NEWEST DEVELOPMENT for you MGF users!!!!

[LakeMountD]

Okay after continued debate between xtraflossy and I on Yahoo and digging through various sutudies we found mounting evidence as to why MGF is ineffective for people continually taking it! I am going to post a few excerpts from some studies then explain them. I apologize that there was one error in the manual stating that MGF proliferates, differentiates, fuses, AND activates these satellite stem cells. Although this information was correct in previous studies, newer studies have come out proving this wrong (yea im pissed too, done by the same damn doctor too! sheesh). I am updating the manual after this.

"MGF [4 and 6], is biologically active and has a distinct activity compared to that of mature IGF-I in that it can increase myoblasts proliferation but it totally inhibits the myotubes formation. Also the selective blocking of the IGF-I receptor provides evidence that MGF increases myoblast proliferation via a different signalling pathway."

"Two of MGF-positive C2C12 clones and two IGF-I Ea clones were used to study the effects of MGF and systemic IGF-I Ea on myoblast proliferation and differentiation. Fig. 1 demonstrates that positive MGF and IGF-I Ea C2C12 clones expressed transfected MGF or IGF-I Ea mRNA, whilst no exogenous MGF mRNA was detected in control C2C12 cells. When cells were induced to undergo myogenesis in the differentiation medium (DM), it was found that positive terminal differentiation was prevented in MGF-positive cells. Even these cells kept in DM for 14 days, remained as myoblasts (Fig. 2A). In contrast, those of the IGF-I Ea-positive clone formed myotubes (Fig. 2B). The normal C2C12 cells showed less cellular proliferation as well as forming myotubes ( Fig. 2C)."

As you can see in these two excerpts MGF actually proliferates the cells by bringing in additional stem cells/nuclei, but actually INHIBITS them from forming myotubes (differentiation). For those of you who don't know the exact definition of differentiation it is: Skeletal muscle differentiation involves myoblast alignment, elongation, and fusion into multinucleate myotubes, together with the induction of regulatory and structural muscle-specific genes.

This means that those of you who were doing MGF day in and day out were actually preventing your body from forming more myotubes. MGF is still an important piece of this puzzle because of its effects on muscle proliferation, but we need exogenous IGF afterwards to activate these things and differentiate the stem cells. This confims my hypothesis for my dosing scheme where I had (xtraflossy said he liked pre workout mgf so thats his idea) pre-post injected MGF as well as ONLY 1 more day of MGF injections which are done two different times the next day, making it ONLY 24 hours of MGF injections. Read the manual to see my exact dosing scheme.

I have attached a graph that is also in the manual showing how your body naturally responds to this stuff. Pay attention the the s/s numbers not the bup numbers since bup is something different. If you notice even your body stops making IGF in large quantities after 24 hours.

 

[jagleaso]

Great information! I want to learn all I can about MGF before I consider putting it in my body.

 

[anabolicandre]

So mgf should be cycled like HGH?? 5on/2off?

 

[xtraflossy]

Thought I'd mention, that its possible that the cession in IGF at day 6ish could be due to the repair process being completed.
In this case, the repair process can be looked at as a balance between proliferation and repair. As MGF expression declines, IGF is ramped up.
When the body needs to create neculi for repair, IGF expression drops, to allow this continous prolifferation

 

[LakeMountD]

So mgf should be cycled like HGH?? 5on/2off?

No, thats not what I am saying. I am saying you probably shouldn't be injecting MGF into any worked muscle (remember its site specific) anytime after 24 hours of working it. Read through the manual at the top. I JUST updated it to include this new information so make sure you guys download the updated copy!!!!!!!!!

 

[xtraflossy]

As a side note I guess, this would say nothing about wether you wasted anything if you went beyone the 24 hours post training. MGF has about a 24 hour expression time period, so, proliferated (donated neculi) would appear to be able to survive that time period of 24 hours before fusion of some type needs to occure.
hint,..hint,..:run:

 

[LakeMountD]

As a side note I guess, this would say nothing about wether you wasted anything if you went beyone the 24 hours post training. MGF has about a 24 hour expression time period, so, proliferated (donated neculi) would appear to be able to survive that time period of 24 hours before fusion of some type needs to occure.
hint,..hint,..:run:

yeah continued proliferation would occur but you are delaying myotube formation. I believe it depends on the size of the muscle. Don't forget the longer you inject MGF the more you are delaying actual muscle growth. Biceps would NOT need to go past 24 hours since it is so small. Legs might need an extra day of MGF injections in various parts of the leg to see an effect.

