Girth theory: glans and corpus cavernosum.

Off topic for this thread. We have quarter of a million members, two and a quarter million posts, and have been going for 14 years. Decide for yourself. The best way is to read around the forums then get started with the Linear Newbie Routine, and judge for yourself. When you see gains, you will believe.

Interestingly, when reading how they(I understand you are in profession too) have to tinker around the muscles and bones to modulate the collagenous tissues properties, we have some advantages having them out the way(of course enter the smooth muscles but they same rather forgiveable)
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They state that heat increases the chances of damaging the collagen.
Less force is needed but that could also turn out unsafe. They state 4 times less force needed to create damage and I guess similar to cause rupture. (Of course only a problem for people doing same intensity heated as “cold”)
Overall heat is a huge benefit. PE Experience,as you and others presented already very well, and science are very clear here I would say. Its a fact that it lowers the needed intensity, I suppose.

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It says tropocollagen bonds are opened and loose their ability to bring the collagen back to zero with heat over 40C.
Now taking this in relation to the prior statements that stretching for over an hour(at rather low tension, without mentioning of added heat) causes permanent changes by melting of the tropocollagen bonds is quiet intruiging.
When talking about higher tension they named it: tearing the gross structure or “disrupting the intermolecular bonds between tropocollagen units.”

So for me I would prefer combining melting and opening instead of disrupting and melting.
Are they just playing with the words “melting” and “opening” or has it a different meaning in the context?
If its different,.. would we want to open and melt at the same time or first open(heat) and then melt(long time low intensity)?
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On another note;
Its interesting how the elastic range is shortened with heat(thus easier to reach plastic range) while it feels like with heat more elasticity is created.

Hope this is comprehensible and not too much at once. I really want to keep it easy to understand.
I really fear loosing my line of thought lol.

More great info dicker. Still haven’t had time to review the book, but I am caught up now on posts.

Doing a little research, tropocollagen bonds are bonds between single collagen molecules. Tropocollagen is the smallest unit of collagen, about 300 nm long, arranged in a thin triple helix strand. Tropocollagen assembles into collagen microfibrils in a winding assembly, in which the end of one tropocollagen is bonded to the beginning of the next. They are parallel, but each starts at the end of the next, and only a small portion, 5-10% is overlapping. The overlapping portion is bound together by what I understand to be a cross-link. So cross links are present in all collagen fibers, as I understand it now. The cross links are not collagen themselves, just a peptide bond. Fibers can be strengthened by having more cross-links than normal, but all fibers contain cross links. The tropocollagen assembles in a helical pattern like this to form microfibrils. The microfibrils assemble similarly to form fibrils, and fibrils make fibers. Fibers assemble into tendons, ligaments, fascia, and for our purposes the tunica.

So breaking a tropocollagen bond would mean causing micro damage at the smallest level, in other words tearing the cross-links within microfibrils. Perhaps the word choice “melting” is in reference to a tropocollagen bond which is opened (broken) under the presence of heat. Otherwise I think they all mean the same thing. When a bond is broken, it’s broken, it’s open, it’s melted, it’s gone. Tearing the gross structure at higher forces - could mean tearing all the bonds through an entire fiber so the fiber breaks. Or it could be referring to breaking the tropocollagen in its helical sturcture, as opposed to the bonds (cross links) from one tropocollagen to the next. Or it could mean breaking bonds between higher level fibers, like the bonds between microfibrils, or between fibrils.

It took some searching but I just found information on ‘tendon healing’ and ‘ligament healing’. Sorry I don’t have links but if you read through the top search results, you’ll find that IPR healing DOES occur in tendons and ligaments, even for micro-damage at the smallest level. This is because an ECM exists within all collagen fibers. Previously this tissue was not thought to regenerate itself in the same way it does during a skin injury. One interesting thought that comes up for me, is that scar tissue within skin is a bad result. The scar tissue aligns itself in only one direction, along the axis of the wound closure. Whereas in healthy skin, the collagen matrix is omnidirectional. Our target tissues in PE are already uni-directional though. In theory, it’s possible that the end stage of tissue remodeling within the tunica results in a tissue very, very similar to the initial structure. The only mention of healing time I saw was approx 1 year to finish remodeling. Another interesting thing I saw was about SRT (soft tissue release) being counterproductive during the first week or two of P-phase. But after that time it was shown to accelerate repair. In other words, massaging the unit or FG rolls could be beneficial during the latter halves of rest periods.

