Manko007's road to big dick land

To test your theory I computed these numbers: : BPFSL beginning of cycle - BPEL end of macro cycle

1st cycle: -0.20
2nd cycle: 0.60
4rd cycle: 0.90

At first cycle the growth in BPEL eclipsed initial BPFSL.
At second the BPFSL lead by 0.60 over the BPEL at end of period.
At third increased by even more, by 0.30.

However gains in BPEL and BPFSL, and the slack of just the gains, and conversion rate respectively, was:

1st cycle: 0.50 , 1.7, 1.3, 29%
2nd cycle: 0.90 , 1.5, 0.6, 60%
4rd cycle: 0.60 , 0.8, 0.2, 75%

We can see slack of actual gains going to 0 it seems. So BPFSL- BPEL should become a 1 to 1 relationship over long term. Gain 0.50 in BPFSL should = 0.50 in BPEL.

However it seems that for me right now the actual conversion for every 1cm gain in BPFSL is 75%. (0.60/0.80)

So slower BPFSL gains but higher conversion basically. Although I gain in gap, the actual conversion to BPEL is higher each cycle.

Also most of my gap avg i.e 1.5 was obtained from 1st cycle. From first cycle data point, my gap was only 0.30. But it increased to 1.5 by end of 1st cycle. So about 1.2cm of my avg. gap is attributed to “newbie” or “first time” hanging. if we remove this first gap data points in the 1st cycle, my avg for 1st cycle is 1.25.

So 1.25, to 1.59, to 1.93. That is about 0.35 gap gain per cycle.

So for my fourth cycle if I extrapolate results and forecast BPEL and BPFSL, and the slack of just the gains, and conversion rate:

4rth cycle should be around: 0.69, 0.62, -0.07, and 100%

Should gain about 0.60 BPEL if I gain 0.60 BPFSL.

Highly unlikely but it is fun to play with numbers and see if things play out that way. We will see.

I’m not suggesting that all of the 1.2 initial gap increase doesn’t get converted though. But yeah I’d be curious of what the 4th cycle numbers reveal, I think graphing that would be very cool. Without being too definitive, I think it’s very useful to consider the process as you’ve broken it down.

You should but those BFSL and BPEL in the same graph and start to look long term. All cycles with the calendar dates and all.

After 3 to 4 cycles you can see the tendency for gap closing when making predictions based on trend line prediction.

My gap is supposed to close in three years.

I will publish mine after Period 3 with the three year goal, which is the point I am exiting.

Dude.. considering how well you gain, in 3 years you might have 15”+ or more…
dont… go.. there… or do?! well, damn.. xD

That would be scary. I can´t even imagine what size shoe I should fit on it. Or what kind of shoe that it won´t look stupid.

Right now staring the steep slope it would be easy to slip in thinking this should continue forever, but the reality is that in three years the gain rate will be stabilized for the modest levels.

Honeymoon starts to be over somewhere between 1 -1.5 years for most of us, and right now I am just trying to keep riding on the crest of the wave as long as possible.

Started my macro cycle on 3rd august.

My ending figures for cycle 3 were BPFSL t0 and t2 22, and 22.7 respectively. My BPEL reached 20.3 all time high for 1 day.

Now my figures starting cycle 4 are 21.2, and 21.8 respectively, and BPEL is 19.7-19.9.

So in summary over my 114 day hiatus break, about 3 plus months, lost 1cm BPFSL, but mantained BPEL.

Not bad, but seems like cycle 3 was a scratch.

I will now post what I believe occurred:

I have two theories:

Theory 1:

I lost 1cm in BPFSL t3 it seems over hiatus, so I am planning to introduce jelquing 10min at the end to help with the conversion of BPFSL to BPEL. BPEL stayed the same almost as my 2nd cycle end, so it seems cycle 3 was a wash even though I briefly saw 20.3cm bpel, it went down back to 19.7-19.9. I think the jequing might be the key to cement BPFSL into BPEL. Otherwise I can’t keep gaining BPFSL and not convert to BPEL. It could be lack of smooth muscle expansion or lack of new length retention at new BPFSL. Maybe I needed to stay at 22.8 for another month to solidify and let BPEL catch up via keep doing my routine. Either one.