 

[xtraflossy]

Well, the thinking LMD, was that that the donated neculi (new cells) could survive UP TO 24 hours, lending support to the Pre workout injections (that I had done in the 12 hour range) protocal. We had discussed the possibility that 12 hours could be too long preworkout,..
IF your thinking that healing needs to begin happening no later then 24 hours after injury, then the pre-workout injections could be a better way to increase cell activity (proliferation) by essentually "cutting" 12 hours from recovery time.
OF course, I would LOVE to do actual feild testing on this vs. post workout + 12
the difference in results MAY be minimul, so the longer the test time frame is (Im thinking about 30 days), the more measureable/noticeable the difference would be.
- This if there was a difference, it would of course make MGF more cost fesable.

 

[LakeMountD]

Well, the thinking LMD, was that that the donated neculi (new cells) could survive UP TO 24 hours, lending support to the Pre workout injections (that I had done in the 12 hour range) protocal. We had discussed the possibility that 12 hours could be too long preworkout,..
IF your thinking that healing needs to begin happening no later then 24 hours after injury, then the pre-workout injections could be a better way to increase cell activity (proliferation) by essentually "cutting" 12 hours from recovery time.
OF course, I would LOVE to do actual feild testing on this vs. post workout + 12
the difference in results MAY be minimul, so the longer the test time frame is (Im thinking about 30 days), the more measureable/noticeable the difference would be.
- This if there was a difference, it would of course make MGF more cost fesable.

Definitely, I wasn't doubting you by any means. In fact as you know in our article I put in there that you should use a pre workout dosage of it and I even explained why that would probably work and it is off the same philosophy. I plan on it, as well, to use pre+post, + 2 the next day + igf for second through 5th days.

Although I plan on doing this whole process for MUCH longer, say 8 weeks. I think I can get downregulation of IGF-1R's (or antibody production whichever it is), down if I use lower dosages. Only time will tell.

 

[Grunt76]

Is the "Manual" is the first post in this thread?

 

[LakeMountD]

Is the "Manual" is the first post in this thread?

Yea, but don't read it off of there, make sure you download the MS Word file at the very bottom, it is MUCH more updated. The links in the word file are interactive too, MUCH better.

 

[dsl]

i will probably never use mgf, but I just wanted to give you props for taking the time to compile this information...GREAT EFFEN JOB!!!!!!!!!!!

 

[LakeMountD]

i will probably never use mgf, but I just wanted to give you props for taking the time to compile this information...GREAT EFFEN JOB!!!!!!!!!!!

Thanks bro. Means a lot hearing this stuff. I spend HOURS every day when I probably should be finishing homework studying this stuff because it absolutely INTRIGUES me. I promise to you guys one thing. I will work my ass off until we get this whole thing figured out. I seriously think this is like the key to some serious growth if we can get a few things figured out (I am working on some of them now in conjunction with a scientist here).

I update that word file quite frequently, too, as I find new information and studies so check back whenever you can and get the updated word file.

Any questions, feel free to contact me via e-mail or PM or anything.

:study:

 

[LakeMountD]

"This factor, called mechano growth factor (MGF), is thus designed to act in an autocrine/paracrine rather than in a systemic fashion. It is possible that MGF is the end product of mechanotransduction signalling pathways in muscle and other cell types. Questions such as whether MGF is up-regulated before membrane damage occurs or whether membrane damage initiates the production of the growth factor can be addressed."


This might explain why pre workout injections are working. I mean this could be placebo effect too, or just "feeling" of a pump that makes us think this but might have some science. I will keep up with it and see what I find.

 

[BodyWizard]

Props for your efforts, dude - way to exemplify the AM motto!
and lookin' mighty hyooge these days, too!

