Maximising Intramuscular IGF-1

[imported_debo]

Sounds like intramuscular IGF-1 is pretty crucial to hypertrophy, but are there any nutritional strategies or minimums to ensure production of adequate levels?
I recall reading in Optimum Sports Nutrition by Dr Michael Colgan (a great book in its day, but starting to date now) that a diet which promoted a constant, high concentration of insulin would encourage production of IGF-1 in the liver. I understand that liver- and intramuscular IGF-1 are different animals, but would this strategy still apply?
I understand that overfeeding increases IGF-1 levels (at least in the liver), and I assume that overfeeding with an adequate percentage of calories coming from carbs would cover your bases, but what about somebody who is dieting and consequently can't afford to use this kind of shotgun approach? Is there a minimum (or optimum) percentage of carbs required? Do carbs have to be consumed at every meal to ensure a steady supply of insulin? Thanks in advance.

 

[Bryan Haycock]

Although you ahve more or less answered your original question, I'll see if I can add a little bit. Rather than thinking of macronutrients as being responsible, try to think of the balance or ratio of anabolic:catabolic hormones floating around. In other words, being in a chronic catabolic state (i.e. dieting or endurance training) will lead to lower levels of all anabolic hormones including MGF (A.K.A. intramuscular IGF-1). So, the key is to ensure that you ahve enough carbs coming in to tip the environement towards anabolism.

A little trick I use during low carb diets is to use glucose polymers during cardio. Drink 50-100 grams during 30-60 minutes of cardio. This will introduce carbs into the system in the least lipogenic way, yet at the same time, tip the system towards anabolism (or at least tilt it back towards anabolism a bit). In short, try to get the muscles burning sugar without having to store too much of it.

 

[stevie]

on a slight tangent...
Growth is dependent upon the fusing of satellite cells with exsisting muscle cells. Which, in a natural trainer, is dependent upon the secretion of a variety of growth factors and cytokines from muscle cells that have been 'disrupted' by the application of load.
Are growth factors IGF-1 etc always secreted from a 'disrupted' muscle cell?
What do catabolic hormones actually do?

I guess im aiming towards this main question....
why should it matter that you are dieting or not? Do the consequences of exposing muscle to an unaccustomed load (cellular 'disruption' which will result in secretion of growth factors, which will in turn result in the fusing of satellite cells and donation of nuclei) not occur regardelss of anabolic:catabolic state? What exactly is going on that prevents the fusing of nuclei in a dieting state?

Also, do the nuclei donated to existing muscle cells remain indefinately?

 

[stevie]

bump

 

[micmic]

In short, I wouldn't say that the rate of protein synthesis drops significantly when you are hypocaloric, it's rather the increased protein breakdown that tends to balance (or even reverse) the overall picture (assuming in both cases the stimulus is the same and protein intake is adequate).

 

[stevie]

Quote[/b] ]it's rather the increased protein breakdown that tends to balance (or even reverse) the overall picture

'protein breakdown' = ?

 

[micmic]

Quote[/b] (stevie @ Nov. 11 2003,6:10)]

Quote[/b] ]it's rather the increased protein breakdown that tends to balance (or even reverse) the overall picture

'protein breakdown' = ?

Yep, protein breakdown, proteolysis. Like when you diet and cortisol goes up, enters the cells, binds its receptor, the resulting complex activates the ubiquitin system and proteolysis increases (muscle breaks down).

Other things may happen that will reduce protein synthesis too (like decreased IGF-1 mRNA expression), but I think muscle breakdown is much more important than reduced muscle building.

 

[stevie]

euxaristo!

 

[micmic]

parakalo!

(if the last two posts sound Greek to the rest of you, it's because they are )

 

[anoopbal]

Protein synthesis and protein break down is always happening in the muscle cell.In this way, cells retain the ability to adapt to a new environment or the diverse demands placed on it.If pprotein were permenanatly placed afer synthesis, there would be no way tp change them.So the proteins are constantly "turning over" to meet the current cellular demands.this mechanism is called proteolysis.


Muscle mass, simply represents the the net balance between protein synthesis and breakdown.Muscle mass could be affected by both degradation and synthesis.For instance, muscle mass can be increased with out any increase in synthesis, if the breakdown is decreased.It has been shown that weigth traianing causes an acute increase in protein synthesis and even protein breakdown.The breakdown might be due to meet the increased demand for protein synthesis. This is exactly the reason for having a post workout protein shake.This exogenous protein will decrease the intracellular protein breakdown.


