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Cell Division

Cell Division

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I am starting this thread to later come back with more stuff I read and write about cells in our body, other bodies, the division process, etc, I hope it’s ok, any help is very welcome.

The videos linked are from the Epstein brothers, very interesting stuff about lab rodents mutating and eventually getting longer repetitive dna sequences at the end of chromosomes that were understood to shorten every time a cell divided, thus making any potential dangerous pharmaceutical tested on them to diminish the tumor risks of the mice, who eventually developed cancer, lab mice specifically. Because of that mutation lab mice, unlike us, can replace their tissues indefinitely. Very interesting stuff…

jelqing before extending, or basically any other more advanced PE exercise than jelqing, done afterwards after a slight pause in jelqing, you know like 30 secs-1 min till you get the extender on or whatnot.

Could it be that when we do this, in order to achieve the final cytokinesis stage of mytosis, we go through interphase when the cell which is basically waiting for cytokinesis is going through a period of REST and grows, like it says on the youtube article: “during interphase the genetical material of the cell increases”

Couldn’t this explain “fat flaccids” post workout?

And/or even the turtling effect?

Maybe when we overdo PE we go through the interphase with the overload and thus making an odd result, schrinkage..

Sorry if this is coverred anywhere else, if it is, I will gladly go to that thread.

Originally Posted by train spot
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I am starting this thread to later come back with more stuff I read and write about cells in our body, other bodies, the division process, etc, I hope it’s ok, any help is very welcome.
The videos linked are from the Epstein brothers, very interesting stuff about lab rodents mutating and eventually getting longer repetitive dna sequences at the end of chromosomes that were understood to shorten every time a cell divided, thus making any potential dangerous pharmaceutical tested on them to diminish the tumor risks of the mice, who eventually developed cancer, lab mice specifically. Because of that mutation lab mice, unlike us, can replace their tissues indefinitely. Very interesting stuff…

You mean telomeres?

Telomeres can be lengthened by more than one method, upregulating telomerase or shuttling it into the nucleous. It’s impractical for increasing lifespan though because of cancer and the loss of a functional immune system. Telomeres are just an element of a cell that correlates with age only because of how well it’s maintained, with younger people tending to have it maintained better than older due to the general functionality of their cells. You could do the same correlation with cytoskeletons or dozens of other things within cells in aged verses the young.

Cancer is actually something that appears throughout your lifespan, normally the immune system recognizes it by aberrations in the proteins presented on cell surfaces. Over time though, the immune system stops functioning correctly. It’s not a matter of how many immune cells there are.

I’m not saying there isn’t a way to defeat aging. Just that telomerase isn’t it. The only real issue right now is the difficulty in synthesizing genomes. We can read DNA easily, synthesizing it is an entirely different matter and the human genome is pretty large. Once technology catches up to our ambition, it will be pretty easy. But we won’t get to that point if our civilization collapses. The USA has basically told 20 years of our brightest minds to wait tables or learn to scam people legally, so I have my doubts on whether or not we’ll make it in time. Maybe if they started paying US scientists the same as athletes and celebrities or broke the pharma cartel up (not all the pharma companies are bad, just most of them) we would have a better chance. Until then, I think we’ll all feel better knowing life has term limits anyway.


Starting: 7"bplx5.2" 2017 (shrunk from disuse)(originally 8"bplx4.5", gained to 9"bplx6")

Current: 9.0"bplx6.125" 2020

Goal: 11.5"bplx7" 2021.

New here, first post.

1st guess: the “fat flaccids” post workout may be due to inflammation from damaged tissue.

2nd guess: “shrinkage” from overdoing PE is due to stiffening of extracellular matrix, I.e. Fibrosis, which in general would strengthen the extracellular matrix to resist the applied stressor. This may happen through a phenotype change of fibroblasts towards myofibroblasts that can contract the tissue with intracellular contractile proteins.

3rd guess: The cell cycle generally takes about 24 hours to complete, interphase taking most of that time, about 22 hours or so.

1st question: How does the PE workout affect the timing of cell division? References would be nice.

Thought: I think of the mechanical strength of the body being mostly due to the extracellular matrix (ECM), not the cells themselves. The cells create, degrade, and rebuild the ECM constantly throughout the body to repair and maintain the “framework” that the cells reside in. Usually, cells in connective tissue are just slowly replacing pieces of the framework to adapt to the mechanical forces experienced by the tissue through mechanoreceptors. However, upon injury, various cytokines and other signaling molecules mediate an inflammatory response during which cells are recruited that help orchestrate a repair process, involving swelling (“fat flaccid?”) and heat from increased blood flow to the injury site. Continued injury before repair is complete can result in a survival response, whereby the tissue is just simply stiffened to avoid further decomposition and ultimately mechanical failure. This would be in contrast to a more high fidelity repair, where tissue elasticity is conserved. Thus, the importance of rest.

