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

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    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
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    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.
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    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.
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    Originally posted by 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 &quot;window&quot;.

    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.
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    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.
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    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.

    ============================== ==============
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    Originally posted by Draven
    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.
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    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******
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    Originally posted by 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)


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

    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.
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    Originally posted by 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 &quot;advanced theory and discussion&quot; section******
    &gt;&gt;&gt;&gt;&gt;&gt;&gt;&g t;&gt;&gt;&gt;&gt;&gt;&gt;&gt; &gt;DEBATE HERE&lt;&lt;&lt;&lt;&lt;&lt;&lt;&l t;&lt;&lt;&lt;&lt;&lt;
    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.
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    link is up to this thread

    All I ask is that you reply if there is a sound argument although it may take time to read over and research any thoughts
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    Originally posted by Bobo




    This also works extremely well in older men... I'm 30 myself and it works very well.
    ... old fart



    I still think this is sticky material.
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    [QUOTE]Originally posted by Bobo
    [B]
    Originally posted by Nelson
    There`s so many studies for &amp;amp; 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.
    mr bobo, high gi carbs dont make a tire around your waist post-workout because the carbs will be stored in muscles not as fat,
    i havent heard of anyone constantly eating high gi carbs for hours after a workout, wich is the only way high gi carbs could cause a spare tire. compared to the same calorie intake to a low gi pw meal.

    imho the best post-workout nutrition is a high g.i./protein shake, followed by a low gi and protein meal, show me a study that shows this instead of all these studies of just low gi or just high gi pw meals, based on cardio workouts and rats.

    frankly, cardio and rats have nothing to do with my weight training.
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    Originally posted by BIGnaturalBROCK


    imho the best post-workout nutrition is a high g.i./protein shake, followed by a low gi and protein meal, show me a study that shows this instead of all these studies of just low gi or just high gi pw meals, based on cardio workouts and rats.

    frankly, cardio and rats have nothing to do with my weight training.
    Shouldn't it be your job to show a study advocating High GI carbs? Bobo has taken a stance on Low-GI carbs, and quite frankly, has proved it quite well, backing it up with studies and the reasoning to follow it. IF you are advocating High-GI carbs, it would be your job to show proof of why it is better, no?
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    Originally posted by jdhar


    Shouldn't it be your job to show a study advocating High GI carbs? Bobo has taken a stance on Low-GI carbs, and quite frankly, has proved it quite well, backing it up with studies and the reasoning to follow it. IF you are advocating High-GI carbs, it would be your job to show proof of why it is better, no?
    it would, i dont see the problem with me asking for a more in-depth study tho
    cheers
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    Originally posted by BIGnaturalBROCK


    mr bobo, high gi carbs dont make a tire around your waist post-workout because the carbs will be stored in muscles not as fat,
    i havent heard of anyone constantly eating high gi carbs for hours after a workout, wich is the only way high gi carbs could cause a spare tire. compared to the same calorie intake to a low gi pw meal.

    imho the best post-workout nutrition is a high g.i./protein shake, followed by a low gi and protein meal, show me a study that shows this instead of all these studies of just low gi or just high gi pw meals, based on cardio workouts and rats.

    frankly, cardio and rats have nothing to do with my weight training.
    [list=1][*]welcome to AM. [*]we do things differently here at AM. We ask people to do more than give unsubstantiated opinion[/list=1]

    ~Todd
    Last edited by tatortodd; 10-15-2003 at 11:57 PM.
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    OK here's some unsubstantiated opinion, sprinkled with some logic.

    1. Low-GI vs High-GI immediately postworkout. Bobo is *RIGHT* Anyone who argues, reread the thread, proof is there.

    BUT

    2. Bobo's point is about GLYCOGEN resynthesis RATE ... and in a secondary manner, AMOUNT.

    WHAT ABOUT

    3. Muscle protein resynthesis.
    4. Muscle GROWTH which is slightly different from point 3.

    This is not adressed in these studies. What I have found is that :

    Paracrine IGF-1 is a very potent generator of muscle satellite cells. These are the cells that fuse with the muscle cell, which increase the myonuclear number (number of nuclei in the myocite) which is responsible for the muscle cell size, as the "myonuclear domain" is pretty constant. Myonuclear domain is how much volume per nucleus a muscle cell has. Exocrine IGF-1 which some people will say "it doesn't grow your muscles, it just makes satellite cells" is had by having insulin while there is GH in the system. GH decreases rapidly after exercise.

    If you don't make satellite cells, your muscles will not grow in SIZE. The fusing part comes from exercise stimulation and testosterone. For strength gains all you need is more contractile protein, which does not require so much fusing of satellite cells, but protein resythesis.

    I thought this was really well known? Shall I start another thread and post studies?

    [EDIT: Er... What I'm saying here is that having a large insulin spike immediately postworkout will not do a thing for muscle glycogen resynthesis but will maximize sattelite cell manufacture, which is an important bottleneck in muscle SIZE. There.]
    Last edited by LunaHotel; 10-20-2003 at 08:08 PM.
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    I think this is definitely relevant to the thread, and would love to see some studies as it is the first I have read along these lines.
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    Gee, there's only one person interested. I guess it's stuff everyone knows. Whatever, I'm writing an article that includes that topic, I'mma have it ready around november 1st.

    I'll post it in another thread though, just in case there happens to be some sort of interest in it.
  

  
 

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