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   Discovered in 1905, L-carnitine is a nitrogen-containing, short-chain carboxylic acid—technically, it is not an amino acid. It is a water-soluble, vitamin-like compound (Kanter & Williams, 1995) that is readily synthesized in the body from lysine and methionine (Cerretelli & Marconi, 1990). Although carnitine is not an essential nutrient because it can be synthesized in the body, it is sometimes considered conditionally essential in that a dietary deficiency may cause adverse side effects in certain circumstances (Broquist, 1994). However, in an industrialized nation, such a deficiency is rare.
   Dietary carnitine can be easily obtained in a number of foods. Perhaps the best source is meat, particularly beef, sheep, and lamb. Other animal foods such as milk, cheese, and poultry contain somewhat less carnitine, while fruits and vegetables have negligible amounts (Kanter & Williams, 1995). In light of this, one must recognize that a diet containing sufficient amounts of essential amino acids will provide the necessary building blocks for our bodies to synthesize sufficient quantities of carnitine.
   L-carnitine functions in a three-part enzyme complex (carnitine acyltransferase I, carnitine translocase, and carnitine acyltransferase II) that is responsible for transport of long-chain fatty acids across the inner mitochondrial membrane to the cristae where ss-oxidative enzymes are active (Pande et. al., 1980).
   However, carnitine supplementation with supraphysiological doses above and beyond that which the body requires, does not result in increased fat oxidation at rest or during exercise in well-nourished individuals; thus, it appears that we can synthesize the necessary amounts from a diet adequate in its precursors (lysine and methionine). Those medically diagnosed as carnitine-deficient may benefit from a supplement, but this condition is uncommon.

Studies On L-Carnitine
   We have established thus far that carnitine plays a vital role in the transport of fatty acids across the inner mitochondrial membrane. Based on this function, it has been postulated that carnitine supplementation will enhance lipid oxidation and thereby improve endurance performance by sparing endogenous carbohydrate. Similarly, in anaerobic activity, it has been purported that oral carnitine will improve performance by inhibiting lactic acid production. The following literature review will address these claims for their validity.
   In a randomized, double-blind crossover study by Decombaz et. al. (1993), nine subjects were given 3 grams/day of L-carnitine for 7 days. Then at the end of the seven days, they completed a 20 minute bicycle exercise at 43% VO2 max. Respiratory quotient (RQ), heart rate (HR), rating of perceived exertion (RPE), and various blood parameters indicated no influence of carnitine supplementation on substrate utilization.
   Otto et al. (1987) completed a randomized, double-blind cross-over study employing 10 conditioned subjects. Participants completed a 4-week carnitine (500 mg/day) loading period prior to beginning a 60-minute endurance event. There were no demonstrable improvements in expiratory ventilation (Ve), VO2, HR, RQ, or work.
   In a separate study by Otto and colleagues (1987), 10 subjects participated in a double-blind crossover study and were randomly assigned to two trials of either 500 mg of carnitine/day or a placebo for 28 days. In this instance the authors were testing its effects on maximal VO2 and serum free fatty acid levels. There were no significant changes in VO2, Ve, anaerobic threshold (AT), HR, or max lactate.
     Fink et al. (1994) studied 8 subjects over 14 days of carnitine supplementation to see what effect it would have on lactate accumulation during high intensity exercise. Subjects performed supramaximal cycling activities at 115% VO2. L-carnitine supplementation had no effect on blood or muscle lactate accumulation.
   Ransone et al. (1994) employed 26 highly trained male distance runners for 14 days of carnitine administration. They completed a 600 m bout of activity and were analyzed for lactate accumulation. The researchers found no effect of carnitine on lactate accumulation during maximal anaerobic effort.
   Kasper et al. (1994) tested the effects of carnitine on running performance. Seven competitive male distance runners consumed 4g/day for two weeks prior to testing. They found no improvement in running performance during a 5k run and no decrease in blood lactate and heart rate.
   Gorostiaga and colleagues (1989) examined 10 subjects over 28 days of supplementation and its effects on respiratory quotient during exercise. This double-blind crossover study found a non significant increase in O2 uptake, blood glycerol, and free fatty acids, and a small down shift in RQ with carnitine supplementation. The authors noted that none of the data were conclusive and that further studies were needed to make any definitive statement on carnitine efficacy.

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