Originally Posted by train spot
Jelqing before extending, or basically any other more advanced PE exercise than jelqing, done afterwards after a slight pause in jelqing, you know like 30 secs-1 min till you get the extender on or whatnot.
Could it be that when we do this, in order to achieve the final cytokinesis stage of mytosis, we go through interphase when the cell which is basically waiting for cytokinesis is going through a period of REST and grows, like it says on the youtube article: “during interphase the genetical material of the cell increases”
Couldn’t this explain “fat flaccids” post workout?
And/or even the turtling effect?
Maybe when we overdo PE we go through the interphase with the overload and thus making an odd result, schrinkage..
Sorry if this is coverred anywhere else, if it is, I will gladly go to that thread.

Originally Posted by Sigmoid
You mean telomeres?

Telomeres can be lengthened by more than one method, upregulating telomerase or shuttling it into the nucleous. It’s impractical for increasing lifespan though because of cancer and the loss of a functional immune system. Telomeres are just an element of a cell that correlates with age only because of how well it’s maintained, with younger people tending to have it maintained better than older due to the general functionality of their cells. You could do the same correlation with cytoskeletons or dozens of other things within cells in aged verses the young.

Cancer is actually something that appears throughout your lifespan, normally the immune system recognizes it by aberrations in the proteins presented on cell surfaces. Over time though, the immune system stops functioning correctly. It’s not a matter of how many immune cells there are.

I’m not saying there isn’t a way to defeat aging. Just that telomerase isn’t it. The only real issue right now is the difficulty in synthesizing genomes. We can read DNA easily, synthesizing it is an entirely different matter and the human genome is pretty large. Once technology catches up to our ambition, it will be pretty easy. But we won’t get to that point if our civilization collapses. The USA has basically told 20 years of our brightest minds to wait tables or learn to scam people legally, so I have my doubts on whether or not we’ll make it in time. Maybe if they started paying US scientists the same as athletes and celebrities or broke the pharma cartel up (not all the pharma companies are bad, just most of them) we would have a better chance. Until then, I think we’ll all feel better knowing life has term limits anyway.


Thank you for clarifying that for me, and providing even more good information.
Yes, it is a much easier way to live, especially nowadays I guess.

Originally Posted by HeatedPipe
New here, first post.

1st guess: the “fat flaccids” post workout may be due to inflammation from damaged tissue.

2nd guess: “shrinkage” from overdoing PE is due to stiffening of extracellular matrix, I.e. Fibrosis, which in general would strengthen the extracellular matrix to resist the applied stressor. This may happen through a phenotype change of fibroblasts towards myofibroblasts that can contract the tissue with intracellular contractile proteins.

3rd guess: The cell cycle generally takes about 24 hours to complete, interphase taking most of that time, about 22 hours or so.

1st question: How does the PE workout affect the timing of cell division? References would be nice.

Thought: I think of the mechanical strength of the body being mostly due to the extracellular matrix (ECM), not the cells themselves. The cells create, degrade, and rebuild the ECM constantly throughout the body to repair and maintain the “framework” that the cells reside in. Usually, cells in connective tissue are just slowly replacing pieces of the framework to adapt to the mechanical forces experienced by the tissue through mechanoreceptors. However, upon injury, various cytokines and other signaling molecules mediate an inflammatory response during which cells are recruited that help orchestrate a repair process, involving swelling (“fat flaccid?”) and heat from increased blood flow to the injury site. Continued injury before repair is complete can result in a survival response, whereby the tissue is just simply stiffened to avoid further decomposition and ultimately mechanical failure. This would be in contrast to a more high fidelity repair, where tissue elasticity is conserved. Thus, the importance of rest.


You make a very interesting point. I am still reading on these topics and I have no education on these matters, but I will read more about the extracellular matrix and how it reacts throughout its’s lifetime in our bodies.
What makes me want to get more info on this is basically the fact that hypertrophy isn’t fully understood to this day…and people have been working with it for so long, getting visible results with either the right or the wrong approach, sort of like I how I see we are getting results from various PE methods and routines, there has to be a simple way to correlate the physical process inside our penis going on with what we are doing when we do PE for so many hours/minutes every day.

