Whole foods PWO?

[dabuffguy]

16 1/4'' arms.


Yeah, I weigh 51 pounds less then you, probably less body fat(when I say probably I mean definitely), and my arms aren't much smaller then yours.

Congratulations. You have less BF because you eat 1500 calories a day. Oh, and almost 2" smaller arms is MUCH smaller bro.

Not to mention I could almost definitely hang with you on core lifts.

Can you pull 545 from the floor? Can you bench 335? Can you squat 405? Not quite, eh? mmmkay.

EDIT:

Oh, and if you really wanna get down to how else I'm better then you, I run a 4.59 40 yard.

Oh, shit! Someone's got an ace up their sleeve. Look the hell out for this son of a bitch. He really means business!

^^^^

 

[dabuffguy]

Milk has a high insulin response. I think milk being listed as Low GI gives people a false sense of security. Milk sugar = lactose. It's 2 simple sugars glucose and galactose bound together by an OH bond. Once the bond is broken, the 2 sugars are monosaccharides and will immediately raise blood sugar. I'm not sure where galactose is on the GI scale because it's generally not listed .. (which is another reason why I generally take issue with milk being listed as low GI)

Good post. People do misunderstand milk.

 

[cobracock1979]

I posted that study today in the other thread
http://www.elitefitness.com/forum/d...give-me-your-advice-618806-7.html#post8557033

It clearly states that the bottom that cortisol and testosterone were unaffected by excess carbs ingested for anabolism
It also states that no significant differences were observed in the types of CHO absorbed

The the above is true then what is the point of spiking insulin PWO. Why not absorb those carbs pre workout to help fuel and reduce muscle microtrama during the workout? This way you could eat more nutrient dense foods instead of eating empty calories such as sugars

Ive already explainend that this is in no way conclusive and that these markers are only an indicator - you would need to physically measure protein absorption to conclude that no protein synthesis took place.

An I already stated Im gonna try ingesting carbs pre workout.

Still waiting for you to prove yopur point here

 

[cobracock1979]

http://62.189.20.9/bst/034/0213/0340213.pdf

Interestind read - mechanisms of protein synthesis and the role of insulin in this

 

[gjohnson5]

Ive already explainend that this is in no way conclusive and that these markers are only an indicator - you would need to physically measure protein absorption to conclude that no protein synthesis took place.

An I already stated Im gonna try ingesting carbs pre workout.

Still waiting for you to prove yopur point here

If you feel you have proof that insulin spike PWO des anything for anabolism, then post it.
There is no proof of that being true...

Hell here's another study which states that glutamine supplementation works just as well as carbohydrates pWO to restore glycogen.

To reiterate the point. carbohydrates are not needed PWO if adequate proteins are present...

Effect of oral glutamine on whole body carbohydrate storage during recovery from exhaustive exercise -- Bowtell et al. 86 (6): 1770 -- Journal of Applied Physiology

However, when the results from the present study are directly compared with those obtained by Varnier and colleagues (36), in a study carried out in our laboratory and using an identical experimental protocol in similar subjects, oral glutamine does appear to promote net resynthesis of muscle glycogen stores relative to control subjects in whom saline or alanine+glycine were infused. We found that after the subjects' consumption of the glutamine-only drink, the rate of muscle glycogen storage was 4.1 ± 1.1 mmol · kg wet wt-1 · h-1, whereas Varnier and colleagues found that the rate of net muscle glycogen storage after infusion of either saline or alanine+glycine fell within the range 0.5-1.0 mmol · kg wet wt-1 · h-1, which is consistent with previously reported results. The effect of glutamine may be due to one or both of two possibilities: first, glutamine has been shown to be an effective substrate for hepatic glycogen synthesis in 72-h fasted rats, i.e., when glycogen is severely depleted (27); such a scenario could also occur in postexercise muscle in which glycogen is low and in which all of the required transporters and enzymes exist. In skeletal muscle, the exogenous glutamine will be rapidly taken up through system Nm (1), where it can be deaminated to form glutamate and then 2-oxoglutarate through the action of either glutaminase and glutamate dehydrogenase or glutamine transaminase and omega -amidase. It is possible, then, for the 2-oxoglutarate to enter the TCA cycle and be removed at the level of malate (by the action either of malate dehydrogenase or of the malic enzyme plus phosphoenolpyruvate carboxykinase and pyruvate kinase); the malate can be converted to oxaloacetate, phosphoenolpyruvate, and finally pyruvate, which may then be used in the glycogenic pathway by reversal of glycolysis to fructose 1,6-bisphosphate. This pathway may be particularly active at the end of exercise, when both the availability of glycogenic metabolites and muscle glycogen concentration are low; comparisons may be drawn to the physiological state in the starved condition, when glutamine has proved to be an effective glycogenic substrate in rat muscle (27). However, only 55 mmol of glutamine were ingested, of which, at most, probably only 47% reached the systemic circulation (15); thus the resultant glycogenic precursor would be of minor importance relative to the 119 mmol of muscle glycogen storage that occurred during the 2-h recovery period.

