Smooth Muscle and PE

I have been thinking about this for a while. I was asked to start a thread on this , so we can kick it around a bit. Feel free to jump in and post any good info or just brainstorm with us.

I’m gonna open with some recent re-posts of mine from some other threads.

I also have a thought that I believe for myself is definitely true, and probably for all other penises.

Thought:
My thought is about the difference of erections, induced by no hand involvement (REM, when you see a hot girl, etc.), versus the edging and masterbating erections induced by hands.

I think the main reason edging and masterbating does take such a tool on our units is the stroking itself. Seriously.

The regular erections are healthy and definitely help gains, while the edging and spanking do not.

end quote

That’s the only difference, so it makes sense. I do have a theory about the parasympathetic nervous system relaxing the smooth muscle more efficiently when you are sleeping, which allows greater girth with less erectile pressure needed, therefore what appears as a thicker unit sometimes when you first wake up…but that’s for another thread…maybe.

Edging and spanking for some guys seems to be PI neutral, in that it doesn’t have negative effects. For some, they can’t do much at all without a negative impact…and everything in between.

The point of the Physiologic Approach (PIs) is that you can’t make hard and fast rules for everyone about stress applied to the penis, such as you can or can’t jack off…some can, some can’t. The point is, everyone must evaluate what it is doing to YOU!!!

For me, and many “hard gainers”, any stress is stress. Its kinda like dieting, ALL the calories count! So what I find is edging and the like is stressful to my unit, and adds to the NET stress load (think total “jelque or stress minutes”), WITHOUT adding any growth potential. So its like being on a 1000 calorie diet, but using those calories on junk food…not a good idea. You want to eat high quality food, or you will lose muscle and your health.

So, I think understanding this will help convert more “non gainers” into gainers if they understand that they are using up there “stress” capacity in non productive ways.

chronostone - Movin On Up

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Hey Remek!

We need to talk more, bro!

My current thinking on most “shrinkage” is smooth muscle contraction. I think that smooth muscle is the most reactive to stress, for what ever reason.

I first noticed this when I had over done PE, and took some Cialis to be ready for the wife that nite. Overtraining would cause the classic contraction, tissue stiffening, decreased EQ etc.

One of the effects of Cialis is relaxation of smooth muscle. When over trained, and I took it, one of the indicators it was working or I had taken an effective dose, was the reversal of the above noted symptoms.

From that, and some other observations, I believe that for most guys (short of connective tissue contraction…which is less easily reversed) the “shrinkage” is due to smooth muscle.

It is something that used to puzzle me when doing bpfsl. My first measurement or two was the longest, but the very act of a hard stretch would cause my smooth muscle to contract, and the measurements would get progressively shorter!

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.

From this I am wondering if maximum bpfsl is a good indicator that the smooth muscle has recovered completely and is ready for further stress? The problem with stressing connective tissue when the smooth muscle wants to hold it in a contracted state, is that it allows it to heal the micro tears in this contracted state and may be counter productive. Most guys report gains when they are also seeing heavy and long flaccid…clear indicator that the smooth muscle isn’t damaged to the point of contraction…which then allows the connective tissue to recover or heal in a more extended state, both length and girth.

I’m gonna stop now, because if I high jack this thread, I will have to send myself a nasty PM…and I don’t want to piss myself off!

Your Secret To Gaining - Focus On What’s Holding You Back (p. 5)

Appendix by Dr. Owens: Physiological cellular events during arousal/erections:
The smooth muscle cells in segments of the penis (corpora cavernosa) can either 1) relax, thereby allowing increased blood flow to the penis, or tumescence, or they can 2) contract, resulting in detumescence, or the flaccid state of the penis. Both events may be initiated in different ways, and it is ultimately the degree of contraction or relaxation of these smooth muscle cells that determines whether the penis is flaccid or erect.

Nerves to the penis release the neurotransmitter noradrenaline (a catecholamine), causing stimulation of alpha-receptors on the surface of adjacent smooth muscle cells. This leads to smooth muscle cell contraction, allowing only limited blood flow into the penis, which is now in the flaccid state, or undergoes detumescence if it was previously erect. Catecholamines can also be released during stressful situations associated with sexual activity such as fear of failure, performance anxiety, anger, shame, or embarrassment (Goldstein, 2000). Or they may be released in painful situations such as genital pain from infection of the prostate, epididymitis, and Peyronie’s disease, or non-genital pain such as headache (Goldstein, 2000). In either case, smooth muscle cells are stimulated to contract, resulting in reduced blood flow to the penis and detumescence.

To complicate matters further, different types of alpha-receptors (alpha-1 and alpha-2-subtypes) are located not only on the smooth muscle cells, but also directly adjacent on the nerve-buds, from where catecholamines and other neurotransmitters are released. From this location alpha-receptors modify how much of the transmitter substance is released from the nerves, and then reaches the smooth muscle cells (Crenshaw and Goldberg, 1996).

