IGF-1 Training protocal: Hyperplasia

[xtraflossy]

I have been doing much thinking about maxamizing the hyperplasia durring an IGF-1 cycle. I really just wanted to share some information that supports my thinking.

My thinking was that (and some of this came from all the other stuff Ive been researching) IGF-1 signals satalite cells. These cells then duplicate (made simple). Now, as I couldnt find any isolated gene, protein, hormone or other factor that specificly sways the new myoblastic cell to join with another vs. hypertrophy. With a lack of this particular expression, I moved on to training variables that might influence.

- Let me start forming a picture:
HOW DOES MUCLE FIBER HYPERPLASIA OCCUR?

There are two primary mechanism in which new fibers can be formed. First, large fibers can split into two or more smaller fibers (i.e., fiber splitting) (6,25,39). Second satellite cells can be activated (11,16,17,43,44).

Satellite cells are myogenic stem cells which are involved in skeletal muscle regeneration. When you injure, stretch, or severely exercise a muscle fiber, satellite cells are activated (16,43,44). Satellite cells proliferate (i.e., undergo mitosis or cell division) and give rise to new myoblastic cells (i.e., immature muscle cells). These new myoblastic cells can either fuse with an existing muscle fiber causing that fiber to get bigger (i.e., hypertrophy) or these myoblastic cells can fuse with each other to form a new fiber (i.e., hyperplasia).

Ok, so the conclusion I came to (man I hope Im just not stating the obvious here) is to eliminate one of the variables I CAN control. That would be the site specific attachment of these new cells to be called upon to do muscle REAPIR (and not form new cells) -hopefully.

Wether or not this will work has yet to be seen: Use IGF-1 site specificly 2 days AFTER training a particular muscle. You will already have IGF in circulation, and you will be signaling anyways due t othe stress from the W/O. Let the muscle heal as much as possible, then shot it with IGF-1. This will (in theory, at least in my head) greatly reduce the chances any newly made cells go twards repairing the damaged fibres. With more cells NOT repairing muscle, they have a greater chance fusing to make new fibers.
If the above were correct, then it is possible you could create even more fibers NOT working out. since almost none of the proliferated cells would be used for repair.
It's all about cell signaling. Work out the muscle, let it signal for a day by itself, then once its almost healed, then administer the IGF-1 (again, just a theory), this will give the muscle a huge boost to signal again, and proliferate. This seems to be the most controll you can have (at this time) as to the differentieation of the cells. This prolonged signaling (amplified by IGF's proliferation propertiers of cvourse) is the basicly the same as other supps on the market now (xfactor being one I can think of right now- all the bennifit of DOMS, but to a much greater extent and less pain).
In other studies I have looked over (and discussed w/ a family member who is a doctor in genetics/research/pedieatrics and specializing in metabolic deseises- yes,.. all of these) it would seem that after the growth factor is removed, the cells will pretty much stop growing, and almost immedieatly form myotubes / new fibers (from what degree this happens 24 hours after injection, I couldnt say, but would be safe to assume it does to some extent)

So my point would be: An 4-5 week IGF-1 cycle would bennifit the user most by primairally following a high rep scheem causing muscle stimulation, hypertrophy, thus allowing your fibres to absord more neutrients, allow for new fibers to be made by NOT being used for muscle repair (at a greater rate), but instead forming bridges between existing muscle threads and forming new fibers on their own.

(Im at the end of my IGF run- I have only recently been following this protocal. I will have to to do another to follow all the way through. The unfortunite part would be that results couldnt be measured durring use, or even right after. AAS could mature the new fibers quickly, but then that would be too many factors to get an exact calculation).


Just wanted some feedback,.. Is this common knowlage? Where are my flaws in thinking? does anyone agree?
Should I just give up now and ban myslef :run:


(Its not so much a study, but a recap of studies- this is where I got my quoted text from- my idea didnt come from this, It just indirectly supported it)http://home.hia.no/~stephens/hypplas.htm

 

[Bionic]

Hey XF, I don't know if you're right or worng on this, as much of the technical knowledge that the geniuses on this board impart, for the most part, goes way over my head. But I do want to commend you for doing your own research and thinking for yourself. VEEERRRY rare these days. Anyways, good luck on your research and I'll be following this thread.

Bionic.

 

[SecretOfSteel]

and what about people using cell mediated IGF with a half life of 48 hours ?