Theory 2:

For the second question. In my understanding, the cyclic loading recruits less fibers than static loading. The cyclic loading recruits the shorter fibers first over and over each cyclic stretch, causing the shorter fibers fatigue and thus breaking. Once broken, the mid length fibers are recruited to support the same load. This happens again and again until a bigger cross section of the tunica is recruited. However, take a look at static stretch, the shorter fibers are elongated until mid are recruited and then long are recruited. Because there is no repetitive fatigue in the short fibers, these may just elongate but not tear to the length of longer fibers. It may not answer the question, but I think with cyclic loading there comes a point where the fibers “snap”. Say you have day 1, day 2, day 3 using 6kg and all are BPFSL at 24cm. And you can’t break through. It may be these shorter fibers have not been fatigued enough to break past 24cm. By increasing the load above normal levels, as the studies show that at 60% UTS cyclic loading causes greater fatigue and shorter fibril rupture, you may break past 24cm by increasing to “60% UTS” (to reference that study) which we don’t know what that would be, but say just for the sake of this example, 10kg (probably nowhere near 60% UTS but still more than 6kg, it may be more or less, whatever is required to break through, this is the point). You fatigue it with 10kg until short fibrils rupture and the mid length fibers are thus fully and primarily recruited. They were secondarily recruited before, now they are primarily recruited. You break past 24cm. Now you have a 24.5 cm dick. There was a displacement that occurred in the stress strain curve to the right, thanks to the larger stress and cyclic fatigue, your shorter fibrils are broken and coiled up (appearing to be crimp but actually just broken, as in that study showed). Now you can go back to your same normal load of 6kg and target the mid range fibers, now that the shorter fibers are out of the picture. Now your mid range fibers may need more than 6kg, because they are longer, they can bear more load before fatigue breaks them. So you may need to increase this to 7kg lets say. Day 1 day 2 day 3 BPFSL is 24.5cm. Repeat the 10+kg fatigue and break through to even longer fibers. Now you at 25cm lets say. Once you are at your larger fibers, there may be diminishing returns. Or simply the weight needed to fatigue these is too painful, etc.

I have a feeling my static loading the shorter fibers never ruptured, they were elongated only, to 22.8 in my case. Then after a break, they recoiled back up to 21.8.

Now with cyclic loading I will aim to break these, so the recoiling can’t happen. And have a permanent length increase.

Both theories I posted in another thread hosted by Kyrpa:
Gaining volume with IPR

So it may sound out of context as I felt lazy to rewrite in this context.

Going forward, this is my protocol which I’ve adjusted based on new insights and suggestions from Kyrpa.

Step1: Precon for 30min using bib hanger via elastic resistance band and luggage scale to monitor weight up to 3kg simply sitting on a rolling chair and pushing back. Band is secured to desk so it allows easy loading and unloading, and variable loading.

Step2: Heat for 10min using US and IR lamp at 6kg. I hold the IR lamp about 8to 12 inches from shaft while heating with US 1mhz 2cm^2 power, or just max power at 1mhz. My target is the lower left ventral area, so I am positioning US probe on upper right. This is according to 1mhz reach of 2.5 to 5cm.

Step 3: Cyclic stretch for 10min at 7.5kg. 1min on 30 seconds off. It is easy because the resistance band and my rolling chair allows me to move around and adjust weight accordingly. The luggage scale confirms the correct weight.

Step 4: Heat with US and IR this time 3mhz to target more surface tissues. Probe over target area this time, not opposite. IR at same distance.

Step 5: Manual stretches with max grip strengh 30seconds on 15 seconds off for 10min.

Step 6: Wet jelq for 10min.

Step 3 and 5 are cyclic stretching to address my theory 2 concerns. And step 6 address my theory 1 concerns.

So far my results are:

BPFSL 21-21.2 and BPFSL T2 21.8-21.9. Strains of 3.8% and 3.3%.

For cycle 4 my aim is to address Theory 1 and Theory 2.

To further address theory 1 my cycle will last 60days. This is a 30 day increase.

Part of this reasoning is seeing how Kyrpas results achieve over 30+ days is possible.

Also, less burn out because my setup is much leaner than before. No more running baths, setting up weights etc. That took a lot of time. Now it’s very simple, resistance band and rolling chair combo. Easy breezey.

Also, based on my theory 2, the rolling chair allows me to increase the weight variable based on how further back I roll on my chair. For my last session I aimed max weight of 7.5kg but I felt comfortable enough after 5min and felt like increasing so I just pushed back and ending weight was 8kg.

I may play a little with the weight based on comfort thanks to this, during the cyclic stretching step 3 only. This is the way I plan to break the shorter fibrils with higher stresses based on feeling.

I can’t think of anything else so that’s all for now.

Have to say that you love them theories, way more than I do :)

For the first one I am in a hope that it would be anecdotal confirmation for what I have been witnessing already.
Whether or not the growth is related on smooth muscle development or not, we can´t get no answer. Not before we take biopsy specimens before and after and have them analyzed.

So on for the theories which we have no possible way for confirming anything, we should not give a that much of investments.
But anecdotal findings are there, continuing with girth orientated workouts after stopping intensive stretching periods I have been able to produce permanent gains on BPEL with better rate.

