[pinoy]

k guys sorry

[Iron Warrior]

****, it looks like I wasted $30 on Dextrose last week

[Sheesh]

Originally posted by Iron Warrior
Shit, it looks like I wasted $30 on Dextrose last week

[Lgoosey]

2. Had there been any study saying the faster muscle glycogen is replenished the better for muscle growth? Not really. They say muscle glycogen resynthesis isn't changed. If we were concerned with replenishing muscle and liver glygogen fast for energy requirements then its a whole different story. We're not concerned with that here. Strickly muscle repair.

We are concerned with the speed at which glycogen is restored in order to take advantage of the optimal, quickly fading, post workout window.

2. Is there any benefit of creating a HUGE insulin spike? IMO, no because muscle gylocgen replenishment in its first phase is independent of insulin. After that its followed by a slower insulin dependent phase. Sound like low GI would be better for that without the risk of excess glucose being present.

Muscle glycogen can be restored without an insulin spike but insulin compounded with carbos raise the rate and effectiveness in which this occurs.


***ALSO in Bobo's first two studies...its is never specified what complex carb is used. Maltodextrin is a complex carb yet we know that it is far from low GI....Complex does not mean low GI, and you are arguing to use oatmeal which has a realtively low GI.

the last study posted by Bobo: we as BB-ers do not conduct is prolonged exaustive exercise. The time frame isnt specifed nor are any numbers given for time frames or amount of carbo ingestion ... also it states simply: "about the same"?!?!?

quantity of carbs used is also not noted in any studies

[Kruger]

Originally posted by Lgoosey


We are concerned with the speed at which glycogen is restored in order to take advantage of the optimal, quickly fading, post workout window.



Muscle glycogen can be restored without an insulin spike but insulin compounded with carbos raise the rate and effectiveness in which this occurs.


***ALSO in Bobo's first two studies...its is never specified what complex carb is used. Maltodextrin is a complex carb yet we know that it is far from low GI....Complex does not mean low GI, and you are arguing to use oatmeal which has a realtively low GI.

the last study posted by Bobo: we as BB-ers do not conduct is prolonged exaustive exercise. The time frame isnt specifed nor are any numbers given for time frames or amount of carbo ingestion ... also it states simply: "about the same"?!?!?

quantity of carbs used is also not noted in any studies

1. Your right and you study you posted claimed nothing about the RATE that resynthesis occured, just the amount. Then I posted one saying it doesn't matter the amount of insulin or glucose present, the rate of resynthesis will occur at the same rate no matter the structure. Just because your muscles are fuller faster doesn't mean the rate of resynthesis is increased. The only thing that say increases resynthesis is the addition of protein and/or aminos.

2. Sorry your second statement isn't accurate. Read the first study posted. Resynthesis is insulin INDEPENDENT.

3. It called depletion. Whether you deplete throuhg edurance training isn't the point. Actually resistance traning depletion is less catabolic since the scecretion of GH is released up to 60 minutes after exercise. This means there is still further reason not to need a large insulin spike.

4. The solution used was a wheat mixture. When studies conducted with maltodextrin its either descibed as malto, or a glucose polymer.

5. Thats the point. Its about the same. If there was a singificant difference, it would be told. If you want just go read the full text and you have all the numbers you want.

6. I liked this part too. "Suggestions have been made that carbohydrate availability is the main limiting factor for glycogen synthesis. A large part of the ingested glucose that enters the bloodstream appears to be extracted by tissues other than the exercise muscle (i.e. liver, other muscle groups or fat tissue) and may therefore limit the amount of glucose available to maximise muscle glycogen synthesis rates." That would explain the numerous cases of increased fat storage with large amount of carbs are present. High GI makes it even worse.

[Lgoosey]

this study states that glycogen sythesis does not require insulin. this by no means implies that insulin has no added effects.

It also states( bold part) that increased insulin is the cause for an increase in glycogen synthesis!!! therefore glycogen sythesis can occur without insulin but the presence of insulin benefits resynthesis which calls for high GI carbs.

