Insulin binding to fat cell receptors

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    Insulin binding to fat cell receptors


    So I understand that insulin will bind to fat cell receptors (as well as other cell receptors) and inhibit fat oxidation, but i want to know if the body has an order or sequence in which cells insulin targets.

    So lets say you spike your insulin, it will bind to receptors and pull glucose into the cell, but will the body target cells that need it most or will it bind to everything? Thanks.


    EDIT: And if anyone knows a good read on the subject i would love it.

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    Insulin inhibits fat oxidation because insulin is released when you consume food in portions that lead to surplus energy. When you supply your body with extra food energy, it has little need to dip into stores. Insulin is the effect not the cause.

    As far as targetting specific cells. Fat deposits are generally larger around the body's center of gravity (mid section). Is that what you mean?
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    insulin is signaled when glucose is elevated in the bloodstream (blood sugar levels which depend on either a rapid increase which is bad and steady which is prefered)...as a result, it pulls the glucose to either muscle cells for energy or if energy is not needed, then it is stored as fat
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    think of it in terms of chemical reaction rates...the rate of uptake into muscle cells is proportional to the concentration of glucose in the blood, the amount of "room" in muscles free to be filled, and the anabolic response from exercise pulling glucose into cells.
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    Quote Originally Posted by Nitrox View Post
    Insulin inhibits fat oxidation because insulin is released when you consume food in portions that lead to surplus energy. When you supply your body with extra food energy, it has little need to dip into stores. Insulin is the effect not the cause.

    As far as targetting specific cells. Fat deposits are generally larger around the body's center of gravity (mid section). Is that what you mean?
    Quote Originally Posted by Jax11 View Post
    insulin is signaled when glucose is elevated in the bloodstream (blood sugar levels which depend on either a rapid increase which is bad and steady which is prefered)...as a result, it pulls the glucose to either muscle cells for energy or if energy is not needed, then it is stored as fat
    So are you both saying that glucose will ONLY be stored as fat once all glycogen stores are filled? Which would seem to me that insulin will bind to cells in a specific order (muscle cells then fat cells, just talking about these at the moment) depending on the state of the body. Basically, the body should not store glucose as fat if there are glycogen stores that need to be filled, correct?
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    I have never read any info that is that definitive. Personally, I don't believe that it works that way; that would be a fairly linear response.

    Different cells in the body have different 'sensitivities' to insulin. The theory is that after training a muscle, it becomes hungry for energy and becomes more sensitive to insulin. However, if you 'spike' insulin to a high enough level (by consuming more food energy than is necessary for replenishment and maintenance) then theoretically you can 'turn on' all the cells and store fat and replenish glycogen at the same time.
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    Muscular contraction causes glucose transporters (GLUT4 to be precise) to transolcate to the outside of the cell membrane and grab glucose molecules out of the bloodstream; this process is completely independent of insulin. This effect tends to diminish rather rapidly post-exercise.

    Unless you are doing a lot of endurance work or really high volume lifting you probably aren't even approaching glycogen depletion. But, any level of glycogen depletion should selectively increase skeletal muscle insulin sensitivity.

    Also, while protein synthesis is elevated for several hours PWO, so is degradation. Elevated insulin levels mitigate the rate of degradation as do elevated levels of Amino Acids in the bloodstream. What all this means is that we can potentially get a significant partitioning effect by ingesting the bulk of our carbohydrate intake and large amounts of protein in the hour before and several hours after our WO's.

    While I am not sold on IF (intermittent fasting) as the most effective nutrient timing strategy for body composition the anecdotal evidence seems to support that it is somewhat effective.

    I am currently experiencing excellent recomp effects by limiting my calorie intake to an ~11 hour window with two training sessions in that period. I am sticking with the same caloric intake I would normally consume in a 15-16 hour timeframe and my total volume of training is only slightly elevated from my previous once daily WO's.

