cranberry juice PW - AnabolicMinds.com

cranberry juice PW

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    cranberry juice PW


    Just wondering if gulping down a cup of cranberry juice PW is a good idea. Not sure the nature of the carbs (low / high GI) but, regardless, wouldn't this be a good idea for a PW insulin spike? You would also get the added benefit of liver/kidney health.
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    Quote Originally Posted by canadian champ
    Just wondering if gulping down a cup of cranberry juice PW is a good idea. Not sure the nature of the carbs (low / high GI) but, regardless, wouldn't this be a good idea for a PW insulin spike? You would also get the added benefit of liver/kidney health.
    cc
    i dont think so - since it is fructose - but i could be wrong - if you want to go high GI route, use dextrose or malto. low GI - well - use a low gi carb like oatmeal or blend up a yam and some protein powder.
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    yeah fructose will, according to most studies, replenish liver glycogen levels as opposed to muscle glycogen. Not bad necessarily, just not optimal.
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    Go w/dextrose if you want the most ideal pwo substance on earth.

    ~SC~
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    Ugh...

    I would opt for a lower GI source.
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    Why? What's the reasoning?

    To purposely have something that is very slow digesting when it's most optimal to ingest something that is very easily digestible immediately?

    I'd say you can include a low gi carb/lean protein as the SECOND meal post-workout, but not right after. Waiting around for absorption is almost like not eating at all in regards to your body and it waiting for the quick uptake of nutrients.

    Again, we all have our methods, and success with each one. So, just curious that's all.

    ~SC~
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    Because glyocgen depletion and catabolism is highly overated post exercise. The hormonal respons to exercise in itself in anti-catabolic in nature. This is also the time when nutrient signaling is at its highest so the need for such a drastic insulin spike is not necessary. There has been no study confirming that the faster you restore glyogen stores the faster protein synthesis occurs. In fact protein synthesis is at its highest 24 hours after exercise. If proper nutrition is followed the need for a large amount of fast acting glucose is not warranted. There is also the the fact the glyocgen synthesis is biphasic and the frist stage (30 minutes post exercise) is insulin indpendent. This stage is more reliable on available amino acids as a substate rather than glucose. Exercise in itself increases glut4 permeability so the increased amounts of insulin are not needed to achieve this to improve trnasport. This is just some of the reasons I recommend a slower more stable release of insulin that will coincided wiht the second phase of glycogen resynthesis. Thjere is also the the reaosn of increased glucose storage due to a high insulin spike. Studies show that not all glucsoe in absorbed by the exercised muscle and there is increase chances of this being utilized by other tissues, adipose tissue being one of them
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    Only if one doesn't know how much dextrose to utilize pwo, would this be problem. As well, you can utilize R-ALA, V.S., etc. to help in this post-workout timeframe. I've tried both on myself and others, and there is no comparison as far as I am concerned. Studies are just that, studies, but I've always been one for REAL world application. So far I've yet to fail. Studies usually don't take real world application into account, and are controlled, negating much of what is practical.

    Thanks for the opinion! Nice to hear sides to everything w/out any flame wars.

    ~SC~
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    How much dextrose do you recommend PWO?
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    I practice what I preach and it has worked on me along with numerous others that have followed the High GI hype marketing by most supplement companies and switched to this style. The benefit? Same LBM gains with less fat in all phases and this has been reported over and over again. Plus I don't agree one needs R-ALA or glucose dispersal agents if someone has normal insulin sensitivity. Glut4 recpetors are already increased drastically post exercise so the need to increase them more is pointless IMO. It would just increase glut4 receptors in fat cells even more so.

    Just because you have yet to fail doens't mean their isn't room for improvement. Plus what would you fail at anyway?
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    Quote Originally Posted by SwoleCat
    Studies usually don't take real world application into account, and are controlled, negating much of what is practical.


    ~SC~
    Studies support basic physiology and are conducted in the real world. What I stated before is basic physiology. I don't undertand why people insist studies are done in a fantasy setting.

    Plus I don't understand how a study on resistant trained athletes in a controlled setting negates what is practical. That doesn't make sense.
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    Quote Originally Posted by SwoleCat
    Only if one doesn't know how much dextrose to utilize pwo, would this be problem.

