Determinants of post-exercise glycogen synthesis during short-term recovery

[bachovas]

Determinants of post-exercise glycogen synthesis during short-term recovery.

Jentjens R, Jeukendrup A.

Human Performance Laboratory, School of Sport and Exercise Sciences, University of Birmingham, Edgbaston, Birmingham, UK.

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.

 

[Dwight Schrute]

This also correlates to the release of GH in that same amount of time. But the supp cpmanies are never wrong. You NEED that HUGE spike of insulin


I was wondering why I couldn't find this. It was just published. LOL...


Benz should like this.

 

[Dwight Schrute]

Here's a follow up on that one.

Regulation of GLUT4 protein and glycogen synthase during muscle glycogen synthesis after exercise.

Ivy JL, Kuo CH.

Department of Kinesiology, The University of Texas at Austin, 78712, USA.

The pattern of muscle glycogen synthesis following its depletion by exercise is biphasic. Initially, there is a rapid, insulin independent increase in the muscle glycogen stores. This is then followed by a slower insulin dependent rate of synthesis. Contributing to the rapid phase of glycogen synthesis is an increase in muscle cell membrane permeability to glucose, which serves to increase the intracellular concentration of glucose-6-phosphate (G6P) and activate glycogen synthase. Stimulation of glucose transport by muscle contraction as well as insulin is largely mediated by translocation of the glucose transporter isoform GLUT4 from intracellular sites to the plasma membrane. Thus, the increase in membrane permeability to glucose following exercise most likely reflects an increase in GLUT4 protein associated with the plasma membrane. This insulin-like effect on muscle glucose transport induced by muscle contraction, however, reverses rapidly after exercise is stopped. As this direct effect on transport is lost, it is replaced by a marked increase in the sensitivity of muscle glucose transport and glycogen synthesis to insulin. Thus, the second phase of glycogen synthesis appears to be related to an increased muscle insulin sensitivity. Although the cellular modifications responsible for the increase in insulin sensitivity are unknown, it apparently helps maintain an increased number of GLUT4 transporters associated with the plasma membrane once the contraction-stimulated effect on translocation has reversed. It is also possible that an increase in GLUT4 protein expression plays a role during the insulin dependent phase.

Publication Types:
Review
Review, Tutorial

PMID: 9578375 [PubMed - indexed for MEDLINE]


Dietary strategies to promote glycogen synthesis after exercise.

Ivy JL.

Exercise Physiology and Metabolism Laboratory, Department of Kinesiology and Health Education, The University of Texas at Austin, Austin, TX, USA.

Muscle glycogen is an essential fuel for prolonged intense exercise, and therefore it is important that the glycogen stores be copious for competition and strenuous training regimens. While early research focused on means of increasing the muscle glycogen stores in preparation for competition and its day-to-day replenishment, recent research has focused on the most effective means of promoting its replenishment during the early hours of recovery. It has been observed that muscle glycogen synthesis is twice as rapid if carbohydrate is consumed immediately after exercise as opposed to waiting several hours, and that a rapid rate of synthesis can be maintained if carbohydrate is consumed on a regular basis. For example, supplementing at 30-min intervals at a rate of 1.2 to 1.5 g CHO x kg(-1) body wt x h(-1) appears to maximize synthesis for a period of 4- to 5-h post exercise. If a lighter carbohydrate supplement is desired, however, glycogen synthesis can be enhanced with the addition of protein and certain amino acids. Furthermore, the combination of carbohydrate and protein has the added benefit of stimulating amino acid transport, protein synthesis and muscle tissue repair. Research suggests that aerobic performance following recovery is related to the degree of muscle glycogen replenishment.

Publication Types:
Review
Review, Tutorial

PMID: 11897899 [PubMed - indexed for MEDLINE]

 

[Dwight Schrute]

Here's one for the amounts of glucose. All were the same so why would cram so much dextrose malto down your throat?

Effect of different post-exercise sugar diets on the rate of muscle glycogen synthesis.

Blom PC, Hostmark AT, Vaage O, Kardel KR, Maehlum S.

Department of Physiology, National Institute of Occupational Health, Oslo, Norway.