    I wouldn't suggest this strategy unless your primary goals are fat loss or steady recomp. I couldn't see myself consuming a true bulking diet in this manner.
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    Quote Originally Posted by Jax11 View Post
    insulin is signaled when glucose is elevated in the bloodstream (blood sugar levels which depend on either a rapid increase which is bad and steady which is prefered)...as a result, it pulls the glucose to either muscle cells for energy or if energy is not needed, then it is stored as fat
    Glucose is transported via GLUT4 primarily into skeletal muscle cells. When an abundance is in the cell formation of glycogen begins. Extra is excreted and NOT stored as fat (if this wasn't true then we would have no need for waste being excreted from the body). This is common misconception, because the typical diet is high in fats as well as carbohydrates. When high fats are consumed with high carbohydrates the carbohydrates will drive their own metabolism first then they will fuel the metabolism of fatty acids (they cannot fuel their own metabolism). Since high carbohydrates have been consumed with high fats, the fats do not get utilized, in which case would be stored.
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    Quote Originally Posted by russy_russ View Post
    Glucose is transported via GLUT4 primarily into skeletal muscle cells. When an abundance is in the cell formation of glycogen begins. Extra is excreted and NOT stored as fat (if this wasn't true then we would have no need for waste being excreted from the body). This is common misconception, because the typical diet is high in fats as well as carbohydrates. When high fats are consumed with high carbohydrates the carbohydrates will drive their own metabolism first then they will fuel the metabolism of fatty acids (they cannot fuel their own metabolism). Since high carbohydrates have been consumed with high fats, the fats do not get utilized, in which case would be stored.
    A large portion of our carbohydrate intake is synthesized into fatty acids.

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    Quote Originally Posted by russy_russ View Post
    Extra is excreted and NOT stored as fat (if this wasn't true then we would have no need for waste being excreted from the body).
    Extra glucose is not excreted - except in the case of diabetics experiencing hyperglycemia. If not burned or stored as muscle/hepatic glycogen it will be converted to fat through DNL (de novo lipogenesis).
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    Glut 4 pathway goes into adipose AND muscle cells. Not just muscle cells

    Posted from my mobile device.
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    Carbohydrates do not turn into fat HUMANS. Studies shown in which carbohydrates turn to fatty acids are not done on humans.

    "The daily protein in take is used to maintain existing tissue protein, hormones, and enzymes. If more is taken in than is needed, the "extra" is oxidized for metabolic needs, and fat mass is not increased. The same is true for carbohydrates. Ingested carbohydrates are used to fill liver and muscle glycogen stores; the excess is oxidized and is NOT converted to fat. Carbohydrate intake promotes its own oxidation. This is a relatively new idea that has major ramifications for our understanding of nutrient and energy balance.The evidence seems to be quite convincing that 'de novo' lipogenesis from carbohydrates (the making of new lipids from other nutrients) is of only minor consequence in humans. Simply, carbohydrates are either stored as carbohydrates or oxidized; they do not add directly to adipose tissue mass. This leaves fat.

    In contrast to carbohydrate and protein, fat intake is not automatically balanced by fat oxidation. When "extra" fat is added to the diet, the same amounts of carbohydrate, fat, and protein are oxidized as before; the extra fat is stored in adipose tissue. Fat intake does not promote its own oxidation."

    Acheson, K. J. 1987. Carbohydrate metabolism and de novo lipogenesis in human obesity. AMERICAN JOURNAL OF CLINICAL NUTRITION 45; 78-85

    Powers, Scott and Edward T. Howley. Exercise Physiology: Theory and Applications to
    Fitness and Performance. New York: McGraw-Hill, 2009.
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    Quote Originally Posted by russy_russ View Post
    Carbohydrates do not turn into fat HUMANS. Studies shown in which carbohydrates turn to fatty acids are not done on humans.
    Yes...they do. In the presence of a caloric surplus, glucose is converted into pyruvic acid and further into Acetyl CoA. That can then be converted into fatty acids(known as lipogenesis). I'm not sure where you think all of that extra glucose goes.

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    Quote Originally Posted by crazyfool405 View Post
    Glut 4 pathway goes into adipose AND muscle cells. Not just muscle cells

    Posted from my mobile device.
    Wrong, GLUT4 is specifically for glucose. GLUT4 opens a gate on the plasma membrane so that glucose can be shuttled into the cell to form glycogen. Insulin suppressed beta-oxidation (oxidation of fatty acids) by directly inhibiting lipase activity. This stops the metabolism of stored fatty acids, it does NOT store fat.
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    Quote Originally Posted by Cinn View Post
    Yes...they do. In the presence of a caloric surplus, glucose is converted into pyruvic acid and further into Acetyl CoA. That can then be converted into fatty acids(known as lipogenesis). I'm not sure where you think all of that extra glucose goes.