 

[LakeMountD]

"A polyclonal antibody to MGF was shown to be specific by using its peptide to block its reaction. Using a proteomics approach we used the antibody to detect a specific MGF-binding protein on two-dimensional electrophoresis gels. The binding protein was then identified by cutting out the spots and by using a mass spectrometer. The binding protein was shown to bind only MGF, and not the systemic types of IGF-I. The muscle-specific binding protein localizes and stabilizes the MGF within the muscle and also acts as a time-release mechanism. It is for this reason and others that we regard MGF as an autocrine growth/repair factor. Also, the discovery of MGF provides a link between the mechanical stimulus and gene expression, although the nature of the mechanochemical coupling process is not yet known."

Haha looks like another update will be coming soon after finding this out. But I need more information on it.

Apparently now they have identified a binding protein for MGF. This is actually a good thing for us, since MGF has a shorter protein chain sequence than IGF-1 (being a spliced variant), it also, therefore, has a shorter half life, bad for us injecting MGF. IGF-1 only has a half life of 20 minutes, LR3 IGF-1 is a little different, however, and is much more stable. Question is then this: Are there enough of these binding proteins available to time release the amount of exogenous mgf we are injecting? There has to be a 'threshold amount' of exogenous MGF that won't be a waste, and that these binding proteins can uptake.

 

[wideguy]

Thankyou bro

 

[LakeMountD]

HERE IS ANOTHER BIGGIE!!!!!



Investigation of insulin-like growth factor (IGF)-I and insulin receptor binding and expression in jejunum of parenterally fed rats treated with IGF-I or growth hormone.

Ney DM, Huss DJ, Gillingham MB, Kritsch KR, Dahly EM, Talamantez JL, Adamo ML.

Department of Nutritional Sciences, University of Wisconsin-Madison, 53706, USA. [email protected]

To investigate the ability of insulin-like growth factor-I (IGF-I), but not GH, to stimulate jejunal growth, we compared indices of IGF-I and insulin receptor expression in jejunal membranes from rats maintained with total parenteral nutrition (TPN) and treated with rhIGF-I and/or rhGH. TPN without growth factor treatment (TPN control) induced jejunal atrophy, reduced serum IGF-I, increased serum insulin concentrations, and increased IGF-I receptor number, IGF-I receptor messenger RNA, and insulin-specific binding to 133% to 170% of the orally fed reference values, P < 0.01. Compared with TPN control, IGF-I or IGF-I + GH stimulated jejunal mucosal hyperplasia; IGF-I treatment increased serum IGF-I by 2- to 3-fold and decreased serum insulin concentrations by 60%, decreased IGF-I receptor number by 50% (P < 0.001), and increased insulin receptor affinity and insulin receptor protein content. Treatment with GH alone increased serum IGF-I concentration, did not alter TPN-induced jejunal atrophy, and decreased insulin-specific binding and insulin receptor protein content (39% and 59%, respectively, of the TPN control values, P < 0.01). We conclude that: 1) jejunal IGF-I receptor content reflects circulating concentration of ligand and is not limiting for jejunal growth; and 2) increased circulating concentration of IGF-I may promote jejunal growth via interaction with jejunal insulin or IGF-I receptors.



The problem with these studies once again is that it uses rhIGF-1 and not LR3 IGF-1. I am thinking the added half life of LR3 IGF-1 as well as its anabolic properties might increase that number slightly to possibly around 65-75%. That means we might be able to start off at lower dosages then double it at some point. Perhaps, start with 20mcg daily and then go to 40mcg daily after 3-4 week and stick there. Another problem, however, is this is talking about intestinal receptors, there are more receptors there as it is.

 

[same_old]

"MGF [4 and 6], is biologically active and has a distinct activity compared to that of mature IGF-I in that it can increase myoblasts proliferation but it totally inhibits the myotubes formation. Also the selective blocking of the IGF-I receptor provides evidence that MGF increases myoblast proliferation via a different signalling pathway."

As you can see in these two excerpts MGF actually proliferates the cells by bringing in additional stem cells/nuclei, but actually INHIBITS them from forming myotubes (differentiation). For those of you who don't know the exact definition of differentiation it is: Skeletal muscle differentiation involves myoblast alignment, elongation, and fusion into multinucleate myotubes, together with the induction of regulatory and structural muscle-specific genes.

LMD - honest, serious questions and issues here:

IGF promotes differentiation such that a delayed IGF injection after MGF administration could potentially mature the new cells created...any idea if MGF causes greater myoblast proliferation than IGF? if not, then MGF is a complete waste.

http://endo.endojournals.org/cgi/content/full/141/1/100 says that proliferation and differentiation are mutually exclusive, so it shouldnt be a big surprise that MGF can only turn one on at a time.

the above study also asserts that IGF promotes both diff and prolif, but they dont know what the signaling pathway is that decides which, at what time.

more to come...