The pattern of muscle glycogen synthesis following glycogen-depleting exercise occurs in two phases. Initially, there is a period of rapid synthesis of muscle glycogen that does not require the presence of insulin and lasts about 30-60 minutes. This rapid phase of muscle glycogen synthesis is characterised by an exercise-induced translocation of glucose transporter carrier protein-4 to the cell surface, leading to an increased permeability of the muscle membrane to glucose. Following this rapid phase of glycogen synthesis, muscle glycogen synthesis occurs at a much slower rate and this phase can last for several hours. Both muscle contraction and insulin have been shown to increase the activity of glycogen synthase, the rate-limiting enzyme in glycogen synthesis. Furthermore, it has been shown that muscle glycogen concentration is a potent regulator of glycogen synthase. Low muscle glycogen concentrations following exercise are associated with an increased rate of glucose transport and an increased capacity to convert glucose into glycogen. The highest muscle glycogen synthesis rates have been reported when large amounts of carbohydrate (1.0-1.85 g/kg/h) are consumed immediately post-exercise and at 15-60 minute intervals thereafter, for up to 5 hours post-exercise. When carbohydrate ingestion is delayed by several hours, this may lead to ~50% lower rates of muscle glycogen synthesis. The addition of certain amino acids and/or proteins to a carbohydrate supplement can increase muscle glycogen synthesis rates, most probably because of an enhanced insulin response. However, when carbohydrate intake is high (>/=1.2 g/kg/h) and provided at regular intervals, a further increase in insulin concentrations by additional supplementation of protein and/or amino acids does not further increase the rate of muscle glycogen synthesis. Thus, when carbohydrate intake is insufficient (<1.2 g/kg/h), the addition of certain amino acids and/or proteins may be beneficial for muscle glycogen synthesis. Furthermore, ingestion of insulinotropic protein and/or amino acid mixtures might stimulate post-exercise net muscle protein anabolism. Suggestions have been made that carbohydrate availability is the main limiting factor for glycogen synthesis. A large part of the ingested glucose that enters the bloodstream appears to be extracted by tissues other than the exercise muscle (i.e. liver, other muscle groups or fat tissue) and may therefore limit the amount of glucose available to maximise muscle glycogen synthesis rates. Furthermore, intestinal glucose absorption may also be a rate-limiting factor for muscle glycogen synthesis when large quantities (>1 g/min) of glucose are ingested following exercise.

========================================


***Also high levels of insulin are beneficial post workout***
Low GI carbs will obviously not provide as much of an insulin response.


Physiologic hyperinsulinemia stimulates protein synthesis and enhances transport of selected amino acids in human skeletal muscle.

Biolo G, Declan Fleming RY, Wolfe RR.

Department of Internal Medicine, University of Texas Medical Branch, Galveston.

We have investigated the mechanisms of the anabolic effect of insulin on muscle protein metabolism in healthy volunteers, using stable isotopic tracers of amino acids. Calculations of muscle protein synthesis, breakdown, and amino acid transport were based on data obtained with the leg arteriovenous catheterization and muscle biopsy. Insulin was infused (0.15 mU/min per 100 ml leg) into the femoral artery to increase femoral venous insulin concentration (from 10 +/- 2 to 77 +/- 9 microU/ml) with minimal systemic perturbations. Tissue concentrations of free essential amino acids decreased (P < 0.05) after insulin. The fractional synthesis rate of muscle protein (precursor-product approach) increased (P < 0.01) after insulin from 0.0401 +/- 0.0072 to 0.0677 +/- 0.0101%/h. Consistent with this observation, rates of utilization for protein synthesis of intracellular phenylalanine and lysine (arteriovenous balance approach) also increased from 40 +/- 8 to 59 +/- 8 (P < 0.05) and from 219 +/- 21 to 298 +/- 37 (P < 0.08) nmol/min per 100 ml leg, respectively. Release from protein breakdown of phenylalanine, leucine, and lysine was not significantly modified by insulin. Local hyperinsulinemia increased (P < 0.05) the rates of inward transport of leucine, lysine, and alanine, from 164 +/- 22 to 200 +/- 25, from 126 +/- 11 to 221 +/- 30, and from 403 +/- 64 to 595 +/- 106 nmol/min per 100 ml leg, respectively. Transport of phenylalanine did not change significantly. We conclude that insulin promoted muscle anabolism, primarily by stimulating protein synthesis independently of any effect on transmembrane transport.

