how fat metabolism works?
- 01-26-2009, 02:32 PM
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?
- 01-26-2009, 02:44 PM
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.
- 01-26-2009, 04:33 PM
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.
01-27-2009, 01:51 PM
[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?
01-27-2009, 02:05 PM
01-27-2009, 02:16 PM
so fasted is just a higher % of fat used while having carbs in your system still uses more fat all together?
01-27-2009, 02:29 PM
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
01-27-2009, 02:39 PM
but my question is which burns more fat overall working out in a fasted state or with carbs
01-27-2009, 03:07 PM
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...
01-27-2009, 03:10 PM
The main thing is to burn more calories that taken in
01-27-2009, 06:44 PM
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.
01-27-2009, 06:59 PM
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.
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?
01-27-2009, 07:18 PM
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.
01-27-2009, 07:26 PM
01-27-2009, 07:37 PM
01-27-2009, 07:45 PM
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.
01-27-2009, 07:55 PM
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...
01-27-2009, 07:59 PM
01-27-2009, 08:04 PM
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).
01-28-2009, 10:55 AM
01-28-2009, 11:11 AM
02-11-2009, 08:28 AM
start reading up on oxidative fat mobilization ...
02-11-2009, 09:39 AM
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