how fat metabolism works? - AnabolicMinds.com

how fat metabolism works?

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    how fat metabolism works?


    I can't seem to find a good answer for this..

    there's common knowledge to how carbs and proteins get metabolized. Carbs break down to glucose eventually, raising blood sugar, signaling insulin, etc.
    Proteins break down to aminos, and also cause a smaller raise in blood sugar and therefore insulin... then insulin jams both into muscles, fat.. though carbs can be stored in liver as the case with fructose.

    what about fat?

    do healthy sources of fat like monounsaturated/polyunsaturated fat get into the blood stream to be used as energy? or do they, as I would expect, simply get stored as fat?

    I have no problem making sure I get my "essential" fatty acids like omega 3s, but i'm starting to wonder what real benefit there is to having a bunch of peanut butter, olive oil, etc, when I don't think the body is going to use it as energy if I'm having carbs as well.

    I'm starting to think I'd do just fine with the trace-fats found in my lean proteins (i have plenty of lean beef), my carbs (even whole wheat has some fat), and supplemented omega 3s or just fish. any thoughts?

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    Quote Originally Posted by pinchharmonic View Post
    I can't seem to find a good answer for this..

    there's common knowledge to how carbs and proteins get metabolized. Carbs break down to glucose eventually, raising blood sugar, signaling insulin, etc.
    Proteins break down to aminos, and also cause a smaller raise in blood sugar and therefore insulin... then insulin jams both into muscles, fat.. though carbs can be stored in liver as the case with fructose.

    what about fat?

    do healthy sources of fat like monounsaturated/polyunsaturated fat get into the blood stream to be used as energy? or do they, as I would expect, simply get stored as fat?

    I have no problem making sure I get my "essential" fatty acids like omega 3s, but i'm starting to wonder what real benefit there is to having a bunch of peanut butter, olive oil, etc, when I don't think the body is going to use it as energy if I'm having carbs as well.

    I'm starting to think I'd do just fine with the trace-fats found in my lean proteins (i have plenty of lean beef), my carbs (even whole wheat has some fat), and supplemented omega 3s or just fish. any thoughts?
    Straight from my ex phys book:

    Sources of Fat During Exercise:
    "When an individual consumes more energy (i.e., food) then he or she expends, this additional energy is stored in the form of fat. A gain of 3,500 kcal of energy results in the storage of 1 pound of fat. Most fat is stored in the form of triglycerides in adipocytes (fat cells), but some is stored in muscle cells as well. The major factor that determines the role of fat as a substrate during exercise is its availability to the muscle cell. To be metabolized, triglycerides must be degraded to FFA (three molecules) and glycerol (one molecule). When triglycerides are split, FFA can be converted into acetyl-CoA and enter the Krebs cycle. Which fat stores are used as fuel source varies as a function of the exercise intensity and duration. For example, plasma FFAs (i.e., FFA from adipocytes) are the primary source of fat during low-intensity exercise. At higher work rates, metabolism of muscle triglycerides increase. At exercise intensities between 65% - 85% VO2 max, the contribution of fat as muscle fuel source is approximately equal between plasma FFA and muscle triglycerides.

    Also note that when carbohydrate stores are low the rate of glycolysis is reduced due to the unavailability of substrate, pyruvic acid levels in the sarcoplams decline, and the levels of Krebs cycle intermediates decrease as well. This decline in Krebs cycle intermediates slows the rate of Krebs cycle activity, with the end result being a reduction in the rate of aerobic ATP production. This reduced rate of muscle ATP production limits musclar performance. The reduction in Krebs cycle intermediates (due to glycogen depletion) results in a diminished rate of ATP production from fat metabolism, since fat can be metabolized only via Krebs cycle oxidation (FFAs are converted to acetyl-CoA through beta-oxidation). Hence, when carbohydrate stores are depleted in the body, the rate at which fat is metabolized is also reduced.

