More Thoughts On Training Frequency...

I wonder if we can treat the micro tears and the stress we place on our penises the same way that one would treat injured ligaments. I found something interesting in these regards as far as the nutritional aspect of treating injured ligaments. Check out the following website.

http://www.chir oweb.com/archiv … s/08/12/03.html

Interesting link, but how does that translate in food, other than to drink orange juice?

SmilingBob,

Your thoughts are very interesting. Especially the skin and priapism related post. I was thinking how PE works a lot myself.

I wonder if one could pump at a very light pressure (to avoid hurting the blood circulation) for a long time (lets say few days) would it cause a permanent gains?

Anyone done this?

1)hey navarro what routine do you follow

2)I agree with everything you say sparkyx

3)Thunderss easy with your mouth you are too tough over the Internet

Oh shit, I’ve been hammered.

Navarro,

Listen to Thunder on this one!

Many newbies stop gaining BECAUSE they quit doing their newbie routine and increase to more!!!!

Sparkyx,

Do you think “light” ADS would be effective after an overtraining period in order to prevent the penis from contracting?

… or I should add remaining in a contracted state.

Yes and no. PE inflicts controlled injury upon the ligaments (suspensory and fundiform) and the tunica. However, we do not want these tissues to simply heal back to their initial lengths. Unlike a knee or a shoulder, the penis is an organ whose ligaments one wants to stretch. I believe we want to do just the opposite of what this article suggests. We want to continually break down the tissues so as to continually elongate them.

Some healing needs to take place to prevent tissue failure, and it invariably will. But one should try to delay healing, I believe. Length before strength.

A couple of things stand out in this article:

1) healing takes several days. It is not until the third day after injury that new collagen is laid down. This means that wearing an ADS in the afternoon cannot possibly help tissues heal in an elongated state—at least not the same tissues that were injured that morning.

2) dietary protein restriction may encourage lysis—breakdown of older proteins in the injured area to provide raw materials for creating newer proteins. Thus, protein-deficient diets may speed gains by forcing the body to break down tissue in the damaged area.

Good stuff.

Can adaptation to a stressor happen without injury that requires healing in the total absence of the stressor?
Or can adaptation be a continual process.

These seem to be important questions relevant to exercise frequency. It may be argued that all adaptation stems from some level of injury. It is my belief that there is a threshold between desirable adaptation and injury.

I read a lot of proponents of the “micro tear” theory of PE. I believe these can and do happen at a certain level of mechanical stretch in the ligaments or/and in the ligament like tissues of the tunica. , but I am not at all sure this is what we want.

Ligaments under increasing load undergo a phase of elasticity as component fibers align in the direction of stress. This results in a small elongation of the ligament until these fibers become fully aligned in the direction of pull, then the ligament becomes rigid (1). Even low amounts of mechanical stretch modifies the composition of extracellular matrix of human ligament fibroblasts (2).

I believe this is the level of “stress” we want to achieve during PE, well below the stress that would cause micro tearing thus require a longer “healing” process, but high enough to cause an adaptation response at a cellular level. This level of stress must be quite low however because cellular damage is induced at ligament strains significantly below the structural damage threshold (3). Injuries to ligaments induce a healing response that is characterized by the formation of a scar tissue that is weaker, larger and biomechanically inferior to the tissue it replaces (4),(5).

It is unsettling to think that by using too high a level of stress and causing “micro tears”, one may be slowly replacing his tunica with inflexible scar tissue.

References;
(1) Biomechanics Journal of Acta Ortopédica Brasileira vol.11-2 72-78, 2003
(2) Hua Xi Kou Qiang Yi Xue Za Zhi. 2001 Jun;19(3):155-7
(3) J Appl Physiol. 2002 Jan;92(1):362-71
(4) Can J Surg. 1998 Dec;41(6):425-9.
(5) J Musculoskelet Neuronal Interact. 2004 Jun;4(2):199-201.

1) WRONG! An ADS applied continuously throughout the healing period will contribute to elongated tissues. Looking at this in a short duration period as in morning and afternoon perspectives is not productive. what is productive is the bigger picture of what happens over many days of ADS application from the time of micro tears and through the healing period several days down the road. Given that another hanging session usually takes place within the cycle of an individuals routine we see that healing never reaches completion. That is the beauty of an ADS of light weights.