    ~SC~
    Its not the amount ingested, its the amount that is circulating. Since there is only around 4-6g of circulting glucose present in the bloodstream at one time taking in a large amount of fast absorbing glucose just increases the chance of LPL storing excess fuel (circulating TGL's) into adipose tissue. Increase glucose = increased insulin = increase lipoprotein lipase = greater chance of adipose storage. Why take the chance when its not needed. Glyocogen synthesis is the same at a 24 hours peroid whether its a high GI or Low GI carb.
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    4-6 grams circulating at one time? U know this to be true w/everyone? Just as everyone has the same insulin sensitivity? Rhetorical questions........

    Been reported over and over again.....where? To you maybe by those you know or work with, but we don't know their diet/habits/sensitivity to slin, etc. Those do play a factor.

    PWO you have an increased uptake, so you can ingest more carbs, whatever the like, and have them be utilized in glucose replacement not fat storage. Lower gi's circulating over a longer period would have more of a chance to get stored, as if you eat too many and they are not shuttled into muscle cells or burned for energy, guess where they go? U can always say that " there wouldn't be excess, you ingest the correct amount" and then you go back to what I said about the right amount of dextrose.

    All good man, like I said you have your beliefs/ways and I have mine. The key is to do what works for you, or for those you assist.



    Cheers!

    ~SC~
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    Quote Originally Posted by Bobo

    Plus I don't understand how a study on resistant trained athletes in a controlled setting negates what is practical. That doesn't make sense.
    Because they study ONE aspect, the one we are discussing, and don't take into account any other types of diet/exercise/insulin sensitivity that can change the meaning of the first aspect. I.E., there are other factors that can have an impact on the result(s) of a study, yet those factors are not addressed when the study is carried out. We don't have any actual studies to look at to see what was taken into account, nor were we there, so we simply don't know what the actions were the other times aside from testing.

    "Studies" can be said all day, fact is there are studies all over earth for both sides of the "argument", but what does that solve? Nothing really....because the fact is both of those studies (the summary of those studies) will work for different kinds of people! Each has to find what works for him/herself. I've found that in what I design, dextrose is far more ideal, but what I have myself and others doing the other 23 hours of the day will be different than others utilizing other forms of pwo materials, so therein lies a reason why some things might not work for others. It's all a part of one's "bigger plan" and cannot be looked @ just pwo.

    What's nice is that you have a method that works for yourself, and I have a method I found works great for myself. You can see below that my method works for me.......

    Hope that's clear.

    ~SC~
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    Quote Originally Posted by SwoleCat
    4-6 grams circulating at one time? U know this to be true w/everyone? Just as everyone has the same insulin sensitivity? Rhetorical questions........

    Been reported over and over again.....where? To you maybe by those you know or work with, but we don't know their diet/habits/sensitivity to slin, etc. Those do play a factor.

    PWO you have an increased uptake, so you can ingest more carbs, whatever the like, and have them be utilized in glucose replacement not fat storage. Lower gi's circulating over a longer period would have more of a chance to get stored, as if you eat too many and they are not shuttled into muscle cells or burned for energy, guess where they go? U can always say that " there wouldn't be excess, you ingest the correct amount" and then you go back to what I said about the right amount of dextrose.

    All good man, like I said you have your beliefs/ways and I have mine. The key is to do what works for you, or for those you assist.



    Cheers!

    ~SC~
    1. Yes it the same for everyone thats why its varying (4-6). Once you hit below that threshold is when metabolic changes occur (hypoclycemia, ketosis, etc..). There is a reaosn glucose tabs are 5g. This can be verified in any physiology book.

    2. Been reported here and on bb.com and on several other boards. Its effects are greater in people over 25 since this is the general area in which natural insulin resistance starts to play a role. So you might try this in your older cleints as the effect might be positive.