 

[LakeMountD]

LMD - honest, serious questions and issues here:

IGF promotes differentiation such that a delayed IGF injection after MGF administration could potentially mature the new cells created...any idea if MGF causes greater myoblast proliferation than IGF? if not, then MGF is a complete waste.

http://endo.endojournals.org/cgi/content/full/141/1/100 says that proliferation and differentiation are mutually exclusive, so it shouldnt be a big surprise that MGF can only turn one on at a time.

the above study also asserts that IGF promotes both diff and prolif, but they dont know what the signaling pathway is that decides which, at what time.

more to come...

I think you are mistaken on the different types of IGF-1. Trust me this happened to me too when I first started really digging through the material. There is a difference between hIGF-1, hIGF-1E, hIGF-1Ea, and hIGF-1Ec (hIGF-1Ec and IGF-1Eb are the same but one is in people and one is in rats, both correspond to MGF).

IGF-1 in a sense DOES proliferate AND differentiate. However, this is how you will see it written in the older studies. As you can see this studies was copyrighted in 2000. Why do we see this in older studies? Before MGF was fully understood, it was said that IGF-1 did both proliferation and differentiation and this was right. But the reason this is right is because IGF-1 is spliced towards MGF. It is kind of like saying hGH is responsible for proliferation and differentiation, in a sense it is because it is what causes a spike in IGF-1, which increases how much MGF can be produced. Make sense?

Although you could easily take LR3 IGF-1 day in and day out, with the use of exogenous MGF, I set up the dosing scheme the way I did for a few reason. 1) attempt to see if I could stop down regulation at any rate, 2) try and save you guys money, your body's natural response is to increase MGF, with IGF-1 levels low, then switch that and begin producing more of the other and less of MGF.

 

[xtraflossy]

Well, thank God you answered that before I did.
Its a "This OR That" kinda thing. not both at the same time.

One clue I missed until I read your post LMD, was that they had previously discovered this IGFBP-rP1, as it is identified by at least 3 other names I beleive. (I need to pay more attention to the dates on these things :study: )

"the above study also asserts that IGF promotes both diff and prolif, but they dont know what the signaling pathway is that decides which, at what time."

-I think that there was a time "limit" on one of the actions,.. up to 24 hours. It means nothing by itslef, but makes me wonder what "counts down" that time frame..

One last thing I guess,.. Does "doubleing time" refer to what I think it does, or is this somehow taken WAY out of context (LMD, you know where Im going with this one Im sure
I posted the text I am refering to below: (also note I could be looking for something that isn't there)

"Growth rates of C2-LX and C2-rP1 myoblasts in 10% FCS/DMEM were indistinguishable (Fig. 4). Estimated doubling times for the two populations were 14.5 ± 1.8 h for C2-LX myoblasts and 14.8 ± 1.5 h for C2-rP1 myoblasts, which were not significantly different (by t test) and which are comparable to that for the nontransduced parental population. "
http://endo.endojournals.org/cgi/content/full/141/1/100

 

[fedaykin]

Feel free to delete my post if it ****s up the flow of the thread *as i am definatly not your your level* but.... heres what im thinkin (might have been said, but nobody said it this simple and some of your language has exceeded my cranial capacity and i just dont understand what you ****ers are sayin scientificly lol)

If none of these studies have been done with LR3 then it doesnt really pertain to what we are trying to do here. If we are using LR3 2x per day, then our IGF-1 levels are pretty much consistently kept at a pretty high level and always available for use instead of trying to time IGF-1 with a 10minute half life to match the MGF.

Knowing we have constant levels (somewhat) of IGF-1 in our body due to LR3.... now wouldnt all we need to do was properly time the MGF in order to utalize the IGF-1's synergistic effects properly.




