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For Science minded PE'ers

Originally Posted by Shiver
Alice,

something I often wonder about is gains in ligs vs tunica with hanging. I’ve never used a hanger as it seems most if its benefits are in lig stretching and I want to keep my ligs exactly where they are (or even tighter). Do you think there is any benefit to be had in the tunica using a hanger (OTS/SO etc)?

I like your question and I will answer it the best I can, but I am not an expert, just trial and error on my part. First of all, I hate OTS and upper angles with a passion, the reason is they limit movement and/or cause too much stress on my shoulder. I’m a jittery kind of fellow that didn’t mind walking around the room or house with weights dangling off my cock, I simply couldn’t set still.

There is, of course, benefit in hanging upper angles, but I do have the belief that when the ligs are elongated to the max, more and more stress is taken up by the inner tunica. This worked for me and extended my time hanging by not driving me cuckoo, you have to somewhat enjoy what you are doing.

I hope this helps a little.

Ah

Shiver,

Yes, most definitely!

All of my hanging of late has been SO with a fulcrum…and that is when I started to make any real gains hanging. I did make some small gains hanging SD, but even though I hung to fatigue the time hanging/reward ratio was very poor for me. Far better once I switched to hanging SO.

I was thinking that I read somewhere that the ratio of collagen to elastin was important…specifically that too much collagen was a reason for ED as men get older. Would too much collagen prevent the normal (and as we age…sub-normal) blood pressure from fully expanding the CC?

Originally Posted by swinglow
I was thinking that I read somewhere that the ratio of collagen to elastin was important…specifically that too much collagen was a reason for ED as men get older. Would too much collagen prevent the normal (and as we age…sub-normal) blood pressure from fully expanding the CC?

Without elastin, the smooth muscles in your CC’s may not be able to relax as effectively. As it turns out, it’s the relaxation, rather than flexing, of these muscles that gives you a hard on.

I’m not that knowledgeable yet about the functioning of the muscles. Maybe WestLA will give you a better answer.

Originally Posted by Shiver
http://www.redwingbooks.com/html/ca…/TL_Extract.pdf

“When the inflammatory process is prolonged, it causes problems for the ligament or tendon that is healing. Continued inflammation leads to excessive adhesion, fibrosis, and scarring. There will be inapropriate cross-linking of the fibers which contributes to dense, inflexible tissue. The developing fiber orientation is often random and scattered (not parallel).”

Shiver,

This sounds terrible, but I don’t believe this is what happens when you PE. I think this type of problem is more what happens with carpal tunnel syndrome or other repetitive motion disorders, where you keep punishing the tendons and they keep swelling, without getting what they need to heal.

It does serve as kind of a warning to PE’ers, however, not to work out to the point of continuous inflammation. Problem is, I’m not sure what “continuous inflammation” means. I think it’s more than just soreness. This is also a good reason to include NSAIDs in your PE toolkit.

Do you feel NSAIDs would hinder healing though? Inflammation is after all part of a healthy response so long as it doesn’t become a cyclical self reinforcing issue.

I mentioned in another thread that verapamil might be something to consider. There are studies showing some impressive results with it for peyronies in topical form (contrasting sharply results using it by injection). I have other experiments to try our first, but I may tinker with making a topical verapamil gel at some point. I think you could home brew a years supply for around $80-90.

Shiver,

Considering how liberally MD’s prescribe massive doses of NSAIDS following surgery, I doubt they do much to inhibit healing.

I sometimes think the human body overdoes its inflammatory responses. A little inflammation is necessary and good; a lot can be damaging. NSAIDS allow you to control the response, to some extent.

The TL_Extract says that new collagen isn’t laid down until after the inflammatory phase. So, I think the real problem with inflammation (i.e., in promoting fibrosis) is only when it becomes chronic.

“Inflammation manifests as swelling, heat, redness, and pain. The
acute inflammatory phase lasts from three to seven days after injury.
Following this acute phase the result is either tissue repair or adhesion
and scarring (see upcoming section on remodeling process).”

The paper goes on to say that adhesions and scarring occur when inflammation becomes chronic. Otherwise, normal tissue repair and remodeling occur.

