# Hyperplasia???



## Delhi (Dec 8, 2005)

Right stupid question time.

If GH and IGF cause hyperplsia (New cell growth), does that mean you will forever have these new cells?

Even if you stop training?

Or will the catabolic state eventually erradicate these cells?


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## supercell (Aug 23, 2005)

Del,

If hyperplasia occurs then these new cells will stay with you. When people stop training they dont lose tissue, this is impossible as you have a pre determined no of muscle cells (different for everyone)

When you train these cells enlarge due to glycogen/water retention and amino acid/nitrogen uptake etc. Steroids do the same but to a greater degree.

This is why when you stop AAS/training or both and then restart some time later, you can get back to where you were before a lot more quickly.

Think of the muscle cell as a balloon. The first time you blow it up its hard but the second, third, fourth time its a lot easier. Thats muscle memory for you. I know its a bit off the topic you asked about but it seemed a logical progression.

J


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## Ziricote (Feb 18, 2007)

What supercell has said, once a new cell is created (eg muscle cell via hyperplasia) it is there for good. It's size is dependant upon a lot of factors such as diet, exercise etc.


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## Five-O (May 21, 2006)

Ive had great gains by running GH a few months before I cycled, I noticed that my gains were a lot more keepable, I put this down to hyperplasia, GH can be utilised in a lot of useful ways, if one runs the right "sweet" dose then I think its better overall than AAS.


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## ajfitness (Mar 13, 2007)

i was under the impression that hyperplasia was not yet possible in people? or at least had not been proven. forgive me if that sounds daft but tests had been inconclusive. the last i heard about hyperplasia, (the forming of NEW cells as opposed to hypertrophy, enlarging of existing muscle cells) it had been proven in rats but not humans,

can someone set me straight here?!


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## 3752 (Jan 7, 2005)

well i would say that it is possible when using peptides i have been training for 18years pretty much the same time as i have used steroids but last year i gained 14lbs of muscle this was made possible via using peptides now i have no scientific data to back it up but i can tell you it is possible...


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## ajfitness (Mar 13, 2007)

ok cheers paul, thanks for clearing that up for me!


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## Delhi (Dec 8, 2005)

Right dumb question 2: (Seem to have lots of these latley)

If IGF is a pre-cursor (By product) of GH why is it reccomended to cycle IGF 4weeks on 4 weeks off, but GH is usually recommended as the longer the better?

Also why would you cycle IGF while on GH (Would this just be like taking IGF in double doses?)


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## 3752 (Jan 7, 2005)

well IGF-1 is created by some of the GH you take and this conversion is moderated by the body when you inject IGF-1LR3 there is no automatic control system and receptor saturation becomes an issue....

i have noticed that you can use a little less IGF-1LR3 when using GH but the half life of IGF-1 from the liver is very very short so i don't feel the impact is much of a benefit.


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## supercell (Aug 23, 2005)

^^^^ Plus Gh has other proerties that igf doesn't i.e more lipotropic actions (fat burning). I read an article in a book that said using igf and gh togther was advantageous and they had a synergistic effect, rather like certain combo's of AAS.

Perhaps Paul can vouch for that as I have never tried the two peptides together?

J


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## 3752 (Jan 7, 2005)

oooh yes mate i can definatly vouch for this theory


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## Nytol (Jul 16, 2005)

supercell said:


> ^^^^ Plus Gh has other proerties that igf doesn't i.e more lipotropic actions (fat burning). *I read an article in a book that said using igf and gh togther was advantageous and they had a synergistic effect*, rather like certain combo's of AAS.
> 
> Perhaps Paul can vouch for that as I have never tried the two peptides together?
> 
> J


I have read the study which showed that too.


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## wogihao (Jun 15, 2007)

Could Peg-MGF also have a synergistic effect on the igf-1/hgh stack?


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## 3752 (Jan 7, 2005)

yes it will have only if you take the pMGF the night before so that the pMGF and IGF do not compete for the same receptor


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## wogihao (Jun 15, 2007)

Ahh i see. Thanks!


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## hackskii (Jul 27, 2003)

Eventually you should cycle the GH too as it can make you a bit insulin resistant.


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## 3752 (Jan 7, 2005)

yep with GHRP-6 and Hexeralin...


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## stow (Jun 5, 2007)

(1st post ever on Uk-M, so hello!)

Delhi, hyperplasia is the splitting of the muscle fibre, its not growth of a new cell. There is still little scientific evidence for it, but it doesn't mean there is a shortage of circumstantial evidence. However, due to the obvious ethical implications, you would struggle to find a significant study which included exogenous supply of GH, IGF etc for non-medical purposes. There is still a huge gap in significant research even on steroid use, for the same reason,most studies have been conducted for medical reasons.