 

[xtraflossy]

Would that be the Oratropin like IGF-1? (Im guessing because you said cell medieated...)
I personally was using the long form of IGF-1, so I had circulating levels just as one would with the orals (almost, I beleive the orals release in waves, extending the circulation time beyond 24h ). The bennifit of site specific is lost in the Oral delivery.

If your using the oral version: The training method I mentioned still should work. Your still hitting receptors, and it still should be real IGF-1 in your body. Even the injected form will circulate 24 hours. The suggestion that injecting the muscle group after recovery, to induce site specif signaling for twice the duration (with the second time it signals-due to injection- there is very minimul damage to repair.)

What Im thinking is IGF-1 can/does cause hyperplasia. (There is an edge with injections IMO.) If hyperplasia does occure, then the two options for the newly formed cell are to:
1) repair damaged muscle tissue. (or be broken down for energy, but lets assume your getting enough carbs, proteins,...)

2) Join with other cells to bridge gaps between fibers or form new fibers (in a way, there kind of the same- new fibers)

When has you body NOT chosen survival over everything else!! It will repair 1st before deciding to make "new" tissue (to be more specific- new tissue in access).

The training method *should* work regardless or circulating time (or delivery).

Again, this is just a theory-

 

[CDB]

I do believe there are studies showing elevated protein synthesis up to eight days after a workout thought. I guess the question would be how much if this is actual repair of myotrauma and how much isn't. I'd recommend you bring this thread here: http://www.hypertrophy-research.com. The guys there have a whole shitload of knowledge that they could bring to bear on this and help you work the theory out, see if it's workable or not. I think the forum is accessible if you mess around a bit with the internal links, because right now the main site is being reconstructed.

My guess off the hip would be that you're right, lighter weight training would be what to go for to increase protein synthesis and satelite cell activity but cause as little actual muscle damage as possible. Something like German Volume Training, or maybe something like Sub7s ACIT/occlusion ideas would good to use here. Id' shoot him a PM or post a thread, I think he and Ron, the guy he worked out ACIT with, have access to some studies that show elevated protein synthesis, satelite cell activation and hypertrophy, but in the absence of muscle damage.

More important than how hyperplasia happens is why it happens though. If you could find out why or under what conditions satelite cells would preferentially form new fibers as opposed to donating their nuclei to damaged fibers that might get you further toward your goal.

 

[xtraflossy]

That is EXACTLY the key I have been searching for!! :jaw:

Science doesnt seem to know yet by me understanding, and this is readily stated in many of the journals and studies Ive read. Although, when searching for "supplements" the "HOW" becomes very important.

Im pretty sure I know WHY it happens though. It just seems fairly obvious, as it applies for every change your body makes.
Ive read studies (and you can also see this in real life, just look at the treadmill) that show swimmers develope larger shoulder muscles (total), although there fiber size is smaller. Your body will change to adapt to the demands.
Now, since the shoulder muscle as a whole increases in size, but the fiber size remains the same, hypertrophy is not the most visable cause. It seems fairly obvious that there are new muscle fibers created, that were not there before. (same with long distance runners.)
Ok, heres where I probably explain things really bad... Endurrence excersize causes stress on the muscles. Not to the extent that weightlifters do, but some stress. This requires contractile proteins to handle that demand (or the movement of the muscle). In the case that the stresses do not cause large tears, the body tries to adapt to the stress.
If the muscles can not hold any more contractile proteins, because the fibers havent hypertrophied enough to allow for the necessasery addition of these proteins, then the body would just simply just grow new fibers; to hold the proteins/energy to meet the demand.
We know that distance runners and such will develope a certine type of muscle fiber much smaller, but greater in number. It would have to,.. maybe it has something to do with muscle cell serface area (for better obsorbtion of energy, proteins and such-= I know this to be true about other things, cillia for one, but I cant remember the science behind why it is better- will think about it and edit later)
I came to this because for the past 8 months, I've walked to work. Its 2.5 miles each way. (and thats before the gym). Now, the size of my legs has gone down some,.. but I continue to make strength gains without putting on size. We know that muscle fiber type can change due to demand as well, and I think this is what happened/is happening. Which is good, because if Im not hypertrophing because the endurrence is outweighing the gym needs, then the only conclusion is Im able to put more contractile proteins (and glycogen) in the same sized container. And it thats true, then what happens when those "containers" become full?? -make more because the ones there cant cary anymore.
What Im liking about this, is when I get a car, and my requirements on my muscle change, all those new fibers I'll be able to blow up into larger ones!!