I just came across this interesting article, which discusses the role of NSAIDS in muscle building. I believe the information here is readily transferrable to PE, especially because the article focuses on connective tissue:

http://www.planetmuscle.com/article…upplements.html

Here’s an excerpt:

While non-steroidal anti-inflammatory drugs (NSAIDs) like aspirin may exert a ‘braking’ effect on inflammation and pain, keep in mind that inflammation is a necessary part of the repair phase following a connective tissue injury. Some forms of mild pain can be a good thing, such as second-day muscle soreness from a hard workout.

A few studies have recently demonstrated that NSAIDs may inhibit protein synthesis in exercised muscle. However, this does not necessarily mean that these drugs will inhibit muscle growth following your workouts.

Dr. Claude Cote, one of the leading researchers on the matter of NSAIDs and inflammation told me that his view is that NSAIDs, that are strong enough to really inhibit inflammatory cell infiltration and activity, can also repress cellular and molecular mechanisms necessary for repair after damage. And, this is part of a hypertrophy response from training. However, he says, NSAIDs theoretically inhibiting muscle growth would only be in a case where these drugs are taken in higher doses for long periods. He suspects aspirin would not do it because it works with a different mechanism of action from a classic NSAID. He suggests that the theory would require highly controlled experimental protocols with human subjects.

Good find Modesto! I guess mild doses where inflamation is a problem should not be too much of an issue then. I’ve never had a case of inflamation was bad enough to require them though, so cannot speak from experience.

As a reply on the very first post of Shiver in this topic,
You are partially right for as far as I consider. However, taking plants as an example, they have something called Cell Turgor (not sure on the translation of it, should be right),
So considering that fact, all this stressing we do to increase the vein’s diameter should induce way more injuries then (from what I’ve read here) there are.

Just my quick 0.02€

Almost 14 years old, but still an interesting read. I now have some L-Carnosine and DMSO on the way. I’m putting a tremendous amount of time and effort into manual exercises, so anything that can potentiate these exercises is worth a shot.


Start 11/30/17: 5.94” BPEL, 4.25 MSEG - My Progress Report

Latest 5/17/18: 6.75" BPEL, 4.75 MSEG - My Progress Photos

“I have a vision. I have disposable income and time. I will reach my goals. It is inevitable. I will not stop otherwise.” - TG

Cross-post from DMSO + Iodine Experimental Treatment for Deflated Glans and Firm Flaccid (p. 49) since this is relevant here as well.

Update: I’m scrapping L-carnosine. It reduces HIF-1α (hypoxia inducing factors), which in theory could inhibit angiogenesis (the creation of new blood vessels).

Effect of L-carnosine on HIF-1α:

Quote
In the current study we found that L-carnosine reduces the HIF-1α protein level affecting its stability and decreases the HIF-1 transcriptional activity. In addition, we demonstrated that L-carnosine is involved in ubiquitin-proteasome system promoting HIF-1α degradation.


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4013086/

The reason this may not be desirable:

Quote
I have stumbled upon the subject of hypoxia inducing factors (HIF), which basically removes oxygen from the cells where it is injected. When the cell is hypoxic (lack of oxygen), it releases a signal to nearby blood vessels to sprout new pathways to the oxygen-deprived cells. This signal is called vascular endothelial growth factor, or VEGF for short. The new blood vessels connect to the existing vascular network, provide oxygen via the red blood cells, and the signalling stops.


http://chemicalpenisenlargement.blo…aking-more.html

Quote
A cell doesn’t have to be starved of oxygen to release VEGF. A number of chemicals can stimulate a cell to release VEGF: these chemicals belong to a group called Hypoxia Induction Factors (hypoxia means ‘lacking oxygen’), or HIF for short. HIFs are currently being tested to revascularize liver, kidney and heart tissue, with very promising results.


http://chemicalpenisenlargement.blo…injections.html

DISCLAIMER: I am not a doctor or researcher. I work in IT. The half baked experiments I do on myself hardly count as research. I’m doing my best to interpret relevant studies and various other sources of information, but I do not have a solid background in chemistry, biology, or medicine. Take anything I say here with a large grain of salt. Feel free to correct or contradict me. Do your own research.


Start 11/30/17: 5.94” BPEL, 4.25 MSEG - My Progress Report

Latest 5/17/18: 6.75" BPEL, 4.75 MSEG - My Progress Photos

“I have a vision. I have disposable income and time. I will reach my goals. It is inevitable. I will not stop otherwise.” - TG

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