Clamping: Advanced Empirical Discussion

Just updating you guys:

I think I’ve concluded that EVO > heat. The reason we apply cold/hot pads or the IR lamp is to encourage blood circulation and healing. I never found it that useful, it helped, but only marginally. Last night I slept with the evo on and used it today in between sessions of clamping - extremely good results. This is the first technique that really helped me with healing.

Sparkx’s comment is important to keep in mind, but so long as you know your limit and are going there anyway, the EVO really helps limit discomfort of clamping. I expect it’s also speeding up healing. I do know that my tool doesn’t feel or look this way unless I take a 2-3 day break usually, and this was just from one night of sleep in EVO.

Highly recommended: but test somewhere else on your skin first to make sure you won’t have a bad reaction. I’m going to keep sleeping in the EVO and using it in between my sessions during the day (I have an 8 hour lapse between the 2 usually).

Edit: If Sparkx is correct and this thing only repairs only the minor blood vessels, why have most of the users (and myself already) experienced an increase in vascularity? I can see the larger blood vessels more clearly. Also, if it works topically, which it seems to, then some of it must be getting into the blood stream. In addition to those 2 things, it repaired a larger blood vessel for EVO (judging by the size of the thrombosed vain he mentioned). So it seems that this solution might be working for even the non-visible larger blood vessels Sparkx.

PE for Life.

Mentions loss of girth after stopping clamping. Maybe there is something to the cementing gains issue? But what does that say about the process we are going through then? Would deformation need to be "cemented"? What process could stagnate and then retract so quickly?

Regarding increasing frequency over time:

Marinera’s post got me thinking (as his posts often do). BG increased his clamping frequency over time. When he saw massive results from clamping, he slowly moved to do clamping marathons on weekends and then even more often, from what I can tell, leading up to doing 16 sets per day. He maintained all set times to 10 minutes throughout, from what I can tell.

The interesting thing is that (from what I can tell - BG correct me if I’m wrong), he seems to have gained most of his gains by 2005. He mentions going to a nudist camp with a clamping/pumping swollen tool that went from 8 inches to level off at 6.5. He continued to clamp for a large amount of time afterward, making his marathons more frequent and intense - yet his EG seems to have remained at 6.5.

What does this say about the underlying process, and how we should affect it? Assume BG gained the majority of his gains, continued to increase daily frequency and even frequency per week, but made no real gains. He called this “cementing,” but lets ignore terminology: the reality is that he continued to clamp and even did it more frequent per day and more days per week and did not gain.

I am thinking that if we are gaining because of Marinera’s theory, that the tool grows in size because it needs to be large enough to maintain oxygen through this time period, it will grow for a 10 minute clamp session more and more until it reaches a limit. It will not grow past that limit, because it no longer needs to - the body responds to incentives. Even if you do the 10 minute clamp 10 more times in a day, the penis has reacted and conditioned itself for the 10 minute clamps. If this theory is true, assuming these empirical results from BG, I believe that once the body has reacted sufficiently to the 10 minute clamps and growth does not continue, the period in clamp must be increased to incentivize more growth.

This might be dangerous and we may not have reason to do if our dicks grow large enough from the 10 minute clamps, but it seems sufficiently logical that if we wanted to grow more at that point, and the oxygenation theory is true, the only way to do so would be to increase time under clamp - frequency would yield no more benefits after a certain amount, frequency should be maintained at the optimal level (which we don’t know, but leave that to later). Clampathons would be completely useless once the penis has grown to its maximum amount given the time under clamp.

This logic seems to hold if we assume the cause of growth to be a need for adjusting to time without oxygen. So if this is the cause, this is the only logically consistent way to grow larger past a maximum determined by sufficient frequency and a certain time under clamp. Agreed?

What I am beginning to think is this: new clampers shouldn’t jump to 10 minutes. There must be some minimum amount of time to induce growth. We need to find out an optimal frequency (it will not be a clampathon - that doesn’t make sense with this assumed cause, if it turns out that growth has a different cause then maybe), and then given that frequency clampers should slowly increase time, beginning at the absolute minimum amount of time under clamp needed to incentivize growth. Clampers would then reach a point of no growth at each time (say starting at 5 minutes), at which point they would need to add time under clamp (say 2 minutes each time they reach a sufficient period of no growth, indicating the body has finished adjusting to the time).

Remember, this model only works if the theory, and its assumption of causality, is true. However, if the cause is deformation for example, then increasing frequency would work, but gains would stop due to needing more growth under clamp, which would be impossible at one point, where we could no longer do anything to induce growth under clamping.

What’s bothering me: the loss of girth after stopping clamping (link posted above). What does this mean? Could smooth muscle grow and then suddenly go back? I expect so. Could collagen grow and then suddenly (within a month) decrease? I doubt it, from my extremely limited knowledge of collagen growth. But how would smooth muscle remain grown after clamping is completely stopped for a long period? From my limited knowledge of hypertrophy, this seems impossible. Maybe if it is muscle growth, then smooth muscle hypertrophy is different than other hypertrophy?

Marinera —- what do you think? Do you agree with the model, assuming the cause? What do you think this loss of girth indicates about causality?

Well, it’s just putting ideas based on near nothing really known (I’m good at this :D ), but:

if the growth is just ‘elastic’ growth (so not significative amount of new tissue is gained), then it makes sense that it last less time than ‘real’ growth.

Supposing smooth muscle hypertrophy causes elastic deformation of connective tissue, once the stimulus isn’t anymore applied consistently enough, smooth muscle hypertrophy tends to go back to previous (pre-PE) size :this is true for striated muscle, why should not be true for smooth muscle? So, it could explain loss of size on both planes : connective tissue is less stretched by the hypertrophied smooth muscle.