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    glucose is either converted to pyruvate or lactate (depending on a few physiological reasons) from there the pyruvate or stored as liver glucose or muscle glycogen. Pyruvate is converted to Acetyl-CoA with the enzyme pyruvate kinase. Acetyl-CoA does NOT convert to fat, instead it enters TCA cycle (kreb's cycle, how ever you call it; it has many names). Beta-Oxidation is the pathway for fatty acids to be converted to Acetyl-CoA to enter the TCA cycle for complete oxidation. This process is not reversible in humans.
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    Quote Originally Posted by russy_russ View Post
    glucose is either converted to pyruvate or lactate (depending on a few physiological reasons) from there the pyruvate or stored as liver glucose or muscle glycogen. Pyruvate is converted to Acetyl-CoA with the enzyme pyruvate kinase. Acetyl-CoA does NOT convert to fat, instead it enters TCA cycle (kreb's cycle, how ever you call it; it has many names). Beta-Oxidation is the pathway for fatty acids to be converted to Acetyl-CoA to enter the TCA cycle for complete oxidation. This process is not reversible in humans.
    You do realize that you are essentially claiming someone eating an increased kcal, high carb, low fat diet can not gain fat...right? Think about how silly you sound.

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    Quote Originally Posted by russy_russ View Post
    glucose is either converted to pyruvate or lactate (depending on a few physiological reasons) from there the pyruvate or stored as liver glucose or muscle glycogen. Pyruvate is converted to Acetyl-CoA with the enzyme pyruvate kinase. Acetyl-CoA does NOT convert to fat, instead it enters TCA cycle (kreb's cycle, how ever you call it; it has many names). Beta-Oxidation is the pathway for fatty acids to be converted to Acetyl-CoA to enter the TCA cycle for complete oxidation. This process is not reversible in humans.
    Acetyl-CoA is most certainly not catalyzed to form fatty acids, but it is highly regulated in fatty acid biosynthesis, via its carboxylation to Malonyl-CoA via the aptly named "acetyl-CoA-carboxylase" [ACC].
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    Quote Originally Posted by Mulletsoldier View Post
    Acetyl-CoA is most certainly not catalyzed to form fatty acids, but it is highly regulated in fatty acid biosynthesis, via its carboxylation to Malonyl-CoA via the aptly named "acetyl-CoA-carboxylase" [ACC].
    The beta oxidation process ends with Acetyl-CoA, which then can either enter the TCA cycle or used in biosynthesis of amino acids.

    http://www.bgsu.edu/departments/chem...dation_angela/

    Which I believe is what you were trying to say. That's why I said the process CANNOT be reversed "acetyl-coa --> fatty acids"
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    I've posted my sources for information. Take what you want from it; I'm out.
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    Quote Originally Posted by russy_russ View Post
    The beta oxidation process ends with Acetyl-CoA, which then can either enter the TCA cycle or used in biosynthesis of amino acids.

    http://www.bgsu.edu/departments/chem...dation_angela/

    Which I believe is what you were trying to say. That's why I said the process CANNOT be reversed fatty acids --> acetyl-coa
    I was illuminating the role of acetyl-CoA in the biosynthesis of fatty acids. Acetyl-CoA is carboxylated into Malonyl-CoA, and this reaction is both the first step in FA synthesis, and the lack of Malonyl-CoA as a substrate is the rate-limiting step for FA oxidation - this reaction, therefore, is a paramount response to the AMP:ATP pathway of energy-reaction. The process of beta-oxidation is not reversible, I was merely illustrating that we must remember Acetyl-CoA is highly involved in FA biosynthesis.
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    Quote Originally Posted by russy_russ View Post
    Wrong, GLUT4 is specifically for glucose. GLUT4 opens a gate on the plasma membrane so that glucose can be shuttled into the cell to form glycogen. Insulin suppressed beta-oxidation (oxidation of fatty acids) by directly inhibiting lipase activity. This stops the metabolism of stored fatty acids, it does NOT store fat.
    Can you point me in the direction of that information as I'd like to read more. I was under the impression glut4 was for glucose uptake into muscle and adipose tissue.

    Posted from my mobile device.
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    Quote Originally Posted by crazyfool405 View Post
    Can you point me in the direction of that information as I'd like to read more. I was under the impression glut4 was for glucose uptake into muscle and adipose tissue.

    Posted from my mobile device.
    It is. You worded it a little funny before but had the right idea.

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    Ok so what I said was rifht

    Posted from my mobile device.
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    Quote Originally Posted by Cinn View Post
    You do realize that you are essentially claiming someone eating an increased kcal, high carb, low fat diet can not gain fat...right? Think about how silly you sound.

