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Understanding force thresholds for growth

I believe the ideas from this site on bodybuilding can be used for PE I hope you can find these excerpts useful.

“Acute vs. Chronic Stimuli
In order for the loading to result in significant hypertrophy, the stimulus must be applied with sufficient frequency to create a new “environment”, as opposed to seemingly random and acute assaults on the mechanical integrity of the tissue.

Progressive Load
Over time, the tissue adapts and becomes resistant to the damaging effects of mechanical load. This adaptation (resistance to the stimulus) can happen in as little as 48 hours (Repeated Bout Effect or Rapid Training Effect). As this happens, hypertrophy will stop

Strategic Deconditioning
At this point, it is necessary to either increase the load (Progressive load), or decrease the degree of conditioning to the load (Strategic Deconditioning). The muscle is sensitive not only to the absolute load, but also to the change in load (up or down). Therefore, you can get a hypertrophic effect from increasing the load from a previous load, even if the absolute load is not maximum, assuming conditioning (resistance to exercise induced micro-damage) is not to extensive. There is a limit to the number of increments you can add to increase the load. You simply reach your maximum voluntary strength eventually. This is why Strategic Deconditioning is required for continued growth once growth has stopped (all things remaining equal).”

I also found this about wound/tissue repair on that site.

“Hunt TK, Hussain MZ.
Can wound healing be a paradigm for tissue repair?
Med Sci Sports Exerc. 1994 Jun;26(6):755-8..
Quote
This paper is written in the hope, if not the conviction, that it will be helpful to investigators of muscle physiology and development. Its thesis is that cell growth, connective tissue matrix deposition, and angiogenesis are stimulated in wounds in response to NAD+ depletion caused by a burst in lactate generation. We surmise that muscle development may also involve this metabolic control.

Hunt TK, Knighton DR, Thakral KK, Goodson WH 3rd, Andrews WS
Studies on inflammation and wound healing: angiogenesis and collagen synthesis stimulated in vivo by resident and activated wound macrophages.
Surgery. 1984 Jul;96(1):48-54.

Hunt TK, Conolly WB, Aronson SB, Goldstein P.
Anaerobic metabolism and wound healing: an hypothesis for the initiation and cessation of collagen synthesis in wounds.
Am J Surg. 1978 Mar;135(3):328-32.
Quote
Total LDH activity corresponded directly to lactic acid concentration and inversely to oxygen availability. LDH isoenzymes in wound fluid were in an anaerobic pattern soon after injury and evolved toward the aerotic pattern as oxygen supply more nearly matched metabolic capacity. Lactate levels in the wound space are elevated soon after wounding and remain elevated far above those in blood. These data again indicate that wound metabolism is characterized by a relatively poor oxygen supply. Current data from several sources indicate that lactate found in the hypoxic area of the wound may stimulate collagen synthesis in fibroblasts lying in the high lactate environment. We postulate that elevated concentration of lactate in wounds is a major signal for collagen synthesis and repair.”

My guess is kegel holds may help flush the area with lactic acid?

Info about stretching I found.
“Passive stretch puts the strain of the load on “structural” proteins (both collagenous and otherwise) and the cell membranes. When the fibers contract, it shifts the load to the contractile proteins (myosin, actin, z-discs, etc). This appears to be crucial for activation of p38, which of course leads to significant fiber hypertrophy.

Long term modulation of protein synthesis involves the activation of myogenic stem cells or satellite cells. This is how existing muscle cells increase the number of nuclei they contain. If you recall, when a muscle is stretched it not only produces mechano growth factor (MGF), but also PGF2α and PGE2. PGE2 is a potent inducer of satellite cell proliferation and fusion. This is important because in order for a muscle to grow rapidly, it must produce more mRNA. This is done in the nucleus of the muscle cell. The more nuclei you have, the more mRNA you can produce. Within the cell, prostaglandins may also be involved in regulating the number of ribosomes. This could have long term implications for hypertrophy. This helps shed light on the ability of prostaglandin inhibitors such as ibuprofen and other NSAIDs to prevent training induced muscle growth.

Is this possibly what is going on when we PE?

Originally Posted by gerrykjohnsons
My guess is that if you hang 40 pounds off your dick for 6 months you’ll have a bigger dick.

I’m just teasing you…

It’s all good. I concur hanging will elect much greater growth.

Originally Posted by reven
I believe the ideas from this site on bodybuilding can be used for PE I hope you can find these excerpts useful.

“Acute vs. Chronic Stimuli
In order for the loading to result in significant hypertrophy, the stimulus must be applied with sufficient frequency to create a new “environment”, as opposed to seemingly random and acute assaults on the mechanical integrity of the tissue.