The effect of repeated ingestions of fructose, sucrose, and various amounts of glucose on muscle glycogen synthesis during the first 6 h after exhaustive bicycle exercise was studied. Muscle biopsies for glycogen determination were taken before and after exercise, and every second hour during recovery. Blood samples for plasma glucose and insulin determination were taken before and after exercise, and every hour during recovery. When 0.35 (low glucose: N = 5), 0.70 (medium glucose: N = 5), or 1.40 (high glucose: N = 5) g.kg-1 body weight of glucose were given orally at 0, 2, and 4 h after exercise, the rates of glycogen synthesis were (mean +/- SE) 2.1 +/- 0.5, 5.8 +/- 1.0, and 5.7 +/- 0.9 mmol.kg-1.h-1, respectively. When 0.70 g.kg-1 body weight of sucrose (medium sucrose: N = 5), or fructose (medium fructose: N = 7) was ingested accordingly, the rates were 6.2 +/- 0.5 and 3.2 +/- 0.7 mmol.kg-1.h-1. Average plasma glucose level during recovery were similar in low glucose, medium glucose, and high glucose groups (5.76 +/- 0.24, 6.31 +/- 0.64, and 6.52 +/- 0.24 mM), while average plasma insulin levels were higher with higher glucose intake (16 +/- 1, 21 +/- 3, and 38 +/- 4 microU.ml-1).(ABSTRACT TRUNCATED AT 250 WORDS)

 

[Dwight Schrute]

I got bored so I'd figure I'd add a couple more.


Comparison of carbohydrate and milk-based beverages on muscle damage and glycogen following exercise.

Wojcik JR, Walber-Rankin J, Smith LL, Gwazdauskas FC.

Department of Human Nutrition, Foods, and Exercise at Virginia Polytechnic Institute and State University, Blacksburg 24061, USA.

This study examined effects of carbohydrate (CHO), milk-based carbohydrate-protein (CHO-PRO), or placebo (P) beverages on glycogen resynthesis, muscle damage, inflammation, and muscle function following eccentric resistance exercise. Untrained males performed a cycling exercise to reduce muscle glycogen 12 hours prior to performance of 100 eccentric quadriceps contractions at 120% of 1-RM (day 1) and drank CHO (n = 8), CHO-PRO (n = 9; 5 kcal/kg), or P (n = 9) immediately and 2 hours post-exercise. At 3 hours post-eccentric exercise, serum insulin was four times higher for CHO-PRO and CHO than P (p < .05). Serum creatine kinase (CK) increased for all groups in the 6 hours post-eccentric exercise (p < .01), with the increase tending to be lowest for CHO-PRO (p < .08) during this period. Glycogen was low post-exercise (33+/-3.7 mmol/kg ww), increased 225% at 24 hours, and tripled by 72 hours, with no group differences. The eccentric exercise increased muscle protein breakdown as indicated by urinary 3-methylhistidine and increased IL-6 with no effect of beverage. Quadriceps isokinetic peak torque was depressed similarly for all groups by 24% 24 hours post-exercise and remained 21% lower at 72 hours (p < .01). In summary, there were no influences of any post-exercise beverage on muscle glycogen replacement, inflammation, or muscle function.

Publication Types:
Clinical Trial
Randomized Controlled Trial

PMID: 11915776 [PubMed - indexed for MEDLINE]

 

[Dwight Schrute]

You high carb dieters are only hurting yourselves!!!

Carbohydrate nutrition before, during, and after exercise.

Costill DL.

The role of dietary carbohydrates (CHO) in the resynthesis of muscle and liver glycogen after prolonged, exhaustive exercise has been clearly demonstrated. The mechanisms responsible for optimal glycogen storage are linked to the activation of glycogen synthetase by depletion of glycogen and the subsequent intake of CHO. Although diets rich in CHO may increase the muscle glycogen stores and enhance endurance exercise performance when consumed in the days before the activity, they also increase the rate of CHO oxidation and the use of muscle glycogen. When consumed in the last hour before exercise, the insulin stimulated-uptake of glucose from blood often results in hypoglycemia, greater dependence on muscle glycogen, and an earlier onset of exhaustion than when no CHO is fed. Ingesting CHO during exercise appears to be of minimal value to performance except in events lasting 2 h or longer. The form of CHO (i.e., glucose, fructose, sucrose) ingested may produce different blood glucose and insulin responses, but the rate of muscle glycogen resynthesis is about the same regardless of the structure.

PMID: 3967778 [PubMed - indexed for MEDLINE]



WHOAH! Where's Draven?

 

[Dwight Schrute]

Here's one for us old folks? Whey could be better? Hmmm....

Type and timing of protein feeding to optimize anabolism.

Mosoni L, Mirand PP.

PURPOSE OF REVIEWThe delivery rate of amino acids to an organism significantly affects protein anabolism. The rate can be controlled by the type and the timing of feeding. Our aim was to bring new insights to the way they may act.RECENT FINDINGSDuring young and adult ages, when food supply is liberal, subjects can adapt to various modes of protein feeding. However, during food restriction, protein anabolism is favored when the delivery of amino acids is evenly distributed over the day, either with frequent meals, or through the use of slowly absorbed proteins like casein. In contrast, during aging, quickly absorbed protein sources become more efficient. During recovery after exercise, the timing of protein feeding after the end of exercise may or may not influence its anabolic effect, depending on the subject's age and the type of exercise.SUMMARYThe synchronization of variations in anabolic capability with amino acid supply partly explains the effects of the type and timing of protein feeding. This effect is modulated by the amount of amino acids required to increase whole-body proteins and by the signaling properties of some amino acids to stimulate protein synthesis. Indeed, the anabolic effect of amino acids is determined by their interaction with other anabolic factors (other nutrients or physiological factors, whose efficiency is mainly related to their effect on protein degradation). It is clear that benefits can be obtained from adapted protein feeding patterns.

