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Smooth Muscle and PE

Originally Posted by avocet8
You are onto something, all of you, and sometimes from different perspectives.

I was a good gainer, and a rather fast one. During my active PE years I made it a rule for myself never to overdo. I broke that rule. But had only three negative events: I went over my acceptable pumping HG pressure once and got a lot of red-dots once; I got a doughnut once. And I thought I could handle Horses but could not with the result of discoloration that lasted two years - but no concomitant erectile issues from the horses. In the first two cases, I backed off totally until whatever cleared; I quit the Horses altogether and reverted to modified (and easier) Ulis for girth. Point is, I have nearly always approached PE from the point of view of “slow and steady wins the race.” Slow and steady did win it for me.

I believe very strongly that nocturnal erections, parasympathetic-system induced, are the single best tool we have in PE - along with our conscious exercises - for healing, and cementing. During these events, all the flood gates are opened; newly-oxygenated blood cleans the plumbing pipes from whatever moderate stresses we applied while awake and tissue cells are encouraged to divide. Some other good stuff happens, too. Wakeful, psychological negatives totally disappear during these unconscious erections.

Many of you think you never get nocturnal erections because you don’t wake to them. Most of you who think you never get them are mistaken. You simply sleep through them. The rest of you don’t get them. There are reasons for not getting them. Multitudinous ones which you can personally take a look at. Among them, lousy sleep patterns, stress in your life, physiological ED, and on and on..

I’m glad you brought this up because it opens up to opportunity to say this.

I had a nocturnal two nights ago that I can’t forget, ouch! It woke me up!

Someone told me a while back I think it was you Avocet8. To let the erection die down to 50% and build it back up to a 100%. I guess this introduces new blood and oxygen and vital nutrients into the penis.

Jelq with a soft grip.
Masturbate with a soft grip.
I have never gotten little red spots in the three years or so that I have been doing PE.
Erection levels got weak a few times either by over PE or not enough sleep.
I think dare I post, that easy does it is the fast way to quick gains. Whether you hang, pump or jelq.
I challenge anyone that is a hard gainer to lighten up the grip! Lighten up the weight, lighten up the pressure.
You can safely jelq for an hour if your gentle on your dick.
But longer jelq requires longer warm up and stretches. So a one hour jelq sessions may not be the thing for you.
So keep it simple.

I predict the next ED drug may be a derivative of Ginkgo,Viagra, and Yohimbe. Remember drugs are often made from plant sources. Viagra may be a derivative of aloe vera or something, who knows.


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

avocet8 - I agree that there has got to be a good physiological reason for NPT’s. Otherwise why do we have them? They tend yo be maximal erections (if your PI’s are good). Does it keep the plumbing primed for future episodes of attempted species perpetuation? Is it like a sigh, which helps to open collapsed air sacs; so simple but so important? These maybe religious questions, but it doesn’t mean they’re not worth asking.

Originally Posted by pudendum
Avocet8 - I agree that there has got to be a good physiological reason for NPT’s. Otherwise why do we have them? They tend yo be maximal erections (if your PI’s are good). Does it keep the plumbing primed for future episodes of attempted species perpetuation? Is it like a sigh, which helps to open collapsed air sacs; so simple but so important? These maybe religious questions, but it doesn’t mean they’re not worth asking.

All I know a lack of them says there is something wrong in the body. I imagine nocturnal erections vary from man to man. Some guys have perhaps 5 a night or more. Perhaps some men only have one or two. Aside from the nocturnal erection that woke me up the other night I thought that maybe I was not having them. I do sleep pretty deep these days.


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

Originally Posted by Iguana
I have never heard of this drug. I wonder what the status is on it. Did the FDA ever approve it?


According to http://www.vasomaxnews.com/, “Clinical Trials in the US have been put on hold awaiting the results of a mechanistic study of brown fat proliferation in rats. Schering-Plough has been given regulatory approval to market the drug in Mexico and Brazil under the trade name Z-Max. Vasomax has been cleared for the go ahead of clinical trials in the UK” This web site, and this information, may be very old; another story refers to Mexico having approved the drug in 1998.