Make sense? If Im wrong about the contractile proteins, I still beleive that the concept is still good. I just had the container contents wrong.

I'll check out the site you mentioned, and see what knowlage can be gained there. I dont expect to be taken very seriously at first though.

 

[CDB]

I'll check out the site you mentioned, and see what knowlage can be gained there. I dont expect to be taken very seriously at first though.

You put a lot more apparent research into this than most people tend to do in their entire lives. My guess is they'll take you seriously. It's a very polite, well moderated board with a heavy emphasis on studies and a science based approach to work outs. Definitely go there, it's too much raw info to miss out on in those guys' heads.

 

[BigCasino]

Your body will change to adapt to the demands.
Now, since the shoulder muscle as a whole increases in size, but the fiber size remains the same, hypertrophy is not the most visable cause. It seems fairly obvious that there are new muscle fibers created, that were not there before. (same with long distance runners.)

If the muscles can not hold any more contractile proteins, because the fibers havent hypertrophied enough to allow for the necessasery addition of these proteins, then the body would just simply just grow new fibers; to hold the proteins/energy to meet the demand.
s!!

I believe you are talking about the difference between fast-twitch vs. slow twitch muscle fibers. You are correct in that typically, athletes that excel in / practice cardiovascular based events (such as long distance running) do in fact tend to have a different ration of muscle fibers, than someone that has spent many years practicing weight lifting. This difference is their contrasting ratios of fast to slow twitch muscle fibers.

However, your theory that this is the result of numerous new muscle cells being created is slightly off course. Genetically, certain people will be predisposed to have certain ratios of these varying fiber types in their body. Some individuals have genetic blueprints that lean heavily towards fast twitch, and vice versa, then againt here are those who have more balanced ratios. You noted something very important though, your body can and will adapt. However this adaptation does not mean that suddently it is creating countless new muscle cells, rather it is developing through stimulation towards a certain ratio. If all you practice is powerlifting your body WILL adapt to meet those demands.

What is so appealing about IGF is the idea of hyperplasia of the muscle cells, and cell division. Ordinarily, we develope a certain number of muscle cells and then that is it, we grow stronger and bigger through hypertrophy of our *existing* muscle fibers, not by readily growing new ones. When you are talking about becoming stronger without gaining additional size or muscle tissue, that has more to do with the training of your Central Nervous System (CNS), that it does with "filling the container". You have a valid point there though, and when you are speaking of glycogen and filling the container versus straight hypertrophy, you are really talking abou the differences between sarcoplasmic and myofibril hypertrophy.

As for the original topic of this thread, muscle cell hyperplasia through IGF-1 is something that occurs over the long term, and when I say long term I mean months and years of continual use. Yes IGF will encourage satillite cell function, and proliferation, but is generally a slow process. Muscle cells are not the most readily to volunteer for division. The islets cells found in your liver are far more eager for that purpose. I think that regardless of the protocols you use, it is still going to take months of continual use eitherway.

 

[xtraflossy]