Originally Posted by train spot
Thank you for clarifying that for me, and providing even more good information.
Yes, it is a much easier way to live, especially nowadays I guess.

Sometimes I wonder if it is actually easier to live with Western technology.

Yes, fewer babies die because various medicines, but increasingly when I look at cities it looks like a factory farm with humans in little pens and everyone looks so sick from chronic conditions and bad food (no one is testing the food for LPS or mycotoxin contamination and I think they’re using rotten grains among other things).


Starting: 7"bplx5.2" 2017 (shrunk from disuse)(originally 8"bplx4.5", gained to 9"bplx6")

Current: 9.0"bplx6.125" 2020

Goal: 11.5"bplx7" 2021.

Originally Posted by HeatedPipe
Continued injury before repair is complete can result in a survival response, whereby the tissue is just simply stiffened to avoid further decomposition and ultimately mechanical failure. This would be in contrast to a more high fidelity repair, where tissue elasticity is conserved. Thus, the importance of rest.

What are your thoughts on the validity of concepts like plastic deformation in permanent ligament extension and the fact that folks like BIB don’t even advocate for rest days when hanging


Life goal: 9x7 inches of pure raging steel, with a small patch of decorative grey hairs.

Much of the soft tissue of the human body can be described as plastic, elastic, or some combination of the two depending on the strain. Knowing which elements have which properties and how best to train them can be important knowledge for a coach to have. Elastic tissue is similar to a rubber band. Stretch it and it will snap back. When we speak of the elastic tissues of the body we’re primarily concerned with the tendons. Plastic tissue doesn’t have that same recoil. If it’s stretched too far it will remain stretched and have a permanent deformation. Cartilage and to a lesser extent fascia is generally thought to be plastic in nature.
*from https://elitetrack.com/blogs-details-5337/ , idk how valid this site is considered to be, I was only searching for fascia information and this came up.

Buck’s fascia is continuous with the external spermatic fascia in the scrotum and the suspensory ligament of the penis.
On its ventral aspect, it splits to envelop corpus spongiosum in a separate compartment from the tunica albuginea and corporal bodies.
Variation *from wikipedia btw*
Sources differ on its proximal extent. Some state that it is a continuation of the deep perineal fascia,[6] whereas others state that it fuses with the tunical albuginea.
The deep dorsal vein of the penis, the cavernosal veins of the penis, and the para-arterial veins of the penis are inside Buck’s fascia, but the superficial dorsal veins of the penis are in the superficial (dartos) fascia immediately under the skin.
Efficient movement requires sufficient mobility in all tissues to permit adequate range of motion at a joint while still being able to take full advantage of the elastic properties of tendons and muscles. (this kind of sounds like not doing too much PE to avoid conditioning)

further on with the website I first mentioned
Very few people have the perfect balance which makes addressing the different structures (and there associated ranges of motion) very important to truly maximize performance. In fact, many excessively asymmetrical movements or inefficient movement patterns can be addressed through diligent mobility work. Unfortunately, in cases like these, traditional static stretching will not suffice. Because we’re looking for plastic deformation of restricted areas the tension has to either be quite high during extreme ranges of motion and / or for extended periods of time. If neither of these is observed any stretching will be primarily for CNS down-regulation and social time and not making lasting changes in the tissue. The trick is that this needs to be done without causing laxity or reducing any of the beneficial elastic properties of the joint. This is where an understanding of functional anatomy really helps. For a quick primer, I suggest picking up The Concise Book of Muscles, Revised Edition by Jarmey.

I can’t understand this one though.

https://www.ncbi.nlm.nih.gov/pubmed/9728682

An experimental protocol was tested to measure elastic properties of connective tissue displaying viscoelastic as well as plastic properties. The protocol consisted of a slow rate, linear elongation (0.88 mms(-1), 8 mm) in combination with a superimposed sinusoidal vibration of small amplitude (50 Hz, 0.1 mm). Using digital filters and mathematical algorithms, the force responses to linear elongation and to vibration were obtained. The method was tested on excised fibromuscular tissue of the vaginal wall obtained from women who suffered a vaginal prolapse. The force-stiffness and force-elongation relationships based on the vibration response were unaffected by any long-term deformation of the specimens. The directly measured force-elongation curves were strongly affected by these deformations. It was therefore concluded that with the new method, it is possible to determine the elastic properties accurately. Furthermore, this method seems more sensitive to small changes in elastic properties than the classic tensile test.

This one might confirm using electrically induced heat, or at least heat during exercises, not just before I guess

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC164307/

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