L-Carnitine exists primarily in skeletal muscle (approx. 95% of approx. 20 g in the body). Carnitine is involved in the transport of LCFAs (long-chain fatty acids) from the cytoplasm across the mitochondrial membranes for subsequent entry into the beta-oxidation pathway in the mitochondrial matrix.  LCFA transport is linked to the CPT (carnitine palmitoyltransferase) complex and the fatty acid transport protein. The important roles of carnitine in energy metabolism have spurred many investigators to examine the effects of oral carnitine supplementation on the ability of skeletal muscle to increase reliance on fat as the principle substrate for energy production during exercise and potentially improve exercise performance. The underlying assumption of these studies is that carnitine limits fat transport into the mitochondria and that the provision of additional carnitine in the diet and appearance in the plasma would result in an increased muscle carnitine content, increased LCFA transport into the mitochondria and increased fat oxidation. It is clear that attempts to increase muscle carnitine content by oral carnitine supplementation have been ineffective in healthy individuals. Not surprisingly, the majority of well-controlled studies on this topic have reported no effect of carnitine supplementation on (i) enhancing fat oxidation, (ii) reducing carbohydrate oxidation, glycogen breakdown or lactate accumulation, (iii) enhancing performance during prolonged endurance exercise.  The review article documents that the only way to raise muscle carnitine contents have been temporarily elevated by 10-20% with infusion-induced plasma hypercarnitinaemia and hyperinsulinaemia may be useful in determining whether muscle carnitine levels limits oxidative metabolism during strenuous exercise.

Spriet LL, Perry CG, Talanian JL. Legal pre-event nutritional supplements to assist energy metabolism. Essays Biochem. 2008;44:27-43.