.
.
.
.
In conclusion, ingestion of glutamine alone appeared to promote muscle glycogen resynthesis during recovery from exhaustive exercise, relative to that expected from studies in which no substrate was provided. The promotion of muscle glycogen synthesis by consumption of glucose polymer and of glutamine was not additive. However, the addition of glutamine to the glucose polymer drink resulted in a greater storage of carbohydrate in sites other than skeletal muscle, the most likely candidate being the liver.

 

[cobracock1979]

If you feel you have proof that insulin spike PWO des anything for anabolism, then post it.
There is no proof of that being true...

Hell here's another study which states that glutamine supplementation works just as well as carbohydrates pWO to restore glycogen.

To reiterate the point. carbohydrates are not needed PWO if adequate proteins are present...

Effect of oral glutamine on whole body carbohydrate storage during recovery from exhaustive exercise -- Bowtell et al. 86 (6): 1770 -- Journal of Applied Physiology

However, when the results from the present study are directly compared with those obtained by Varnier and colleagues (36), in a study carried out in our laboratory and using an identical experimental protocol in similar subjects, oral glutamine does appear to promote net resynthesis of muscle glycogen stores relative to control subjects in whom saline or alanine+glycine were infused. We found that after the subjects' consumption of the glutamine-only drink, the rate of muscle glycogen storage was 4.1 ± 1.1 mmol · kg wet wt-1 · h-1, whereas Varnier and colleagues found that the rate of net muscle glycogen storage after infusion of either saline or alanine+glycine fell within the range 0.5-1.0 mmol · kg wet wt-1 · h-1, which is consistent with previously reported results. The effect of glutamine may be due to one or both of two possibilities: first, glutamine has been shown to be an effective substrate for hepatic glycogen synthesis in 72-h fasted rats, i.e., when glycogen is severely depleted (27); such a scenario could also occur in postexercise muscle in which glycogen is low and in which all of the required transporters and enzymes exist. In skeletal muscle, the exogenous glutamine will be rapidly taken up through system Nm (1), where it can be deaminated to form glutamate and then 2-oxoglutarate through the action of either glutaminase and glutamate dehydrogenase or glutamine transaminase and omega -amidase. It is possible, then, for the 2-oxoglutarate to enter the TCA cycle and be removed at the level of malate (by the action either of malate dehydrogenase or of the malic enzyme plus phosphoenolpyruvate carboxykinase and pyruvate kinase); the malate can be converted to oxaloacetate, phosphoenolpyruvate, and finally pyruvate, which may then be used in the glycogenic pathway by reversal of glycolysis to fructose 1,6-bisphosphate. This pathway may be particularly active at the end of exercise, when both the availability of glycogenic metabolites and muscle glycogen concentration are low; comparisons may be drawn to the physiological state in the starved condition, when glutamine has proved to be an effective glycogenic substrate in rat muscle (27). However, only 55 mmol of glutamine were ingested, of which, at most, probably only 47% reached the systemic circulation (15); thus the resultant glycogenic precursor would be of minor importance relative to the 119 mmol of muscle glycogen storage that occurred during the 2-h recovery period.

.
.
.
.
In conclusion, ingestion of glutamine alone appeared to promote muscle glycogen resynthesis during recovery from exhaustive exercise, relative to that expected from studies in which no substrate was provided. The promotion of muscle glycogen synthesis by consumption of glucose polymer and of glutamine was not additive. However, the addition of glutamine to the glucose polymer drink resulted in a greater storage of carbohydrate in sites other than skeletal muscle, the most likely candidate being the liver.

Where have I been unclear on this? I have never said I have proof that insulin spikes increase anobolism PWO, quite the opposite.

It is you that have said, in black and white "I can definatively prove that insulin spikes PWO have no positive effect on protein synthesis PWO" - see the link below.

The impetus is on you to prove this definatively. Let me repeat the important word here again - definatively. If you can't then fine - dont make such comments in future.

Dont get me wrong, you have raised some interesting fundamental points and have provided some studies which indicate thay MAY have some validity, so thats something. I have stated in my latest thread that I will be potentially trying some new whole food workout regimes. But I guess you will continue stating that I am not open to other peoples viewpoints...cos you just dont listen.


