Smooth Muscle and PE

Phentolamine has been around for too long - no longer patent protected. So noone will invest money because everybody can manufacture and sell the drug.

To answer these questions, you have to answer this one: Are NPT’s restorative (dust off the cobwebs) or recuperative (part of a healing process)? Without real explanation for why we have NPT, we must be empirical.

After evening or early night-time intercourse or masturbation, I have my 1st NPT within 2 - 3 hrs after going to sleep. It tends to be very hard, long lasting and sometimes uncomfortable. After evening PE, my first NPT can be delayed. The intensity of the erection is inversely related to the intensity of the workout, if I have one at all (consistent with negative PI’s).

If NPT was an important recuperative process, wouldn’t you think that they would be more frequent after moderate to intense PE? Experience tells us otherwise. For evening PE within positive PI limits, I think you are right that blood flow and expansion here are restorative. Probably allows ongoing tension-induced connective tissue remodeling to occur at the “new” erect length and/or girth. Cement gains? I’m not sure what that means on an anatomical/physiological level.

AM PE after a night full of NPT’s is probably optimal. Your penis is in prime shape to take your routine and it gives time during the day for recuperation, be that through increased blood flow, remodeling and/or inflammatory processes. This leads to the do you or don’t you let it turtle debate which I won’t touch here. I agree with you proposition here as well.

I personally do both morning and evening routines.

Agree and this why a pill form will probably never be approved by the FDA and probably most European pharmaceutical regulatory bodies as well.

This is why I love getting you and T3 involved in these discussions…thats some AWESOME info there buddy!

Very cool, ok…gonna plug that info into my brain.

Yeah, I don’t propose its the ENTIRE method of normal contraction, just a significant addition to what I already understood or DIDN’T understand before.

The macroscopic structure of the tunica accounts for a whole bunch of the normal movement we see, but I think the smooth muscle accounts for what doesn’t seem to make sense in terms of contractility of the penis due to stimulation such as temperature, stress, PE stress and the like.

Like I previously mentioned, even with mild stress like doing a stretch flaccid bone pressed measurement, I get immediate contraction enough to throw off my measurements my 1/4 inch. I used to be totally confused by that.

Also, if I wake up from a nap, most times I will have a pretty full flaccid, but 1 minute after standing up, it immediately begins to shrink.

So, it makes sense to me that it is a mechanism other than the macroscopic structure of the tunica. The tunica is pretty much an mechanical stress dependant structure, no real structures ( that I know about) than can cause any significant changes due to factors like psychogenic stress…whereas the smooth muscle seems to fit that bill.

Unless there is a safety mechanism involved, which I believe there is.

What follows is pure wild ass speculation on my part.

My best guess is that with enough trauma, some type of chemical signal is released ( I’m thinking smooth muscle is the most likely canidate) which inhibits smooth muscle relaxation, therefore erections, in order to protect an already compromised tissue from further stress from the normal erectile stress.

I feel that’s what leads to decreased EQ and is a strong indicator that the tissue has been traumatized, at least enough to produce this “protective” effect. I also believe when EQ returns, it is a strong indicator that the damaged tissue has healed enough for the body to allow normal function.

I believe this return of EQ is a great indicator that your penis is ready for further PE stimulus.

I heard a lot of reports from guys that say if they don’t use enough PE stress to cause at least a small drop in EQ, they don’t gain as well. In my mind, this tends to bolster my tissue trauma concept.

Like I said, this is wild speculation…for all I know it could be entirely controlled by the nerves in the penis and no tissue trauma or chemical messengers are involved at all, but this is my current thinking on it.

You answered your own question.

I think that is a great definition of “cementing gains”…”it allows ongoing tension-induced connective tissue remodeling (and smooth muscles hyperplasia[?] ) to occur at the “new” erect length and/or girth.”

If the tissue damage is great enough to cause a decrease in NPT, its a strong indicator to modify that level of stress and/or wait until the return of your baseline NPT before you restress the penis.

Further thoughts.

Girth work tends to drop EQ quicker than pure stretching, in general. IF smooth muscle trauma is the initiating mechanism of the “protective reaction” resulting in decreased EQ…do you think girth work tends to create greater stress to the smooth muscle than pure stretching?

To put it in a less convoluted way, why to you think girth work tends to be harder on EQ than stretching…or do you disagree with that generalization?

Girth work can drop EQ level, it is that way with me that is why I only do it 2-3 days per week. Seems to work good this way I grew 3mm of an inch in girth this year and another tenth is evolving right now. If the new girth gain sticks that will be 4mm. That 5.9” may be a 6” in a few weeks.

Really good thread on smooth muscle, hadn’t read it until now.

The Penis (smooth) Muscle Theory

The mechanism here is smooth muscle related.

Standing up activates pressure sensing receptors known as baroreceptors. The most important ones are in the carotid arteries. These receptors normally fire (that is send nerve activity to the brain stem) with increases in blood pressure, as with every heart beat. (If you take electrodes on the nerve leaving one of these receptor areas and amplify the activity, it sounds like a railroad steam engine.)