    PS: The glycerol molecule from the breakdown of triglycerides can be converted to glucose in the liver and transported through blood circulation to contracting muscles as fuel; this is a minute percent though.
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    First of all, insulin does not transport or jam anything in to cells. Insulin stimulates the GLUT cells to be more sensitive to glucose through a whole range of mechanisms. Sorry, I just really wish people would stop calling or referring to insulin as some kind of a shuttle. It doesn't do that.

    Fat is different from glucose in the fact that it goes to the liver before the body gets a crack at the energy from it. The liver converts the FFA into TAGs and chylomicrons for circulation in the blood. TAGs can't cross the cell membrane so have to be broken down and repackaged in the cell. When they enter the cell, they are in the form of free fatty acids (FFA). From there, depending on whether the cell is expressing hormone sensitive lipase or not determines whether it will be stored as a TAG in the cell or burned for fuel. Basically, the body doesn't know whether or not the energy it is using is coming from a healthy or unhealthy fat. That is more seen in the levels of circulating TAGs and cholesterol levels among other things.

    Now, for each FFA, there are different properties. This is where Omegas and the like come in. This is a pretty dense topic but it basically comes down to your body needing fat to function. It needs fat for hormones and other things as well. Low fat diets are not as healthy as previously believed. It would be better to limit the amount of saturated fats if you're worried.
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    [QUOTE=russy_russ;1775377]Hence, when carbohydrate stores are depleted in the body, the rate at which fat is metabolized is also reduced.QUOTE]

    so working out on an empty stomach doesnt burn as much fat as working out with carbs in your system?
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    [QUOTE=Dyou;1777252]
    Quote Originally Posted by russy_russ View Post
    Hence, when carbohydrate stores are depleted in the body, the rate at which fat is metabolized is also reduced.QUOTE]

    so working out on an empty stomach doesnt burn as much fat as working out with carbs in your system?
    In a fasted state, your body has less glycogen to draw on, and which utilize a higher % of fatty acids for energy vs. training in a fed/glycogen rich state.
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    so fasted is just a higher % of fat used while having carbs in your system still uses more fat all together?
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    Without carbohydrate stores the fat : carb : protein ratio will shift mostly to protein then fat, which is why working out fasted dcreases performance. Since fat metabolism is slowed more protein will be broken down and used as the most available substrate

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    but my question is which burns more fat overall working out in a fasted state or with carbs
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    Carbs but moderate amount too much causes the body to use it as main substrate ~50% total cal is recommended

    Also note that consuming a HIGH carbohydrate meal 30-60 minutes before exercise results in a significant amount of insulin to be released which directly inhibits lipase activity...

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    The main thing is to burn more calories that taken in

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    Where did you get that fat metabolism is slowed from not having carbs? Due to the TCA cycle intermediates not being available? Fat metabolism is slowed only during starvation. If you have enough proteins available to enter gluconeogenesis there will continue to be carbon backbones fed in to the TCA cycle to continue to push fat metabolism along. It will take a day or two of fasting to cause the proteins to metabolize slower.

    If you're doing cardio on an empty stomach, lipoprotein lipase, which helps store fats, will be low and hormone sensitive lipase (which is expressed in the presence of glucagon aka a fasted state) will be relatively high, mobilizing fat stores. If you keep your intensity low (50-60% HR) your body will also prefer to be utilizing fats for energy. Theoretically, you will burn a greater amount and greater relative amount of fat on an empty stomach. The only problem is, you will also mobilize proteins, some in muscle, to keep up with the TCA cycle. The amount needed for that would again be theorectically low compared to the amount of fat you're burning. Its good to have protein turnover anyways so the meal you consume after the workout should replenish any broken down muscle anyways. Your muscles can't get bigger without a little bit of catabolism first as far as I know.
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    Quote Originally Posted by wearedbleedblue View Post
    Where did you get that fat metabolism is slowed from not having carbs? Due to the TCA cycle intermediates not being available? Fat metabolism is slowed only during starvation. If you have enough proteins available to enter gluconeogenesis there will continue to be carbon backbones fed in to the TCA cycle to continue to push fat metabolism along. It will take a day or two of fasting to cause the proteins to metabolize slower.
    Proteins must be broken down, and only alanine can be directly converted to glucose in the liver and transported via circulation to contracting skeletal muscles to resynthesize ATP. Protein or amino acids CANNOT enter the Krebs Cycle (Citric Acid Cycle) directly; they must be converted into acetyl-CoA first.

