I am also under emotional stress right now and have been for 6 months. Personal issues. So that could coincide with what you are saying above.
The Penis (smooth) Muscle Theory
- Thread starter remek
- Start date
In reference to the post, your wording was dead-on with what I was thinking - that "the smooth muscle volume isn't sufficent to press firmly against the tunica." I changed the wording around and added a little bit more. It's still a rough draft at this point, but I wanted to make sure that we were accounting for all the things that could be causing weaker erections. Let me know what you think.
I noticed that thread and haven't had a chance to check it out. I just finished PMing sparky, and we're thinking similarly in that we're all wondering: How can we focus our routines more? There have to be clues the penis is giving off!
He does, however, have a few differences in opinion. Chiefly, he thinks that the tunica is the MAIN limiting factor and that once we expand that, the smooth muscle will just come automatically.
In any regard, I absolutely think that when we overtrain we're stressing our smooth muscle. It makes the most sense. The smooth muscle becomes "fatigued," like regular muscle, and thus it can't work as effectively - and in a sense creating a "gap," as it can't relax enough to press against the tunica. Skeletal muscle acts similar when it is overtrained; the muscle becomes sore and nearly unusable in some cases.
I'm not sure how much this would affect our BPEL, though. I think it would affect it to some degree, as weaker erections lead to a smaller penis. What do you think?
Yea, I think this has a lot to do with your slightly weaker and inconsistent erections. Stress can play a tremendous roll on erection strength - especially if something has been stressing you for that long.
Interesting article in Circulation research about Smooth Muscle growth.
Changes in blood pressure or flow induce arterial remodeling that normalizes mechanical loads that are imposed on arterial tissue. Arteries are also under substantial longitudinal stretch (axial strain) that may be altered by growth or atrophy of tissues to which they are attached. We therefore tested whether axial strain is also regulated in a negative feedback manner through arterial remodeling. Axial strain in rabbit carotid arteries was increased from 62±2% to 97±2% without altering other mechanical loads on wall tissues. Strain was reduced within 3 days and completely normalized by 7 days. Remodeling involved tissue elaboration, endothelial cell replication rates were increased by >50-fold and smooth muscle cell replication rates were increased by >15-fold, and substantially elevated DNA, elastin, and collagen contents were recorded.
Wall Tissue Remodeling Regulates Longitudinal Tension in Arteries -- Jackson et al. 90 (8): 918 -- Circulation Research
Changes in blood pressure or flow induce arterial remodeling that normalizes mechanical loads that are imposed on arterial tissue. Arteries are also under substantial longitudinal stretch (axial strain) that may be altered by growth or atrophy of tissues to which they are attached. We therefore tested whether axial strain is also regulated in a negative feedback manner through arterial remodeling. Axial strain in rabbit carotid arteries was increased from 62±2% to 97±2% without altering other mechanical loads on wall tissues. Strain was reduced within 3 days and completely normalized by 7 days. Remodeling involved tissue elaboration, endothelial cell replication rates were increased by >50-fold and smooth muscle cell replication rates were increased by >15-fold, and substantially elevated DNA, elastin, and collagen contents were recorded.
Wall Tissue Remodeling Regulates Longitudinal Tension in Arteries -- Jackson et al. 90 (8): 918 -- Circulation Research
Another one:
Mechanical Stretching Stimulates Smooth Muscle Cell Growth, Nuclear Protein Import, and Nuclear Pore Expression through Mitogen-activated Protein Kinase Activation*
Vascular smooth muscle cells that were mechanically stretched exhibited an increase in proliferating cell nuclear antigen expression, cell number, and cell size within 24–48 h.
Vascular smooth muscle cells (VSMCs)3 within the vessel wall are continuously exposed to mechanical cyclic strain due to changes in blood flow and pressure. Under normal conditions, the vessel wall is subjected to hemodynamic forces that can stretch the large arteries up to 10% (1–3). During conditions of hypertension, physical stress on the arterial vessel walls can increase to 30% (2, 4–6). This stretch directly leads to the growth of VSMCs (2, 7–10). Cell growth in the form of hyperplasia and/or cell hypertrophy is an active process that requires cells to enter the cell cycle through the induction of cell cycle regulatory proteins (11–14).
