sharp like a razor blade. Stay tuned.. I like it that way.

And check my new thread “pumping and pussy pumping - together”.


Later - ttt

Originally Posted by pudendum
Girth is basically circumferential length, if that makes any sense. There are a significant number of the tunica fibers that are arranged circumferentially. So a decrease in tunica girth is a decrease in tunica circumferential length. In my mind, the same processes would apply for decon regarding fiber size reduction vs. fiber length reduction here as for longitudinally arranged fiber length.

I hope this makes some sense.

I basically agree, but…aren’t we forgetting something? We are speaking of three-dimensional things. Can’t fibers become thicker? TA can’t go getting wider? Or this 3th dimension is negligible reported to the whole penile volume?

This lead me to another point : is reported by many that getting older gains are way harder to achieve.
As you know, I suspected that the cause of that was lessen of elasticity in older men. But maybe thickening of tunica is the (con)cause of this lessen in gains AND of harder gains when PE work is done for a significative amount of time.

I’ve done some homeworks:

Effect of aging on penile ultrastructure
Zhou-Jun SHEN, Xiao-Dong JIN, Zhao-Dian CHEN, Yuan-He SHI

Department of Urology, First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou

310003, China

Asian J Androl 2001 Dec; 3: 281-284

Abstract
Aim: To clarify whether there are anatomical changes in tunica albuginea and corpora cavernosa in

aged rats. Methods: Seventeen male Sprague-Dawley rats were divided into three groups based on age.

Group A consisted of young rats (9 weeks), Group B, middle aged rats (14 weeks) and Group C, old

rats (62 weeks). The penile samples were obtained and observed under a scanning electron microscope.

Results: The thickness (mean±SD) of the tunica albuginea was 0.14±0.02, 0.16±0.03 and 0.06±0.02 mm

in Groups A, B and C, respectively. The tunica albuginea of group C was significantly thinner than

those of the other two groups (P<0.05) and the elastic fibers were diminished in the old rats. In

the corpora cavernosa of old rats, the intracavernous pillars were irregular, in which many large

collagen fibers could be observed, and the smooth muscle and elastic fibers were reduced.

Conclusion: In old rats, the tunica albuginea became thinner with diminished elastic fibers; the

collagen fibers of corpora cavernosa were increased while the smooth muscle and elastic fibers were

reduced.
……………..
Jevtich[8] reported that there were more interstitial matrix and fewer smooth muscle cells in the

corporeal tissue of impotent individuals compared to normal men. Wespes[9] measured the percentage

of smooth muscle cells in patients of different ages with normal erection, using computerized image

analysis. Under 40 years of age, the percentage was 46%, between 41 and 60 years it was 40%, and

over 60 years it was 35%. The authors suggested that the decrease in smooth muscle content would

have caused the decline in erection in older men. In the present study, the reduction of smooth

muscle fibers in the elderly rats may affect the sinusoidal relaxation and arterial dilatation.

http://www.asiaandro.com/1008-682X/3/281.htm

Immunocytochemical and quantitative study of the tunica albuginea testis in young and ageing men
Journal Histochemistry and Cell Biology
Publisher Springer Berlin / Heidelberg
ISSN 0948-6143 (Print) 1432-119X (Online)
Issue Volume 107, Number 6 / June, 1997

Pages 469-477

Authors
M. Isabel Arenas1, Fermín R. Bethencourt2, Benito Fraile1, R. Paniagua1
1Department of Cell Biology and Genetics, University of Alcalá, E-28871 Alcalá de Henares (Madrid),

Spain
2Department of Urology, Hospital Príncipe de Asturias, E-28871 Alcalá de Henares (Madrid), Spain

Abstract

A light and electron microscope immunohistochemical study of the tunica albuginea from both young

and elderly men was carried out to determine the distribution of the cells that contain actin,

vimentin and/or desmin, and to evaluate the possible variations with ageing by means of quantitative

studies. Testicular volume and testicular parenchyma volume decreased significantly with age whereas

the tunica albuginea volume remained unchanged. These results agree with the scanty quantitative

changes observed in the testicular connective tissue with age, and the notion that age-related

changes in testicular volume are principally restricted to the seminiferous tubules. Three

connective tissue layers could be distinguished in the tunica albuginea in both young and elderly

men. The middle and inner layers increased in width with age while the width of the outer layer

decreased. The average width of the tunica albuginea increased significantly with ageing. The tunica

albuginea of young men and elderly men presented two types of fusiform cells: (1) fibroblast-like

cells, which immunoreacted to actin and vimentin, but not to desmin; and (2) myoid cells, which