"You noted something very important though, your body can and will adapt. However this adaptation does not mean that suddently it is creating countless new muscle cells, rather it is developing through stimulation towards a certain ratio. If all you practice is powerlifting your body WILL adapt to meet those demands."
Of course, you are right. I didnt mean (If I came off as such) anything would happen "suddenly", happen, or be exclusively all new fibers. This is why I mentioned my personal situation, which seems to have evolved over the better part of a year- naturally though.
Personally, I really dont buy the "we have a predetermined number of cells thing. It would be hard to beleive that your body stops growing new tissue when the situations are right for it. What I WILL give ya though, is yes, we have a static number of satallite cells when were matured. I have been looking into ways to modify this number (MyoD inhibbition, othrer growth factors like fibroblast growthfactor (I have another post on this in this section, along wit hthat, I think I have found the factor responsable for growing new androgen receptors.,... but nowhere near commenting on it yet). In studies though, satalite cell division seems to have a seperation limit- around 60 divides in its life cycle. This has to do with the DNA strands getting shorter. And I havent found a reason why your body would A) Let this number totlly max out, I mean, yes, those cells might max out on divisions, but that wouldnt happen normally, so your body wouldnt want to reach that number on its own. And if it did, Im sure it would compensate by other means, possible by creating new dividable cells. But, this is more a personal opinion as to why I dont beleive in the notion of preconceived fiber count. But, this be a discussion on altering those factors, so...
I was planning on on a total of a 3 month run of IGF, not consecuitive though, 1 month on, one off. So, My intention wasnt for it to be all magic.
I would like to comment that the reason for other organs growing much more faster, would be like your skin, organs have a rate at which they renew themselves. For instance (these times are just made up, as I dont know/havent checked the exact numbers) your might get a new liver every 6 years, new skin every few years and so on. NOW- wether this would be because those organs are more receptable to IGF and other factors or theyre just designed to do that on their own anyways is up in the air for me. This type of knowlage can be used to determin medical abmnormalities, and explain seeming random sysmptoms in disorders by the time seperated between each lenght of time an organ is effected- I dont really have the best way to explain this right now. I'll try to edit later.
But, yes growing of new fibers using IGF-1 WILL take months, it will happen in 1 month to some small degree, and a greater degree after long term use.
But I do beleive that my training protocol enhances the rate. Simply because cell signaling in the fassion were using is for the body to repair itself. And IGF-1 will cause hyperplasia also. So, if no repair is needed, while muscle stimulation is still present, I beleive that would influence the outcome.
The studies done on regrowing damaged tissue in living organisms suggest that since the growth stops after the original amount is repaired/replaced. While normal, healthy muscle tissue is subjected to exogenous IGFwhen the cells are generated/replicated because of the signaling, what else would they do if they had "nowhere" to go??

(Sorry, I really need to stay more on topic here :blink:
But, if youve done a bunch or research and stuff, one thing leads to another... )

 

[BigCasino]

After reading your latest post, and re-reading your previous ones it is apparent to me that you have spent a great deal of effort researching and educating yourself on this topic. In case I did not acknowledge it in my first post, I do respect your opinion and share your interest in this area.

Personally, I really dont buy the "we have a predetermined number of cells thing. It would be hard to beleive that your body stops growing new tissue when the situations are right for it. What I WILL give ya though, is yes, we have a static number of satallite cells when were matured. I have been looking into ways to modify this number (MyoD inhibbition, othrer growth factors like fibroblast growthfactor (I have another post on this in this section, along wit hthat, I think I have found the factor responsable for growing new androgen receptors.,... but nowhere near commenting on it yet).

I concur, MyoD inhibition is certainly a factor that in its regulation, or lackthere of, can determine muscle cell proliferation. In general though I do believe that your average, non-chemically enhanced, human truly has a predetermine number of muscle fibers based on their genetic make up. Now when I say this, I do not necessarily mean that it is a pre-defined set number in the sense that by looking @ genetics, subject A will have X amount of fibers @ the time of maturation, and subject B will have Y amount of fibers. Rather I am talking about a relative quanatative amount. Given there are certainly abnormalities that take place in everyday cell activities within our bodies, and of course there are external elements such as diet, exercise, stress, age. That being said, I do not believe this number of muscle fibers from the point of maturation onward can be tangibly manipulated through exercise type alone.


Of course with IGF-1 and other "theraputic" elements you and I both agree this manipluation certainly can take place.

I am glad you mentioned the following though:

In studies though, satalite cell division seems to have a seperation limit- around 60 divides in its life cycle. This has to do with the DNA strands getting shorter. And I havent found a reason why your body would A) Let this number totlly max out, I mean, yes, those cells might max out on divisions, but that wouldnt happen normally, so your body wouldnt want to reach that number on its own. And if it did, Im sure it would compensate by other means, possible by creating new dividable cells.

You are correct sir, you are speaking about the telomeres, the "capped" end of DNA chromosomes. These telomeres can be visualized as the hard compressed pointed ends of your shoelaces. Like the end of your shoelaces they eventually become frayed after repeated use, eventually rendering them useless. When this happens on the cellular level, essentially the telomere is becoming uncapped which the body will recognize and will eventually lead the cell to programmed cell death, apoptosis. Really this is just the body being programmed to age and eventually expire, but there is another reason. Think cancer. The telomeres serves as a type of fuse, a preventative measure against an absurd number of divisions. Cancer just loves cells that natively divide constantly, such as the skin and liver cells you pointed out. What seems to us to be such a frustrating question of why won't our body just let us grow more fibers given prime conditions really has a lot to do with tumor supressor genes, and natural hardwired preventive measures your body takes against "unnatural" cell division.