Mechanical Stretch of VSMCs Stimulates Cell Growth—VSMCs were mechanically stretched to stimulate cell growth. After 48 h of stretch, the cells exhibited a significant 5-fold increase in proliferating cell nuclear antigen expression when compared with non-stretched control cells (Fig. 1A). This would suggest that the stretched cells were actively entering the cell cycle. Cell counts confirmed that the cells were completing the cell cycle. There was a significant increase in cell number in a time-dependent manner as a function of the stretch stimulus (Fig. 1B)
Cell hypertrophy is another type of cell growth that may be stimulated by cell stretching. Cell hypertrophy was determined using the cytoplasmic probe calcein AM to measure total cell volume. Cells stimulated by stretching exhibited a significant increase in cell size compared with the non-stretched control group (Fig. 1C). This too was blocked in the presence of 1 µ[SIZE=-2]M[/SIZE] PD98059. These results demonstrate that mechanical stretching is capable of inducing both hyperplasia and hypertrophy in the SMCs and that this appears to occur in an MAPK-dependent manner.
Mechanical Stretching Stimulates Smooth Muscle Cell Growth, Nuclear Protein Import, and Nuclear Pore Expression through Mitogen-activated Protein Kinase Activation -- Richard et al. 282 (32): 23081 -- Journal of Biological Chemistry
Mechanical Stretching Stimulates Smooth Muscle Cell Growth, Nuclear Protein Import, and Nuclear Pore Expression through Mitogen-activated Protein Kinase Activation*
Vascular smooth muscle cells that were mechanically stretched exhibited an increase in proliferating cell nuclear antigen expression, cell number, and cell size within 24–48 h.
Vascular smooth muscle cells (VSMCs)3 within the vessel wall are continuously exposed to mechanical cyclic strain due to changes in blood flow and pressure. Under normal conditions, the vessel wall is subjected to hemodynamic forces that can stretch the large arteries up to 10% (1–3). During conditions of hypertension, physical stress on the arterial vessel walls can increase to 30% (2, 4–6). This stretch directly leads to the growth of VSMCs (2, 7–10). Cell growth in the form of hyperplasia and/or cell hypertrophy is an active process that requires cells to enter the cell cycle through the induction of cell cycle regulatory proteins (11–14).
Mechanical Stretch of VSMCs Stimulates Cell Growth—VSMCs were mechanically stretched to stimulate cell growth. After 48 h of stretch, the cells exhibited a significant 5-fold increase in proliferating cell nuclear antigen expression when compared with non-stretched control cells (Fig. 1A). This would suggest that the stretched cells were actively entering the cell cycle. Cell counts confirmed that the cells were completing the cell cycle. There was a significant increase in cell number in a time-dependent manner as a function of the stretch stimulus (Fig. 1B)
Cell hypertrophy is another type of cell growth that may be stimulated by cell stretching. Cell hypertrophy was determined using the cytoplasmic probe calcein AM to measure total cell volume. Cells stimulated by stretching exhibited a significant increase in cell size compared with the non-stretched control group (Fig. 1C). This too was blocked in the presence of 1 µ[SIZE=-2]M[/SIZE] PD98059. These results demonstrate that mechanical stretching is capable of inducing both hyperplasia and hypertrophy in the SMCs and that this appears to occur in an MAPK-dependent manner.
Mechanical Stretching Stimulates Smooth Muscle Cell Growth, Nuclear Protein Import, and Nuclear Pore Expression through Mitogen-activated Protein Kinase Activation -- Richard et al. 282 (32): 23081 -- Journal of Biological Chemistry
Last edited:
Does the above article about stretching and smooth muscle indicate that sparkyx is correct in his theory that the tunica is the main limiting factor and when stretched the SM will follow? Therefore stretching indeed helps a lot..By the way just ignore me if you feel the need just find this interesting, always good to know whats happening to my penis when I pe.
Interesting. Perhaps stretching/hanging causes SM hypertrophy (to some degree, as the tunica will take the blunt of the stress) and uli, clamping, etc causes SM hyperplasia. Or perhaps girth exercises also causes SM hypertrophy, as they are stretching the tunica outward. What do you think about all this, Iguana?
I quickly glanced over this, so tell me if I missed something. . . But from what I gather, an increase in blood flow actually increased cell devision of smooth muscle cells.
I imagine that this has many applications to PE. Here's one:
- What does the Kegel do?!?! It increased blood flow/blood pressure to the penis. What does increased blood pressure do (or according to this study)? It increases smooth muscle cells. What does increased smooth muscle cells do? It increases 1) Hardness 2) Size (if the smooth muscle is the limiting factor). This could possible explain why Kegels increases both of these and why more men should Kegel - especially if they want hardness or if their smooth muscle is their limiting factor.