Slightly off-topic, but interesting; fat cells work on a similar principle. You start with a certain number, which can grow in size. When they reach a certain size, they multiply and you grow more. Once you have these new ones, they are there for life (unless you have them sucked out).

They can decrease in size, but the total number stays at the new higher level. Number 1 reason for not getting fat in the first place.


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## hackskii (Jul 27, 2003)

stow said:


> Slightly off-topic, but interesting; fat cells work on a similar principle. You start with a certain number, which can grow in size. When they reach a certain size, they multiply and you grow more. Once you have these new ones, they are there for life (unless you have them sucked out).
> 
> They can decrease in size, but the total number stays at the new higher level. Number 1 reason for not getting fat in the first place.


Welcome and I didnt now that about fat cells.

I hear the test to determine hyperplasia is hard to determine.


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## Ziricote (Feb 18, 2007)

stow said:


> Slightly off-topic, but interesting; fat cells work on a similar principle. You start with a certain number, which can grow in size. When they reach a certain size, they multiply and you grow more. Once you have these new ones, they are there for life (unless you have them sucked out).
> 
> They can decrease in size, but the total number stays at the new higher level. Number 1 reason for not getting fat in the first place.


PGF-2(a) causes cell death in adipose tissue.


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## stow (Jun 5, 2007)

The main problem with proving hyperplasia in human subjects is the lack of baseline data.

As someone mentioned, everyone is different, so proving that a bodybuilder has more fibres per cross-sectional area of muscle than he did say 10 years ago, for a large enough group of people to make it statistically sound, is near impossible, (because the collection of baseline data prior to the program hasn't taken place).

And thanks for the welcome, I hope I'll be able to contribute something to the discussions, even if its just interest!


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## 3752 (Jan 7, 2005)

in my opinion the only real way it can be proved to an extent is for a bodybuilder to compete one year then compete 1yr later at a higher bodyweight but at the same or lower BF%...


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## stow (Jun 5, 2007)

That would prove hypertrophy, but not hyperplasia.

STOW


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## Ziricote (Feb 18, 2007)

stow said:


> That would prove hypertrophy, but not hyperplasia.
> 
> STOW


Surely without taking samples it would only prove increased mass rather than hypertrophy or hyperplasia. A double blind thingy majigger over a course of 6 months to a year with different test groups (exercise, non-exercise, diet, non-diet, placebo, non-placebo etc) taking tissue samples at set intervals seems in my mind the best way to see whether or not hyperplasia occurs.


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## stow (Jun 5, 2007)

Sort of agree. But at a lower or same bf, and a higher body mass, lean mass growth would have had to occur, and that would most likely be muscle. I'm just speaking very broadly, it wouldn't necessarily PROVE hypertrophy, but what Paul says would definitely suggest it. (But it wouldn't disprove hyperplasia either).

Yes - a real study would have to be over a long period of time, with a large group, all training the same, taking the same gear, eating the same, etc etc and then even then, one part of the muscle may act differently to another, and differently to other subjects. So the biopsies would need to be from exactly the same site etc etc.

Its a very complex hypothetical situation.

We are getting bogged down in hypothesis.

I think it probably can occur, under the right range of stimuli, for SOME people, in SOME circumstances. Thats genetics for you.

Manipulation of the myostatin gene is more likely to produce genetic freaks, but its probably years off and the most ethically unsound idea ever!

STOW (gotta love this part of the forum, v interesting)


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## Ziricote (Feb 18, 2007)

What I was thinking with the increased mass in my last post was water weight, although, most could guess that hypertrophy had occurred probably wouldn't be wrong to assume so.

Forgot to say it earlier but welcome to the site Stow, good to have more of this type of discussion on the site.


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## stow (Jun 5, 2007)

A good deal of muscle is made up of water, and hypertrophy of the muscle cells could be due to intra-cellular fluid.

Low bodyfat would suggest less fluid retention outside the muscle.

STOW


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## mrmasive (Dec 30, 2005)

stow said:


> (1st post ever on Uk-M, so hello!)
> 
> Slightly off-topic, but interesting; fat cells work on a similar principle. You start with a certain number, which can grow in size. When they reach a certain size, they multiply and you grow more. Once you have these new ones, they are there for life (unless you have them sucked out).
> 
> They can decrease in size, but the total number stays at the new higher level. Number 1 reason for not getting fat in the first place.


Damn it


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## hackskii (Jul 27, 2003)

Ziricote said:


> PGF-2(a) causes cell death in adipose tissue.


Hey bro, do you got any more information on this stuff?


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## Ziricote (Feb 18, 2007)

hackskii said:


> Hey bro, do you got any more information on this stuff?


Hmmm, as in PGF-2a analogues or just about PGF-2a? I had read into it a while back but not enough to be able to explain the process in which it works to cause cell death.