By blocking alpha-receptors on the smooth muscle cells with drugs like phentolamine (Regitine, Vasomax, mentioned on page 136), contraction of the smooth muscle cells can be prevented or at least reduced, allowing an erection to persist longer. This is why the drug phentolamine is effective in the treatment of ED and is currently being tested for possible FDA-approval as such a treatment option (Goldstein, 2000). The drug is already used as a blood pressure lowering medication for people with pheochromocytoma, a condition where excess catecholamines are produced in the body.

Alpha-2-receptors are blocked by Yohimbine, an alkaloid obtained from the bark of the African tree, Coryanthe yohimbe (Crenshaw and Goldberg, 1996; Morales, 2000). For over a century Yohimbine has been used as an aphrodisiac, and only recently has it become clear that Yohimbine has central effects (in the brain), increasing sexual arousal, as well as peripheral effects, blocking the catecholamine induced contractility in the smooth muscle of the penis (Bancroft, 2000). Alpha-2 receptors are located throughout the body on blood vessels and in the intestines as well, which explains some of the side effects (indigestion, nausea, dizziness, headache) experienced following the intake of Yohimbine (Crenshaw and Goldberg, 1996).

There are other ways smooth muscle cells in the penis can relax, resulting in an erection: During sexual arousal penile nerves release nitric oxide (NO), which activates the smooth muscle cells to release the messenger cyclic guanosine monophosphate (cGMP) inside the cells. It is this messenger signal which tells the contractile proteins inside the smooth muscle cells to stop contracting and to relax. The more of the messenger cGMP that is available inside the cells, the more they relax, and the more blood is channeled to the penis through widened pass ways, causing tumescence and erection.

Viagra enhances erections by increasing cGMP levels in erectile tissue smooth muscle cells. It increases the amount of intracellular cGMP by inhibiting its breakdown through the enzyme type 5 phosphodiesterase (PDE 5). Viagra only works in men who are sexually aroused (take a Viagra, mow the lawn, and nothing happens) and who produce some cGMP on their own. The drug can enhance a minor erection by making sure that the cGMP produced stays around in the cells for a while longer, instead of being removed by PDE 5. For men taking heart medication such as nitrates, Viagra can fatally potentiate the medicine effect and the cGMP released upon medicine intake may be increased to dangerous levels, causing a potentially deadly drop in blood pressure. It is important to emphasize that this only applies to situations where men take Viagra while simultaneously being on nitrates, and that Viagra otherwise is a safe drug to use. It is of utmost importance that Viagra is prescribed by a doctor and is not shared or taken without a doctor’s consent.

References:
Bancroft, J. (2000) Effects of alpha-2 blockade on sexual response: experimental studies with Delequamine (RS15385); International Journal of Impotence Research; Vol. 12, Suppl. 1, S64-S69
Crenshaw, T. L. & Goldberg, J. P. (1996) Sexual Pharmacology. Drugs That Affect Sexual Function. W. W. Norton & Company. New York. London; ISBN: 0-393-70144-1
Goldstein, I. (2000) Oral phentolamine: an alpha-1, alpha-2 adrenergic antagonist for the treatment of erectile dysfunction; International Journal of Impotence Research; Vol. 12, Suppl. 1, S75-S80
Morales, A. (2000) Yohimbine in erectile dysfunction: the facts; International Journal of Impotence Research; Vol. 12, Suppl. 1, S70-S74
Muller, J.E. et al. (1996) Triggering myocardial infarction by sexual activity. Low absolute risk and prevention by regular physical exertion; Journal of the American Medical Association; 275, 1405-1409

http://www.ejhs … lume3/book8.htm

From the * Microsurgical Potency Reconstruction Center, Taiwan Adventist Hospital, Taipei Medical University Hospital, the {ddagger} Department of Anatomy, College of Medicine, Taipei Medical University, and the {dagger} Department of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei, Taiwan, Republic of China.

Correspondence to: Dr Geng-Long Hsu, Microsurgical Potency Reconstruction Center, Taiwan Adventist Hospital, 424 Pa-Te Rd, Sec 2, Taipei 10558, Taiwan, Republic of China (e-mail: glhsu@tahsda.org.tw).