PMID: 12690263 [PubMed - in process]

 

[bachovas]

Wow BOBO, slow down man.

 

[jweave23]

lmao, once he starts bro, he doesn't stop! This is Bobo's bread and butter right here. Great thread though, yet another reason to not utter the word malto..... whoops I almost said it

 

[Nelson]

Dietary strategies to promote glycogen synthesis after exercise.

Ivy JL.

Exercise Physiology and Metabolism Laboratory, Department of Kinesiology and Health Education, The University of Texas at Austin, Austin, TX, USA.

It has been observed that muscle glycogen synthesis is twice as rapid if carbohydrate is consumed immediately after exercise as opposed to waiting several hours, and that a rapid rate of synthesis can be maintained if carbohydrate is consumed on a regular basis. For example, supplementing at 30-min intervals at a rate of 1.2 to 1.5 g CHO x kg(-1) body wt x h(-1) appears to maximize synthesis for a period of 4- to 5-h post exercise. If a lighter carbohydrate supplement is desired, however, glycogen synthesis can be enhanced with the addition of protein and certain amino acids. Furthermore, the combination of carbohydrate and protein has the added benefit of stimulating amino acid transport, protein synthesis and muscle tissue repair. Research suggests that aerobic performance following recovery is related to the degree of muscle glycogen replenishment.

[/B][/QUOTE]

Good info Bobo & Bachovas.
I`m trying to figure out approximately how many carbs/protein to aim for using the low-GI method post/w.
In regards to a `lighter carbohydrate supplement` being consumed with protein & bcaa`s:
What amounts do you feel would be best to enhance glycogen synthesis in the meals/shakes following a workout, bearing in mind that it is better to supplement at 30 minute intervals?

 

[Dwight Schrute]

I know all these studies seem to make it more complicated but through trial and error I've found that around 30-50g pre workout of Oatmeal and 30-50g post workout has worked best for me. This is also dependent on weight, type of exercise, etc...So their really isn't just one answer. As for protein I usually do about 20-30g pre and at least 30 post. Once again its all dependent on your personal criteria...

 

[Nelson]

Thanks Bobo.
Some of the studies go over my head.

 

[Biggs]

phew, damn. this one really came on fast, nice stuff Bobo... so, from what I can gather here, and what you mean to say... is that gayners doan mak u b swole?!

 

[Nelson]

There`s so many studies for & against high-GI post-exercise.
Which study do you base your diet on?

Burke L. M., G. R. Collier, and M. Hargreaves. Muscle glycogen storage after prolonged exercise: effect of the glycemic index of carbohydrate feedings. Journal of Applied Physiology 75: 1019-1023, 1993.

abstract

The effect of the glycemic index (GI) of postexercise carbohydrate intake on muscle glycogen storage was investigated. Five well-trained cyclists undertook an exercise trial to deplete muscle glycogen (2 h at 75% of maximal O2 uptake followed by four 30-s sprints) on two occasions, 1 wk apart. For 24 h after each trial, subjects rested and consumed a diet composed exclusively of high-carbohydrate foods, with one trial providing foods with a high GI (HI GI) and the other providing foods with a low GI (LO GI). Total carbohydrate intake over the 24 h was 10 g/kg of body mass, evenly distributed between meals eaten 0, 4, 8, and 21 h postexercise. Blood samples were drawn before exercise, immediately after exercise, immediately before each meal, and 30, 60, and 90 min post-prandially. Muscle biopsies were taken from the vastus lateralis immediately after exercise and after 24 h. When the effects of the immediate postexercise meal were excluded, the totals of the incremental glucose and insulin areas after each meal were greater (P < or = 0.05) for the HI GI meals than for the LO GI meals. The increase in muscle glycogen content after 24 h of recovery was greater (P = 0.02) with the HI GI diet (106 +/- 11.7 mmol/kg wet wt) than with the LO GI diet (71.5 +/- 6.5 mmol/kg). The results suggest that the most rapid increase in muscle glycogen content during the first 24 h of recovery is achieved by consuming foods with a high GI.

 

[Lgoosey]

Not the low GI advocates

Regulation of glycogen resynthesis following exercise. Dietary considerations.