As we progress with gene therapy manipulations I have no doubt that we will be able to switch off many of these factors, but in the mean time I agree IGF-1 is still your best bet for inducing hyperplasia.

I am eager to hear the results of your IGF protocols, please continue to keep us posted and share your research and ideas :type:


p.s. I'm aware that you know most of this already, but I tried to explain a few things in an easily digestible fashion for others that are following along and may not be familiar with some of these concepts :cheers:

 

[Bionic]

p.s. ...but I tried to explain a few things in an easily digestible fashion for others that are following along and may not be familiar with some of these concepts :cheers:

And for that, I'm very appreciative!

 

[BigCasino]

Glad to hear that bro!


Knowlege is power :dance:

 

[Dan Moore]

I'd recommend you bring this thread here: http://www.hypertrophy-research.com. The guys there have a whole shitload of knowledge that they could bring to bear on this and help you work the theory out, see if it's workable or not.

I think the forum is accessible if you mess around a bit with the internal links, because right now the main site is being reconstructed.

More important than how hyperplasia happens is why it happens though. If you could find out why or under what conditions satelite cells would preferentially form new fibers as opposed to donating their nuclei to damaged fibers that might get you further toward your goal.

Thanks for the link and very nice things you've said, I appreciate it.

The main website is back up an accessible and you can link to the forum there.

That's the unanswerable part. Although there was a recent study that saw something, IE possiblitly of new fibers. If I run across it again I'll post it.

It's not that hyperplasia doesn't happen, the problem is the measuring of it. Either way it has been shown that hypertrophy happens before hyperplasia.

Here is a list of references you guys may want to view.
Start with these reviews

Adaptation of muscle size and myofascial force transmission:
a review and some new experimental results
Scand J Med Sci Sports 2005: 15: 349–380

Control of the Size of the Human Muscle Mass Annu. Rev. Physiol. 2004. 66:799–828

Mechanical Signals, IGF-I Gene Splicing,and Muscle Adaptation
PHYSIOLOGY 20: 232–238, 2005

Autocrine and/or paracrine insulin-like growth factor-I activity in skeletal muscle.
Clin Orthop. 2002 Oct;(403 Suppl):S188-96

Growth Hormone and the Insulin-Like Growth Factor
System in Myogenesis
Endocrine Reviews Vol. 17, No. 5

Exercise Effects on Muscle Insulin Signaling and Action
Invited Review: Intracellular signaling in contracting skeletal muscle
J Appl Physiol 93: 369–383, 2002

Dan Moore
www.hypertrophy-research.com
[email protected]

 

[BigCasino]

Dan Moore,

Great to have you here sir! Thank you very much for posting those references. Most of my knowledge on hyper plasia and cell proliferation comes from my research in the Cancer biology / Oncology field, so I always am looking to diversify my sources of information on the topic.

So you agree that the body will place a natural priority on hypertrophy over hyperplasia. What do you think of xtraflossy's ideas on how to work around this tendency?

 

[xtraflossy]

Well, Im glad to see some interest in the subject. I spent some of the weekend thinking of ways I could test this protocal. I wanted to reiterate, that following this protocal doesn't guarentee any significant advantage over another training protocal, if would might be best compared to the difference between being a defensive driver or not. Defensive driving Im sure has helped avoid accidents, but theres no telling how many. But its the best thing you can do to avoid them.

Now that I have my "disclaimer" out of the way :study: here are my thoughts on testing it:
With one month use, theres no telling directly after what the results are. Yoiu could do a cycle of AAS to mature what new fibers you do have and see the results. However, theres no controll for this test. If you used the same anabolic, who's to say (even after a long amount of time) that if you used the same anabolic after your second run that using the same same anabolic the second time would taint the results. Becasue some extent of "tolerence" (wrong word- but you get the idea) would exist on the secong go around.
Using a different anabolic would yeild different results simply because it may never have been used, also your predisposittion of response might be greater or less then the first anabolic.
Ok, those are the reason I beleive that wouldnt work. Heres what I beleive might.

The best way I can think of (and this may sound expream to some, but thats another issue) is to take a biopsy. What I am thinking, is there is a small cylindricial tube, thinner then a pincle. This tube (It has a name, its what they take skin biopsys with) has a razor edge. Take a slightly deeper sample from your leg, where there is minimul bodyfat, to get a very very small muscle tissue sample. This sample would also be the spot of injection for all, or the majority (or maybe just another part in the rotation) of use. You take one before, and another about a week after finishing.
This would eliminate the hypertrophy due to glycogen storrage. Check out both samples under a microscope and compare.