Progressive Load
Over time, the tissue adapts and becomes resistant to the damaging effects of mechanical load. This adaptation (resistance to the stimulus) can happen in as little as 48 hours (Repeated Bout Effect or Rapid Training Effect). As this happens, hypertrophy will stop

Strategic Deconditioning
At this point, it is necessary to either increase the load (Progressive load), or decrease the degree of conditioning to the load (Strategic Deconditioning). The muscle is sensitive not only to the absolute load, but also to the change in load (up or down). Therefore, you can get a hypertrophic effect from increasing the load from a previous load, even if the absolute load is not maximum, assuming conditioning (resistance to exercise induced micro-damage) is not to extensive. There is a limit to the number of increments you can add to increase the load. You simply reach your maximum voluntary strength eventually. This is why Strategic Deconditioning is required for continued growth once growth has stopped (all things remaining equal).”

I also found this about wound/tissue repair on that site.

“Hunt TK, Hussain MZ.
Can wound healing be a paradigm for tissue repair?
Med Sci Sports Exerc. 1994 Jun;26(6):755-8..
Quote
This paper is written in the hope, if not the conviction, that it will be helpful to investigators of muscle physiology and development. Its thesis is that cell growth, connective tissue matrix deposition, and angiogenesis are stimulated in wounds in response to NAD+ depletion caused by a burst in lactate generation. We surmise that muscle development may also involve this metabolic control.

Hunt TK, Knighton DR, Thakral KK, Goodson WH 3rd, Andrews WS
Studies on inflammation and wound healing: angiogenesis and collagen synthesis stimulated in vivo by resident and activated wound macrophages.
Surgery. 1984 Jul;96(1):48-54.

Hunt TK, Conolly WB, Aronson SB, Goldstein P.
Anaerobic metabolism and wound healing: an hypothesis for the initiation and cessation of collagen synthesis in wounds.
Am J Surg. 1978 Mar;135(3):328-32.
Quote
Total LDH activity corresponded directly to lactic acid concentration and inversely to oxygen availability. LDH isoenzymes in wound fluid were in an anaerobic pattern soon after injury and evolved toward the aerotic pattern as oxygen supply more nearly matched metabolic capacity. Lactate levels in the wound space are elevated soon after wounding and remain elevated far above those in blood. These data again indicate that wound metabolism is characterized by a relatively poor oxygen supply. Current data from several sources indicate that lactate found in the hypoxic area of the wound may stimulate collagen synthesis in fibroblasts lying in the high lactate environment. We postulate that elevated concentration of lactate in wounds is a major signal for collagen synthesis and repair.”

My guess is kegel holds may help flush the area with lactic acid?

Info about stretching I found.
“Passive stretch puts the strain of the load on “structural” proteins (both collagenous and otherwise) and the cell membranes. When the fibers contract, it shifts the load to the contractile proteins (myosin, actin, z-discs, etc). This appears to be crucial for activation of p38, which of course leads to significant fiber hypertrophy.

Long term modulation of protein synthesis involves the activation of myogenic stem cells or satellite cells. This is how existing muscle cells increase the number of nuclei they contain. If you recall, when a muscle is stretched it not only produces mechano growth factor (MGF), but also PGF2α and PGE2. PGE2 is a potent inducer of satellite cell proliferation and fusion. This is important because in order for a muscle to grow rapidly, it must produce more mRNA. This is done in the nucleus of the muscle cell. The more nuclei you have, the more mRNA you can produce. Within the cell, prostaglandins may also be involved in regulating the number of ribosomes. This could have long term implications for hypertrophy. This helps shed light on the ability of prostaglandin inhibitors such as ibuprofen and other NSAIDs to prevent training induced muscle growth.

Is this possibly what is going on when we PE?

Good info thanks.

There has been lots of good info that may or may not be whats going on.

I feel we could go on endlessly speculating or all chip in about $100,000.00 each and do the studies.

I don’t know about you, but I don’t have it to spend on a bigger dick.

The alternative is to observe physiologic responses and apply forces and time off in a way that gives us the best responses and growth.

For example, I increased my time using 10 oz from 2 hours to 8 hours…the next day my bpfl was decreased by over 1/4 inch.

I assumed this was a contraction reaction, took most of this day off, and will remeasure bpfl tomorrow.

If I’m correct, that it was a contraction reaction…I should start seeing a return of my max bpfl. This has shown me that that was too much stimulus to recover within my one day time frame.

On the other hand, when I have taken one day off, bpfl stayed the same…when I extended that to 2 days, I started to get shortening.

I assumed that was because of UNDER STIMULATION and only used one day off with that level of stimulus.

So, by having a few basic observations of your own reaction based on stimulus and rest, I think we can begin to tune our workouts for the best responses.

This is the direction I believe one needs to go if you want a big dick in the near future.

These other discussions are good, I think its good to try and extrapolate from available literature, but its important not to let it replace good old fashioned observation.

The key is recording of those observations and scientifically manipulating the force/time parameters to achieve the best results.

This can be done now, with our current understanding.