I will have to read this book, sounds like a great resource. I’m not sure how much I can say without it being gross conjecture. I think higher forces likely tear these bonds at a much higher rate than lower forces (to notice PE growth we’re probably talking about breaking millions, billions, or trillions of these bonds). I also think we should be open to the idea that what is considered “injury” in a tendon or ligament may not disrupt the function of the tunica in the same way. I used to be resistant to this idea, but have now embraced it. Whether the damage is at the micro level, or a higher level, I do believe permanent PE growth happens from what the book calls “permanent damage” to these collagen fibers. Permanent damage to me means permanently bigger in our context - if given the chance to heal.

Targeting the smallest level microfibers with low intensity, long time, heated workouts reminds me of Bib’s theories. It makes me think of tropo-bonds breaking at the smallest levels, slowly but surely. And as they break, more of the force is passed on to the remaining bonds. And then they break. And so on, until some of the higher structure bonds (fibrils and fibers) are breaking. Maybe force is increased slightly along the way to target the higher levels bonds. As long as they are broken sequentially, from weakest and smallest structures, to strongest and biggest structures, it will be a kind of controlled damage that Bib talked about. Never shearing the molecules themselves, but always breaking the next strongest bond. Kind of a clean break so to speak, that is perhaps more easily repaired.

I have officially reached babbling. Very glad to have found confirmation that IPR occurs in tissues fully comprised of connective tissue. Good night.

Didn’t sleep, kept thinking. One thought is the rate of change in the stress v strain graphs. ds/dn. It starts at zero, rises to a positive constant, then falls and goes negative. This could be the effect of bonds breaking. As one bond breaks, relatively less additional force is required to break the next bond - because there are less bonds overall resisting the force. Their strength in numbers has decreased by 1. Very Bib.

Now, having there be one less bond does not mean that the next bond will require less force to break. Each bond requires more force than the last to break, up until the ultimate stress. But each bond does require marginally less additional force than the last bond to break.

Going back to the discussion of how to interpret the ultimate stress points and failure in this comparison of metals and tendons to PE, I think there’s a confusion because we can think of two different target tissues. One tissue is a single tropo-C-bond. We want it to fail. In this context, micro-damage occurs and then heals, causing PE growth. The other context is to think of the entire connective tissue, the tunica albuginea. We do not want it to fail. In this context, the ultimate stress would mean a tipping point, at which so many (billions or perhaps trillions) of tropo-C-bonds have failed, and the next bond to fail requires less absolute force than the last, and the tunica itself is ripped clear across. This would be the equivalent of ripping our dicks off. In the first context, we want to go to failure. In the second context, we want to stay a very safe distance away from the ultimate stress level.

Other thoughts.

I currently practice PE in search of strain. A longer stretch / more expansion during the routine = better work out to me. This discussion has raised the idea to me: perhaps I should be practicing in search of breaking bonds. The powerpoint link on tendons showed a stretch / recoil response called hysteresis, which I take to mean that progressively higher amounts of strain are achieved at the same amount of stress by simply releasing and repeating the stretch. Obviously with diminishing returns. It also showed a graph showing that strain was dependent on speed of stretch. Now, maybe not all bonds are broken equally, and there is some value to stretching slowly and repeatedly, to break bonds at the longest point possible. Common sense would say that’s the case. Experienced PE’ers tend to employ these tactics of slower stretches, repeated stretches, stretches at heat - all getting more strain at lower forces. But going back to strain vs breaking bonds. Maybe the slope of the relationship matters as much as the strain achieved.

