Just Say No To Soy!

[fightbackhxc21]

crap, i been eating a lot of soy protien in my bars. I liked them cuz they were tastey and cheap. Anyone got any other good bars that are cheap and non soy?

[will-work4andro]

Originally Posted by President Wilson

Good point, AMPK activation definately is strongly associated with decrements in hypertrophy in aged muscle.

AMPK is also activated with resistance training but this blunts the protein synthesis response to resistance training.

Nutritionally we can turn on AMPK a number of ways, but the main way appears to be by simply lowering the energetic state of the cell (glycogen depeltion) or in this case some component of the soy is actually able to activate AMPK, and thus it is hindering overall protein synthesis

is there any difference though, other than the way it is turned on? is the activation of AMPK in response to resistance training, the fact that muscle is using fuel? so let me know if have this right....if you would lift weights, AMPK is activated, but upon eating AMPK is turned back off...however, if your meal is SOY...it will stay activated...am i thining this right?

[Layne Norton]

Originally Posted by will-work4andro

Jacob i'm not as clear on this issue as you are...so i'm basically asking what you think....i'm not a proponent of soy in the least bit, but isn't AMPK activated in response to resistance training in the healthy? I know they think chronic AMPK activation is one of the reasons why aged muscle doesn't hypertrophy...so i guess what i'm asking is, would the effects on mTOR from soy mostly depend upon how long AMPK is activated, acutely or chronically?

yes it is. The other side of the coin is that AMPK will increase fat oxidation but you don't want it doing that at the expense of muscle mass.

My recommendation is if you take soy, don't take it by itself, have it with some whey or supplemental BCAAs so that you can overcome the negative regulation of AMPK on mTOR

[President Wilson]

Originally Posted by will-work4andro

is there any difference though, other than the way it is turned on? is the activation of AMPK in response to resistance training, the fact that muscle is using fuel? so let me know if have this right....if you would lift weights, AMPK is activated, but upon eating AMPK is turned back off...however, if your meal is SOY...it will stay activated...am i thining this right?

Yes that seems to be the case. For example studies which start with lower muscle glycogen stores get a greater AMPK response than when the individual starts with high muscle glycogen stores, same goes for creatine phosphate levels which may be one mechanism creatine consumption increases lean mass, by increasing the energetic state of the cell and lowering AMPK.

Basically anything that creates an energy deficit will increase AMPK.

So you are correct after exercise, by consuming a meal you should shut down AMPK, particularly by improving the energetic state of the cell, but Soy appears to counter this, by a mechanism that I do not believe has been identified.

[dashforce]

Pres --

Are adipocyte phosphocreatine stores influenced by supplementation? If so, could C theoretically impede fat loss? I've seen a few studies where creatine shifted substrate oxidation away from fat toward carbs, but nothing mind-blowing.

And while I'm at it, do you know of any estimate for adipocyte glycogen stores? I know they have very little, but I'm curious as to a whole-body estimate.

[President Wilson]

Hmmm all great questions. What I know is that 98 % of creatine stores are in skeletal muscle tissue, so this is the main area supplementation would effect.

In terms of hindering fat metabolism, the main study I am aware of is from Huso and colleagues, their results seemed to indicate that creatine supplementation did hinder fat metabolism by shifting fuel utilization to a higher reliance on carbohydrates. So if creatine does decrease fat metabolism then this would be the main area it mediates the effect.

http://jap.physiology.org/cgi/content/full/93/6/2018

[Ben2285]

wow excellent stuff guys

[Ordo Ab Chao]

Klosey and I were talking about soy in another thread and he mentioned this, now I see what he is talking about. It says that mice on the high-PE diets consumed 198ppm daidzein and 286 ppm genistein. So what does this equate to in a standard diet? How much soy needs to be consumed to to activate AMPK? Is this really of any concern?

For awhile people were raving about soy raising estrogen, but it turns out that it takes about 20mg of phytoestrogens per kg of bodyweight to raise estrogen (in mice subjects). Considering that the average 3 oz. serving of tofu only contains 20 mg and a 3.5 oz. scoop of soy protein concentrate has 100 mg, it's hard to consume enough soy to be worried about raising estrogen. I wonder if this is also the case here.

[klosey]

Originally Posted by Ordo Ab Chao

Klosey and I were talking about soy in another thread and he mentioned this, now I see what he is talking about. It says that mice on the high-PE diets consumed 198ppm daidzein and 286 ppm genistein. So what does this equate to in a standard diet? How much soy needs to be consumed to to activate AMPK? Is this really of any concern?

For awhile people were raving about soy raising estrogen, but it turns out that it takes about 1700 mg of phytoestrogens to raise estrogen (in mice subjects). Considering that the average 3 oz. serving of tofu only contains 20 mg and a 3.5 oz. scoop of soy protein concentrate has 100 mg, it's hard to consume enough soy to be worried about raising estrogen. I wonder if this is also the case here.

ampk activation is a concern as this stops protien synthesis which means no growth

[Ordo Ab Chao]

Originally Posted by klosey

ampk activation is a concern as this stops protien synthesis which means no growth

I gathered that. I meant is soy consumption really a concern or is it difficult to consume enough to receive a PE dose high enough to activate ampk.