    3. Thats just not true at all. Nutrient uptake is increased but there is a threshold that can be easily passed. Like I already said insulin usually serves a purpose of increasing permeability in glut4 recpetors helping increase nutrient uptake during normal feeding patterns. This already occurs just from resistance training alone so the need for such a dratic spike in a short amount of time is not needed and the studies done on ahtletes reveal that insulin does not react in the same fashion post exercise.(1) Lower GI never has an increased chance of being stored over High GI because of fuel availability. Its also does not effect LPL levels like a high insulin spike would. Basically the lower the LPL the less chance of adipose storage and this is always the case when you compare low to high GI. This is basic physiology.


    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.
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    Quote Originally Posted by SwoleCat
    Because they study ONE aspect, the one we are discussing, and don't take into account any other types of diet/exercise/insulin sensitivity that can change the meaning of the first aspect. I.E., there are other factors that can have an impact on the result(s) of a study, yet those factors are not addressed when the study is carried out. We don't have any actual studies to look at to see what was taken into account, nor were we there, so we simply don't know what the actions were the other times aside from testing.

    "Studies" can be said all day, fact is there are studies all over earth for both sides of the "argument", but what does that solve? Nothing really....because the fact is both of those studies (the summary of those studies) will work for different kinds of people! Each has to find what works for him/herself. I've found that in what I design, dextrose is far more ideal, but what I have myself and others doing the other 23 hours of the day will be different than others utilizing other forms of pwo materials, so therein lies a reason why some things might not work for others. It's all a part of one's "bigger plan" and cannot be looked @ just pwo.

    What's nice is that you have a method that works for yourself, and I have a method I found works great for myself. You can see below that my method works for me.......

    Hope that's clear.

    ~SC~
    No they don't study one aspect. They study glucose and aminos uptake, synthesis rates for both glyocgen and protein and a host other effects. The list goes on and on depending on what study you use. These are in resistance trained athletes. The exercise is the same. The diet is the only factor that could be different and in that case would only help my arguement. A proper diet minimizes catabolic activity so the need to create such drastic spikes is even more uneccesary. Insulin resistance is also another key area that would favor my approach. When you take all factors into account the need for a drastic spike is uneccesary. THe ONLY reason you would dop this if you had glyocgen dpendent activity (lets say football practice) after a weight training session would glyocgen stores be restored fast. Other than that there is no activity which requires a fast replenishment of glyocogen stores for a BB'er.

    And we still are forgetting that glycogen synthesis is insulin INDEPENDENT post exercise for up to 30 minutes. Why would ingest fast acting carbohydrates when glyocgen resythesis is insulin independent anyway? It doesn't make sense at all.


    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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    Thanks for the response to the pm, I just hit ya back.

    What do you think about dextrose for those w/normal insulin responses who do not store fat easily, even w/the 30 minute non-slin dependent window after exercise?

    (I already know we have two diff methods of replinishing muscle glycogen as whole, lol)

    Thanks,
    ~SC~
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    Hit ya right back


    Well I think it does depend on the individual. When I was younger I could eat just about anything and wouldn't gain a lb of fat anywhere. The benefits of a fast metabolism So my recommendations are certainly not for everyone as some get easily get away with the dextrose option but I thnk the sooner one learns to choose the right foods and whats most beneficial for overall health, the better off they will be down the line when age starts to creep in the equation.

    Its an ugly scene when you eat just about anything for most of of your life and stay lean yet as 25 you look down and a little pouch is starting to form. Confusion sets in.....

    Although adding quality muscle tends to be easier....
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    Yeah, I hear that 100%!

    ~SC~
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    Good stuff Bobo, I haven't really looked at it that way. When I first started...and after reading about the window of opportunity, greater uptake of nutrietns and aminos, it was just set in stone in my head...jack the Dextrose and the Whey postworkout. I think the best part about what you wrote was the over rated factor of glycogen deprivation post workout. Baring cardiovascular activity, I doubt that I am depleted which makes you question adding a bunch of sugar after a workout
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    I found this in researching more of this issue, and it supports dextrose/malto/etc. pwo and gives reasoning as well. Just curious of what you think Bobo, or anyone else for that matter.

    Q: What are the properties of glycogen? And why are these properties so vital post workout?