Now in theory that exo MGF does not suppress natural MGF levels, and they are highest post workout, wouldnt it hinder our natural pulse to take it pre-workout when post workout our natural pulse is highest? What we would want to do is PROLONG that pulse of MGF... which would mean allow the natural pulse of MGF post workout, and shoot MGF maybe 1-2hrs post workout (wish we knew the levels of the pulse of post workout MGF and how long it takes to wind down, so we could more properly time the exo MGF) in order to prolong the MGF signal in the body to keep repairing the damaged muscle at a higher rate (and probably administer again first thing in the AM).Now considering the natural pulse is very high(theory), you are wasteing less MGF since it is not needed at this point, and using less exo. MGF for a shorter period of time which i would guess would lead to far less suppression and a more potent effect every time its administered

Another idea is that the exo MGF will greatly exceed the natural pulse of MGF the body will produce post workout, in that case we would want the MGF to hit hardest post workout for the muscle we just hit, and be sustained for another 24-36hrs. We also want it to hit alittle preworkout in order to which would more effeciently PRIME the muscle for growth, as well as prolong it with the next two doses (PWO and next early AM).

The reason for MGF not really working after a few days is most likley because as many of you said... MGF is useless without a damaged muscle. Those of you who tried it without hittin the muscle got **** out of it. Well what is MGF doing? Its repairin that muscle at a higher rate than usual to a much larger extent. That means that after 24-36hrs.. there really is no more damaged muscle. Its repaired. Maybe if we want extreme effects on a muscle we need to hit it more than 1x per week, more like 2x per week if its gonna repair this quickly, that way we can utalize the MGF on a damaged muscle more often and have more growth periods for it.

Hmm.... Makes me wonder about my 1 on 2 off idea again.

 

[LakeMountD]

I answered his questions on the other thread, I don't know why he posted it twice, read the MGF users thread.

 

[LakeMountD]

my apologies just wanted to make sure someobody got to it. I can delete if you wish.

It's all good, the mods just HATE double posts and double threads. I sorta do too because it is hard to consolidate info and get everyone on the same page.

 

[anabolicandre]

This is all so mind boggling and I cant wait to put these theories to the test.

 

[xtraflossy]

As LMD will happily point out ( I know from expirence); LR3 doesnt splice to MGF. Consider LR3 a different compound when it comes to cellular interactions, because most of the studies were working with are not using LR3.

I also sure you could use a large pre workout dose. Also, the maintenence levels your refering to afterwards are the exact same thing as Pre/post+. (Especially when say your pre-WO shot is full dose, and the post is half dose and the morning one is as well.) Bigger dose, "mini dose" x2
However, the change your proposing is mostly dose related then,.. and a very safe assumption is that your not naturally expressing 30+mcg of MGF after tissue damage in your bicept.
So these doses should be already high.

You are right about wanting to have MGF "leave" after it has done its job. But, remember, natural expression is for just over 24 hours POST injury. So,
The pre-workout shot, adds to the prolifferation time frame.
The post workout and AM shot are taken with time to spare (so to say).
If your training at 6:30pm:.....
1st shot: Noon that day
2nd shot: 8:00 after workout
3rd shot: 6:00am -next morning
Then that is 12 hours from workout, + how ever many hours pre-workout + how long the last shot MGF remains active.


I cant remember if you have used LR3 before, but 80mcg is a moderately high amount, especially for first time. You could get away with half that and not even notice a difference. Look at some of the older IGF threads. Most people did not notice any difference from their first time at say, 40mcg, and there second run at 80mcg.

Just friendly advise....:run:

 

[LakeMountD]

The point of using LR3 is to DIFFERENTIATE as you yourself pointed about 2 posts ago.

I think you guys have the wrong idea of the word splice. We are talking RNA transcription splicing here. That may be the wrong "terminology" but that is sort of how it works.

 

[LakeMountD]

No one on this board is an expert bro. We may know more than others about the aspects of it but there are only a handful of experts on it. I just want to make that clear first.

But I mean you have to remember bro it is too early to tell. None of us truly know. THere are SO MANY hidden variables out there that they don't know about that it is impossible to tell what will happen. Natural MGF expression stays pretty elevated until like day 4, although it stops peaking after day 1 and starts a steady decline until that day 4 when it sharply drops off. I read into this as the fact that the body doesn't produce much of this stuff so it needs more MGF to create a greater pool of myoblasts. The IGF-1Ea begins its steady rise at day 3-4 and continues for a few more days to complete repairs and begin differentiation.

