Does hyperplasia really happen with IGF1 LR3?

[Elexecution]

I was told by someone in the AAS section that hyperplasia is a lengthy process and will not occur in a 4 week cycle of IGF LR3 using 60mcg/ed. I was going to do this before my upcoming cycle, hoping for splitting of the muscle cells, and then the growth of them by AAS. the mod told me that i'd be better off running it during my cycle...

Should I run it before or during? Does hyperplasia really occur?

[Gear]

Hyperplasia is defenitely a lenght process, and it's not that it won't happen in a 4 week cycle, it's just that you won't be able to notice anything in that time.

I usually cycle IGF during AAS and after AAS (through PCT).

-Gear

[MuscleScience]

nope doesnt happen in humans its a exercise myth.

[Spyeyes007]

show me your proof that muscle hyperplasia does not occur.

[MuscleScience]

show me your proof that muscle hyperplasia does not occur.

with one post I bet you can google scholar it on your own. In fact here I will give you a key words to search. Look up Terminal differentiation, G0 cell cycle phase, satelite cell metaplasia, mitogenic factors, mitosis. Those should get you started.

[Spyeyes007]

I hope this helps. I am not trying to be a D-Bag here man, or step on toes or have a power trip. I am Biochemistry major at the University of Kansas, and even though I have no interest in this field as a career, I have a strong interest in skeletal muscle hyperplasia as a hobby. I feel these few studies more than prove that SMH is possible, and the cause could definately be IFG-1. If you want to discuss biochemical pathways in more detail, I am interested.
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http://jap.physiology.org/cgi/content/full/81/4/1584

Journal of Applied Physiology
Vol. 81, No. 4, pp. 1584-1588, October 1996
EXERCISE AND MUSCLE

ABSTRACT

Kelley, George. Mechanical overload and skeletal muscle fiber hyperplasia: a meta-analysis. J. Appl. Physiol. 81(4): 1584-1588, 1996.With use of the meta-analytic approach, the purpose of this study was to examine the effects of mechanical overload on skeletal muscle fiber number in animals. A total of 17 studies yielding 37 data points and 360 subjects met the initial inclusion criteria: 1) "basic" research studies published in journals, 2) animals (no humans) as subjects, 3) control group included, 4) some type of mechanical overload (stretch, exercise, or compensatory hypertrophy) used to induce changes in muscle fiber number, and 5) sufficient data to accurately calculate percent changes in muscle fiber number. Across all designs and categories, statistically significant increases were found for muscle fiber number [15.00 ± 19.60% (SD), 95% confidence interval = 8.65-21.53], muscle fiber area (31.60 ± 44.30%, 95% confidence interval = 16.83-46.37), and muscle mass (90.50 ± 86.50%, 95% confidence interval = 61.59-119.34). When partitioned according to the fiber-counting technique, larger increases in muscle fiber number were found by using the histological vs. nitric acid digestion method (histological = 20.70%, nitric acid digestion = 11.10%; P = 0.14). Increases in fiber number partitioned according to species were greatest among those groups that used an avian vs. mammalian model (avian = 20.95%, mammalian = 7.97%; P = 0.07). Stretch overload yielded larger increases in muscle fiber number than did exercise and compensatory hypertrophy (stretch = 20.95%, exercise = 11.59%, compensatory hypertrophy = 5.44%; P = 0.06). No significant differences between changes in fiber number were found when data were partitioned according to type of control (intra-animal = 15.20%, between animal = 13.90%; P = 0.82) or fiber arrangement of muscle (parallel = 15.80%, pennate = 11.60%; P = 0.61). The results of this study suggest that in several animal species certain forms of mechanical overload increase muscle fiber number.
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TITLE: Muscle-specific inactivation of the IGF-I receptor induces compensatory hyperplasia in skeletal muscle
AUTHOR, EDITOR, INVENTOR: Fernandez,-Ana-M [Author]; Dupont,-Joelle [Author]; Farrar,-Roger-P [Author]; Lee,-Sukho [Author]; Stannard,-Bethel [Author]; Le-Roith,-Derek [Reprint-author]
SOURCE: Journal-of-Clinical-Investigation. 2002; 109(3): 347-355
ABSTRACT: During the development of skeletal muscle, myoblasts withdraw from the cell cycle and differentiate into myotubes. The insulin -like growth factors IGF-I and IGF-II, through their cognate tyrosine kinase receptor (IGF-I receptor), are known to play a role in this process. After withdrawal of myoblasts from the cell cycle, IGF-I promotes muscle differentiation by inducing the expression or activity of myogenic regulatory factors (MyoD, myogenin) and effectors (p21). However, little is known about the intracellular mechanisms by which the IGF-I system regulates these factors during the process of myogenesis. Here we show that MKR mice, which express a dominant negative IGF-I receptor specifically in skeletal muscle, have marked muscle hypoplasia from birth to 3 weeks of age. This hypoplasia occurs concomitantly with a decrease in ERK immunoreactivity levels and decreases in MyoD and myogenin expression. BrdU immunocytochemistry showed a compensatory hyperplasia as MKR mice grew to adulthood. Interestingly, hyperplasia occurred concomitantly with an increase in p38, MyoD, myogenin, and p21 immunoreactivity levels, as well as a decrease in Twist levels. These findings suggest that regulation of these cellular elements by IGF-I may play a role in the development and differentiation of skeletal muscle in vivo.
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TITLE: Skeletal muscle fiber hyperplasia
AUTHOR, EDITOR, INVENTOR: Antonio,-Jose [Author]; Gonyea,-William-J [Reprint-author]
SOURCE: Medicine-and-Science-in-Sports-and-Exercise. 1993; 25(12): 1333-1345
ABSTRACT: Skeletal muscle enlargement in adult animals has been ascribed primarily to changes in fiber cross-sectional area (i.e., fiber hypertrophy); however, recent evidence from several laboratories suggests strongly that fiber hyperplasia contributes to muscle mass increases in adult animals and possibly human athletes. Scientists have used three models to study the cellular mechanisms of muscle enlargement: compensatory hypertrophy, stretch, and exercise. Each of these models has provided direct as well as indirect evidence supporting the occurrence of muscle fiber hyperplasia. Direct counts of muscle fibers using nitric acid digestion techniques have shown that both exercise and stretch overload result in significant increases (range = 9-52%) in fiber number. Indirect fiber counts using histological cross-sections have suggested fiber hyperplasia (range = 10-82%) in all three models. Additionally, the expression of embryonic myosin isoforms have provided indirect evidence for new fiber formation in stretch overloaded muscle. Furthermore, satellite cells have been shown to be involved in muscle fiber hyperplasia in stretch and exercise.