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    russyruss--this is precisely what I thought when I read your theory that excess carbs are excreted and not stored as fat. For clarity's sake, are you actually claiming that someone who managed to eat above maintainence on an all CHO and PRO diet could not possibly increase their adipose stores. Are you seriously claiming this?
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    Quote Originally Posted by russy_russ View Post
    Wrong, GLUT4 is specifically for glucose. GLUT4 opens a gate on the plasma membrane so that glucose can be shuttled into the cell to form glycogen. Insulin suppressed beta-oxidation (oxidation of fatty acids) by directly inhibiting lipase activity. This stops the metabolism of stored fatty acids, it does NOT store fat.
    GLUT4 is certainly found in both muscle tissue and adipose cells. A series of cellular phosphorylations (ranging from the phosphorylation of tyrosine residues and tyrosine kinase activity within cytoplasmic proteins, to insulin receptor substrate activation of phosphatidylinositol-3-kinase, to activation of GTP-binding protein ras, and ultimately to the mitogen-activated protein kinase system (MAPK)) induce several effects, including the translocation of glucose transporter proteins, especially GLUT4, to the cell membrane, leading to glucose uptake, higher glycogen formation, increased activity of the glucose synthase enzyme, activation of transcription factors leading to improved DNA synthesis, and so on. In fact, GLUT4 is one of the only GLUT proteins specifically present in adipose cells.
    For those interested, GLUT1, for instance, is found in all tissues, especially in red cells, and in the brain. It is mainly involved in glucose uptake and transport across the blood-brain barrier. GLUT2 is mainly found in the liver, in the gut, in the kidney, and in the B cells of the pancreas, and is involved in the transport of glucose and fructose, as well as in glucose homeostasis, especially in the regulation of the release of insulin. GLUT3 is primarily found in the brain, in the placenta, in the kidney, and in some other tissues. It is involved in glucose uptake in neurons and other tisues. GLUT5 is found in the gut and kidney, and is involved in the absorption of fructose. While GLUT5 is not the only protein that transports fructose, it is the only GLUT protein that transports fructose.
    Altogether, 14 GLUT proteins have been identified. Only 1-5 have been well characterized.
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    Quote Originally Posted by Mulletsoldier View Post
    I was illuminating the role of acetyl-CoA in the biosynthesis of fatty acids. Acetyl-CoA is carboxylated into Malonyl-CoA, and this reaction is both the first step in FA synthesis, and the lack of Malonyl-CoA as a substrate is the rate-limiting step for FA oxidation - this reaction, therefore, is a paramount response to the AMP:ATP pathway of energy-reaction. The process of beta-oxidation is not reversible, I was merely illustrating that we must remember Acetyl-CoA is highly involved in FA biosynthesis.
    Agree.
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    Quote Originally Posted by russy_russ View Post
    The beta oxidation process ends with Acetyl-CoA, which then can either enter the TCA cycle or used in biosynthesis of amino acids...
    Generally correct. Mitochondrial fatty acid oxidation (beta-oxidation) generally produces one mole of NADH, one mole of FADH2, and mole of acetyl-CoA. Acetyl-CoA, the end-product of each cycle of beta-oxidation, enters the TCA (Krebs) Cycle where it is oxidized, along with further NADH and FADH2, to ultimately generate the energy currency, ATP. This process holds for lipids with an even number of carbon atoms. For lipids with an odd number of carbon atoms, acetyl-CoA is still yielded as an end product of beta-oxidation. However, in addition to this, a single mole of propionyl-CoA is also produced. This propionyl-CoA is then converted to succinyl-CoA (via the enzymatic actions of propionyl-CoA-carboxylase, methylmalonyl-CoA epimerase, and methlymalonyl-CoA mutase), which enters the Krebs Cycle for further ATP- dependent oxidation. Finally, unsatuirated fats. Here, the same process as for saturated fats occurs. The only exception is when a double bond is present. In this case, isomerization of the double bond occurs via an enoyl-COA isomerase. Once this occurs, oxidation continues as in saturated fats.
    The entire process is also different in cases of methylated fats. Here, alpha, not beta-oxidation, occurs.
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    Quote Originally Posted by scherbs View Post
    russyruss--this is precisely what I thought when I read your theory that excess carbs are excreted and not stored as fat. For clarity's sake, are you actually claiming that someone who managed to eat above maintainence on an all CHO and PRO diet could not possibly increase their adipose stores. Are you seriously claiming this?
    Believe what you wish; I have scientific data backing my claim.

    BTW: lipids are stored in adipose tissue as triglycerides, not glucose or glycogen.
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    Quote Originally Posted by russy_russ View Post
    Believe what you wish; I have scientific data backing my claim.