[Kruger]

Originally posted by Lgoosey
this study states that glycogen sythesis does not require insulin. this by no means implies that insulin has no added effects.

It also states( bold part) that increased insulin is the cause for an increase in glycogen synthesis!!! therefore glycogen sythesis can occur without insulin but the presence of insulin benefits resynthesis which calls for high GI carbs.



========================================


***Also high levels of insulin are beneficial post workout***
Low GI carbs will obviously not provide as much of an insulin response.


Physiologic hyperinsulinemia stimulates protein synthesis and enhances transport of selected amino acids in human skeletal muscle.

Biolo G, Declan Fleming RY, Wolfe RR.

Department of Internal Medicine, University of Texas Medical Branch, Galveston.

We have investigated the mechanisms of the anabolic effect of insulin on muscle protein metabolism in healthy volunteers, using stable isotopic tracers of amino acids. Calculations of muscle protein synthesis, breakdown, and amino acid transport were based on data obtained with the leg arteriovenous catheterization and muscle biopsy. Insulin was infused (0.15 mU/min per 100 ml leg) into the femoral artery to increase femoral venous insulin concentration (from 10 +/- 2 to 77 +/- 9 microU/ml) with minimal systemic perturbations. Tissue concentrations of free essential amino acids decreased (P &lt; 0.05) after insulin. The fractional synthesis rate of muscle protein (precursor-product approach) increased (P &lt; 0.01) after insulin from 0.0401 +/- 0.0072 to 0.0677 +/- 0.0101%/h. Consistent with this observation, rates of utilization for protein synthesis of intracellular phenylalanine and lysine (arteriovenous balance approach) also increased from 40 +/- 8 to 59 +/- 8 (P &lt; 0.05) and from 219 +/- 21 to 298 +/- 37 (P &lt; 0.08) nmol/min per 100 ml leg, respectively. Release from protein breakdown of phenylalanine, leucine, and lysine was not significantly modified by insulin. Local hyperinsulinemia increased (P &lt; 0.05) the rates of inward transport of leucine, lysine, and alanine, from 164 +/- 22 to 200 +/- 25, from 126 +/- 11 to 221 +/- 30, and from 403 +/- 64 to 595 +/- 106 nmol/min per 100 ml leg, respectively. Transport of phenylalanine did not change significantly. We conclude that insulin promoted muscle anabolism, primarily by stimulating protein synthesis independently of any effect on transmembrane transport.

1. You seem to missing the point once again. Insulin obviously helps but tell me why you need A HUGE spike to do this. Do you think I'm advocating no carbs here? Please understand these points if you wish to continue this debate. GI measure's the rate, not the amount. Your not listening to everything I have to say and looking at the big picture. Nobody every said High GI doesn't work. Your just saying Low GI doesn't work as effectively. I've given studies to state the opposite.

2. If you take 50g of Oatmeal vs 50g of Dextrose guess what happens? The same amount of insulin is produced but at a faster rate with dextrose. According to that study excess amounts of glucose will NOT be used by the exercised muscle. Guess where that goes. So your study says nothing about the GI. It measuring glycaemic load. Who ever said insulin is bad?

3. As for your study and bold print you still seem to missing the point that the first phase is insulin INDEPENDENT! Whether you consume carbs or not muscle glycogen will not be effected by insulin since it doesn't utlize this until the second phase. I don't understand why you aren't readin this. The addiotion of protein along with an insulin spike will help during the second phase where it a "slower insulin dependent rate of synthesis". What do we want with a slower insulin dependent rate of synthesis? A lower GI that will creat a stable, slower release of insulin to faciliate synthesis.

[New Body]

Great post guys. I've surely learned a lot reading all the responses.

thanks and BOBO I'll give the Oatmeal + whey a try.

