REVISITING THE ERGOGENIC PROPERTIES OF LCARNITINE
F. Stephens Ann Nutr Metab 2013;63(suppl 1):30
More than 95% of the body’s carnitine is found in skeletal muscle where it translocates fatty acids into the mitochondrial
matrix for β-oxidation via carnitine palmitoyltransferase 1 (CPT1), and buffers excess acetyl-CoA from the pyruvate dehydrogenase complex (PDC) during high glycolytic flux as a via carnitine acetyltransferase. Not surprisingly oral L-carnitine feeding has been advocated as an ergogenic aid.
However, scientific interest in L-carnitine as an ergogenic aid declined during the 1990s when it became apparent that oral (2-6 g per
day for 1 day to 4 months) or intravenous (up to 5 g) administration of L-carnitine alone does not increase muscle carnitine content or alter fuel utilisation during exercise.
We have recently demonstrated that insulin stimulates muscle carnitine uptake, and that 12-24 weeks of L-carnitine feeding in combination with a carbohydrate beverage in order to stimulate insulin release (1.4 g L-carnitine + 80 g carbohydrate twice
daily) can increase the muscle carnitine store by 20-30% and have some remarkable effects upon fuel utilisation compared to
carbohydrate feeding alone.
For example, the increase in muscle carnitine content in these studies resulted in reduction in muscle glycogen utilisation, and an increase in whole-body fat oxidation and energy expenditure during low intensity exercise (cycling at 50% VO2max), which is consistent with the premise that carnitine availability is limiting to CPT1. On the other hand, during high intensity exercise (cycling at 80% VO2max) an increase muscle carnitine content results in greater buffering of acetyl groups and a better matching of glycolytic flux to mitochondrial ATP production, as evidenced by increased muscle PDC activation and reduced muscle lactate accumulation. Manipulating both of these metabolic roles of carnitine will have implications for exercise performance.