In the end for me, I find the science fasanating, and am also tring to get the most bang for my buck. At closer to $200 a month, (%150, but I think I got durring a sale) doing 3 months can get a little expensive. You know, I just thought about it though... I do kinda have access to a medical research facility, and a doc, who has done many skin biopsies. I know by the end of the 3 months use (with time off of course) I could get samples done, with analysis - free of course. Its just the "before" sample I would have difficulty with.-

I would like to thank BigCasino for "translating" my posts. As I have a tendency to remember the big picture made from the smaller ones but dont remember all the details and correct names. -I wish my rep points were worth more....

I am also hoping that I am able to continue this discussion further as last night was my last dose of IGF-1. I think I can say that Ive been feeling more "Einsteinian" lately, so its effects on memory are, for me, concluded. I just hope I dont go dumb in the next 24 hours (anyone see mthat Seignfeild eppisode where George goes without sex and thinking about wemen and becomes supersmart?? Starts teaching physics to kids, doing expirements. Then as soon as he gets some, he gets "stupid" again.... )

 

[Dan Moore]

Dan Moore,

Great to have you here sir! Thank you very much for posting those references. Most of my knowledge on hyper plasia and cell proliferation comes from my research in the Cancer biology / Oncology field, so I always am looking to diversify my sources of information on the topic.

So you agree that the body will place a natural priority on hypertrophy over hyperplasia. What do you think of xtraflossy's ideas on how to work around this tendency?

Although interesting, I think he's shooting in the dark. Several researchers have used recombinant IGF and to my knowledge they haven't produced when used alone in healthy individuals.

Now I'm not saying it won't work but it doesn't look all too promising.

For example in one study they used IGF on rats and found that even thgouh it help reduced overall body catabolism it did nothing for growth. In humans their have been substantial weight gain when IGF is administered but the weight has been predominantly water retention not protein synthesis.

In the only study I know of that used IGF in combination with exercise and or GH, again although it showed some mass change a lot of this was water increase and fat mass actually increased.

Lastly the side effects of IGF injections may not be all that grand or wanted, skin irritation, disturbance of the somatropic axis and bloating.

So even though injections may very well increase the plasma levels of IGF, it's a shot in the dark as to how muscle tissue will respond. Remember it's not the plasma IGF that is needed it's the two splice variants that constitute the mechanical sensitive IGF that we are after.

Hyperplasia, it's hard to say, the animal models don't truly represent the human condition but the relatively few studies that may have reported increased cell muscle number seem to point that it's more a matter of how long you've been working out rather than how you've been working out. Also let's not discount the importance of copious amounts of test. Which have been shown to work on so many levels, AR mRNA, IGF, Sat Cells and so on.

Dan Moore

www.hypertrophy-research.com
[email protected]

 

[CDB]

Thanks for the link and very nice things you've said, I appreciate it.

CDB=xahrx=Rich, Dan.:burger:

I turns out I'm traveling to Baltimore tonight to meet with some clients tomorrow and do some work for them. I can hit the university when I get back Wednesday/Thursday and see about the study you asked for. The bad part about this is the one suit I own is crumpled up in my friend's trunk. I'm meeting him today to see if I can get an emergency clean and press. Otherwise the client better be okay with business casual.

I think recently Bryan actually posted on the HST boards, haven't seen him there in a while, in response to a similar question and his answer was the same, hypertrophy first with hyperplasio being a distant, not too reliable second. No details though.

 

[xtraflossy]

Can some one elaborate a little on:

"Remember it's not the plasma IGF that is needed it's the two splice variants that constitute the mechanical sensitive IGF that we are after."

 

[Dan Moore]

Can some one elaborate a little on:

"Remember it's not the plasma IGF that is needed it's the two splice variants that constitute the mechanical sensitive IGF that we are after."

If you can download these and read them.

Control of the Size of the Human Muscle Mass Annu. Rev. Physiol. 2004. 66:799–828

Mechanical Signals, IGF-I Gene Splicing,and Muscle Adaptation
PHYSIOLOGY 20: 232–238, 2005

Autocrine and/or paracrine insulin-like growth factor-I activity in skeletal muscle.
Clin Orthop. 2002 Oct;(403 Suppl):S188-96

In a nutshell there are different forms of IGF-1 (there is also IGF-II which also acts on skeletal muscle but it's much less researched, each has a different action on cells as related to it's origin (heptatic or muscle specific). These two forms are IGF-1Ea and 1Ec (sometimes refered to as 1Eb if looking at research in rodents).