The “brown fat in rats” study results were released in 2001: http://www.allbusiness.com/company-…/6194752-1.html

1998 (!) CNN story on Vasomax: http://www.cnn.com/HEALTH/9806/02/viagra.alternative/
2002 study on Vasomax: http://www.nature.com/ijir/journal/…l/3900885a.html

There does not seem to be any recent news about Vasomax for the U.S.


For Lampwick, becoming hung like a donkey was the result of a total commitment.

Originally Posted by stagestop
Hi Sparkyx,

I am a bit confused about the premise of the tread.

Just a very broad discussion of the role of smooth muscle in PE. I originally addressed how I speculate that smooth muscle is the primary mechanism of “shrinkage” that most guys see with too much PE. I futher speculated that it is probably the tissue most easily injured, and that damage results in the contraction of it.

This is all speculation, so I thought I’d just kick it out there and see what comes up.

Originally Posted by pudendum
I’ve recently read numerous medical papers studying nocturnal penile tumescence (NPT: “night wood” or dream-related erections). There appear to be distinct differences between it and psychogenic/arousal/”I want to show that hot honey my new long and fat dick” erections. NPT is associated with more frequent and more sustained bursts of spontaneous IC/BC muscle contractions. This drives up CC and CS pressures. There is also good evidence that nerve stimulation patterns in nerves to the penis (parasympathetic vs. sympathetic) are different between the two erection types. This may explain the differences we note; NPT erections can be harder, girthier (CS expansion?) and more intense (almost painful at times). Guys with psychogenic impotence have normal NPT’s. Guys with true organic impotence have very few if any NPT’s.

Is smooth muscle relaxation in the erectile chambers or large feeding arteries any different between NPT vs. arousal erections. Possibly, but I’ve seen no specific mention of it.


Pudendum:

Do you have any thoughts on how NPTs relate to the timing/scheduling of one’s PE program?

For a while now, I’ve thought that PE before bedtime was good, as the NPTs reinforced whatever expansion had taken place.

I’ve also thought that PE first thing after getting up was good, as the NPTs had warmed things up and may have set the stage for better subsequent expansion from PE.

I’m not hearing anything here that contradicts my approach, and I’d be interested in your perspective.

Avocet’s post #15 is along the same line of thought I had about PE before going to sleep,and the beneficial effects of NPT on healing and cementing post-PE:

Originally Posted by Avocet
I believe very strongly that nocturnal erections, parasympathetic-system induced, are the single best tool we have in PE - along with our conscious exercises - for healing, and cementing. During these events, all the flood gates are opened; newly-oxygenated blood cleans the plumbing pipes from whatever moderate stresses we applied while awake and tissue cells are encouraged to divide. Some other good stuff happens, too. Wakeful, psychological negatives totally disappear during these unconscious erections.


SparkyX’s first post in this thread also suggests that PE on waking might mean working with tissue that is already ‘warmed up’ and potentially amenable to better stretching/expansion from PE:

Originally Posted by SparkyX
I also think this answers the mystery of the thicker girth from a sleeping erection. Sleep activates the parasympathetic system which in turn relaxes smooth muscle. I think this may be a more effective relaxation of smooth muscle than a waking erection, which will allow it to get girthier with less internal pressure, because the tension from smooth muscle is less. Its kind of like blowing up a stretched out balloon vs a newer tighter one.


For Lampwick, becoming hung like a donkey was the result of a total commitment.


Last edited by Lampwick : 01-26-2008 at .

What is the hypothesis?


originally: 6.5" BPEL x 5.0" EG (ms); currently: 9.375" BPEL x 6.75" EG (ms)

Hidden details: Finding xeno: a penis tale; Some photos: Tiger

Tell me, o monks; what cannot be achieved through efforts. - Siddhartha Gautama

Originally Posted by pudendum
Sparkyx - I have limited writing space on my PDA so I can’t quote. I have been thinking and reading about smooth muscle in the penis and have been scratching my head about the premise that it is smooth muscle contraction that brings about flaccid penis retraction. The smooth muscle of the penis resides in blood vessels. The vast majority is in the erectile chambers associated with the trabecular walls of the sinusoids. We all are familiar with parasympathetic/nitrous oxide/cGMP/testosterone mechanisms of smooth muscle relaxation with erection and the sympathetic nervous system effect on smooth muscle causing loss of erection.