So even if satellite cells donate nuclei, without sufficient protein muscle mass will be compromised.Also, enough ATP should be prodeuced in the mitochondria to regulate protein synthesis.


Anoop

 

[imported_ilFacell]

Inject IGF-1 locally...(you can, but im jk)

 

[stevie]

Quote[/b] ]If pprotein were permenanatly placed afer synthesis, there would be no way tp change them.

yes of course, but you are replying to my question at the wrong level of detail. One particular protein will be continually created, destroyed, but that doesnt matter as long as the machinery for making those proteins is still there.
What i was asking was whether the satellite cell donated nucleus will remain in light of the fact that cells arent in the habit of loosing their nucleus!!!! ie when the muscle cell replicates does the donated nucleus also replicate?

Quote[/b] ]So even if satellite cells donate nuclei, without sufficient protein muscle mass will be compromised

well,
if satellite cells donate their nuclei and remain there, then the muscle cell will possess greater hypertrophy potential (there is a positive relationship between the number of nuclei present in the cell and the size of the muscle cell). This potential would exsist regardless of proetins being made/broken down within the cell...unless of course we are talking about muscle cell apoptosis?
what i was wondering was whether nuclei get donated even during diet. then when it comes to bulking, the muscle building potential gets realised.
however, as micmic pointed out,

Quote[/b] ]Other things may happen that will reduce protein synthesis too (like decreased IGF-1 mRNA expression

therefore, there would be a reduction in the production of the molecular signals for satelite cell differentation and proliferation (IGF-1 etc).

 

[anoopbal]

Quote[/b] ]if satellite cells donate their nuclei and remain there, then the muscle cell will possess greater hypertrophy potential (there is a positive relationship between the number of nuclei present in the cell and the size of the muscle cell).

Increase in myonuclei number to hypertrophy and decrease in myonuclei to atrophy is basically an additional mechanism for increasing or decreasing the protein synthesis mechanism.So,if there is no protein available for synthesis there is no reason for the muscle to maintain those additional nucleous.So I guess it will naturally eliminate those nuclei(maybe by apoptosis).Also,since muscle atrophies due to decrease in protein synthesis or increase in breakdown, few myonuclei may be deleted to maintain that constant nucleous to cytoplasmic ratio. As Bryan commenetd, decreased calorie intake can reduce the IGf1 thereby avoiding or decreasing the myonuclei donation.
I might be a bit off topic here.If there is constant ratio of myonuclei to cytoplasmic volume how does slow fibershave greater number of nucleous than fast twitch fibers.Fast twitch fibers are supposedly larger than slow titch fibers.So how is this possible.
Anoop

 

[micmic]

Quote[/b] (anoopbal @ Nov. 13 2003,7:59)]I might be a bit off topic here.If there is constant ratio of myonuclei to cytoplasmic volume how does slow fibershave greater number of nucleous than fast twitch fibers.Fast twitch fibers are supposedly larger than slow titch fibers.So how is this possible.

The myonuclear number to cytoplasmic volume ratio is constant only in the context of a certain fiber type. In general, myonuclei in slow twitch fibers are more crowded, they have less cytoplasmic personal space. Look at the following:

Tseng BS, Kasper CE, Edgerton VR - Cytoplasm-to-myonucleus ratios and succinate dehydrogenase activities in adult rat slow and fast muscle fibers

... and this pdf (200KB):

ROSSER B, MALCOLM SD, BANDMAN E - Myonuclear domain size varies along the lengths of maturing skeletal muscle fibers

It has also been proposed that the increase in myonuclei of the fast twitch fibers may be a prerequisite for their conversion to slow twitch ones.

 

[anoopbal]

Thanks, micmic.I have also read that myonuclei number is related to the mitochondrial number.And fiber size is inversely propotional to the oxidative capacity.So,I supppose fibersize, oxidative capacity and myonuclei number are all depenedent and competeing with each other for space.


So, for instance, if a person performs aerobic training or cardio training and if there is an increase in oxidative capacity(Mitochondrial number), there should be a increase in myonuclearr number according to the ratio.Am i right?

Anoop