Here are some things we don't know:

-Whether a single over expression of MGF will create a massive pool of myoblasts for continuous use or if there is some critical dose that will no longer bring in more myoblasts

-How much MGF actually inhibits myotube formation

-Whether or not these two things can happen at the same time even with the inhibition, etc.

-Whether differentiation inhibits proliferation (instead of vice versa). This might already be known but I have yet to find a study on it yet so this is what I don't know yet.

The way I see it is, with these large amounts and over expressions of growth factors you don't need to run it for 4 days like your body does, it should exponentially speed up this process. LR3 IGF-1 can be run all week since it does nothing but good (from the studies shown).

 

[fedaykin]

-Whether differentiation inhibits proliferation (instead of vice versa). This might already be known but I have yet to find a study on it yet so this is what I don't know yet.

The way I see it is, with these large amounts and over expressions of growth factors you don't need to run it for 4 days like your body does, it should exponentially speed up this process. LR3 IGF-1 can be run all week since it does nothing but good (from the studies shown).

I thought you said that you don't know if it is differentiation inhibits proliferation or if it is vice versa. So wouldn't that mean that IGF-1 could actually cause problems/interfere with the MGF? Wouldn't that make sense considering the fact that IGF doesn't rise in the body until 3-4 days post exercise?

So, by using IGF for a month strait or MGF for a month strait people could actually be shooting themselves in the foot(figuratively speaking)?
:blink:

 

[Grunt76]

That's what he's saying. Unless they're actually shooting their feet, which although strange would make them shot in the feet BOTH figuratively and properly speaking, surely a first among MGF users.

 

[LakeMountD]

I thought you said that you don't know if it is differentiation inhibits proliferation or if it is vice versa. So wouldn't that mean that IGF-1 could actually cause problems/interfere with the MGF? Wouldn't that make sense considering the fact that IGF doesn't rise in the body until 3-4 days post exercise?

So, by using IGF for a month strait or MGF for a month strait people could actually be shooting themselves in the foot(figuratively speaking)?
:blink:

I am speaking hypothetically. NOTHING is known about this stuff so you have to consider every possibility, although I seriously doubt they inhibit each other. The reason I say that is because IGFBP-Pr1 has something to do with the inhibition of differentiation as well and I believe it also has to do with MGF, meaning there is some unknown pathway that MGF inhibits differentiation, I don't think that there is a hidden pathway for the IGF-1 since the reason it is unknown for the MGF is because we don't really know how MGF is working, it doesn't bond to the IGF-1 receptor. Plus I believe the only reason why IGF-1Ea is low during the times that MGF is high is because more of it is being spliced to form MGF not because it actually inhibits.

All this is yet to be seen.

 

[xtraflossy]

I am speaking hypothetically. NOTHING is known about this stuff so you have to consider every possibility, although I seriously doubt they inhibit each other. The reason I say that is because IGFBP-Pr1 has something to do with the inhibition of differentiation as well and I believe it also has to do with MGF, meaning there is some unknown pathway that MGF inhibits differentiation, I don't think that there is a hidden pathway for the IGF-1 since the reason it is unknown for the MGF is because we don't really know how MGF is working, it doesn't bond to the IGF-1 receptor. Plus I believe the only reason why IGF-1Ea is low during the times that MGF is high is because more of it is being spliced to form MGF not because it actually inhibits.

All this is yet to be seen.

There ya go! Its not so much that IGF and MGF counteract each other it seems. Running LR3 would not appear to hinder the MGF.
MGF, is a splice varient of IGF-1Ea. The mechanical workload of training releases "factors" that splice the muscle tissue reserve of IGF-1Ea, into MGF.
Your body always tries to keep equlebreium, so it should try to replenish that lost (spliced) IGF-1Ea. This may explain why you have the increase in IGF 3-4+ days AFTER damage.
Again, as said before though, we dont know why it takes that long for the body to "get the message" that IGF-1Ea needs to be replaced, or what keeps keeps it from being expressed at peek levels the same time MGF levels are high.