    Also, when Krebs Cycle intermediates are low; entering acetyl-CoA does not have anything to react with to complete the cycle. That is why it is slowed down.

    Quote Originally Posted by wearedbleedblue View Post
    If you're doing cardio on an empty stomach, lipoprotein lipase, which helps store fats, will be low and hormone sensitive lipase (which is expressed in the presence of glucagon aka a fasted state) will be relatively high, mobilizing fat stores. If you keep your intensity low (50-60% HR) your body will also prefer to be utilizing fats for energy. Theoretically, you will burn a greater amount and greater relative amount of fat on an empty stomach. The only problem is, you will also mobilize proteins, some in muscle, to keep up with the TCA cycle. The amount needed for that would again be theorectically low compared to the amount of fat you're burning. Its good to have protein turnover anyways so the meal you consume after the workout should replenish any broken down muscle anyways. Your muscles can't get bigger without a little bit of catabolism first as far as I know.
    Yes, glucagon promotes gluconeogensis and FFA mobilization in to the blood cycle (they must enter the cell to be utilized, not circulate in the blood); however, The FFA must then be beta-oxidized to acetyl-CoA which is the only molecule that can enter the Krebs Cycle. And, again we come back to the issue of low levels of Krebs Cycle intermediates which was explained up top. Also, at 20% VO2 max your body uses about 60% FFA as substrates for fuel; while at 50% - 60% your body uses 40% FFA as substrates, but at the higher intensity below the lactate threshold the total rate of fat oxidation is at its greatest.

    I got my information from a few exercise physiology books; as well as I've talked with many professors (which have PhD's in Ex Phys) about these issues.

    Where did you get your information from?
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    Pubmed, personal research in two different labs and discussion with a few PIs. I also have exercise physiology books, which I'm looking through now. Check out "Fatty acid oxidation is directly regulated by carbohydrate metabolism during exercise" by Coyle EF, et al.

    Also, CHO increases malonyl CoA which stores fat, not oxidizes it. It directly inhibits lipid transport into the mitochondria. "During exercise in a fasted state adipose tissue lipolysis exceeded skeletal muscle fat oxidation" straight out of the text book I'm referencing coming from I believe the same study I referred to before. That means that its mobilizing the fat faster than it can even be used during a fasted state.
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    Quote Originally Posted by wearedbleedblue View Post
    Pubmed, personal research in two different labs and discussion with a few PIs. I also have exercise physiology books, which I'm looking through now. Check out "Fatty acid oxidation is directly regulated by carbohydrate metabolism during exercise" by Coyle EF, et al.

    Also, CHO increases malonyl CoA which stores fat, not oxidizes it. It directly inhibits lipid transport into the mitochondria. "During exercise in a fasted state adipose tissue lipolysis exceeded skeletal muscle fat oxidation" straight out of the text book I'm referencing coming from I believe the same study I referred to before. That means that its mobilizing the fat faster than it can even be used during a fasted state.
    So is my information... I've also have lab experience.

    I cannot find anything that carbohydrates increases malonyl CoA. Malonyl CoA is used in fatty acid synthesis, not during beta-oxidation; which is what I was referring to.
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    Quote Originally Posted by russy_russ View Post
    Proteins must be broken down, and only alanine can be directly converted to glucose in the liver and transported via circulation to contracting skeletal muscles to resynthesize ATP. Protein or amino acids CANNOT enter the Krebs Cycle (Citric Acid Cycle) directly; they must be converted into acetyl-CoA first.
    Yes only they can be broken down to glucose but the only things that need glucose are the brain and red blood cells. You don't need glucose to enter the TCA cycle to synthesize ATP. Proteins CAN enter the TCA cycle (citric acid cycle, more often referred to as tricarboxylic acid cycle) without being converted to acetyl-CoA. They can also be converted in to alpha ketoacids which would then be glucogenic aminos. Alanine enters at the level of pyruvate, 5 others are ketogenic and enter where ketones would, ARG and GLN enter at AKG level, 4 more enter at the succinyl-CoA level, 2 enter at the fumarate level and even more enter at the oxaloacetate level.