2)Anti-inflammatory OTC’s can and do contribute to the prevention of healing. From NSAIDS to the simple Aspirin, they slow down the healing process. It is important to understand the healing process.

The first phase is called acute inflammation and is about one hundred hours long. This step begins at the time of the injury, when the ligament and the adjacent cells are broken open and their contents spill at the wound site. The ligamentous and cellular debris and a number of chemicals in the fluid or plasma around the broken-open cells attract an influx of white blood cells called leukocytes. Their job is to clean out the bacteria and prevent infection at the injury site. Many of the chemicals released during this phase will be broken down into messengers or chemical signals that tell cells to become active or inactive during this phase of inflammation. Some of these chemicals are called prostaglandin’s, which can cause pain at the injury site.

The leukocytes also secrete hormones which attract an important cell called the “macrophage”. The arrival of the macrophages at the injury site signals the beginning of the next phase in the healing process, the granulation phase. As the macrophages arrive at the injury site, they begin to “clean up” the area through a combination of digesting the broken-down cell parts and secreting enzymes, which break down many of the damaged ligament molecules. The macrophages also release a number of hormones which will bring more cells to the injury site.

The macrophages also release chemicals (growth factors) which stimulate the growth of new blood vessels, intercellular matrix, and the cells that will make new ligaments. These specialized cells which make ligaments are called fibroblasts. The fibroblasts will be responsible for the actual repairing of the sprained ligament. The combination of all of these cells and the new blood vessels being formed causes the thickness and fullness that can be felt at the injury site. The granulation phase will be present for ten days to two weeks.

Having said all that NSAIDS and/or Aspirin tend to inhibit the 1st phase of the process. Those of us that take an aspirin a day for cardio reasons didn’t really realize the side benefits to our regimen.

So there’s 2cents worth.

Monty,

Are those “stealth” PE Weights on the way yet? ;)

My comment was directed toward people on this forum who falsely believe that wearing an ADS in the afternoon promotes healing of tissues stretched the same morning. The negative cast of the statement reflects my general suspicions about ADS. I’m not sure it works, as a general matter.

It’s plausible that ADS can help to heal tissues in an elongated state based on heavy stretching done on prior days. This makes perfect sense, although I think it’s speculative.

Your description of the healing process is terrific. Not to highjack this thread, but do you have any idea where ADS might enter the picture? In other words, do you have a biochemical basis for thinking ADS works, which fits in with your description?

As I understand it, th problem is that the tissues adapt by becoming stronger, not longer. Levels of stress lower than those required to plastically deform tissues only make them thicker and more resistant to elongation.

If this were true, PE would get progressively easier over the course of one’s PE career, as stronger tissue is replaced by weaker tissue. However, just the opposite happens. Gains become harder to attain.

My understanding is that macro-injuries cause scar tissue to form, whereas micro-injuries (i.e., micro-tears) do not. The tissue is repaired with no trace left behind.

Check this out:

From page 23,

Note that this is an either-or proposition. Either there’s tissue repair, or there’s adhesion and scarring.

Later, at page 26,

Interesting stuff Monty, however I don’t believe we are causing an injury of that magnitude (of a sprain), or at least we should not be. If so, one would have to wait at least three or four days before hanging or jelqing again. Quote form the aforementioned article:

Obviously this is not what we seeing in successful PE. I believe the type of “adaptation” we are experiencing is a slow change in the composition of the extracellular matrix of fibroblasts. The same thing that is experienced by people undergoing various types of traction therapy daily.

If one was to “sprain” his tunica tissue or supporting ligaments, I doubt an ADS would be tolerated very well if at all. Besides, as I cited in the above references, this type of injury would produce a lot of scar tissue in the ligament itself. Not a desirable thing.

Wow, a great find ModestoMan! Thank you for the link.

Perhaps that is a good illustration of what I meant by the difference between “adaptation” and “injury”. All my blather in two sentences! :)

It would seem to be that we need to not only find the type and amount of stress to cause a significant amount of micro-injuries without causing any macro injury, but also examine the time required for the complete healing of these so that we can better determine the best training frequency.