See post 57 http://www.elitefitness.com/forum/diet-bodybuilding/mass-please-give-me-your-advice-618806-6.html

 

[cobracock1979]

If you feel you have proof that insulin spike PWO des anything for anabolism, then post it.
There is no proof of that being true...

Hell here's another study which states that glutamine supplementation works just as well as carbohydrates pWO to restore glycogen.

To reiterate the point. carbohydrates are not needed PWO if adequate proteins are present...

Effect of oral glutamine on whole body carbohydrate storage during recovery from exhaustive exercise -- Bowtell et al. 86 (6): 1770 -- Journal of Applied Physiology

However, when the results from the present study are directly compared with those obtained by Varnier and colleagues (36), in a study carried out in our laboratory and using an identical experimental protocol in similar subjects, oral glutamine does appear to promote net resynthesis of muscle glycogen stores relative to control subjects in whom saline or alanine+glycine were infused. We found that after the subjects' consumption of the glutamine-only drink, the rate of muscle glycogen storage was 4.1 ± 1.1 mmol · kg wet wt-1 · h-1, whereas Varnier and colleagues found that the rate of net muscle glycogen storage after infusion of either saline or alanine+glycine fell within the range 0.5-1.0 mmol · kg wet wt-1 · h-1, which is consistent with previously reported results. The effect of glutamine may be due to one or both of two possibilities: first, glutamine has been shown to be an effective substrate for hepatic glycogen synthesis in 72-h fasted rats, i.e., when glycogen is severely depleted (27); such a scenario could also occur in postexercise muscle in which glycogen is low and in which all of the required transporters and enzymes exist. In skeletal muscle, the exogenous glutamine will be rapidly taken up through system Nm (1), where it can be deaminated to form glutamate and then 2-oxoglutarate through the action of either glutaminase and glutamate dehydrogenase or glutamine transaminase and omega -amidase. It is possible, then, for the 2-oxoglutarate to enter the TCA cycle and be removed at the level of malate (by the action either of malate dehydrogenase or of the malic enzyme plus phosphoenolpyruvate carboxykinase and pyruvate kinase); the malate can be converted to oxaloacetate, phosphoenolpyruvate, and finally pyruvate, which may then be used in the glycogenic pathway by reversal of glycolysis to fructose 1,6-bisphosphate. This pathway may be particularly active at the end of exercise, when both the availability of glycogenic metabolites and muscle glycogen concentration are low; comparisons may be drawn to the physiological state in the starved condition, when glutamine has proved to be an effective glycogenic substrate in rat muscle (27). However, only 55 mmol of glutamine were ingested, of which, at most, probably only 47% reached the systemic circulation (15); thus the resultant glycogenic precursor would be of minor importance relative to the 119 mmol of muscle glycogen storage that occurred during the 2-h recovery period.

.
.
.
.
In conclusion, ingestion of glutamine alone appeared to promote muscle glycogen resynthesis during recovery from exhaustive exercise, relative to that expected from studies in which no substrate was provided. The promotion of muscle glycogen synthesis by consumption of glucose polymer and of glutamine was not additive. However, the addition of glutamine to the glucose polymer drink resulted in a greater storage of carbohydrate in sites other than skeletal muscle, the most likely candidate being the liver.

I know this - I have already stated glutamine and BCAA's are effective for this.

But we are taking about skeletal protein synthesis, and how it is effected by insulin spikes and protein ingestion. We are not discussing the most effective method of reglycogenation.

 

[cobracock1979]

Please also see the newest thready I started - it is on this subject and this subject alone.

What do you think on the stuff about insulin spikes curbing cortisol production and increasing IGF-1 production significantly at high levels of insulin PWO?

 

[jwo02]

^^^^

Dude I weigh 51 fucking pounds less then you WITH A LOWER BODY FAT. I didn't say I could lift with you pound for pound, I said I can hang with, which I can.


Bench: 285
Squat: 355
Power: 240
Hang: 235


Not to mention I'm not even training for strength like you are, nor have I ever taken anything even remotely close to abombs.


Just admitt you've been out done.


This will be my last post in this thread because I know how you're going to answer back, the same way you answer EVERYTHING...you're going to say "see bro I'm stronger then you bro I eat a shit ton bro you need to eat more bro bro bro I know everything about diet bro that's why I look like shit on a white rag bro I have 18'' biceps bro and only 1 3/4'' of those inches is my layer of rhino fat bro."


Admitt your diet blows. You don't need all those fucking carbs. You're just eating them cause you want to eat and don't have the self discipline not to.


</tellingbroherewhateveryonewantstosaycausehesanarrogantlittleprick>

 

[OneBreath]

this thread is cursed. Everyone gets in a fight that posts.