To investigate the anatomy of the ischiocavernosus muscle, bulbospongiosus muscle, and tunica albuginea and to determine their relationships to smooth muscle, which is a key element of penile sinusoids, we performed cadaveric dissection and histologic examinations of 35 adult human male cadavers. The tunica of the corpora cavernosa is a bilayered structure that can be divided into an inner circular layer and an outer longitudinal layer. The outer longitudinal layer is an incomplete coat that is absent between the 5-o’clock and 7-o’clock positions where 2 triangular ligamentous structures form. These structures, termed the ventral thickening, are a continuation of the anterior fibers of the left and right bulbospongiosus muscles. On the dorsal aspect, between the 1-o’clock and 11-o’clock positions, is a region called the dorsal thickening, a radiating aspect of the bilateral ischiocavernosus muscles. In the corpora cavernosa, skeletal muscle contains and supports smooth muscle, which is an essential element in the sinusoids. This relationship plays an important part in the blood vessels’ ability to supply the blood to meet the requirements for erection, whereas in the corpus spongiosum, skeletal muscle partially entraps the smooth muscle to allow ejaculation when erect. In the glans penis, however, the distal ligament, a continuation of the outer longitudinal layer of the tunica, is arranged centrally and acts as a trunk of the glans penis. Without this strong ligament, the glans would be too weak to bear the buckling pressure generated during coitus. A significant difference exists in the thickness of the dorsal thickening, the ventral thickening, and the distal ligament between the potent and impotent groups (P <= .01). Together, the anatomic relationships between skeletal muscle and smooth muscle within the human penis explain many physiologic phenomena, such as erection, ejaculation, the intracavernous pressure surge during ejaculation, and the pull-back force against the glans penis during anal constriction. This improvement in the modeling of the anatomic-physiologic relationship between these structures has clinical implications for penile surgeries.

Key words: Corpora cavernosa, corpus spongiosum, bulbospongiosus muscle, ischiocavernosus muscle, distal ligament, tunica albuginea

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

Great info spark! Very interesting!

Clearly explains “performance anxiety.”

So that’s why Yohimbine works

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

It would be interesting to know if and to what extent physical stress affects smooth muscle relaxation. You may be right,
excess stress (maybe due to over-training) could lead to SM atrophy.

Doesn’t that depend on how sexy your lawn is?

:couch:

My penis has been overtained/overwanked for a long time. My erections are mostly crap but when I take yohimbe or viagra my erections are throbbing, stronger and longer and thicker (bout 0.5” longer, head full and hard rather than small and soft and shaft bit thicker) and remain hard for hours. I rarely achieve this without these pills and I’m only 24. I hope one day again it’ll be possible to get erections like this without these pills. But I’m a chronic masturbator and I believe never get a chance to repair unless I give it a long term break, but it’s too hard ;-) Even one week without touching it is tough going. I think I need 1 month of no touching but my brain would explode so??????

Maybe some sex addict therapy?

Sounds like the equipment is fine, just overworked (or overwanked :leftie: ).

May I ask how old you are?

This is really outside of the scope of this thread, but look into the fleshlight. The problem isn’t the masturbation, but the amount of stress you induce doing it. If you use the fleshlight, and lay off PE for a couple weeks, it should fix the problem.

The other thing is read this;

Movin On Up

It will give you an idea of how little may be needed to gain. But really, if its totally compulsive, the fleshlight will greatly decrease the wear and tear that excessive hand pressure can cause. Just google fleshlight.

Well said sparkyx.

Now. About your sexy lawn…

Phentolamine has been around for a long time, so long in fact most docs and pharmacists have forgotten its brand name.

It is a very strong alpha blocker and is reserved mainly for treating the blood pressure spikes in people with pheochromocytoma (a epiphrine/adrenaline secreting tumor that causes astronomical spikes in blood pressue) and cocaine overdoses. Its use in routine blood pressure management is rare. It can cause severe drops in blood pressure particularly when you stand up. I wouldn’t prescribe it. I have used it in an intravenous form for the 2 problems I described, but there are much better drugs used now. I’m away from my sources to tell you whether it is available now in an oral form.

Sorry didn’t mean to crash the thread with my problems, just ignore. Just really mentioning here about how viagra etc has enabled my penis too be bigger than normal. However this is? I’m thinking it’s just because my penis is overwoked and therefore not achieving its full natural potential without chemicals. What this means I don’t know? Why can viagra lead an overworked penis to a super full erection one day and the next day this penis wont achieve the same standard of erection. Viagra shows my penis is capable of it and at only 24 it should be like this always? Anyways.

Cool, I actually spoke with you before on another thread a few times. Gave some good advice before. I have bought a fleshlight and it has been of great use in cutting down on hand masturbation and in fact leads to better erections and better orgasms. But the only problem IMO is it’s not so handy and convienent as your hand. But I suppose you have to work your way into a girl’s pants so you could look at preparing the fleshlight as the equivelant LOL.

As for complusive masturbation, my job (security type thing) is so quiet and boring I often sit in a cupboard or empty room and masturbate as there is nothing else to do, can’t take my fleshlight to work LOL. Or maybe I could.

Boss: ‘Hey. What’s that on your desk there?’
Security: ‘Hey gaffer. It’s just my new torch. In times of darkness it will be of great use.’

HAHA.

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

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?

Yohimbine has both alpha-1 and alpha-2 receptor actions. This is why it increase blood pressure. People with high blood pressure are warned not to use it unless under the recommendations and care of a doctor.

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.

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…