Friedman JE, Neufer PD, Dohm GL.

Department of Biochemistry, School of Medicine, East Carolina University, Greenville, North Carolina.

With the cessation of exercise, glycogen repletion begins to take place rapidly in skeletal muscle and can result in glycogen levels higher than those present before exercise. Understanding the rate-limiting steps that regulate glycogen synthesis will provide us with strategies to increase the resynthesis of glycogen during recovery from exercise, and thus improve performance. Given the importance of muscle glycogen to endurance performance, various factors which may optimise glycogen resynthesis rate and insure complete restoration have been of interest to both the scientist and athlete. The time required for complete muscle glycogen resynthesis after prolonged moderate intensity exercise is generally considered to be 24 hours provided approximately 500 to 700g of carbohydrate is ingested. Muscle glycogen synthesis rate is highest during the first 2 hours after exercise. Ingestion of 0.70g glucose/kg bodyweight every 2 hours appears to maximise glycogen resynthesis rate at approximately 5 to 6 mumol/g wet weight/h during the first 4 to 6 hours after exhaustive exercise. Further enhancement of glycogen resynthesis rate with ingestion of greater than 0.70g glucose/kg bodyweight appears to be limited by the constraints imposed by gastric emptying. Ingestion of glucose or sucrose results in similar muscle glycogen resynthesis rates while glycogen synthesis in liver is better served with the ingestion of fructose. Also, increases in muscle glycogen content during the first 4 to 6 hours after exercise are greater with ingestion of simple as compared with complex carbohydrate. lycogen synthase activity is a key component in the regulation of glycogen resynthesis. Glycogen synthase enzyme exists in 2 states: the less active, more phosphorylated (D) form which is under allosteric control of glucose-6-phosphate, and the more active, less phosphorylated (I) form which is independent of glucose-6-phosphate. There is generally an inverse relationship between glycogen content in muscle and the percentage synthase in the activated (I) form. Exercise and insulin by themselves activate glycogen synthase by conversion to glycogen synthase I. Although small changes in the activity ratio (% I form) can lead to large changes in the rate of glycogen synthesis, glycogen synthase I appears to increase very little (approximately 25%) in response to glycogen depletion and returns to pre-exercise levels as glycogen levels return to normal. Thus glycogen resynthesis, which may increase 3- to 5-fold, may also be influenced by glucose-6-phosphate, which can activate glycogen synthase in the D form.

 

[RaulJimenez]

I want to give some personal opinion based on glycogen resynthesis. I remember a while ago I argued with Bobo and we kinda swapped each other with abtracts and studies, but somehow he convinced me with his studies to try and add oatmeal, a complex carbohydrate with protein. After trying it out for 4 weeks now, I'm afraid to say it is really working, first of all my pumps last longer, my muscles are feeling replenished, I have more stamine after a workout, specially after legs day, and my gut hasn't increased due to the maltodextrin, I used to consume an ultra-fuel which is 100grams of maltodextrn post workout, gave me a gut even though it really replenished my muscle glycogen stores, not a good idea for bulking, if you guys haven't tried Bobo's recipe, give it a try im sure you won't regret it, i didn't.

 

[Jay Mc]

uh oh...bring on the GLUT4 supplements

J

 

[RaulJimenez]

hmm whatever that means jay!?

 

[Sheesh]

hmm whatever that means jay!?

He means that supplement companies are going to start exploiting this new study (the one bachovas posted) for their own profit....


Bachovas - nice find! Muchas gracias!

 

[RaulJimenez]

Thanks sheesh, had to read over the top again !!!

 

[Dwight Schrute]

Not the low GI advocates

Yeah, the low GI advocates.


Effect of different types of high carbohydrate diets on glycogen metabolism in liver and skeletal muscle of endurance-trained rats.

Garrido G, Guzman M, Odriozola JM.

Department of Human Performance, National Institute of Physical Education, Madrid, Spain.

Male Wistar rats were fed ad libitum four different diets containing fructose, sucrose, maltodextrins or starch as the source of carbohydrate (CH). One group was subjected to moderate physical training on a motor-driven treadmill for 10 weeks (trained rats). A second group received no training and acted as a control (sedentary rats). Glycogen metabolism was studied in the liver and skeletal muscle of these animals. In the sedentary rats, liver glycogen concentrations increased by 60%-90% with the administration of simple CH diets compared with complex CH diets, whereas skeletal muscle glycogen stores were not significantly affected by the diet. Physical training induced a marked decrease in the glycogen content in liver (20%-30% of the sedentary rats) and skeletal muscle (50%-80% of the sedentary rats) in animals fed simple (but not complex) CH diets. In liver this was accompanied by a two-fold increase of triacylglycerol concentrations. Compared with simple CH diets, complex CH feeding increased by 50%-150% glycogen synthase (GS) activity in liver, whereas only a slight increase in GS activity was observed in skeletal muscle. In all the animal groups, a direct relationship existed between tissue glucose 6-phosphate concentration and glycogen content (r = 0.9911 in liver, r = 0.7177 in skeletal muscle). In contrast, no relationship was evident between glycogen concentrations and either glycogen phosphorylase activity or adenosine 5'-monophosphate tissue concentration. The results from this study thus suggest that for trained rats diets containing complex CH (compared with diets containing simple CH) improve the glycogenic capacity of liver and skeletal muscle, thus enabling the adequate regeneration of glycogen stores in these two tissues.