(BUT- when you think about it,.. another "theory" could be that ,.. lets assume IGF-1Ea and MGF are one in the same. Example: if there is going to be 3mcg of total "factor" in a given muscle, then it can be at any ratio, and not cause a deficite,..
EX: -using made up 3mng number- 3mcg total Factor. Then we train, 1 mcg of that factor (IGF-1Ea ) becomes broken down into MGF by the "splicing factors" involved in the process. Now, there is 2mcg IGF-1Ea, and 1mcg MGF in that tissue, still totaling the "3mcg".
Then MGF does it prolifferation, and I am sure that the body either: uses MGF in that proliferation process, further degrades it until is can be carried/flushed from the body, or picked up by a binding protein or something...
This could cause the defficite I was refering to earlier. So, now the tissue is down about 1mcg "factor". That space will be filled with more IGF-1Ea (this would be a few days after training, which would mean the IGf spike).
This could explain why IGF and MGF are not expressed at peek levels at the same time.
Also, The process I mentioned, seems just to damn logical to me. I mean, .. given the current information.

Sorry I keep pulling crap outta my ass and throwing it everywhere.:blink:
But, The first part of what I said was my main point.

 

[same_old]

just to clarify - i believe the study that concluded that MGF totally inhibits myotube formation was done in vitro, with the myoblasts being subjected to JUST MGF...in your body, those recently proliferated myoblasts will have IGF (or some other factor) causing them to differentiate once MGF has brought them in. all that study is saying is that MGF is probably THE splice variant that causes proliferation, and is missing the capacity that IGF has to provoke myoblasts to differentiate.

make sense? (i'm not asserting that as fact, just telling you all what i got from it)

if this is indeed true, a person would be able to activate satellite cells (presumably at a higher rate than IGF because it's the ONLY thing MGF does) at ANY time, and along with IGF administration, mature those new cells, regardless of training or timing.

i am curious how slow this all happens - does the muscle tissue really not shift from activation to maturation for several days afterwards? if that's the case, you could get several MGF injections in PWO and proliferate the he11 out of that muscle before the IGF would need to be administered heavily to mature the new cells...again, just thinking out loud.

when the study i posted earlier claimed that proliferation and differentiation are mutually exclusive pathways, i took it at face value. IGF may be able to compel the tissue to do both, but not at the same time. perhaps IGF operates on various pathways depending on the biological stimulus and apparent need, shifting from an MGF bias to a variant more conducive to maturation.

 

[LakeMountD]

if this is indeed true, a person would be able to activate satellite cells (presumably at a higher rate than IGF because it's the ONLY thing MGF does) at ANY time, and along with IGF administration, mature those new cells, regardless of training or timing.

I agree, this is pretty much what I was posting previously, was that i believe that the use of LR3 throughout is fine because it would make sense that LR3 can mature myoblasts at anytime independent of proliferation. The only reason I put LR3 in my dose scheme on days 2-5 was so people could save some and run it longer. But I did specify a bunch of times that it could easily be run throught. The off days could help up regulate receptors again, too, IF that is even a big concern, which we don't really know yet.

i am curious how slow this all happens - does the muscle tissue really not shift from activation to maturation for several days afterwards? if that's the case, you could get several MGF injections in PWO and proliferate the he11 out of that muscle before the IGF would need to be administered heavily to mature the new cells...again, just thinking out loud.

What I got out of that graph was the reason MGF is expressed for so long is because of the VERY low dose that your body is producing. It would also seem that differentiation is much easier than proliferation, since your body heals quite fast after MGF drops off, or so the graph suggests. The graph stops at day 7, which is the same day IGF-1 peaks (and still continues to rise past day 7). MGF drops off exponentially at day 4. They study stated that complete rehabilitation of the muscle was accomplished on day 7. Seems like proliferation might take a little longer, either because it needs to continue to replenish the pool and heal at the same time or the dosages are so low that it just takes a long time to bring in enough myoblasts for healing. You must also note that these are natural expressions and in NO WAY are they near the dosages we could use exogenously which is why I advocated for 4 injections of MGF in the worked muscle per week over 2 days.

 

[xtraflossy]

What I got out of that graph was the reason MGF is expressed for so long is because of the VERY low dose that your body is producing. It would also seem that differentiation is much easier than proliferation, since your body heals quite fast after MGF drops off, or so the graph suggests. The graph stops at day 7, which is the same day IGF-1 peaks (and still continues to rise past day 7). MGF drops off exponentially at day 4. They study stated that complete rehabilitation of the muscle was accomplished on day 7. Seems like proliferation might take a little longer, either because it needs to continue to replenish the pool and heal at the same time or the dosages are so low that it just takes a long time to bring in enough myoblasts for healing. You must also note that these are natural expressions and in NO WAY are they near the dosages we could use exogenously which is why I advocated for 4 injections of MGF in the worked muscle per week over 2 days.