I asked previously about the expansion through pumping: I have very little experience with pumping, but I’d say the expansion (neat of fluid build-up) is bigger with pumping (at least with high pressures) than with clamping. So, micro-tears are created more likely through pumping than through clamping. Micro-tears require healing - so, rest.

That’s why pumping everyday, expecially with high pressures, gives no gains : too much trauma, too little recover.

It’s a group of hypothesis I’m posing : they seem consistent to my eyes, but I don’t have any kind of back-up.

First thing first: we should search for studies that could proove the link - [lack of oxygenation -> smooth muscle growth]; this link seems to be sustainable (basing on some studies) for striated muscle. Anyone who could help doing this ‘homework’?

P.S.: I’m pretty on a hurry right now, so if this post isn’t understanble, I apologize in advance.

1. What I meant about hypertrophy of smooth muscle was exclusive to the hypertrophy, in that I don’t think deformation is related to cartilage - the muscle hypertrophies and the dick grows from that. That would explain why there is no or close to no length gains. Also, many notice gains heavier on the bottom side of the penis, where that line (anatomy? don’t know the name of it) is: does this have more smooth muscle? If so, it would support the conjecture.

2. Clamping everyday causes better gains, that is pretty close to established. The major gainers clamped ED, plus we have Kaan’s hypothesis (tried ED and not ED and had better results ED). This is the part that screws with our hypertrophy of smooth muscle issue, for the hypertrophy to occur, we need tears, and for tears to heal, we need time off. So why don’t we need, better yet, why is it better to clamp ED?

There is some function that we don’t understand (how the penis grows through oxygen starvation), but it is a reasonable cause from what I can tell. There may not be any tears at all, the incentive may be the lack of oxygen. In striated muscle, hypertrophy occurs through tears. We may simply be dealing with a process that is incentivized through oxygen starvation. IF that is the case, ED clamping would at least not be less beneficial than taking breaks.

For the guys not interested in the causality or process of growth, what we are assuming so far is telling us this:

First, there should be an optimal level of clamping sets per day (dependent on the person), likely between 2-16. Second, clampers would want to start at the minimal time under clamp for all sets (between 1-10 minutes) and then ramp up time under clamping only once gains stop at the current time under clamping. Increasing the frequency from the optimal time should yield no additional results. IE = if this causality theory is true, clampathons would be useless (unless optimal frquency is actually a clampathon, but this is refuted by BG’s growth under less frequency and lack of additional growth under clampathons). Pressure under clamp could also be a variable factor, but it isn’t easily measured, so for convenience lets constrain it in the model to full pressure (rock hard glans). So under this theory of causality, the variable factor to be manipulated is time under clamp, with frequency per day (ED) constrained to some optimal number of sets (unknown).

Lets set TUC as time under clamp for discussion and CF as clamping frequency for day, to make it easier to discuss.

I’m referring to connective tissue when speaking of growth as consequence of micro-tears, not to smooth muscle.

The base girth could be explained by lack of oxygen as well, and pressure exerted by the clamp on that zone.

So what you are saying, clamping might be a form of self induced priapism?

Taken from pegym:

I didn’t say “minor”, I said SUPERFICIAL, by that I mean vessels of the surface or close to it. I don’t think it penetrates very deeply so I don’t think it will strengthen deeper vessels or tissues and it might give you a false sense of security.

Then again, as long as you don’t use it to significantly up your pressure, the larger AND deeper vessels should be fine.

When you quote BG and his gains and procedures its CRITICAL to realize that BG himself admits to damaging his unit more than he should have, and now denounces that approach.

I would agree with sparkyx on that, for sure.

This popular(?!) idea is the same hypothesis I’m speaking of.

“Thus spake marinera!”

I like it! It could be a tone poem.

Thank you Hap. :)

I’ve done a fast search on google:

Continuous Nitric Oxide Inhalation Reduces Pulmonary Arterial Structural Changes, Right Ventricular Hypertrophy, and Growth Retardation in the Hypoxic Newborn Rat

Jesse D. Roberts, Jr, Carole T. Roberts, Rosemary C. Jones, Warren M. Zapol, Kenneth D. Bloch

(Circulation Research. 1995;76:215-222.)

"……………

Breathing low oxygen levels for several weeks produces progressive pulmonary artery hypertension and smooth muscle hypertrophy and hyperplasia in many species…."

Link 1

Mild hypoxia induces hypertrophy of cultured neonatal rat cardiomyocytes: a possible endogenous endothelin-1-mediated mechanism.

Ito H, Adachi S, Tamamori M, Fujisaki H, Tanaka M, Lin M, Akimoto H, Marumo F, Hiroe M.

"Hypoxic or ischemic stresses on cardiomyocytes may cause a variety of compensatory responses including cell hypertrophy. In this study, we examined whether hypoxia induces hypertrophy of cardiomyocytes in vitro …………..These data suggest that mild hypoxia induces hypertrophy of cardiomyocytes .."

J Mol Cell Cardiol, 1996 Jun;28(6):1271-7.

Link 2

I still have to find something specific on smooth muscles of the penis.

Just a side note: hanging with a Bib’ cause also base girth. Bib’ hanger also cuts blood-flow; could it be that local ischemia has a role in base girth gains both in clamping and hanging?

I feel that this is the case. Our de-oxygenation cause might case the area that is cut off to grow larger to hold more blood when clamped. Makes sense?