Simple and complex carbohydrate-rich diets and muscle glycogen content of marathon runners.

Roberts KM, Noble EG, Hayden DB, Taylor AW.

Faculty of Physical Education, University of Western Ontario, London, Canada.

The effects of simple-carbohydrate (CHO)- and complex-CHO-rich diets on skeletal muscle glycogen content were compared. Twenty male marathon runners were divided into four equal groups with reference to dietary consumption: depletion/simple, depletion/complex, nondepletion/simple, and nondepletion/complex. Subjects consumed either a low-CHO (15% energy [E] intake), or a mixed diet (50% CHO) for 3 days, immediately followed by a high-CHO diet (70% E intake) predominant in either simple-CHO or in complex-CHO (85% of total CHO intake) for another 3 days. Skeletal muscle biopsies and venous blood samples were obtained one day prior to the start of the low-CHO diet or mixed diet (PRE), and then again one day after the completion of the high-CHO diet (POST). The samples were analysed for skeletal muscle glycogen, serum free fatty acids (FFA), insulin, and lactate and blood glucose. Skeletal muscle glycogen content increased significantly (p less than 0.05) only in the nondepletion/simple group. When groups were combined, according to the type of CHO ingested and/or utilization of a depletion diet, significant increases were observed in glycogen content. Serum FFA decreased significantly (p less than 0.05) for the nondepletion/complex group only, while serum insulin, blood glucose, and serum lactate were not altered. It is concluded that significant increases in skeletal muscle glycogen content can be achieved with a diet high in simple-CHO or complex-CHO, with or without initial consumption of a low-CHO diet.

PMID: 3342797 [PubMed - indexed for MEDLINE]

 

[Dwight Schrute]

Not the low GI advocates

Forgot this one.


Carbohydrate nutrition before, during, and after exercise.

Costill DL.

The role of dietary carbohydrates (CHO) in the resynthesis of muscle and liver glycogen after prolonged, exhaustive exercise has been clearly demonstrated. The mechanisms responsible for optimal glycogen storage are linked to the activation of glycogen synthetase by depletion of glycogen and the subsequent intake of CHO. Although diets rich in CHO may increase the muscle glycogen stores and enhance endurance exercise performance when consumed in the days before the activity, they also increase the rate of CHO oxidation and the use of muscle glycogen. When consumed in the last hour before exercise, the insulin stimulated-uptake of glucose from blood often results in hypoglycemia, greater dependence on muscle glycogen, and an earlier onset of exhaustion than when no CHO is fed. Ingesting CHO during exercise appears to be of minimal value to performance except in events lasting 2 h or longer. The form of CHO (i.e., glucose, fructose, sucrose) ingested may produce different blood glucose and insulin responses, but the rate of muscle glycogen resynthesis is about the same regardless of the structure.

 

[Dwight Schrute]

There`s so many studies for & against high-GI post-exercise.
Which study do you base your diet on?


Well then lets look at all the facts then.

1. Will muscle glycogen be replenished with either form of carbohydrate? Yes.

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.

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.


So after lookin at those points deduced from the studies above it seems both methods work. One method just has a bigger risk of creating a nice little tire around your waist

You guys judge for yourselves.

 

[Sheesh]

I'm with you Bobo....

 

[RaulJimenez]

Bump for BOBO, both shits work, but in our aesthethic purposes, I think LOW GI plus Protein is the most adequate for our bodies, my 2cents.

 

[jeepthang]

Great posts guys. I've always been on the dextrose/malto post-workout band wagon. I'll try oatmeal+whey post-workout for the next few months and let you know how things go.

Again, great posts.

 

[pinoy]

wouldn't oatmeal take too long to digest (fiber) for post workout? isn't it best to replenish muscles asap?

 

[Biggs]

wouldn't oatmeal take too long to digest (fiber) for post workout? isn't it best to replenish muscles asap?

been readin this shiot? take another look bro.

 

[Sheesh]

wouldn't oatmeal take too long to digest (fiber) for post workout? isn't it best to replenish muscles asap?