Standing causes blood to travel to your lower body and your blood pressure suddenly dips. The nerve activity from these receptors also drip suddenly. This activates a reflex that immediately increases sympathetic nerve activity to raise blood pressure so your brain gets blood and you don’t pass out. This burst of activity causes vessels (particularly veins) to constrict via vascular smooth muscle contraction to send blood back to the heart to keep the pressure up.

This burst will cause the smooth muscle in the corpora to contract and take your somewhat fluffy flaccid penis and make it less fluffy and shorter. After the body accommodates to the upright position, sympathetic nerve activity falls back towards normal levels allowing some dilation of sinusoidal smooth muscle and your penis starts to hang prouder.

Very interesting all that.

Let’s try to approach a little the complex ‘smooth muscl & PE’.

If smooth muscle is so important than becasue it forms part of the vessel and sinusoid walls in our dicks. The discussion so far has clearly shown that the vessels - becasue of their smooth muscle wall component are by far not passive elastic tubs but actively regulate their tone in dependence of multiple factors .

Now I would like to address the crucial question: how can we make our vessels/sinusoids grow.

The phenomenon is known as angiogenesis (vessel formation) and we would have to look for angiogenetic factors (those which promote growth).

What I know of hands?

Angiogenetic factors:

- Are secreted by malignant tumors in order to form pathological blood vessels in order to feed the tumor.

- Similarly, a baby in the mother creates blood vessel growth to feed it self

- Ischemia (absence/reduction of blood flow and with subsequent oxygen lack) produces new / bigger vessels.

There are many more, we just have to collect them. The physiologic effects are mediated by chemically identifiable (angiogenetic) substances. Once we know them pe could become a lot easier if the vascular system plays a major role in PE.

There’s a thread going in the Main Member Forum about the merits of infrared (IR) for PE. The original poster was concerned that IR could cause nerve damage. Mile-long-dong found this recent news item about the use of IR to treat Alzheimer’s:

BBC NEWS | Health | Alzheimer’s helmet therapy hope

From the article: "Low level infra-red red is thought to stimulate the growth of cells of all types of tissue and encourage their repair. It is able to penetrate the skin and even get through the skull."

More from the article:

"We age because our cells lose the desire to regenerate and repair themselves. This ultimately results in cell death and decline of the organ functions - for the brain resulting in memory decay and deterioration in general intellectual performance.

"But what if there was a technology that told the cells to repair themselves and that technology was something as simple as a specific wavelength of light?"

And note that the treatment in question was only ten minutes, which they claimed was long enough to have an effect.

Tissue regeneration/repair would seem to be something of potential interest in encouraging healthy tissue growth. So, is IR something that potentially should be added to the list?

For what it is worth, my nocturnal erections seemed to have really increased since I started PE. I am late into the second month, and I started noticing this about 1 or 2 weeks into the second month.

Before I was aware of one or two erections a night. Now it seems that my first one is about an hour after going to sleep, and then it is as if I am erect or semi-erect for most of the night.

Maybe I am just more aware of them and there is really no change. But on the other hand, I usually wake up for a couple minutes every hour or two when I sleep. So I do think there has been a real change.

An example:

The angiogenetic effect of intramuscular administration of b-FGF and a-FGF on cardiac muscle: The influence of exercise on muscle angiogenesis
Authors: Efthimiadou, Anna1; Asimakopoulos, Byron1; Nikolettos, Nikos1; Giatromanolaki, Alexandra2; Sivridis, Efthimios2; Lialiaris, Theodoros3; Papachristou, Dimitrios4; Kontoleon, Eleni1

Source: Journal of Sports Sciences, Volume 24, Number 8, August 2006 , pp. 849-854(6)

Publisher: Taylor and Francis Ltd

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Abstract:

Although angiogenetic therapy using recombinant growth factors holds much hope for the treatment of ischaemic diseases, there are still many unanswered questions, including the method of administration, the correct dose of these factors, and the duration of the therapeutic approach. Exercise has also been suggested to induce neovascularizaiton in muscles. We evaluated the angiogenetic effects of the intramuscular administration of basic-fibroblast growth factor (b-FGF) and acidic-fibroblast growth factor (a-FGF) in rat heart, compared with rats who exercised daily. In conclusion, both the intramuscular administration of b-FGF and exercise increased significantly angiogenesis in the heart in contrast to the intramuscular administration of a-FGF, which was ineffective.
Keywords: Angiogenesis; b-FGF; a-FGF; exercise; cardiac muscle

Document Type: Research article

DOI: 10.1080/02640410500245629

Affiliations: 1: Departments of Physiology 2: Pathology 3: Genetics 4: Medicine-Division of Endocrinology, School of Medicine, Democritus University of Thrace, Alexandroupolis, Greece