    A: Glycogen is a polysaccharide, (C6H10O5)n that is the main form of carbohydrate storage in animals and humans and occurs primarily in the liver and muscle tissue. It is readily converted to glucose as needed by the body to satisfy its energy needs (21), such as during intense training.

    To enhance the progress of muscular strength and size with heavy-resistance body building programs, optimal conditions for recovery from training sessions are imperative, primarily glycogen re-synthesis (22).

    Recovery occupies the coordinated operation of multiple physiological processes that are heavily influenced by the accessibility and actions of exclusive hormones and nutrients (16, 17).

    Both qualitative and quantitative modifications in skeletal muscle contractile proteins are all supported and signaled by a horde of systematic -trophic influences from hormones to nutrient availability (18, 19).

    Markedly, concentric and eccentric contractions disrupt or damage certain muscle fibers that must undertake a remodeling restoration process. Dietary nutrients, hormones, and growth factors interact to regulate this remodeling of skeletal muscle proteins (5).

    One primal factor associated with muscular fatigue is depletion of muscle glycogen (1).

    These stores must be replaced rapidly during the post-workout initial recovery phase in order for performance to be reproducible in a subsequent exercise bout(s).

    Glycogen synthesis may be restricted by blood glucose concentration, glucose transport, and the activity of the enzymes involved in the pathway, particularly glycogen synthase (10).

    Body building training programs provide conditions within skeletal muscle to support the rapid synthesis of glycogen.

    Glycogen synthase action is inversely relative to glycogen intensity (23); as a result of the glycogen-depleted state post-training, skeletal muscle (24) and hepatic glycogen synthase activity are raised (13).

    Basal glucose transport within skeletal muscle occurs via GLUT-4 (A powerhouse effect of insulin is the stimulation of glucose transport via the translocation of the insulin responsive glucose transporter, GLUT4, to the plasma membrane) (14).

    Nevertheless, the ability of skeletal muscle to take up glucose is relative, due to adjustments in the GLUT-4 content of the sarcolemal membrane.

    Image 1. Atrophic muscle fibers. The sarcolemal membranes of these two atrophic fibers have a wavy appearance. Courtesy: Department of Pathology; Virginia Commonwealth University;

    There are hypothesized to be one or more intracellular pools of GLUT-4 proteins, which are translocated to the sarcolema in response to both increased insulin concentration (20) and prior exercise (9); these effects are additive (6).









    In the post-workout period, therefore, muscle membrane permeability to glucose is high, thus favoring the accretion of glycogen replacement. However, if rapid carbohydrate distribution is not provided during recovery, glycogen synthesis will be limited because the rate of endogenous glucose production from gluconeogenic precursors such as alanine and glycerol is inadequate to support maximal rates of glycogen synthesis (15).

    The ingestion of high GI carbohydrates increases glycogen synthesis in two ways.

    The first (12) is increased substrate availability through the increased blood glucose concentration, which results in an increased glucose uptake due to mass action.

    Moreover, the resultant increase in systemic insulin concentration stimulates the translocation of GLUT-4 transporters from an intracellular pool to the sarcolemal membrane (7).

    The hormone insulin is also a powerful activator of glycogen synthase and inhibitor of glycogen phosphorylase (2).

    The effectiveness of a specific carbohydrate in encouraging resynthesis of the carbohydrate stores is reliant on the insulin and glucose response to the carbohydrate load (4).

    This is directly linked to gastric emptying and intestinal absorption rates. It is also associated with the insulinogenic potential of the carbohydrate, as indicated by the glycemic index (GI) of a carbohydrate.

    The development of glycogen synthesis relies upon the accessibility of glycogenic substrate (8) and the activity of the enzymes implicated in glycogen synthesis. These include hexokinase and glycogen synthase.