Slanker, it's really hard to say. The study involved stretching arterial smooth muscles (arteries) which are very very similar to the CC and CS chambers in the penis. Unfortunate for us, but fortunate for them, they were not hindered by the tuncia and could freely stretch the smooth muscle. I think there's no doubt the tunica is the main limiting factor. But this doesn't not always mean that the tunica is what is preventing gains (according to our theory.) As remek correctly pointed out, when manual stretching or hanging the tunica probably absorbs most of the stress and therefore the smooth muscle is not worked as efficiently as with other exercises that generate internal pressure such as jelqing and clamping. I have a feeling that when you effectively stretch out the tunica it doesn't just spill over to fill up the added space. Smooth probably needs to grow and expand to catch up with it.
Very possible! Note that both hyperplasia and hypertrophy were included as a growth response to stretching. It looks like mechanical stretch induces the cells to grow and increase in number. This could explain why hangers report an increase in base girth? It would be interesting to know if both happen simultaneously, or one precedes the other.
No, but that's because I don't talk to anyone who only does Kegels (most guys who PE and measure are also doing jelqs, stretches, etc). I have talked to several men who report that they strongly believe Kegels helped them gain on the ruler, though.
Quick note/more on this later: I wonder if the length before girth theory holds any ground, especially in conjunction with this theory. Tunica first. Smooth muscle second. This would hold ground if the SM was easier (or even slightly easier) to enlarge than the tunica.
I was talking to someone about this theory, and he threw in an unexplainable experience that he thinks might relate:
They certainly can hurt. I just started back up with kegels recently after reading your benefits topic again.
I know my PC muscle has certainly become weaker over the last few years. Hopefully, these will help.
remek said:
Interestingly, Base on this assumption, I had always planned on reaching my length goal first and then working on girth. In fact, when compared to length, I have done very little girth work. If our theory holds true, the only problem I can see with trying to reach your length goal before girth would be weakened erections. Which is exactly what I was experiencing. This could happen if the tunica gets too far out ahead of the SM.
remek said:
That is an interesting experience. Especially the part about the flaccid gains coming quickly. This brings up several questions; Is he a newbie? Was he doing any exercises other than fowfers? Were his gains only flaccid? Did he have any girth gains? Did he happen to say what he was doing over the two week period where his EQ started improving?
I think experiences like are very helpful in gaining insight and gathering data. Might make a good thread. I don't know how you would solicit them though?
Yea, I'm curious about the EQ for the many men who've only focused on length for a long period of time and gained it. It would be interesting to see if this also correlates with our theory.
He wasn't a newbie. I'm not sure about the other questions, but I think his gains were only in the flaccid state.
I think once we release the theory there will be plenty of useful data coming in
This is the first time I've seen this thread but I've been intuitively thinking the same thing about loss of EQ through lengthening of the tunica without any increase of vein size (which is naturally done through girth work) to increase blood flow to it. I'm focusing on length right now before I start on my girth and my erections have been of the same quality on average which I think is from doing kegel work. However, I do believe that if you keep lengthening the tunica without increasing the size of of the veins or power of the blood flow it naturally will take longer for you to get erect and also might lead to loss of EQ. I think it might be worth looking into if our bodies naturally produce more blood and blood cells to compensate for the extra flesh that we're creating. If it does then EQ should remain constant if gains are slow, or if tunica length gains are quick and a loss of EQ occurs then once the body produces the extra blood needed for the body to function properly again the EQ should return back to normal. What do you guys think?
Meh, I've gained over 2" in length with weight hanging in the past, and never had a problem with erection quality.
how long can you do pe before you have to taper off
how long can you do pe before you have to taper off
I saw the info on cementing your gains. I can only do pe two times a week one week, and twice the next because of my crazy work schedule. I was wonder how long I can do pe until I need to cement my gains.
how long can you do pe before you have to taper off
I saw the info on cementing your gains. I can only do pe two times a week one week, and twice the next because of my crazy work schedule. I was wonder how long I can do pe until I need to cement my gains.
SWM: I'd like to dissect you a little bit (figuratively, not literally), as you may offer some more insight into the theory.
When you did your hanging, were you exclusively focusing on length, or was that when you were clamping too?
When you did your hanging, were you exclusively focusing on length, or was that when you were clamping too?