[hugovsilva]

And the debate goes on...

[MuscleScience]

The results of this study suggest that in several animal species certain forms of mechanical overload increase muscle fiber number.



Again the key word is in humans, those are all animal studies. The model for hyperplasia research is in cat's, to be more specific most of the research has focused on the calf muscles of cats where it has been to some extent shows the ability for hyperplasia.

Secondly if you look at the body of medical research you would see that in humans the vast majority of papers show no hyperplasia to take place. If it could be shown to be induced in humans with regularity then it would be of great medical value. Its been looked at countless times.

[chainsaw2]

So you must feel IGF-1 is useless because that is what I thought the main purpose of IGF was, hyperplasia.

[MuscleScience]

So you must feel IGF-1 is useless because that is what I thought the main purpose of IGF was, hyperplasia.

Nope you have it backwards, intracellular IGF is one of the main factors that induces hypertrophy.

[Gear]

Hyperplasia may also be induced artificially by injecting hormones such as IGF-1 and human growth hormone . Perhaps the most interesting and potent effect IGF has on the human body is its ability to cause hyperplasia.

References
^ Ramzi Cotran, Vinay Kumar, Tucker Collins (1999). Robbins Pathologic Basis of Disease, Sixth Edition. W.B. Saunders. ISBN 072167335X.
^ Antonio, J, et al. (1994) "Muscle fiber splitting in stretch-enlarged avian muscle". Medicine & Science in Sports & Exercise, 26:8, 973-7.
^ Tavassoli FA (2005). "Breast pathology: rationale for adopting the ductal intraepithelial neoplasia (DIN) classification". Nature clinical practice. Oncology 2 (3): 116-7. doi:10.1038/ncponc0109. PMID 16264885. 

-Gear

[MuscleScience]

The key word there is MAY cause, which is different than what everyone else is saying on here. There isnt enought evidence to say that it does which is what people are saying on here. There is more evidence to say that it doesnt when you look at the body of evidence.

You cant tell someone if the take IGF or HGH that it will cause hyperplasia, the evidence isnt very clear that it does at all. You can say there is some speculation or some evidence to elude to the fact that possible IFG or HGH may induce moderate amounts of hyperplasia.

Plus everyone is quoting animal studies, or cancer studies which is not being debated. Find human studies, they are they just you just have to search extinsively.