immunoreacted to actin, vimentin and desmin. In both young men and elderly men, the total number of

desmin-positive cells (myoid cells) was significantly lower than that of fibroblasts. However, the

total number of desmin-positive cells was significantly increased in ageing men. In young testes,

desmin-positive cells were more abundant in the outer layer of the tunica albuginea, whereas in

elderly men these cells predominated in the middle layer. The increased desmin immunoexpression in

the tunica albuginea of ageing men contrasts with the decrease in desmin immunoreaction in other

myoid cells of the testis, the peritubular myoid cells, but only in seminiferous tubules that showed

severe germ cell depletion. This suggests that changes in intermediate filament immunoexpression in

peritubular cells are focalised, and thus, under local control, whereas changes in the tunica

albuginea cells are generalised and possibly related to factors also affecting the connective tissue

in other organs

from:
http://www.springerlink.com/content/pymaqd4ywf20rv6h/

Any comments?


Last edited by marinera : 12-30-2007 at .

Originally Posted by marinera
I basically agree, but…aren’t we forgetting something? We are speaking of three-dimensional things. Can’t fibers become thicker? TA can’t go getting wider? Or this 3th dimension is negligible reported to the whole penile volume?

Good point, there is a 3rd dimension. Do you surmise that increased fiber diameter circumstantially is the cause of longitudinal gains? There are fibers arranged in a more longitudinal direction as well which are stressed by other lengthening PE methods. I do not rule out that some of the lengthening may be due to increased fiber diameter of circumferential arranged tunica collagen fibers, but I do not believe it is the major contributor.

Originally Posted by marinera
This lead me to another point : is reported by many that getting older gains are way harder to achieve.
As you know, I suspected that the cause of that was lessen of elasticity in older men. But maybe thickening of tunica is the (con)cause of this lessen in gains AND of harder gains when PE work is done for a significative amount of time.

First, who are you calling old? I resemble that. :)

But seriously, if anything the evidence is that connective tissue atrophies with age. In the case of the penis this is reflected in a small retracted penis in the sexually inactive oldster (that’s older than me, if you were interested). If anything, gains should be easier in this population. Hmm…maybe that’s why my gains have been so good.

As far as decreased elastic fiber component in the older penis (that you have shared with us), I believe it represents part of an overall disuse atrophy of the tunica that includes both collagen fibers and elastic fibers.

Originally Posted by marinera
Effect of aging on penile ultrastructure
Zhou-Jun SHEN, Xiao-Dong JIN, Zhao-Dian CHEN, Yuan-He SHI
Asian J Androl 2001 Dec; 3: 281-284

The tunica albuginea of group C was significantly thinner than those of the other two groups (P<0.05) and the elastic fibers were diminished in the old rats. In
the corpora cavernosa of old rats, the intracavernous pillars were irregular, in which many large collagen fibers could be observed, and the smooth muscle and elastic fibers were reduced.
Conclusion: In old rats, the tunica albuginea became thinner with diminished elastic fibers; the collagen fibers of corpora cavernosa were increased while the smooth muscle and elastic fibers were reduced.

Increased collagen fibers within the cavernosa represent “cobwebs” in an old unused “warehouse” which is what it would be in an older (I mean older) man who does not use his unit for anything other than urine.

They found thinner tunicas in their “old man” rats. Again not unexpected in the case of disuse atrophy.

It is not surprising that if an older man does not have erections, that the component of smooth muscle in the cavernosa is decreased; specifically in the trabeculum walls that line the venous sinusoids where blood pools when the penis engorges. Smooth muscle in these walls is necessary to push the pooled blood out of the penis as the erection subsides.

Smooth muscle content in the cavernosa may play an important role in erection, particularly regarding ED (and is interesting), but has little to do with our discussion regarding connective tissue (specifically the tunica) remodeling with regards to PE.

Originally Posted by marinera
Immunocytochemical and quantitative study of the tunica albuginea testis in young and ageing men
M. Isabel Arenas, Fermín R. Bethencourt, Benito Fraile1, R. Paniagua
Histochemistry and Cell Biology 107 (1997) 469-77.

Any comments?


The tunica albuginea that they are talking about in this report is in the testis not the penis. This is a totally different structure covering the testicle and is related in name alone (at least for our discussion).

A question for Pudendum:

Where exactly are the androgen receptors in the penis. I’m thinking jelqing stimulates this somehow and causes the outward and forward expansion of the cavernosa bodies?
Not all growth is lig growth.

I remember when I was a bit younger say about 26. I was jerking off and I looked down I had both hands wrapped around my dick but the head did not reach the first finger and the thumb but came short of this land mark.