    Prior exercise enhances skeletal muscle glucose transport (3) because of the translocation of GLUT-4 transporters from an intracellular pool to the sarcolemal membrane.
    The inclination for skeletal muscle to extort blood glucose will thus be increased, and the glucose will tend to be directed toward glycogen synthesis because glycogen synthase is activated during recovery due to the low intramuscular glycogen concentration (23).
    These conditions favoring the resynthesis of glycogen can be exploited (8) by the provision of a quality carbohydrate source.
    The consequential amplification in glucose availability and the insulin response to the glucose load would tend to stimulate (7) a further increase in the GLUT-4 content of the sarcolemal membrane.
    Research has demonstrated (11) that there is a direct correlation between the rate of glycogen storage during recovery and total muscle GLUT-4 protein content.
    On a side note, observational and empirical evidence makes it plainly obvious that the endocrinal state of the body builder post-workout is nothing like that of a sedentary individual.
    A red herring argument is an attempt to offer evidence to support one proposition by arguing for a different one entirely, or dodging the main argument by going off on a tangent.
    Oftentimes opponents of high GI carbohydrate supplementation post-workout will point to the dangers of excess insulin-spiking and glucose intake; however, this is a red herring argument. This claim is like comparing apples to oranges.

    ~SC~
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    Quote Originally Posted by SwoleCat
    I found this in researching more of this issue, and it supports dextrose/malto/etc. pwo and gives reasoning as well. Just curious of what you think Bobo, or anyone else for that matter.

    Q: What are the properties of glycogen? And why are these properties so vital post workout?

    A: Glycogen is a polysaccharide, (C6H10O5)n that is the main form of carbohydrate storage in animals and humans and occurs primarily in the liver and muscle tissue. It is readily converted to glucose as needed by the body to satisfy its energy needs (21), such as during intense training.

    To enhance the progress of muscular strength and size with heavy-resistance body building programs, optimal conditions for recovery from training sessions are imperative, primarily glycogen re-synthesis (22).

    Recovery occupies the coordinated operation of multiple physiological processes that are heavily influenced by the accessibility and actions of exclusive hormones and nutrients (16, 17).

    Both qualitative and quantitative modifications in skeletal muscle contractile proteins are all supported and signaled by a horde of systematic -trophic influences from hormones to nutrient availability (18, 19).

    Markedly, concentric and eccentric contractions disrupt or damage certain muscle fibers that must undertake a remodeling restoration process. Dietary nutrients, hormones, and growth factors interact to regulate this remodeling of skeletal muscle proteins (5).

    One primal factor associated with muscular fatigue is depletion of muscle glycogen (1).

    These stores must be replaced rapidly during the post-workout initial recovery phase in order for performance to be reproducible in a subsequent exercise bout(s).

    Glycogen synthesis may be restricted by blood glucose concentration, glucose transport, and the activity of the enzymes involved in the pathway, particularly glycogen synthase (10).

    Body building training programs provide conditions within skeletal muscle to support the rapid synthesis of glycogen.

    Glycogen synthase action is inversely relative to glycogen intensity (23); as a result of the glycogen-depleted state post-training, skeletal muscle (24) and hepatic glycogen synthase activity are raised (13).

    Basal glucose transport within skeletal muscle occurs via GLUT-4 (A powerhouse effect of insulin is the stimulation of glucose transport via the translocation of the insulin responsive glucose transporter, GLUT4, to the plasma membrane) (14).

    Nevertheless, the ability of skeletal muscle to take up glucose is relative, due to adjustments in the GLUT-4 content of the sarcolemal membrane.

    Image 1. Atrophic muscle fibers. The sarcolemal membranes of these two atrophic fibers have a wavy appearance. Courtesy: Department of Pathology; Virginia Commonwealth University;

    There are hypothesized to be one or more intracellular pools of GLUT-4 proteins, which are translocated to the sarcolema in response to both increased insulin concentration (20) and prior exercise (9); these effects are additive (6).









    In the post-workout period, therefore, muscle membrane permeability to glucose is high, thus favoring the accretion of glycogen replacement. However, if rapid carbohydrate distribution is not provided during recovery, glycogen synthesis will be limited because the rate of endogenous glucose production from gluconeogenic precursors such as alanine and glycerol is inadequate to support maximal rates of glycogen synthesis (15).

    The ingestion of high GI carbohydrates increases glycogen synthesis in two ways.

    The first (12) is increased substrate availability through the increased blood glucose concentration, which results in an increased glucose uptake due to mass action.