    Quote Originally Posted by russy_russ View Post
    Also, when Krebs Cycle intermediates are low; entering acetyl-CoA does not have anything to react with to complete the cycle. That is why it is slowed down.
    We're talking a fasted state, not a starved state. In a fasted state, there are still enough carbon backbones like I mentioned before, to continue the cycle. It needs OAA and there is plenty from GNG and from the excess glycogen leftover.



    Quote Originally Posted by russy_russ View Post
    Yes, glucagon promotes gluconeogensis and FFA mobilization in to the blood cycle (they must enter the cell to be utilized, not circulate in the blood); however, The FFA must then be beta-oxidized to acetyl-CoA which is the only molecule that can enter the Krebs Cycle.
    AcCoA isn't the only molecule that can enter the "krebs cycle." You should also reference some sources other than exercise phys sources. Nutri Sci is its own discipline, imagine that. Sorry for coming off as a ****, no personal attacks are meant here. Just trying to sift out the science.
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    Malonyl coa is used in FA synthesis and is a direct inhibitor of FFA oxidation. Any increase in insulin which would occur with even a moderate amount of CHO would elevate Mal-CoA and decrease HSL activity.
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    Some amino acids can be converted to pyruvate, some to acetyl-coa. If glycogen stores are still present, glycolysis and krebs cycle are not hindered. It is when glycogen stores become insufficiently low / depleted which I believe I mentioned in my first couple posts. Acetyl-CoA starts the Krebs Cycle when it combines with oxaloacetate to form citrate. The cycle continues through a series of reactions where hydrogens are removed and combined with NAD and FAD to enter the electron transport chain. Eventually, the cycle will end with the conversion of Malate to Oxaloacetate. And the cycle starts over again. But, I know you know this so really no point in explaining it...
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    Quote Originally Posted by wearedbleedblue View Post
    Malonyl coa is used in FA synthesis and is a direct inhibitor of FFA oxidation. Any increase in insulin which would occur with even a moderate amount of CHO would elevate Mal-CoA and decrease HSL activity.
    Of course, it makes logical sense that if malonyl coa is used for FA synthesis it would directly inhibit FFA oxidation. Insulin spikes and high lactic acid concentrations hinder FFA mobilization and insulin inhibits lipolysis by directly inhibiting lipase activity. However, insulin levels decline (especially during exercise when epinephrine levels are elevated) and carbohydrate & fat metabolism rises. Carbohydrates drive its own metabolism, while fatty acids do not (they must rely on carbohydrates).
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    With science out the window, and from person experience alone. I used to be a big advocate of high protein, low carb diet. I saw ok decrease in weight (a lot being water since carbohydrate intake was limited) and eventually (6-8 weeks) I would hit a plateau and strength and muscle would decline.

    Since I have switched to high carbohydrate, lower protein diet. I've noticed it's much easier to eat under maintenance; My appetite is suppress. And, strength and muscle have not decline much at all and I am still losing fat (I've actually never been as lean as I am eating high carbohydrates).
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    Quote Originally Posted by russy_russ View Post
    Also, at 20% VO2 max your body uses about 60% FFA as substrates for fuel; while at 50% - 60% your body uses 40% FFA as substrates
    Hey Russ, Could you post up your source to that one? Thanks.
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    Quote Originally Posted by pinchharmonic View Post
    I can't seem to find a good answer for this..
    Here is a good diagram of nutrient metabolism

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    start reading up on oxidative fat mobilization ...
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    great info.......
  

  
 

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