[Lgoosey]

Being a prik but 50 grams of dextrose and 50 grams of oatmeal will not produce the same insulin repsonse. There are not 50 grams of carbs in 50 grams of oatmeal

I still don't buy the fact that insulin doesn't effect glycogen synthesis in the first 30-60 minutes. I can see that resynthesis WILL occur without insulin but it never states that insulin, if added, will not effect the situation. It simply states "does not require", nothing about "is not effected".
I don't have my bookmarks because I am in school but I may have a study....

The study I posted is in a new direction, maybe you overlooked my point but I posted it in order to try and point out that a LARGE insulin spike will increase protein synthesis in the all important time post workout, a large insulin spike that Low GI will not provide in the optimal time.

pressed on time, sorry

[Kruger]

Well if you choose not to believe the studies, then thats fine. I have real world results that back it up not only in me but several members on this board and other boards that have tried it.

Your right, it would be a little under a cup of Oatmeal. You knew what I was referring too.

The study you postsed talked about hyperinsulinemia. This refers to the total AMOUNT of insulin prodcued over a peroid of time. Supraphysiological levels of insulin will alwasy be anabolic but a large spike is not needed. You keep associating GI with the total amount of insulin produced and its two seperate issues. The point is to keep a stable release of insulin for a longer peroid of time to account for both phases.


Once again a LARGE spike does NOTHING for muscle resysthesis. It refills glycogen faster but in no way does that equate to a faster rate in which resynthesis will occur. I never said an insulin will not have an effect in the first phase but since muscle glycogen is insulin independnent, there is even a much greater chance of adipose storage since we already see that not all glucose is utilized by the exercised muscle.

You seem to forget exercise alon induces a greater insulin sensitivity. The need for such a high GI is not necessary. Low GI is a smarter and wiser choice.


I did find this one however...

Physiological hyperinsulinemia impairs insulin-stimulated glycogen synthase activity and glycogen synthesis. Iozzo, Patricia, Thonchai Pratipanawatr, Hanno Pijl, Christoph Vogt, Vineeta Kumar, Ruben Pipek, Masafumi Matsuda, Lawrence J. Mandarino, Kenneth J. Cusi, and Ralph A. Defronzo. Division of Diabetes, Departments of 1Medicine and Biochemistry,2 The University of Texas Health Science Center at San Antonio, San Antonio, Texas 78284
--------------------------------------------------------------------------------
APStracts 8:0018E, 2001.
--------------------------------------------------------------------------------
Although chronic hyperinsulinemia has been shown to induce insulin resistance, the basic cellular mechanisms responsible for this phenomenon are unknown. The present study was performed 1) to determine the time-related effect of physiological hyperinsulinemia on glycogen synthase (GS) activity, hexokinase II (HKII) activity and mRNA content, and GLUT-4 protein in muscle from healthy subjects, and 2) to relate hyperinsulinemia- induced alterations in these parameters to changes in glucose metabolism in vivo. Twenty healthy subjects had a 240-min euglycemic insulin (plasma insulin concentration = 121 ± 9 or 143 ± 25 pmol/l) clamp study with muscle biopsies and then received a low-dose insulin infusion for 24 (n = 6) or 72 h (n = 14). During the baseline insulin clamp, GS fractional velocity (0.075 ± 0.008 to 0.229 ± 0.02, P < 0.01), HKII mRNA content (0.179 ± 0.034 to 0.354 ± 0.087, P < 0.05), and HKII activity (2.41 ± 0.63 to 3.35 ± 0.54 pmol•min«minus»1•ng«minus»1, P < 0.05), as well as whole body glucose disposal and nonoxidative glucose disposal, increased. During the insulin clamp performed after 24 and 72 h of sustained physiological hyperinsulinemia, the ability of insulin to increase muscle GS fractional velocity, total body glucose disposal, and nonoxidative glucose disposal was impaired (all P < 0.01), whereas the effect of insulin on muscle HKII mRNA, HKII activity, GLUT-4 protein content, and whole body rates of glucose oxidation and glycolysis remained unchanged. Muscle glycogen concentration did not change [116 ± 28 vs. 126 ± 29 µmol/kg muscle, P = nonsignificant (NS)] and was not correlated with the change in nonoxidative glucose disposal (r = 0.074, P = NS). In summary, modest chronic hypernsulinemia may contribute directly (independent of change in muscle glycogen concentration) to the development of insulin resistance by its impact on the GS pathway.