    Moreover, the resultant increase in systemic insulin concentration stimulates the translocation of GLUT-4 transporters from an intracellular pool to the sarcolemal membrane (7).

    The hormone insulin is also a powerful activator of glycogen synthase and inhibitor of glycogen phosphorylase (2).

    The effectiveness of a specific carbohydrate in encouraging resynthesis of the carbohydrate stores is reliant on the insulin and glucose response to the carbohydrate load (4).

    This is directly linked to gastric emptying and intestinal absorption rates. It is also associated with the insulinogenic potential of the carbohydrate, as indicated by the glycemic index (GI) of a carbohydrate.

    The development of glycogen synthesis relies upon the accessibility of glycogenic substrate (8) and the activity of the enzymes implicated in glycogen synthesis. These include hexokinase and glycogen synthase.

    Prior exercise enhances skeletal muscle glucose transport (3) because of the translocation of GLUT-4 transporters from an intracellular pool to the sarcolemal membrane.
    The inclination for skeletal muscle to extort blood glucose will thus be increased, and the glucose will tend to be directed toward glycogen synthesis because glycogen synthase is activated during recovery due to the low intramuscular glycogen concentration (23).
    These conditions favoring the resynthesis of glycogen can be exploited (8) by the provision of a quality carbohydrate source.
    The consequential amplification in glucose availability and the insulin response to the glucose load would tend to stimulate (7) a further increase in the GLUT-4 content of the sarcolemal membrane.
    Research has demonstrated (11) that there is a direct correlation between the rate of glycogen storage during recovery and total muscle GLUT-4 protein content.
    On a side note, observational and empirical evidence makes it plainly obvious that the endocrinal state of the body builder post-workout is nothing like that of a sedentary individual.
    A red herring argument is an attempt to offer evidence to support one proposition by arguing for a different one entirely, or dodging the main argument by going off on a tangent.
    Oftentimes opponents of high GI carbohydrate supplementation post-workout will point to the dangers of excess insulin-spiking and glucose intake; however, this is a red herring argument. This claim is like comparing apples to oranges.

    ~SC~

    Not a bad article but way too many generalizations and speculations just not based on accurate interpretations of available studies.

    1. Glyocgen resynthesis has nothing to do with how fast glucose is made readily availalble. Big misconception. IT occurs at the saem rate regardless of CHO.

    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.

    2. Insulin does increase Glut4 permeability but exercise in itself does this quite efficiently. Also the role of insulin in increasing Glut4 receptors during post exercise does not react in the same fashion as it would in normal feeding patterns. Muscle contraction in itself producing the initla increase in Glut 4 permeability followed by an insulin dependent phase.

    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


    3. THis statement is completey wrong. All of the follwing studies contradict this. This is what WAS thought but has recently been proven false.

    "The effectiveness of a specific carbohydrate in encouraging resynthesis of the carbohydrate stores is reliant on the insulin and glucose response to the carbohydrate load (4)"


    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.


    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.

    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.


    Type and timing of protein feeding to optimize anabolism.
    Mosoni L, Mirand PP.


    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.

    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.






    4. Another completely false statement:


    "The development of glycogen synthesis relies upon the accessibility of glycogenic substrate (8) and the activity of the enzymes implicated in glycogen synthesis"


    Amino's are the substrate, not glucose. It is also the nutrient signal for ptein synthesis after exercise.

    Amino acids stimulate translation initiation and protein synthesis through an Akt-independent pathway in human skeletal muscle.

    Liu Z, Jahn LA, Wei L, Long W, Barrett EJ.

    Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908, USA. zl3e@virginia.edu

    Studies in vitro as well as in vivo in rodents have suggested that amino acids (AA) not only serve as substrates for protein synthesis, but also as nutrient signals to enhance mRNA translation and protein synthesis in skeletal muscle. However, the physiological relevance of these findings to normal humans is uncertain. To examine whether AA regulate the protein synthetic apparatus in human skeletal muscle, we infused an AA mixture (10% Travesol) systemically into 10 young healthy male volunteers for 6 h. Forearm muscle protein synthesis and degradation (phenylalanine tracer method) and the phosphorylation of protein kinase B (or Akt), eukaryotic initiation factor 4E-binding protein 1, and ribosomal protein S6 kinase (p70(S6K)) in vastus lateralis muscle were measured before and after AA infusion. We also examined whether AA affect urinary nitrogen excretion and whole body protein turnover. Postabsorptively all subjects had negative forearm phenylalanine balances. AA infusion significantly improved the net phenylalanine balance at both 3 h (P < 0.002) and 6 h (P < 0.02). This improvement in phenylalanine balance was solely from increased protein synthesis (P = 0.02 at 3 h and P < 0.003 at 6 h), as protein degradation was not changed. AA also significantly decreased whole body phenylalanine flux (P < 0.004). AA did not activate Akt phosphorylation at Ser(473), but significantly increased the phosphorylation of both eukaryotic initiation factor 4E-binding protein 1 (P < 0.04) and p70(S6K) (P < 0.001). We conclude that AA act directly as nutrient signals to stimulate protein synthesis through Akt-independent activation of the protein synthetic apparatus in human skeletal muscle.



    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 (&gt;/=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 (&lt;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 (&gt;1 g/min) of glucose are ingested following exercise.


    5. Here is another one not based on the lit.

    "Oftentimes opponents of high GI carbohydrate supplementation post-workout will point to the dangers of excess insulin-spiking and glucose intake; however, this is a red herring argument. This claim is like comparing apples to oranges."

    Well it might be apples to oranges to him but not according to the lit.

    "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.





    6. THis statement is true to an extent but glycogen stores are not that depleted.

    "One primal factor associated with muscular fatigue is depletion of muscle glycogen (1)."

    Thats something seem more in a ketogenic state to where the purpose is to depletd glycogen stores. This takes usually around 48 hours to accomplish, not a an hour workout with resistance training. Highly exaggerated.


    7. The basis for his theory is the presumption that hyperinsulinemia increases glycogen and protein synthesis. His findings are based on in vitro studies and for some reason everyone likes to quote these studies withouth knowing the complete difference in effets amino's and/or peptides have when given in vitro compared to a natural physiological response. This study is a clear explample.

    Physiological hyperinsulinemia stimulates p70(S6k) phosphorylation in human skeletal muscle.

    Hillier T, Long W, Jahn L, Wei L, Barrett EJ.

    Department of Internal Medicine, Division of Endocrinology, University of Virginia School of Medicine, Charlottesville, Virginia 22908, USA.

    Using tracer methods, insulin stimulates muscle protein synthesis in vitro, an effect not seen in vivo with physiological insulin concentrations in adult animals or humans. To examine the action of physiological hyperinsulinemia on protein synthesis using a tracer-independent method in vivo and identify possible explanations for this discrepancy, we measured the phosphorylation of ribosomal protein S6 kinase (P70(S6k)) and eIF4E-binding protein (eIF4E-BP1), two key proteins that regulate messenger ribonucleic acid translation and protein synthesis. Postabsorptive healthy adults received either a 2-h insulin infusion (1 mU/min.kg; euglycemic insulin clamp; n = 6) or a 2-h saline infusion (n = 5). Vastus lateralis muscle was biopsied at baseline and at the end of the infusion period. Phosphorylation of P70(S6k) and eIF4E-BP1 was quantified on Western blots after SDS-PAGE. Physiological increments in plasma insulin (42 +/- 13 to 366 +/- 36 pmol/L; P: = 0.0002) significantly increased p70(S6k) (P: < 0.01), but did not affect eIF4E-BP1 phosphorylation in muscle. Plasma insulin declined slightly during saline infusion (P: = 0.04), and there was no change in the phosphorylation of either p70(S6k) or eIF4E-BP1. These findings indicate an important role of physiological hyperinsulinemia in the regulation of p70(S6k) in human muscle. This finding is consistent with a potential role for insulin in regulating the synthesis of that subset of proteins involved in ribosomal function. The failure to enhance the phosphorylation of eIF4E-BP1 may in part explain the lack of a stimulatory effect of physiological hyperinsulinemia on bulk protein synthesis in skeletal muscle in vivo.