For the number two theory, once again concentrating on practical applications we can reach the understanding what brings us the permanent elongation.
But what is happening at the fibril level, we can not get any answers unless specimens are examined.

I will get back on this one better on the original context, as this one is in the center of my focus ,trying to find the amount of stress crucial for permanent elongation.

Is step 4 heat applied under traction. Monty I remember would hang with a traction band, great idea!

Is your bib modified? I’m just wondering because step 1 is 30 min long.

Yeah step 4 is under traction. Doing US and IR without traction may accomplish the opposite if the heat is really high of causing the tissue to shorten, like meat does when it is cooked. Also, I’ve been thinking that all this heat may have on effect on the water molecules dissipating if the heat is prolonged, which may have a good or bad effect I am not sure. But I’ve often felt that over prolonged periods of US my dick becomes rubbery, which doesn’t sound very good.

The bib is modified. I should have said 20min with bib or 30min with vac ads. I could probably do 30min with the bib but it’s been ingrained in me that 20min should be the max, even though Xeno reported hanging indefinitely with the modified version, he did so I believe only without therawrap or anything. That is a bit too much for me lol

Well theory is the reason for why we got this far. So it is important at some level :)

I am not big into theories as most of it is just speculation, but I only have theories when I need them to explain things that I cannot explain, and to use as a way to improve.

Anyway, there is no way of knowing for sure. But theory 2 is based on that study’s “theory” which is written on the discussion. It is a theory based on a theory, but they are scholars who are experts in tissue, there is also some micro pictures that show the recoiling of broken fibers from the 60% UTS cyclic stretch. I think it is not in that study you have seen, but I will try to find it and post it here.

Yes of course they mean something, being the base of all this.

I just like to stay with applied sciences, with the approach which has been from the start to be very pragmatic and application orientated.

Phenomenological modelling is more fitting description for what I have been trying to construct here.
To establish direct relations between the external stimuli via stretching and the observed tissue response without trying to explain the mechanisms behind the observations.

Anyways I will get to it at my log, it touches that much the debate started with Tutt (still floating in the air Tutt being absent), I need to sort it out in a long posting.

I see what you mean. I have a strong need to understand what is happening. Just my incessant curiosity and need to know I guess.

Anyway, here is the study I was basing my theory 2 on:
Ligament creep recruits fibres at low stresses and can lead to modulus-reducing fibre damage at higher creep stresses: a study in rabbit medial collateral ligament model - PubMed

You will need to access it via PDF somewhere somehow.

The study was:
-doing cyclic stretch first and then static stretch right after at 4, 7 , 14, and 28 MPa.
-" In each cyclic creep test, the
ligament was loaded for 30 cycles at 1 Hz from “ligament zero” to the
prescribed stress for that particular test. For each static creep test,
the ligament was then loaded immediately to the same stress used in
the cyclic creep test and held in load control for 20 min."

Based on this setup the main interesting points are:

on Fig 5.:
-creep strain from cyclic component and static component were same at 4 and 7 MPa
-creep strain from cyclic component increased and static component stayed same above, for 14 MPa. This point could mean cyclic has some benefit as static strain increase stayed the same. IOW for static change was 0%, for cyclic increase was near 100%. This is over 4 and 7 MPa increases. But question is whether static was done first and then cyclic what would be the resuts.
-Strain increased for both cyclic and static components at 28 MPa. For static nearly 100% increase. For cyclic about 66% increase.

So weirdly cyclic strain increased at 14MPa by 100%, but only 66% at 28MPa. And Cyclic strain increased by 66% and static by 100%, for same stress respectively.

On Fig 6:
-at cycle 6 the ligaments had a discontinuity (tear of short fibrils) and curve shift to the right.
-this was true for 6 out of 12 ligaments
-of which 3 out of 6 were during cyclic portion and other 3 during static I am assuming
-out of the 3 of cyclic portion the discontinuity occurred before cycle 15
-the discontinuity only occured for tests at 28MPa

So this part I concluded that on my theory 2 the high stress would cause the discontinuity that allows the dick to grow past a wall.

On Fig 8:
-The crimp images show the percent of crimp areas as level of crimp and straightened.
-in the Fig 8b one can see that there is higher percentage of crimp in the 28 MPa post creep with discontinuity than straightened.
-compared to fig 8a of 28 MPa post creep without discontinuity the crimp is much less, and much more straightened.

This above fig proves that there are short fibrils breaking and recoiling at the micro level which look like crimp under a microscope but are actually just coiled up fibrils that have ruptured, as speculated in the discussion of the study.

So based on this above study my theory 2 is based upon.