Now I can wrap all 8 fingers around it and the head and part of the shaft sticks out well above the two hands wrapped around my dick with a third inch gap between both hands. My hands measure 3.5” at the knuckle line. This is a comparison I make often.


Speak softly carry a big dick, I'm mean stick!

Originally Posted by kingpole
A question for Pudendum:

Where exactly are the androgen receptors in the penis. I’m thinking jelqing stimulates this somehow and causes the outward and forward expansion of the cavernosa bodies?
Not all growth is lig growth.

May I try to answer? - Thanks.

The purpose of the androgen receptors is to induce penis growth, as early as in mom’s uterus. In the absence of testosterone, all babies look like females whether XX or XY. It’s the testosteron and it’s interaction with the testosterone receptors that induces growth.

Unfortunately, the sensitivity of the receptors fades away during puberty and is practically completely down-regulated in adults. That’s why bodybuilders even when using huge amounts of androgens don’t get penis growth.

For us pe-community it would be the true HAMMER to find a way to up-regulate the testosterone receptors in our dicks.


Later - ttt

Originally Posted by ticktickticker

The purpose of the androgen receptors is to induce penis growth, as early as in mom’s uterus. In the absence of testosterone, all babies look like females whether XX or XY. It’s the testosteron and it’s interaction with the testosterone receptors that induces growth.

Unfortunately, the sensitivity of the receptors fades away during puberty and is practically completely down-regulated in adults. That’s why bodybuilders even when using huge amounts of androgens don’t get penis growth.

Spot on.

It is why DHT creams do not really work when topically applied to the penis as adults.

There are direct correlations between pe and bodybuilding imo.

Focus on stretching the tunica(as one would with the similar muscular sheath that encapsulates muscle bodies).
Focus on training the soft tissue to adapt and to expand with blood capacity.

That is the two pronged approach.

IMO - the ONE main reason why gear users EXPLODE with growth is that the influx of water weight has a direct effect on the stretching on the muscular sheath. That tough sheath is usually the number one thing limiting growth on a purely structural level.

That stretching allows for more growth tissue expansion and is the number one reason why gear users never go back down to the pre-gear size.

Same with PE - the key is stretching the tunica which allows for more “soft tissue” expansion.

Once that stretch becomes “cemented”, then PE guys dont go back to their original size either.

Someone posted about rest periods allowing the penis to become “weaker.”.

One takes rest periods to allow the body to catch up from an over-training standpoint, and I truly think that most PE’ers SEVERELY over-train.

Again - direct correlations with bb’ing.

One sign of over-training in the gym is LACK OF PUMP….sound familiar in regards to lagging EQ?

The correlations go on and on and on, and I have adapted my pe routine to my 15 years of PT experience to look to the PI for a path on when to
increase(or in my case) to decrease the intensity.

Again - as in bodybuilding - folks range from the shallow end to the deep end of the gene pool, and recovery ability is no different.

Some folks can handle HUGE amounts of intensity in the gym, and in PE.

Most, including myself, just cannot.

I hope I made sense in that.


06/21/07 NBP = 7.75(tape) FSL = 7.875 EG = 5.00 Volume= 15.42

09/13/07 NBP = 8.375 FSL = 8.75 EG = 5.38 Volume = 19.29 (+25%)

12/26/07 NBP = 8.625 FSL = 8.75 EG = 5.50 Volume = 20.82 (+35%)

Originally Posted by kingpole
A question for Pudendum:

Where exactly are the androgen receptors in the penis. I’m thinking jelqing stimulates this somehow and causes the outward and forward expansion of the cavernosa bodies?
Not all growth is lig growth.

I remember when I was a bit younger say about 26. I was jerking off and I looked down I had both hands wrapped around my dick but the head did not reach the first finger and the thumb but came short of this land mark.

Now I can wrap all 8 fingers around it and the head and part of the shaft sticks out well above the two hands wrapped around my dick with a third inch gap between both hands. My hands measure 3.5” at the knuckle line. This is a comparison I make often.


Great gains. I’ve seen similar changes, but not to your extent; yet.

And you are absolutely correct that all growth is not ligament. If you’ve maxed out ligament stretch (LOT Theory) then PE must be directed to other growth (which is also requires connective tissue remodeling).

Testosterone is a steroid-based hormone.

Proteins hormones and other substances (like the substances released by nerves) that don’t mix well in fats (fat insoluble) have specific receptors on the cell surface that activate internal signaling through other messenger substances. An example is adrenaline (epinephrine). Some cells have the receptor (like blood vessels for adrenaline) and others don’t.