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## pauly7582 (Jan 16, 2007)

stow said:


> (1st post ever on Uk-M, so hello!)
> 
> Delhi, hyperplasia is the splitting of the muscle fibre, its not growth of a new cell. There is still little scientific evidence for it, but it doesn't mean there is a shortage of circumstantial evidence. However, due to the obvious ethical implications, you would struggle to find a significant study which included exogenous supply of GH, IGF etc for non-medical purposes. There is still a huge gap in significant research even on steroid use, for the same reason,most studies have been conducted for medical reasons.
> 
> ...


Welcome to the boards mate. Growing new muscle cells and the splitting of muscle cells is the same thing, the only way a more cells are produced anywhere in the body is through simple cell division- mitosis. Hyperplasia occurs where existing muscle cells divide producing new ones.

A little additionaly info regarding the fat cells. where adipose tissue used to be thought of as a passive storage site, we now know that it is a complicated organ with important endocrine and metabolic functions.

From the pre determined number of adipocytes that we have at birth, the number inceases far more rapidly during childhood and puberty. Hence obese children usually= obese adults. Proliferation of new adipocytes in adulthood is a slower process (thankfully). However, just as the number of fat cells can increase, so they have been proven to decrease. Key regulators of adipocyte division are insulin, corticosteroids (involved in stress response, immune response and regulation of inflammation, carbohydrate metabolism, protein catabolism, blood electrolyte levels, and behavior)and retinoids (sunstances chemically similar to Vit A- are somtimes used to suppress tumour growth) but the exact mechanisms of control are not entirely understood.

Adipocyte apoptosis is the disintegration of fat cells into particles that are usually disposed of by immune cells. There is some evidence that leptin (hormone produced by adipocytes) can induce this but as always, this has only been investigated in rodents. Basically, high levels of body fat induce high levels of circulating leptin. Where exogenous (additional) leptin was administered adipocytes were destroyed. There is also research that has shown adipocytes are capable of dedifferentiation, where they regress into a simpler less specialised form without storage capacities. This is currently being researched at the Uni of Cambridge and more can be read in the Journal of Lipid Research.

Basically, the extent to which fat gain or loss is attributed to an increase or decrease in adipocyte number is largely unknown in humans but an increase and decrease of the number of fat cells in mammals has been demonstrated.

Interesting stuff!


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## pauly7582 (Jan 16, 2007)

Bloody hell.

i didn't realise I'd went on that much.

:doh:

:rockon:


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## 3752 (Jan 7, 2005)

This is getting way to complicated for me, i don't know how it does what it does but i do know that you will gain muscle using GH/IGF-1LR3 (although not a huge amount) i know this because i have done it and so has many other guys i know have but and this is the big but you only get these real gains from being specific about everything you do not just whack some peptide into your arm and hope for the best which i am afraid to say most guys do....


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## hackskii (Jul 27, 2003)

pauly7582 said:


> Welcome to the boards mate. Growing new muscle cells and the splitting of muscle cells is the same thing, the only way a more cells are produced anywhere in the body is through simple cell division- mitosis. Hyperplasia occurs where existing muscle cells divide producing new ones.
> 
> A little additionaly info regarding the fat cells. where adipose tissue used to be thought of as a passive storage site, we now know that it is a complicated organ with important endocrine and metabolic functions.
> 
> ...


I enjoyed reading that, gave you some reps for it and it gave you two green ones. :bounce:


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## stow (Jun 5, 2007)

Enjoyed reading it too. V interestung and learnt something. I think Paul has some physiology qualifications - right Paul?


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## hackskii (Jul 27, 2003)

stow said:


> Enjoyed reading it too. V interestung and learnt something. I think Paul has some physiology qualifications - right Paul?


I wonder what he does for a living.


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## pauly7582 (Jan 16, 2007)

hackskii said:


> I wonder what he does for a living.


Ah the attention! :humble:lol I feel like a man of mystery. Thanks for the greenies too mate!

I'm a lecturer in anatomy, physiology and biomedicine. :thumb:


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## stow (Jun 5, 2007)

Brilliant.

Am sure we can have some interesting threads.

I have an anatomy and physiology background, many years ago, but now work in IT.

STOW


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## Delhi (Dec 8, 2005)

Stick around guys


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## hackskii (Jul 27, 2003)

pauly7582 said:


> I'm a lecturer in anatomy, physiology and biomedicine. :thumb:


Looking fwd to seeing some more of your posts mate.

If you see me off base then please correct me at any time.



stow said:


> I have an anatomy and physiology background, many years ago, but now work in IT.
> 
> STOW


Looking fwd to seeing your posts as well.....

Iron sharpens iron as one man sharpens another..............


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## misterC (Jul 31, 2007)

Pscarb said:


> yes it will have only if you take the pMGF the night before so that the pMGF and IGF do not compete for the same receptor


Could you please tell me where to find the study,I'm spending hours on pubmed,but still not getting the info I want.


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