Girth theory: glans and corpus cavernosum.

SteadyGains, muscle undergoes fiber hypertrophy with very little (if any) increase in fiber numbers. Muscle fibers are muscle cells; they are alive. Collagen fibers in connective tissue are not. Increases in fiber length or fiber diameter comes from stimulation of fibroblasts to make more collagen subunits which spontaneously assemble when dumped outside the cell. The best stimulus is tension induced.

Short, intense tension will probably add some length initially but more than likely fiber diameter will increase at a faster rate (stronger, not that much longer).

I’ve been thinking about the understanding that collagen assembly is spontaneous. This would suggest to me that PE maneuvers that give longer, sustained stretch at moderate forces or ADS after intense forces to give stretch to the collagen fibers which might allow for spontaneous assembly into existing fibers at a longer fiber length without the need for IPR.

Just a thought.

I totally agree that pressure is important, but so is blood volume when it comes to the glans. When the volume is high enough to pinch off the draining veins in the head, it mushrooms to full size. Further pressure expands the size because its prominent elastic fiber component keeps the glans compliant. Do elastic fibers expand in length to give even greater expansion. We know from experience it does, we just don’t know the mechanism. I don’t think that stretching makes them more compliant. Is it tension induced elastic fiber remodeling? Don’t know yet

It is also important to note that collagen fibers align in the direction of stress. If stimulation is short and intense, the secretion of the c. Fibres thereafter will be random if there is no stress. Random distribution means thickening. If there is still stress applied during the orientation phase of the c. Fibres they will align in parallel to the stress orientation and there will be a potential for growth.

This holds for both girth and length work.

There comes a time when collagen fiber normal stress manifests growth, albeit radial, more reliably than does continued longitudinal stress application. Excepting the phenomenally precise application of IPR principles to maximize elasticity potential/minimize contraction response…strongly advise against this pursuit unless you’re prepared to be more critically analytical than me…believe that to be practically impracticable…well, length gains become very difficult. Stress induced collagen speciation results in a tunica structure that simply has too low a modulus of elasticity to accomplish elongation in the direction of fiber growth…2 years of 200-300lb. hanging = 0.125” EL gain so indicate. Rather advise that one achieve what they can length-wise…and DO USE IPR PRINCIPLES…and then seek to maximize girth…and use IPR principles here too. Use distraction principles too…longitudinal strain (which may require significant longitudinal stress) to develop potential for radial strain.

Might write a more complete treatise that includes suggested training protocols some day.

Very interesting.

The interdependence between girth and length is somehow in contradiction to pudendum’s anatomical sketch of the tunica with two layers, one circumferential and one longitudinal.

However, this is certainly overly simplistic, because one strength factor of collagen are the CROSS-LINKS which run more or less perpendicular to the main fiber orientation. These cross links give the circ. Fibers a longitudinal component and vice versa - more like a meshwork which would explain much better - in my eyes - the interdependence between girth and length.

Can some one explain how the CC is built?
I mean what is inside, and how does the CC grows?
I’m going to use IGF1-lr3 in my CC, and I want to know what is going to happen, IGF-1lr3 causes cell division = more cells, but I’m afraid to get a mutation penis, I just want to know what supposed to be divided in the CC?

Thanks.

Go check the chemical pe-threads.

Continuing my thought:

So when you are in a length routine, e.g. Hanging it might be interesting to crack these cross-links by clamping every once in a while.

Incidentally, vitamin c is known to strengthen the cross links.

Please make my head bigger Mr.ticktickticker!

xeno seems to be developing a case of the dots….

Exactly.

Photomicrographs do not support your contentions of extensive horizontal cross-links between collagen fiber bundles. There are occasional hinge-like fibers found in the relaxed tunica. I cited a study in another thread where tunica segments were place over a thin cylinder and stretched by pressure to simulate elevated CC pressures (some to over 300 mm Hg). The bundles within these tunica undergo biaxial stretch. They were then fixed in this position and prepared for viewing under a microscope. The collagen fiber bundles (not individual collagen fibers) exhibited significant splay (“creep”) between bundles.

IMO the circumferential inner layers splay longitudinally with stretch (biaxial to the long axis of the fiber bundles) and the longitudinal bundles in the outer layers splay circumstantially with tumescence.

I don’t consider this simplistic. I consider it functionally elegant.

We are working on it :) .

I don’t know where the cross links are located exactly. May be not between the fiber bundles but between individual collagen molecules. These would not be visible on microscopic images.

Here - I just found it: "The biological function of fibrillar collagen is to provide the tissue with tensile strength. The tensile strength is due to the covalent bonds, known as collagen cross-links, that develop between individual collagen molecules in a collagen fiber. \" Check this link if you like:

http://herkules .oulu.fi/isbn95 … /html/x383.html

I am not sure though whether these cross links can be broken through mechanical interaction.

I totally agree that like any other protein, collagen has multiple interactions (covalent, van der Waals, electron) that bind individual collagen fibers to one another to form discrete collagen bundles. I am talking about collagen bundle cross-links and splay, not individual fibers.

I dare say you will rip your penis off your body before you can apply enough force (energy) to break the covalent bonds between the collagen fibers. You could hang cars and you wouldn’t affect these bonds. You’ll rip the collagen bundles apart but not the fiber interactions.

IMO collagen bundle splay in one layer allows semi-independent PE work in the other (we know that hanging increases girth as well). The resistance and plateau we observe over time comes from increase in the collagen bundle diameter in the direction of our efforts and not from cross-links between the fibers running perpendicular in the other TA layer.