Testosterone is fat-based so it easily crosses into the cell. I know this has been well presented numerous times in this forum, but for those of you who don’t want to use the search button here is a reference which paints the picture of testosterone actions inside a target cell.

Quote
“When it leaves the circulation, it rapidly crosses the cell membrane. In the cytoplasm [the fluid within the cell] of most androgen target cells, testosterone is then converted to the more potent DHT by 5-reductase. Both testosterone and DHT bind to an intracytoplasmic receptor protein. The genes encoding this protein are located on the X chromosome. The androgen receptor is expressed in almost all mammalian tissues. Although DHT binds to the same intracellular receptor as testosterone, the DHT-receptor complexes are more stable than the testosterone-receptor complexes. Thus, DHT formation serves to amplify the action of testosterone in target tissues…The binding of the hormone-receptor complex to the DNA results in synthesis of messenger RNA (mRNA). The mRNA is then transported to the cytoplasm, where it facilitates transcription [making DNA into mRNA] of various genes, permitting synthesis of new proteins responsible for androgenic effects.”

Normal Structure & Function of the Male Reproductive Tract Chapter 23. Disorders of the Male Reproductive Tract. Stephen J. McPhee, MD in
Lange Pathophysiology. McGraw-Hill Companies. From Access Medicine.


So you ask, where are the androgen receptors in the penis? The answer is every cell in the penis. The question is what does it do there; specifically to penis growth after 20 years old. We know it increases erection frequency, libido and testes size (and all the other non-sex organ effects).

There are no reports of adult penis growth with androgens anywhere in the medical literature that I could find on Science Citation Index (ISI Knowledge Finder) from 1900 to present.

The text books are dogmatic. No penis growth after 20 years old, no matter what the androgen levels.

The only information I could find that even mention the effects of testosterone on the penis talk about its importance in erection control:

Quote
“Animal experiments and, to a much more limited degree, human observations suggest that androgens are necessary to maintain the integrity of the anatomical structures of the penile erectile tissue and, furthermore, that androgens are significant in the biochemical mechanisms subserving penile erection.’

Gooren LGJ, Saad F. Recent insights into androgen action on the anatomical and physiological substrate of penile erection. Asian Journal of Andrology 8 (2006) 3–9.


Quote
“In conclusion, our results clearly demonstrate that T acts intracellularly in corpus cavernosum SMC [smooth muscle cells] to regulate relaxation.”

Alcorn JF, et al. The effects of castration on relaxation of rat corpus cavernosum smooth muscle in vitro. Urological Research 26 (1998) 265-70


I will try to answer your question about jelqing effect on the androgen receptor in the cavernosa.

Masturbation to erection and intercourse cause an increase in testosterone. So you are increasing the amount of testosterone to your cavernosa. This will cause the binding of more of the testosterone receptors, most importantly in the smooth muscles cells in the walls of the venous sinusiods. This causes them to relax. You are increasing the blood capacity of the cavernosa by stopping the smooth muscle from contracting and pushing blood out of the penis.

By increasing the blood volume you are pressure stroking towards the head, you might very well be causing the outward and forward expansion of the cavernosa bodies.

In a real twist, it is becoming increasingly evident that estrogens are involved with penis function as well:

Quote
“In the past decade, interest and knowledge in the role of estrogen in male reproduction and fertility has gained significant momentum. More recently, the cellular distribution and activity of estrogen receptors (alpha and beta)(ER) and aromatase (estrogen synthesis) has been reported in the penis, making the penis the latest “frontier” in the study of estrogen in male reproduction. ER and aromatase are broadly and abundantly expressed in various penile compartments and cell types (erectile tissues, urethral epithelia, vascular and neuronal cells), suggesting the complexity and significance of the estrogen-ER system in penile events. Unraveling this complexity is important and will require utilization of the various resources that are now at our disposal including, animal models and human lacking or deficient in ER and aromatase and the use of advanced and sensitive techniques. Some of the obvious areas that require our attention include: 1) a comprehensive mapping of ER-alpha and -beta cellular expression in the different penile compartments and subpopulations of cells, 2) delineation of the specific roles of estrogen in the different subpopulations of cells, 3) establishing the relationship of the estrogen-ER system with the androgen-androgen receptor system, if any, and 4) characterizing the specific penile phenotypes in human and animals lacking or deficient in estrogen and ER. Some data generated thus far, although preliminary, appear to challenge the long held dogma that, overall, androgens have a regulatory monopoly of penile development and function.”

Mowa CN, et al. The penis: a new target and source of estrogen in male reproduction. Histology and Histopathology 21 (2006) 53-67.


Maybe there is some truth to the adage that we need to get in touch with our feminine side.

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