That's the whole point of this thread and these studies buddy. (No and no)

 

[Sheesh]

been readin this shiot? take another look bro.

beat me to it....

 

[pinoy]

k guys sorry

 

[Iron Warrior]

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

 

[Sheesh]

****, 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

 

[Dwight Schrute]

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.

 

[Dwight Schrute]

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 < 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.

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

 

[Dwight Schrute]

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.

 

[Dwight Schrute]

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.

 

[Dwight Schrute]

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.

1. Once you again you miss the point. GI relates to the response, not the total amount. THere is a reason for the new Insulin Index.

2. Yes it is anabolic but its not utilized during the first phase like it would during other times of the day. Whats the point of creating a huge spike if its not used for synthesis to begin with. Please re-read the thread if you still have problems understanding what I'm saying.

3. Once again you don't underatand. Now either your not reading the studies or just choosing not beleive them. Where does is say in any study the the amount of glycogen present increases the rate? It doesn't. If fact is says there is no difference at all. Do I have to cut and past the same statement a million times?

4. Oh so now it necessay but in smaller doses. Well then there goes your whole theroy of increase insuslin producing anabolic effects. You keep telling me things the supp cpmanies have said for year with no backup at all. You've posted one study talking about the AMOUNT of insulin, not the response. I suggest you re-read them for a better interpretation.

Sorry a HUGE spike in not anabolic. Please refer to these.
"Physiological hyperinsulinemia impairs insulin-stimulated glycogen synthase activity and glycogen synthesis."

"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."

"The form of CHO (i.e., glucose, fructose, sucrose) ingested may produce different blood glucose and insulin responses, but the rate of muscle glycogen resynthesis is about the same regardless of the structure."


Once again, its the amount of insulin produces, not how fast its produced. Now if you can counter these points with some sort of reference I would gladly continue. If not, I have other things I would like to work on. We seem to be going in a circle because you don't seem to be thinking about this from my side. I've done this from your side for years.

 

[hardasnails1973]

other supplement company is on same page

Nonsense. One hundred grams of sugar? If you want to do that, eat 5 or 6 Snickers Bars, as they taste the best. I don't buy this 100-g crap. You need slow burn or low glycemic carbs if your quest is maximum muscle gain, even after workouts. The window of opportunity does not mean window of stupidity. If you want to lose fat or build muscle and lose fat at the same time you'd be much advised to utilize a body process known as neoglucogenesis (the utilization of fats and / or proteins instead of carbs or glucose to replenish your glycogen stores.) Your body has the ability to convert fat into glycogen through this process. And if you are trying to burn fat, then this should be your whole goal, and the way to achieve it is by NOT consuming carbs (no more than 25 grams anyway) after your workout. On the flip side, if you ingest a big load of carbs (especially simple sugars) after your workout, any fat burning you stimulated from the workout will be stopped dead in its tracks. Naturally, we feel that the hydrolysates or predigested proteins and BCAA's that you find in Muscle Provider or Mass Aminos, work best. When you eat a large amount of sugary carbs, you release a large amount of insulin. Insulin does it's best to stabilize things by driving sugar, or glucose, into muscle cells (in the very best case scenario). The trouble is, like paper grocery store sacks filled to the breaking point with Twinkies, the muscle cells can only hold so much. Excesses of glucose are converted into fatty acids and triglycerides by the liver and fat tissue. The high insulin and glycogen concentrations induce the production and storage of fat. As if that weren't bad enough, insulin counteracts the effects of Human Growth Hormone (HGH). Although insulin is mildly anabolic (it probably should be called FAT-ABOLIC), HGH is significantly anabolic and promotes fat loss. Of the two, you'd much rather have high levels of HGH circulating through your blood.

 

[Lgoosey]

Alright I pissed now...Looks like the quaker guy might be gettin a boost in profit from my wallet

I just jumped into this argument not ready so i apologize for my scattered repsonses.

Looks like I'll have ot bring it to the home board and see what they say

(bold part in 1st study)

Muscle glycogen storage after prolonged exercise: effect of the glycemic index of carbohydrate feedings.

Burke LM, Collier GR, Hargreaves M.

Department of Sports Medicine, Australian Institute of Sport, Australian Capital Territory.