In the flaccid state, blood flow to the erectile chambers is minimal. Smooth muscle is in an intermediate state, neither maximally dilated or contracted. The trabecular walls do not span the cavernosa or spongiosum. There are column extensions of the tunica that span across the penis but not longitudinally to act as a penis skeleton for erection and are in the relax position (undulated) like the tunica. There is no smooth muscle component to the tunica. So I ask this question: how does vascular smooth muscle contraction cause shrinkage of the flaccid penis?

My read of Hsu et al.’s entire article (which I don’t have at this time) is that they say nothing about this phenomenon. Neither do the several other sources I’ve read on the subject. Why doesn’t the penis shrink to smaller flaccid lengths when the erection dissipates after intercourse or masturbation when smooth muscle contraction is maximal? Yes, I know when we’re scared or stressed the penis retracts, but there’s got to be more to this than just smooth muscle contraction. Your thought?

Maybe I’m reading the literature wrong, but there seems to be quite a lot of smooth muscle comprising THE WALL ITSELF! Smooth muscle and elastin seem to be a large component (smooth muscle anyway) of the trabecular walls…and this would make sense if correct, and account for the rapid and large changes that are seen in the penis, from full expansion to shrinkage as in cold water or high stress situations.

What is your understanding on the trabecular wall composition?

Originally Posted by stagestop
Hi Sparkyx,

I am a bit confused about the premise of the tread. If the thread is about “cementing” of gains, that would seem one point. If we are talking about hormonal response during erection, that would seem to be a different issue, and if we are discussing what it takes to gain girth, that would seem to be a third issue.

Assuming that the thread is basically about the latter, which is what it takes to get an increase in girth, I would think that an examination of those people that had girth gains would be the place to start.

Perhaps before going there, we should look at what part of the penis actually grows. Certainly skin would not seem relevant, and I doubt that the tunica, even if expanded a bit would change much in thickness. A ligament may grow a bit, but that would not seem to have any great potential. This would seem to indicate that growth in girth is related mostly to growth in the CC, or perhaps a small bit of growth in the CS.

The common thread in PE is stress induced cell division. In my own case, it would be stress induced cell division aided by IGF-1, GH, DHT and PGE-1. Of the four, the one that is not really applicable would be GH. The reason for that is that I am on an anti aging program and my GH levels are put to the level of the average 30 year old. The most active (for growth) of those compounds is IGF-1. When I used higher dosages, (60 mcg a day) the effect was quite noticeable in two weeks time. I should mention here that this dosage is WAY too much, and caused me grief in my prostate at the two week mark. A slow and more effective dosage of 10 to 20 mcg per injection, 3 to 4 days a week. This has given me a 1” + increase in circumference in less than 6 months.

The first. question is how do we differentiate those who achieve a good dose of cell division (growth) trough strictly stress induction of one form or another, and those that have no benefit. I am kind of at a loss on that one. Perhaps some statistical analysis of board members that grow, versus those that have not grown may be of value, but developing a plan as to what to sample would seem to be a challenge. I suspect that there are many more variables than the mere application of stress to the penis, but again, defining what they may be is another challenge.

Regarding the “cementing” of gains, and the fact that sometimes erect lengths can vary, I tend to think that the variables that we all have to contend with, such as vascular sufficiency, pressure inside the penis, hormonal sufficiency on any particular day, etc, etc, would account for the minor variations in erect length and girth that we all get. True growth, which I would define as having additional cells in the various parts of the penis, is only obtained by actually getting those cells. Cementing, as a concept would just be a continued effort that caused the cell division in the first place and reflects not the maintenance of what has already been achieved so much as a slow growth that compensates for the differences in length and girth caused by the effort of the stress application.

Perhaps a survey of a good number of people, that lists all the the variables that seem reasonable in girth expansion would be of benefit to the members? If we had some statistical analysis of what worked, and what did not, perhaps the variables in PE would become more apparent to the membership?

Stage

Hey brother! Always good to see you check in, great post as usual.