    BTW: lipids are stored in adipose tissue as triglycerides, not glucose or glycogen.
    It's called lipogenesis, buddy. Fatty acids can be synthesized from glucose.
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    Well great discussion, thanks for the information... although i'm surprised that there is any question over the existence lipogenesis, specifically from glucose. Now i just need to reread everything to see if my answer is in there somewhere
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    Quote Originally Posted by Cinn View Post
    It's called lipogenesis, buddy. Fatty acids can be synthesized from glucose.
    Yes. That is possible; however, only under very rare circumstances does it in humans.
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    Quote Originally Posted by russy_russ View Post
    Yes. That is possible; however, only under very rare circumstances does it in humans.
    It is certainly not rare by any means! The conversion of glucose into triglycerides in humans is facilitated via the enzymatic action of glycerol-3-phosphate dehydrogenase, leading to an increase in adipocyte size.
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    Quote Originally Posted by strategicmove View Post
    It is certainly not rare by any means! The conversion of glucose into triglycerides in humans is facilitated via the enzymatic action of glycerol-3-phosphate dehydrogenase, leading to an increase in adipocyte size.
    Like I said before; believe what you want. Just keep in mind science is always changing
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    Quote Originally Posted by russy_russ View Post
    Like I said before; believe what you want. Just keep in mind science is always changing
    As it turns out, the science here is fairly well understood. Nothing here has anything to do with belief!
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    Quote Originally Posted by russy_russ View Post
    Carbohydrates do not turn into fat HUMANS. Studies shown in which carbohydrates turn to fatty acids are not done on humans.
    Yeah, I guess you're right...

    Acheson KJ, Schutz Y, Bessard T, Anantharaman K, Flatt JP, Jéquier E.
    Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man. Am J Clin Nutr. 1988 Aug;48(2):240-7.

    Hellerstein MK. De novo lipogenesis in humans: metabolic and regulatory aspects. Eur J Clin Nutr. 1999 Apr;53 Suppl 1:S53-65.

    Minehira K, Vega N, Vidal H, Acheson K, Tappy L. Effect of carbohydrate overfeeding on whole body macronutrient metabolism and expression of lipogenic enzymes in adipose tissue of lean and overweight humans. Int J Obes Relat Metab Disord. 2004 Oct;28(10):1291-8.
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    Quote Originally Posted by crazyfool405 View Post
    Glut 4 pathway goes into adipose AND muscle cells. Not just muscle cells
    Not sure the presence or absence of GLUT4 in adipose tissue is relevant to the discussion unless you are suggesting that they translocate in response to exercise as they do in skeletal muscle.
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    Quote Originally Posted by zaosha View Post
    Yeah, I guess you're right...

    Acheson KJ, Schutz Y, Bessard T, Anantharaman K, Flatt JP, Jéquier E.
    Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man. Am J Clin Nutr. 1988 Aug;48(2):240-7.

    Hellerstein MK. De novo lipogenesis in humans: metabolic and regulatory aspects. Eur J Clin Nutr. 1999 Apr;53 Suppl 1:S53-65.

    Minehira K, Vega N, Vidal H, Acheson K, Tappy L. Effect of carbohydrate overfeeding on whole body macronutrient metabolism and expression of lipogenic enzymes in adipose tissue of lean and overweight humans. Int J Obes Relat Metab Disord. 2004 Oct;28(10):1291-8.

    lol

    In one of your earlier post you mentioned intermittent fasting, could you explain that a little more?
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    Quote Originally Posted by Burner View Post
    lol

    In one of your earlier post you mentioned intermittent fasting, could you explain that a little more?
    leangains.com is probably the best resource to learn about IF from a body composition perspective.

    Basically, IF protocols completely contradict the widely accepted notion that you should eat frequently from the time you awaken until you are ready to sleep. Instead, you limit your calorie intake to certain window, e.g. if you workout at 7am you might restrict your intake to the 8 hours between 6am and 2pm. The idea would be to provide yourself with a decent pre-WO meal so that you have amino acids and glucose available while you are working out and then to consume the rest of your calories in the several hours post-WO.

    IF is really a catch-all term for any plan which incorporates consistent periods of fasting. There are plenty of life extensionists experimenting with EOD fasting who have little interest in body comp goals.
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    Quote Originally Posted by strategicmove View Post
    As it turns out, the science here is fairly well understood. Nothing here has anything to do with belief!
    Actually, there is many topics still precisely unknown to exercise physiologist; research continues and new findings are present continually.
  

  
 

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