 

[Dan Moore]

CDB=xahrx=Rich, Dan.:burger:

I turns out I'm traveling to Baltimore tonight to meet with some clients tomorrow and do some work for them. I can hit the university when I get back Wednesday/Thursday and see about the study you asked for. The bad part about this is the one suit I own is crumpled up in my friend's trunk. I'm meeting him today to see if I can get an emergency clean and press. Otherwise the client better be okay with business casual.

I think recently Bryan actually posted on the HST boards, haven't seen him there in a while, in response to a similar question and his answer was the same, hypertrophy first with hyperplasio being a distant, not too reliable second. No details though.

Richard, I think it's time you buy another suit, I have plenty to spare since I gave up on corporate America

Alway, Gonyea, Antonio, Kadi have all looked real hard at hyperplasia, but it's just so very hard to quantify new fibers in humans. I mean it definatley happens in mammals and lil birdies(so it seems), but to 1. Get an existing count to start with then 2. Wait the extremely long time it would take with training and 3. Then get another accurate count, would be incredible in humans. Just think the human biceps (relatively small) has thousands of fibers, now just imagaine trying to count the human lats (a common muscle used in fowl studies).

Dan

 

[CDB]

Richard, I think it's time you buy another suit, I have plenty to spare since I gave up on corporate America

I buy generally buy a new suit whenever I gain or lose enough weight to justify the purchase. Not the best system, but it's served me thus far.

Alway, Gonyea, Antonio, Kadi have all looked real hard at hyperplasia, but it's just so very hard to quantify new fibers in humans. I mean it definatley happens in mammals and lil birdies(so it seems), but to 1. Get an existing count to start with then 2. Wait the extremely long time it would take with training and 3. Then get another accurate count, would be incredible in humans. Just think the human biceps (relatively small) has thousands of fibers, now just imagaine trying to count the human lats (a common muscle used in fowl studies).

Dan

If I piss these clients off when I tell them there's really nothing we can do for them, I'll probably have enough free time to spare to count muscle fibers. If they like me, I might have a lot of free ice cream. Benefits of occasionally working for the food industry.

 

[xtraflossy]

IF hyperplasia did occure, why wouldnt a sample of an area reflect the muscle as a whole? I wasnt planning on counting thousands or millions of fibers of course. But, the fibers would be really small to begin with,.. so a small sample should show an indication,.. at the cellular level

"These two forms are IGF-1Ea and 1Ec (sometimes refered to as 1Eb if looking at research in rodents)."

-Thanks!! When talking about these things, and discovery when breaking down proteins to a certin level, those 2 forms could easily turn into a huge list if I were to guess :woohoo:

- In the past, there have always been things man couldnt quantify. If you cant ditect the direct result of something, doesnt mean it's unknown. (just a little personal hype,.. I dont like answers that end in "theres just no telling".. :twisted:

 

[Dan Moore]

IF hyperplasia did occure, why wouldnt a sample of an area reflect the muscle as a whole? I wasnt planning on counting thousands or millions of fibers of course. But, the fibers would be really small to begin with,.. so a small sample should show an indication,.. at the cellular level

A biopsy would tell but only if the sample contained new fibers than a previous count. So you are trying to find a needle in a haystack and it may take several biopsies in order to truly find a change. How are we to know which fiber split and at which area of the muscle. In the case of mitogenesis this would be the same situtation, where and when do you perform the biopsy. This is the problem currently it's too hard to test with it being very very painful and that's one reason why it has not been shown conclusively in humans, who wants to sit for multiple biopsies over and over again.

 

[CDB]

This is the problem currently it's too hard to test with it being very very painful and that's one reason why it has not been shown conclusively in humans, who wants to sit for multiple biopsies over and over again.

Has it been shown conclusively in some animals though, rats or monkeys?

 

[xtraflossy]

I wouldn't need to know exactly which fiber split, the area of the biopsy would be a constant. One sample taken before a cycle and one after.
The sample would be small- I have seen it performed many times, only a slightly deeper sample would be needed.