[Kruger]

Amino acids regulate skeletal muscle PHAS-I and p70 S6-kinase phosphorylation independently of insulin. Long, W., L. Saffer, L. Wei, and E. J. Barrett. Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908
--------------------------------------------------------------------------------
APStracts 7:0077E, 2000.
--------------------------------------------------------------------------------
Refeeding reverses the muscle protein loss seen with fasting. The physiological regulators and cellular control sites responsible for this reversal are incompletely defined. Phosphorylation of phosphorylated heat-acid stabled protein (PHAS-I) frees eukaryotic initiation factor 4E (eIF4E) and stimulates protein synthesis by accelerating translation initiation. Phosphorylation of p70 S6-kinase (p70S6k) is thought to be involved in the regulation of the synthesis of some ribosomsal proteins and other selected proteins with polypyrimidine clusters near the transcription start site. We examined whether phosphorylation of PHAS-I and p70S6k was increased by feeding and determined the separate effects of insulin and amino acids on PHAS-I and p70S6k phosphorylation in rat skeletal muscle in vivo. Muscle was obtained from rats fed ad libitum or fasted overnight (n = 5 each). Other fasted rats were infused with insulin (3 muU×min«minus»1×kg«minus»1, euglycemic clamp), amino acids, or the two combined. Gastrocnemius was freeze-clamped, and PHAS-I and p70S6k phosphorylation was measured by quantifying the several phosphorylated forms of these proteins seen on Western blots. We observed that feeding increased phosphorylation of both PHAS-I and p70S6k (P < 0.05). Infusion of amino acids alone reproduced the effect of feeding. Physiological hyperinsulinemia increased p70S6K (P < 0.05) but not PHAS-I phosphorylation (P = 0.98). Addition of insulin to amino acid infusion was no more effective than amino acids alone in promoting PHAS-I and p70S6k phosphorylation. We conclude that amino acid infusion alone enhances the activation of the protein synthetic pathways in vivo in rat skeletal muscle. This effect is not dependent on increases in plasma insulin and simulates the activation of protein synthesis that accompanies normal feeding.

Received 25 October 1999; accepted in final form 8 March 2000
APS Manuscript Number E509-9.
Article publication pending Am J Physiol Endocrinol Metab
ISSN 1080-4757 Copyright 2000 The American Physiological Society.
Published in APStracts on 26 May 2000

[Lgoosey]

Yes insulin will always be anabolic and I think that a huge spike, obviously more anabolic, is needed postworkout to take advantage of the quickly fading "window".

I know GI does not neceesary predict insulin response but they are closely related nonetheless.

So it is agreed that insulin DOES benefit the first phase.

Insulin is obviously anabolic for muscle but then you state that is does nothing for MUSCLE synthesis in the first phase.

Insulin does indeed refill glycogen faster as stated so more insulin will benefit the much needed postworkout resynthesis by making it occur MORE QUICKLY, thus taking advantage of the P-workout window more effectively than the lower levels of insulin from low GI use.

The only people that gain a gut from high GI carbs are foolish and use too much.

High GI is NECESSARY post workout but in far lower dosages than currently used.

[Draven]

Can we find a few studies to support that lgoosey? Bobo has done a good job backing up his stance, it would be nice to see some from the other side.

Also, perhaps once we get all the studies here someone can go through them, without bias, and create an article to sum up all of the findings and try to deduce the best course of action. Perhaps the answer lies somewhere in between with timing being the solution. Kind of like this; 5 mintues after workout a small dink of high GI and whey is consumed and then 20 mins later a low GI/ Whey combo to sustain inslulin levels. Just a thought. I'm not saying the previous is correct, just an example.