The effect of the glycemic index (GI) of postexercise carbohydrate intake on muscle glycogen storage was investigated. Five well-trained cyclists undertook an exercise trial to deplete muscle glycogen (2 h at 75% of maximal O2 uptake followed by four 30-s sprints) on two occasions, 1 wk apart. For 24 h after each trial, subjects rested and consumed a diet composed exclusively of high-carbohydrate foods, with one trial providing foods with a high GI (HI GI) and the other providing foods with a low GI (LO GI). Total carbohydrate intake over the 24 h was 10 g/kg of body mass, evenly distributed between meals eaten 0, 4, 8, and 21 h postexercise. Blood samples were drawn before exercise, immediately after exercise, immediately before each meal, and 30, 60, and 90 min post-prandially. Muscle biopsies were taken from the vastus lateralis immediately after exercise and after 24 h. When the effects of the immediate postexercise meal were excluded the totals of the incremental glucose and insulin areas after each meal were greater (P < or = 0.05) for the HI GI meals than for the LO GI meals. The increase in muscle glycogen content after 24 h of recovery was greater (P = 0.02) with the HI GI diet (106 +/- 11.7 mmol/kg wet wt) than with the LO GI diet (71.5 +/- 6.5 mmol/kg). The results suggest that the most rapid increase in muscle glycogen content during the first 24 h of recovery is achieved by consuming foods with a high GI

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

don't know if this was posted but is sure in interesting.


Role of insulin during exercise-induced glycogenesis in muscle: effect on cyclic AMP.

Ivy JL.

Skeletal muscle cyclic AMP (cAMP) content and glycogen synthesis were investigated in male rats subjected to exhaustive exercise, alloxan diabetes, and combinations of these conditions. After an exhaustive swim or control treatment of wading, randomly selected animals were administered 500 mg glucose via stomach tube. Two hours after glucose administration, gastrocnemius glycogen levels rose from 1.31 to 10.67 mg/g wet wt in fatigued nondiabetics (FND), producing a 94% supercompensation above control values. Glycogen of fatigued diabetics (FD) increased from 0.88 to 4.21 mg/g wet wt during the first 2 hr after glucose administration and did not reach control values for 24 h. In conjunction with these glycogen changes, cAMP increased from 1.23 to 2.59 and 1.47 to 2.81 pmol/mg wet wt for FND and FD, respectively (P less than 0.05). No difference in cAMP levels between diabetics and nondiabetics was found. These in vivo data suggest that insulin may not be essential for muscle glycogen synthesis, but that after glycogen depletion it plays a prominent role in supercompensation. Also, this hormone's mechanism of action in skeletal muscle does not appear to be mediated through alteration in the tissue cAMP concentration.
=============================================

Regulation of GLUT4 protein and glycogen synthase during muscle glycogen synthesis after exercise.

Ivy JL, Kuo CH.

Department of Kinesiology, The University of Texas at Austin, 78712, USA.

The pattern of muscle glycogen synthesis following its depletion by exercise is biphasic. Initially, there is a rapid, insulin independent increase in the muscle glycogen stores. This is then followed by a slower insulin dependent rate of synthesis. Contributing to the rapid phase of glycogen synthesis is an increase in muscle cell membrane permeability to glucose, which serves to increase the intracellular concentration of glucose-6-phosphate (G6P) and activate glycogen synthase. Stimulation of glucose transport by muscle contraction as well as insulin is largely mediated by translocation of the glucose transporter isoform GLUT4 from intracellular sites to the plasma membrane. Thus, the increase in membrane permeability to glucose following exercise most likely reflects an increase in GLUT4 protein associated with the plasma membrane. This insulin-like effect on muscle glucose transport induced by muscle contraction, however, reverses rapidly after exercise is stopped. As this direct effect on transport is lost, it is replaced by a marked increase in the sensitivity of muscle glucose transport and glycogen synthesis to insulin. Thus, the second phase of glycogen synthesis appears to be related to an increased muscle insulin sensitivity. Although the cellular modifications responsible for the increase in insulin sensitivity are unknown, it apparently helps maintain an increased number of GLUT4 transporters associated with the plasma membrane once the contraction-stimulated effect on translocation has reversed. It is also possible that an increase in GLUT4 protein expression plays a role during the insulin dependent phase.

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

 

[Nelson]

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.

That`s exactly what I`ve been doing since Bobo, Benz, RippedUp et al promoted the idea of low-GI post/W.
I get my spike with the dextrose, protein, creatine & amino`s, then I have some oatmeal & chicken 30 mins later to stabilise things.
It also means that I don`t have to waste that dextrose I`ve already bought.
When I finish the dextrose, I will just use oatmeal & become a Low-GI Jedi.

 

[Lgoosey]

I just started a thread on Avant:

I made a clear note and gave credit where credit is due.

I started a thread before but it did not take off as there was no advocates for low GI postworkout

Bobo along with any others wishing to debate: your imput will be greatly appreciated and respected.

It may take some time before anyone has the research to rebuttle but I hope it will turn out to be a good thread.

Please come even as spectators

i will be dissapointed in anyone who uses Low GI and does not voice their opinion.