If wort comes to wors, I could count cells from a grid from the sample. Multipul samples... ? I would only take 2. before and after. I mean, really, it just seems no one is even tring to test this in humans like we want, a real worl sample.
These samples are quick and painless- only small injection of numbing (if your a pussy, and Im going to be)

If getting a fiber or cell count before and after a months use (times 3, for the 3 months) is "useless or yo ufind it would be inconclusive,.. for the love of God, tell me.

I guess if worse comes to worse, I can grow my fibers the old fassioned way,.. in a dish :jaw:

Get a sample of my own muscle tissue, include some growth factors, (they shouldn't bind together until the growth factor is removed) and maybe a local injection of the new fiber "buds"??? -thoughts on this? (I just know Im going to regret this post....)

 

[Dan Moore]

I wouldn't need to know exactly which fiber split, the area of the biopsy would be a constant. One sample taken before a cycle and one after.
The sample would be small- I have seen it performed many times, only a slightly deeper sample would be needed.

If wort comes to wors, I could count cells from a grid from the sample. Multipul samples... ? I would only take 2. before and after. I mean, really, it just seems no one is even tring to test this in humans like we want, a real worl sample.
These samples are quick and painless- only small injection of numbing (if your a pussy, and Im going to be)

If getting a fiber or cell count before and after a months use (times 3, for the 3 months) is "useless or yo ufind it would be inconclusive,.. for the love of God, tell me.

I guess if worse comes to worse, I can grow my fibers the old fassioned way,.. in a dish :jaw:

Get a sample of my own muscle tissue, include some growth factors, (they shouldn't bind together until the growth factor is removed) and maybe a local injection of the new fiber "buds"??? -thoughts on this? (I just know Im going to regret this post....)

Again you are assuming that the fiber split or new fibers would be in the sample area you are measuring and this may not be the case. Please understand that simply because hyperplasia is happening it doesn't mean that every fiber in the muscle is splitting or creating new fibers. If it were this easy don't think research would have proven conclusively that hyperplasia occurs in humans already.

I thought I had already said that in my opinion you are shooting in the dark, how much more speciifc do I need to be.

1. IS 3 months enough time to show hyperplasia?

2. Will IGF injections improve this chance?

3. You can't be sure that the biopsy pulled is an area where hypothetical hyperplasia occurs.

So yes, I think you are wasting your time.

Dan

Kelley G.
Mechanical overload and skeletal muscle fiber hyperplasia: a meta-analysis.
J Appl Physiol. 1996 Oct;81(4):1584-8.


McCall GE, Byrnes WC, Dickinson A, Pattany PM, Fleck SJ.
Muscle fiber hypertrophy, hyperplasia, and capillary density in college men
after resistance training.
J Appl Physiol. 1996 Nov;81(5):2004-12.


Sinha-Hikim I, Artaza J, Woodhouse L, Gonzalez-Cadavid N, Singh AB, Lee MI, Storer TW, Casaburi R, Shen R, Bhasin S.
Testosterone-induced increase in muscle size in healthy young men is associated
with muscle fiber hypertrophy.
Am J Physiol Endocrinol Metab. 2002 Jul;283(1):E154-64.


Klein CS, Marsh GD, Petrella RJ, Rice CL.
Muscle fiber number in the biceps brachii muscle of young and old men.
Muscle Nerve. 2003 Jul;28(1):62-8.

 

[xtraflossy]

Well,.. I understand that I may be shooting in the dark, but if I fire enough bullets, somethings gonna hit hopefully. The sample would be from the injection points (both calves- only place Im going to pin next time) So the effect should be recoginizable if there is one. There is no other way I can up the odds on getting an accurate sample. So many questions... With so many unknowns,.. no one could really say if it would be a waste of time or not I guess.

Basicly, Id rather just try and get no results insted of not knowing (the tests would be free- the IGF is not). With everyone thinking that it just cant be seen, no one is tring.
Not tring to seem childish or anything,.. Im just interested in the research. And have access to the proper tools. If it yeilds no results, then Ive done my part in researching the best I can. If I do see results,..

 

[Dan Moore]

Like I said, "not saying it won't work" but I think the odds are against you.

Let me say this, I would suggest you read the studies I just posted before you start sticking yourself. But that's up to you. I would be interested in knowing how you fair though. If you don't mind keep me updated.

 

[xtraflossy]

Well, I already finished the first month,.. so

Ive already done made the mistakes (or almost did- helpfull people here

I did plenty of research before I started though. And will continue t.

I will read all those studies though