I’m also currently practicing IPR and going hard at it right out of the gate in I-phase. This discussion makes me think that what matters is how many bonds are broken by the end of I-phase. It is necessary to reach high force levels by the end of I-phase, but it’s not necessary to start with them. Perhaps I-phase is best started with low-intensity, long time exercises, that gradually shift and culminate the cycle in high force exercises - progressively breaking stronger and stronger bonds throughout the cycle.

I was also thinking about Rootsnatty’s stress/relxation robocock extender, and the stretch / recoil response, hysteresis - from the powerpoint. It’s different than most stretches, because a force is applied, and then as the tissues relax. Strain is held constant, and stress decreases as the tissue relaxes. I do not understand the physiology of what’s happening there yet. Perhaps bonds are lengthening without breaking. In contrast, most stretches would apply a constant stress over time, and strain would gradually increase as the tissues “relaxed” into the force, until it got maxed at that stress. This could be a benefit of the stress-relaxation method. Get everything completely strained out at a low force, all the next bonds in line to break are all stretched out and very weak. Then very relatively smaller additional increases in force will break the next bond.

Now I am signing out. Again great info dicker, knowledge brings results.

Superb easy to follow thoughts BD! More food for thoughts yummy.

The tropocollagen bonds: I think The different means of how they are broken and how they used differet names for it, must mean something. Suddenly I like referencing to the metal. You could tear the metal, high force-lowtime or melt it and then stretch to failure or longer.

I think the permanent damage thing ties into this too. Cause there seem to be several ways to arrive at permanent damage.
In the book there is a great picture: Figure 3.7
I think it shows where want to go regarding permanent damage. (you are right about what is injury to them isnt to us, but the rupture declared there is still a rupture we dont want I suppose)
At least at the “end of the range” declared there which puts us into the plastic relm. From where we reach micro trauma where we can be sure to have had an impact on the tissue that is beyond elastic.

And the best basic way, as I intepret it, is heat and long time at rather low force.(but enough to reach the plastic and/or micro trauma range, also called linear region here.).

It goes on to say: In the plastic range tension need to be sustained, And I think that ties into what you said about one bond failling and then the next and so on.. (but not sure)

Well I will read the pages in one sitting to make a whole picture of what they want to say.

As I recall xeno used a ratio of something like 1.1 to increase the intensity of his workouts in the I phase.

You just need to think of connective tissue like fiberglass in a flexible resin.
You can heat it and stretch it lightly and the resin softens and breaks down so the attachment point of the fibers shifts or stretch it hard and break fibers.
Probably with PE both are happening to some degree but I know which end of the spectrum will be the healthier.

BD, you have snatched the pebble.

xeno

:)

Of note:

Priapism (erection longer than 4 hours) — is KNOWN to cause permanent size increase. Unfortunately, it is often uncontrolled and disfiguring.

But, it is prima fascie evidence than even under normal physiological pressures withing the CC, permanent deformation will occur over TIME.

I think this may point to why some members who have consistently pumped for an hour or more at a time under low pressure (3”-5” Hg) have seen tremendous length and girth changes — especially when using heat.

And then there are those who have joined here on Thunders after months of pumping and are frustrated with no gains at all.

How many of them are pumping for an hour, under low pressure, multiple times a day?

I think only a handful of members on the board approach 3 hours a day with sessions an hour long.

This is the reported regimen of one poster.

Right. Makes total sense.
Thats what the research over the last pages and its references in literature also suggests.

I would always choose low intensity long time over anything else if the circumstances allow that.
Cause it seems that it would help maximizing total gains. With short high intensity chances are the tissue gets either hard and doesnt grow or it grows but the threshold to grow more gets too high.

Another option is to mix it up and have some higher intensity at the end of long time lwo intensity or the other way around.
Not sure what indicators would speak for which scenario.

I gained length through rather intense but short manual stretches followed by immediate long time low intensity extending.

This is a very interesting thread! I would love to see more follow ups with all the great material here?

Yeah it’s a great would like to see any new updates.

Has there been any research in chemicals that would weaken the tunica to allow it to expand or lengthen? The reason I ask is because, if you get too many cortisone shots around or in ligaments they weaken and can over stretch . Which may not be so bad in what we are trying to achieve with the stubborn tunica.