    So he basically tried to give you a physioliogy lesson using studies that don't support his case. This looks more like a marketing tactic and supp companies tend to this this a lot. It never ceases to amaze me how one can distort studies to try and make a case. You would think I'm back in law school. Leave the distoring of cases to the lawyers
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    Also most of his studies are based on the Tipton studies in which he himself concluded that more recent information indicate that High GI provided no benfit and it would take over two years with constant perfect training conditions to have a statistical difference with any pre/post nutrient schemes.

    So I prefer the one that has less chance of adipose storage as the study shows can clearly happen.
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    Thanks for your input/critique, much appreciated!

    ~SC~
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    Yes, nice debate but now I'm looking at my tub of gatorade and my pwo bottle and feel so confused.
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    Well, I know Bobo and I will agree on this:

    If you are doing something now that is working just fine for you, keep it as is. If you wish to experiment w/other ways, then you can do so, but just remember what has always worked for you so that you may come back to it.

    Science helps us, yes, but there are always exceptions to the rules and sometimes the way things work for some and not others is totally unexplainable. Stick w/what works for you if you are getting results, and if you aren't, simply try something else.

    I'll experiment w/my programs and altering carbs pwo by way of no dextrose, total dextrose, 2nd high GI meal or make it a low GI meal, etc. etc. I'll do this AFTER I am done prepping for pics, because my pwo fest which does utilize dex and carbs in the second pwo meal, has never failed to get me in great shape. So, I am going with that for now for this next round of pics.

    After that, I'll experiment, as being that I help 100's, and they are all successful, I may be able to even make the trips of success they see, even quicker. Who knows, but I'd be silly for not giving it a shot, it only serves to make what I do/teach better, and I've already got an impeccable track record. So, as Bobo said, you have absolutely nothing to lose, but a lot to gain.

    Hope that helps to ease your anxiety over the gatorade issue.

    ~SC~

    ~SC~
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    I agree with that too. It was just a light-hearted way of saying that you both make great arguments and this has been a good read.
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    I know, we suck don't we!

    LOL!!

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    Bobo and crew.

    I am a new poster to the board. I have been around a long time, but until today, didnt have much to add to the brain trust you guys have here. Great board BTW.

    I have read this thread with much interest and I hope your still following it.

    My question is this:

    What is your LOW GI carb/pro PW meal consist of. I seem to fall into the "put on fat easy camp." When I was young I could EAT ANYTHING and EVERYTHING I saw without gaining fat OR MASS. Today, being 34...I look at food during a mass up phase and plump up like a dough boy. I have been trying to figure out WHERE the fat gain comes from and I have isolated it to the PW drink. I, like MOST everyone in here, have been doing the fast carbs w/ protein after the workout. As soon as I start that phase of my training I start to put the fat on real fast. So to make a short story really long, I agree with you completely about the PW drink consisting of the fast carbs is NOT needed and can lead to fat gain. Still, that Is what evryone says you NEED to do. So I still do it. But...something has got to change in my philosophy so I dont get fat. I was thinking about apples with protein after the workout, then 1-2 hours later, repeat with LOW GI carbs and protein again.

    Yours and anyones comments are appreciated.
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    I like to use a coffee grinder to ground raw oats into a powder. Throw that in with your protein shake and it mixes pretty good.
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    Quote Originally Posted by TooL
    I like to use a coffee grinder to ground raw oats into a powder. Throw that in with your protein shake and it mixes pretty good.
    Bump on that Tool. That's exactly what I do.
  32. PC1
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    Bobo..............

    I've been adding uncooked oatmeal in my pwo shake, but I've also been putting in a couple pieces of raw fruit as well. I understand it's fructose, and doesn't give a quick benefit to muscles. But I like to put it in for the sake of the natural source of vitamins/micronutrients that we get from eating fruit.

    Aside from the vitamins/micronutrients angle, is this a bad practice in any sense from a fat accumulation perspective?

    Thanks bro. And great thread btw.
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    this might be totally irrelevant but why not combine them both, such as if one ingested 60grams dex or 60grams oats, just use both, 30g dex and 30g oats post workout.
  

  
 

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