As to what is actually happening…it may be a while…unless you guys start sending my those checks for $100,000.00! :)

Well, a lot of thoughts have been mentioned some of it is something I need to get in my head now!!!!!


Started :BPEL 7.0 x 5.5 Now: BPEL 7.6 x 5.8 Goal: NBPEL 8.6 x 6.3 "Don´t let yourself get attached to anything that you are Not willing to walk out on in 30 seconds flat if you feel the HEAT around th corner." --Robert De Niro (talking to Al Pacino in a caffe in the Movie HEAT)

Ans apply at the same time.


Started :BPEL 7.0 x 5.5 Now: BPEL 7.6 x 5.8 Goal: NBPEL 8.6 x 6.3 "Don´t let yourself get attached to anything that you are Not willing to walk out on in 30 seconds flat if you feel the HEAT around th corner." --Robert De Niro (talking to Al Pacino in a caffe in the Movie HEAT)

Any progess with this thread? I’ve read how vitamin E helps to correct a curvature- has anyone used this with a short decon break and seen a good effect? Does anyone take vitamin E and knows that it has a good effect?

Or has anyone who found it hard to gain at first/overtrained and didn’t realise until later taken vitamin E and seen an improvement?

I have read many many posts, theories,other’s experiences etc etc. about PE and I must tell you, this is one mother f***** SCIENCE! I must also tell you that I enjoy reading and learning from you so I could PE smart and see some good gains one day. I learn from your mistakes!

I was wondering one thing, why do the educated doctors tell you that the PE without surgerry is imposible?!

and in the other hand there are people like you who have gained from 0.5” to 2”+ in lenght and girth through natural way(exercising) and you trained your penises like bb’s train their muscles, and we all know that penis is not a muscle.

So how come, despite your results, the doctors,medical science and other “specialists” don’t admit that natural PE without surgerry is POSIBLE and everything that is not medically approved is bullshit for them ??


/

Originally Posted by sparkyx
I definitely think less force can produce gains where more force hasn’t…but I believe in most cases, a decon is needed.


Do you think this is individual specific or do you think this applies to everyone? The reason I ask this is because I’m kind of following in your footsteps in the over-training department.

After seeing minimal gains in my first two months, I started using an extender, fowfer, jelq and stretch every day without rest on an average of 8.04 hours each day for the past 29 days and I’ve had my best gain last month when I began doing this.


Starting: BPEL 6.125 (15.55 cm) / EG 4.75 (12.07 cm) / NBPFL 2.750 (6.99 cm)

Current: BPEL 7.000 (17.8 cm) / EG 4.75 (12.07 cm) / NBPFL 3.750 (9.52 cm) Goal: BPEL 7.0 / EG 5.0

Call me NSG!!! My Equipment: Phalosan, KR Extender

bump

Great read that hasn’t been bumped in years. What gives. Sparkyx always makes a lot of sense. I laughed, I learned, I pulled my dick. Thanks for the tips!

I think the deconditioning makes a lot of sense.

Also, LOL at “beef jerky like condition of my dick”. You slay me.


2009-05-01: BPEL ~8.25", EG ~5.5" (start) / 2009-08-25: BPEL ~9.00" / EG ~6.0". 2010-02-06: BPEL ~9.25", EG ~6.2" / 2010-08-23: BPEL ~9.4", EG: ~6.25"

I like this quote.

Originally Posted by ModestoMan
.The best force to use is the one just large enough to give you a “stretched” feeling.

Also with jelqing, how erect should you be? Low level, high level?

I have been at PE for 3 months and I use extreme force with a home-made stretcher. I have gained 5/8” in length in the process and have recently began to clamp as well. I will persist with this until I see a lack of growth. The only injury I`ve sustained has been while dry-jelqing. I managed to pull as small patch of skin off the top of my penis near the base. It should heal in a week or so and I will be able to return to jelqing at that time. That`s what you get for jelqing while half asleep!

I’m surprised no one mentioned the smooth muscle! The muscle of the penis is just like a rectum or intestine (which is why cialis can cause acid reflux or anal leakage). My theory at this point is the muscular reaction could be just as significant as the hardening of tissues. Think of how quickly the turtling effect happens! Overtraining makes the penis shrink up immediately which makes me suspect that its compensatory (i.e. protective) function is always active… not only during training but during every erection. The only way a viagra erection can be larger than normal is if the muscle it has effect on was contracting by default. Extrapolate this to PE and not only does it support low level chronic PDE5 inhibitors, it means we need to be conscious of all aspects of muscular relaxation. Heat is a big one, and decon breaks could be a means of allowing atrophy of that smooth muscle. I personally focus my jelqing on relaxing and massing with muscle in mind, rather than using it for pure expansion.

I’m definitely curious to learn more about optimal balance between acute and chronic force though… that’s one area that still seems fairly uncharted.


2014: 8.4 x 5.5

2022: 9 x 6.2

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