That girth survey sounds like a good idea.

Thanks to all you guys that posted here, good discussion. Sorry I posted and ran, but my life keeps interfering with this penis building stuff….sigh.

Avocet, I think you are one of the first people I read that talked about the importance of NPT (nite wood) and I have since come to believe it is a critical sign that you are in the “zone” for growth, AND even a critical element IN growth…thanks.

This is a picture of the sinusoid in the corpus cavernosum. Its from a study entitled;The Effect of Electrocoagulation on the Sinusoids in the Human Penis.

I put it up because they are showing the difference between a normal and healthy sinusoidal wall and an unhealthy one.

http://www.andrologyjournal.org/cgi…l/25/6/954/FIG3

This is the orginal page;

http://www.andrologyjournal.org/cgi…t/full/25/6/954

A lot of articles on smooth muscle and the penis state that it is in the arteries and arterioles. Yet, others seem to indicate a high concentration in the wall of the small compartments that make up the Cavernosal sinusoids.

This is excerpted from;
http://www.ajmc.com/Article.cfm?Menu=1&ID=2526

quote
“The cavernosal nerves enter erectile bodies (corpora cavernosa) (Figure 1). Here, their nerve endings release a second messenger, nitric oxide. Nitric oxide activates the enzyme guanylyl cyclase, which lyses guanosine triphosphate (GTP) to produce a third messenger, the intracellular cyclic guanosine monophosphate (cGMP). Ultimately, the result is a decrease of intracellular calcium and an opening of potassium channels with the resultant relaxation of vascular smooth muscle in the arteries, aterioles, and SINUSOIDS of the corpora cavernosa.”

close quote (emphasis is mine)

Once again, it seems to be indicating that the sinusoids themselves are at least partially comprised of smooth muscle. This again to me explains a lot of the action and reaction we see in the penis.

sparkyx - I do not at all dispute the existence of vascular smooth muscle along the entire surface of the venous sinusoids of the corpora of the penis. With the exception of capillaries, all blood vessels have a middle layer (tunica media), which is entirely made up of smooth muscle. The venous sinusoids of the penis are no exception.

The point I’m trying to address is I find it hard to understand how the contraction of vascular smooth muscle in the sinusoids can lead to penis retraction. Let me be more clear: I mean as the sole mechanism. This is why:

The organ that is most comparible with penis tumescence and detumescence is the dog spleen. The red pulp (ignore the white pulp which is involved with immunity) has venous sinusoids with trabecular walls lined with smooth muscle just like in the corpora. The spleen in the dog (and several other mammals) has an amazing ability to dilate and store lots of blood (smooth muscle relaxation). The dog spleen is covered by a fibroelastic dense connective tissue capsule much like the tunica of the penis. However unlike tunica, the capsule of the spleen has a significant smooth muscle component. So when the dog’s body needs to mobilize this store blood volume, sympathetic nerves fire and cause the contraction of both the vascular smooth muscle and capsular smooth muscle. It is an amazing sight to see it shrive in response to this stimulation. The spleen of man has only minimal storage capacity. It still has red pulp with sinusoids, but it has a less elastic capsule and minimal capsular smooth muscle. It changes only a little in size with sympathetic nerve stimulation (the smooth muscle of the spleen sinusoids in man does contract).

This is why I have difficulties envisioning sinusoid smooth muscle contraction being the sole mechanism for penis retraction.

BTW, the dog spleen is a great model for the study of erection. I am investigating.

Iguana and Lampwick - The only FDA approved preparation of phentolamine in the US is for intravenous or intramuscular use under the brand name Regitine (finally remembered it; been too long since I used it) and its generic equivalent. No oral form has been approved. It seems unusual to me that formal clinical trials have not been conducted or completed in the last 9 or so years in the US. It does take a lot to get the FDA to approve a new drug or new preparation application, if one has even been submitted. Can’t see why one wouldn’t, except because it is a very expensive process.

It has been used “off label” (use of an approved drug for an unapproved use) as an injectable into the cavernosa for erections. Ouch!!

If you want the oral form, you will have to get it from Mexico, Brazil or maybe UK (though I’m not sute it has been approved there)

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