[Spyeyes007]

i completely disagree, the studies saw an increased number of muscle cells. And the studies I posted are on human beings, even though I cannot see how mammalia would differentiate significantly though. Re-read the studies I have posted.

[MuscleScience]

the first two say that they used animal models. The third doesnt specifically say, I would need the whole article to read the methods section. Also the third study attributes some hyperplasia to satellite cell, which is technically wrong based on most medically definitions. When a satellite cell donates is nucleus to a muscle cell for repair its called metaplasia not hyperplasia. I can't believe that got by the reviewers in MSSE which is a good journal.

Lastly we must define hyperplasia as described by most medical journals. Because donation of cellular components from satellite cells and actual muscle cells entering back into mitosis are two different things entirely.

I guess I should correct myself and my stance when I say that hyperplasia doesnt exist. Skeletal muscle cells in humans based on current evidence does not undergo Mitosis. I agree that there is evidence that muscle cells can increase in number after embryonic development.

In a sense I was incorrect because different fields define hyperplasia differently than others, so I will admit I was wrong on my blanket statement that it doesnt exist. I still believe that there isnt conclusive evidence that muscle cells can go back into mitotic division after differentiation.

[MuscleScience]

BTW if you dont have any cell physiology and I have lost you on something LMK. And I will try to explain what I am talking about.

[DRAMACYDAL]

with one post I bet you can google scholar it on your own. In fact here I will give you a key words to search. Look up Terminal differentiation, G0 cell cycle phase, satelite cell metaplasia, mitogenic factors, mitosis. Those should get you started.

so youre saying that using igf is useless if your goals are to gain more muscle through hyperplasia?
then igf is just complete bs?

[MuscleScience]

so youre saying that using igf is useless if your goals are to gain more muscle through hyperplasia?
then igf is just complete bs?

No IGF works via Hyperthropy and works well, In animals you can do things to them that you cant humans. Meaning you can pump them full of all kinds of chemicals and growth factors and then maybe you will see some slight increase in fiber number. You cant do that in humans so you wil not see a direct correlation from animal studies to human studies. Not to mention that you can make an animal exercise at an intensity that even lance armstrong couldnt maintain.

[DRAMACYDAL]

No IGF works via Hyperthropy and works well, In animals you can do things to them that you cant humans. Meaning you can pump them full of all kinds of chemicals and growth factors and then maybe you will see some slight increase in fiber number. You cant do that in humans so you wil not see a direct correlation from animal studies to human studies. Not to mention that you can make an animal exercise at an intensity that even lance armstrong couldnt maintain.

everything ive ever read on igf says it can cause hyperplasia,new muscle cells,which is why its diffrent than AAS bc they only work throuch hypertrophy,the increase in size of an organ
where did you read that igf works through hypertrophy?

[MuscleScience]

everything ive ever read on igf says it can cause hyperplasia,new muscle cells,which is why its diffrent than AAS bc they only work throuch hypertrophy,the increase in size of an organ
where did you read that igf works through hypertrophy?

I was doing research (for school and my degree's) in this general area for about 5 years, not specifically hyperplasia but lots of physiology.So I have read more damn boring papers than I care to remember.

Organs are different than muscle tissue in there ability to regenerate. The liver for example under extreme circumstances such as pieces of it being removed for transplant can grow in size both via hypertropy and hyperplasia.

With Igf we get into satellite cell activation. The donation of a nucleus from a statellite cell to a muscle cell is not the same thing as hyperplasia by some definitions. Which I concede probably does happen in humans, I have never seen a human study that showed that muscle cells could be forced back into mitosis unless a cancer causing agent or a virus of some sort was introduced in vitro. It is entirely possible that it could be done, but for practical purposes i dont think it could be a method that the normal person such as you and I would ever benefit from.

For example in rats in vitro experiments have been shown to regenerate cardiac tissue. When they try to do this in vivo it does not work and the rat often times dies. If the body cant do it under extreme circumstances, then how could we possible do it. Cardiac regeneration is a big deal if it can be done when you think about the leading cause of death is via heart disease. Cardiac muscle and striated skeletal muscle have a much similar physiology than that of smooth muscle.

If you do a lit search for hyperplasia you probably have seen lots of papers that talk about smooth muscle hyperplasia. Smooth muscle if you think about it needs the ability to regenerate in case of injury. Plus it can afford to shut down all its cellular functions to divide into new cells. A muscle or cardiac cell doesnt have the luxury to shout down and divide.