[b said:
Quote[/b] ]No real befit is highly debatable. first CPT is most certianly rate limiting in fat oxidation. yes the body can make more but the real concern if dieting is going to be whether or not the carnitine pool becomes acytlated. should the carnitine pool become acytalated that can prevent LCPUFA oxidation by reducing formation of CoA.
carnitine is certianly not the best bang for the buck supplement but I would not say it has no value either.
highly debatable unless you look at the research that shows no benefit of carnitine supplementation in increasing fat oxidation or increasing bodyfat loss.
You notice I never said CPT is the rate limiting step, I was actually meaning that carnitine wasn’t the rate limiting item of the process. There are potentially many rate limiting steps if fatty acid metabolism.
I mean, once HSL has been activated and actively allowing breakdown of adippcyte tags into glycerol and fatty acids, which are then released into circulation. Once into circulation they are normally bound from the likes of albumin, then they float around until they get to the likes of the muscle. Before it can make it into the muscle, it has to pass from the vascular space into the interstitial space thru the endothelium. From here it has to make it thru the sarcolemma, with the likes of the plasma membrane fatty acid binding protein (FABPpm), fatty acid translocase (FAT) and fatty acid transport proteins (FATP). Certain training raises levels of certain proteins (ie endurance raises FABP and Type I muscle fibres have higher levels of FABP), bringing about the thought of a relationship between fatty acid binding capabilities and oxidative metabolism ability of muscle. Once the fatty acid actually makes it past this and into the muscle cell, it can be esterified and stored (intermusclur tags) or the tag can be bound to FABPc (cytosolic) for transport to the site of oxidation ie activated to acyl-CoA by acylCoA synthase funnily enough.
Once it is converted to Acyl-CoA-FA it cannot get thru the mitochondrial outer layer. The acylcoA is picked up by carnitine palmitoyltransferase I (CPT1) transferring the acyl to carnitine which is then translocated thru to the inner membrane where it is attached back to the coA and onto beta oxidation.
There is many many steps involved in getting the (what I should say is long chain) fatty acid to the point of oxidation, which point is the rate limiting
,
At rest rate of appearance (ie lipolysis) of fatty acids is greater than requirements, once you start exercising, especially >65%VO2max. During high intensity exercise, contribution of FA to energy is diminished. This is because lipolysis cannot really keep up with the muscle ie – lipolysis is the rate limiting step in this circumstance. But, if you infuse lipids above the muscle requirements, it doesn’t burn as much as you would think, because when there is an increase in Acyl-CoA formation (and pyruvate from glucose during extremes of glycolysis) CPT1’s activity is reduced therefore the entry of LC fatty acids is reduced. Ie its not carnitine that is the rate limiting item is CPT…and infused lipids is not a standard practice any one exercising.
Hereditary and acquired conditions of carnitine deficiency will result in a accumulation of FA in the muscle, but this isn’t a normal healthy person (and is relatively rare-less than PKU). If you supply supplemental carnitine to these people it helps. But they have an extreme lack of carnitine, whereas most people do not.
Most studies of carnitine supplementation have used ~2-6g carnitine perday, and time periods from 5days to around 4 odd weeks. These studies confirm that carnitine has no effect on fat oxidation during exercise or performance.
Lipid metabolism during exercise is unchanged, as is glucose metabolism (Vukovich et al, Carnitine supplementation: effect on muscle carnitine and glycogen content during exercise. Med Sci Sports Exerc 1994;26:1122-9). Even if you deplete people before hand to try and maximise fat oxidation, it still doesn’t have any effect, even during submax exercise. (Decombaz et al. Effect of Lcarnitine on sub-maximal exercise metabolism after depletion of muscle glycogen. Med Sci Sports Exerc 1993;25:733-40)
I mean, studies have shown little or no loss of carnitine (From muscles) at high or low intensity exercises, and even massive doses of carnitine only raises muscle content by 1-2%, so it works out as very little effect.
There is potential for carnitine to do other things, like act as a sink for AcylCo-A, which would maintain Co-A availability and this could enhance flux thru the citric acid cycle. And it could increase the activity of PDH which is inhibited by high levels of acylCo-A. This would increase the oxidation of glucose (which might allow increases in exercise performance, but obviously doesn’t)
In terms of carnitine and weight loss the results is largely negative
Villani et al. L-Carnitine supplementation combined with aerobic training does not promote weight loss in moderately obese women. Int J Sport Nutr Exerc Metab. 2000;10:199-207.
Or even massive doses on rats – 5g/kg!!!
Brandsch C, Eder K. Effect of L-carnitine on weight loss and body composition of rats fed a hypocaloric diet. Ann Nutr Metab. 2002;46:205-10.
Sure there has been a little positive research, in rats at least, but it was a combination supplement and not just carnitine.
Hongu N, Sachan DS. Caffeine, carnitine and choline supplementation of rats decreases body fat and serum leptin concentration as does exercise. J Nutr 2000;130:152-7
And those authors also have some other research in humans, but it shows very little at this stage.
The effect of carnitine on fat loss is insignificant.