So, a few things to take note of regaurding the studies we looked at, is that most of the time, they were inducing chemical damage to the muscle, and as LMD and I discussed, this may produce much greater tissue damage then the training, or the damageing effect took longer to create the effect, which could have resulted in the 7 day healing time.

Originally Posted by same_old
i am curious how slow this all happens - does the muscle tissue really not shift from activation to maturation for several days afterwards? if that's the case, you could get several MGF injections in PWO and proliferate the he11 out of that muscle before the IGF would need to be administered heavily to mature the new cells...again, just thinking out loud..

OUR time slots should be altered (abbrevieated) some for these compounds because:
-We are "trained" individules, this isnt a one time muscle trauma
-Were are expressing much higher levels of MGF when we do Exogenous administration.
-Our diets are more tuned to muscle repair then "normal" people.
-We are not rats. (well, most of us arn't anywyas :twisted: )

Also, if our more rapid recovery corolates with an incline of IGF, then our "prolifferation" periods would be reduced as well,.. to only 24 hours perhaps.
Hence the pre-workout injection. That was my thinking about it as well

One thing I wonder though. If complete restoration of the muscle was accomplished at day 7, why did IGF levels continue to rise beyond that time frame?
If its sole purpose was to repair, why not "level off" as opposed to continue to increase?
Could this be a part of the Adaptation process? Initually I dont see how, as all rebuilding has allegidly been done.
Unless maybe the muscle is replenishing glycogen stores after the new fibers have expanded some.. ?

 

[same_old]

OUR time slots should be altered (abbrevieated) some for these compounds because:
-We are "trained" individules, this isnt a one time muscle trauma
-Were are expressing much higher levels of MGF when we do Exogenous administration.
-Our diets are more tuned to muscle repair then "normal" people.
-We are not rats. (well, most of us arn't anywyas :twisted: )

LMD's 2-day post-WO window for proliferation is about what i was thinking earlier....of course we are guessing - none of the factors you listed will necessarily shorten our recovery times (plus i would expect there to be alot of variation among us)

Also, if our more rapid recovery corolates with an incline of IGF, then our "prolifferation" periods would be reduced as well,.. to only 24 hours perhaps.
Hence the pre-workout injection. That was my thinking about it as well

i am personally still not sold on the pre-WO injection, at least not more than an hour beforehand. i get your point, about priming for myogenesis and culling available myoblasts, but you're going to bring them in and THEN damage the muscle and that's not at all what the body does naturally. i dont know if the fresh myoblasts would survive the damage...nor do i see a way to find out.

 

[xtraflossy]

I hear ya about the never being able to find out if the neculi will be destroyed or not durring the workout... I wouldnt think so. (just based on that the neculi themselves wont be involved for the workload. plus, I have had damaged body parts that have had to endure more damage the next day,.. If the process of proliferation is to facilitate in restoration of the muscle, I dont see the body allowing those building blocks (neculi) to be destroyed. An example would be starting a new hard labor job. If you have to carry things all day, every day, ...and tuesday's workload destroyed Monday's neculi, you would really never be able to repair,.. much less adapt to that demand. ... just my thoughts)

That aside,
Yes, (to the part about " but you're going to bring them in and THEN damage the muscle and that's not at all what the body does naturally")
I know thats not the natural cycle of things,.. but, technically speeking, the body doesnt have a way to "predict" or anticipate tissue damage, beyond adaptation.. but WE know when were going to tear it up! :hammer: SO, I guess it could be looked at as a way to give the body a "heads up".

(that last part sounded retarded to me,.. If I can think of a way to be more clear I will come back and edit this.)

Anyways,. Im not tring to sell ya on the Pre-W/O shot, .. I just noticed a big difference in my recovery time when I did it that way compared to post workout only.

 

[anabolicandre]

In reference to the pre w/o shot, isnt that what its all about tricking the body out of homeostatisis?? Finding new ways to get the body to grow??

 

[xtraflossy]

That would be the core principel in exogenous administration outside of HRT.