Smooth Muscle and PE

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..

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.

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

Hi Sparkyx,

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

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.

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.

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.

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?

What is the hypothesis?

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?

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