*******Its in the "advanced theory and discussion" section******
>>>>>>>>>>>>>>>>DEBATE HERE<<<<<<<<<<<<<

 

[Dwight Schrute]

Alright I pissed now...Looks like the quaker guy might be gettin a boost in profit from my wallet

I just jumped into this argument not ready so i apologize for my scattered repsonses.

Looks like I'll have ot bring it to the home board and see what they say

(bold part in 1st study)


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

don't know if this was posted but is sure in interesting.


Role of insulin during exercise-induced glycogenesis in muscle: effect on cyclic AMP.

Ivy JL.

Skeletal muscle cyclic AMP (cAMP) content and glycogen synthesis were investigated in male rats subjected to exhaustive exercise, alloxan diabetes, and combinations of these conditions. After an exhaustive swim or control treatment of wading, randomly selected animals were administered 500 mg glucose via stomach tube. Two hours after glucose administration, gastrocnemius glycogen levels rose from 1.31 to 10.67 mg/g wet wt in fatigued nondiabetics (FND), producing a 94% supercompensation above control values. Glycogen of fatigued diabetics (FD) increased from 0.88 to 4.21 mg/g wet wt during the first 2 hr after glucose administration and did not reach control values for 24 h. In conjunction with these glycogen changes, cAMP increased from 1.23 to 2.59 and 1.47 to 2.81 pmol/mg wet wt for FND and FD, respectively (P less than 0.05). No difference in cAMP levels between diabetics and nondiabetics was found. These in vivo data suggest that insulin may not be essential for muscle glycogen synthesis, but that after glycogen depletion it plays a prominent role in supercompensation. Also, this hormone's mechanism of action in skeletal muscle does not appear to be mediated through alteration in the tissue cAMP concentration.
=============================================

Regulation of GLUT4 protein and glycogen synthase during muscle glycogen synthesis after exercise.

Ivy JL, Kuo CH.

Department of Kinesiology, The University of Texas at Austin, 78712, USA.

The pattern of muscle glycogen synthesis following its depletion by exercise is biphasic. Initially, there is a rapid, insulin independent increase in the muscle glycogen stores. This is then followed by a slower insulin dependent rate of synthesis. Contributing to the rapid phase of glycogen synthesis is an increase in muscle cell membrane permeability to glucose, which serves to increase the intracellular concentration of glucose-6-phosphate (G6P) and activate glycogen synthase. Stimulation of glucose transport by muscle contraction as well as insulin is largely mediated by translocation of the glucose transporter isoform GLUT4 from intracellular sites to the plasma membrane. Thus, the increase in membrane permeability to glucose following exercise most likely reflects an increase in GLUT4 protein associated with the plasma membrane. This insulin-like effect on muscle glucose transport induced by muscle contraction, however, reverses rapidly after exercise is stopped. As this direct effect on transport is lost, it is replaced by a marked increase in the sensitivity of muscle glucose transport and glycogen synthesis to insulin. Thus, the second phase of glycogen synthesis appears to be related to an increased muscle insulin sensitivity. Although the cellular modifications responsible for the increase in insulin sensitivity are unknown, it apparently helps maintain an increased number of GLUT4 transporters associated with the plasma membrane once the contraction-stimulated effect on translocation has reversed. It is also possible that an increase in GLUT4 protein expression plays a role during the insulin dependent phase.

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

1. The bold part still concentrates on glycogen storage, not the rate at which synthesis occurs. Nobdy arguing that storage is increased with high GI. Its also been proven to do the same thing with a light carbs w/ the addition of protein and/or aminos.

2. The second study is the same I posted in the beginning of the thread that stated the glycogen storage is insulin independent.


No beef here bro...We're all here to learn new things. Where would we be if we didn't question what the supp companies tell us. The evidence points in the direction that such a large spike just isn't necessary. You still get one with a lower GI, just not as drastic. The total amounts will still be the same. This also works extremely well in older men with the natural insulin resistance we will all encounter later in life. I'm 30 myself and it works very well. Other's my age or older have experienced the same results.

 

[Dwight Schrute]

I just started a thread on Avant:

I made a clear note and gave credit where credit is due.

I started a thread before but it did not take off as there was no advocates for low GI postworkout

Bobo along with any others wishing to debate: your imput will be greatly appreciated and respected.

It may take some time before anyone has the research to rebuttle but I hope it will turn out to be a good thread.

Please come even as spectators

i will be dissapointed in anyone who uses Low GI and does not voice their opinion.

*******Its in the "advanced theory and discussion" section******
>>>>>>>>>>>>>>>>DEBATE HERE<<<<<<<<<<<<<

Hopefully you'll post our link over there. I've done this debate so many times sometimes it just gets tiring. If someone brings in something new I will certainly participate. Most of arguement are on several threads but the most recent research is posted in this one.