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Elizabeth M. Broad, Ronald J. Maughan and Stuart D.R. Galloway

In a randomized, placebo-controlled, double-blind crossover design, 15 trained males undertook exercise trials during two 4 wk supplementation periods, with either 3 g L-Carnitine L-tartrate (LCLT) or 3 g placebo (P) daily. Total carbohydrate and fat oxidation during 90 min steady state cycling were not different between 0 or 4 wk within LCLT or P trials (mean ± standard deviation: carbohydrate oxidation P0 99 ± 36, P4W 111 ± 27, LCLT0 107 ± 33, LCLT4W 112 ± 32 g, respectively; fat oxidation P0 99 ± 28, P4W 92 ± 21, LCLT0 94 ± 18, LCLT4W 90 ± 22 g, respectively). Subsequent 20 km time trial duration was shorter after P (P0 31:29 ± 3:50, P4W 29:55 ± 2:58 min:s, P < 0.01), with no significant change over LCLT (LCLT0 31:46 ± 4:06, LCLT4W 31.19 ± 4.08 min:s). Four weeks LCLT supplementation had no effect on substrate utilization or endurance performance.

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Weronika N. Abramowicz and Stuart D.R. Galloway

Twelve healthy active subjects (6 male, 6 female) performed 60 min of exercise (60% VO2max) on 3 occasions after supplementing with L-Carnitine L-tartrate (LCLT) or placebo. Each subject received a chronic dose, an acute dose, and placebo in a randomized, double-blind crossover design. Dietary intake and exercise were replicated for 2 d prior to each trial. In males there was a significant difference in rate of carbohydrate (CHO) oxidation between placebo and chronic trials (P = 0.02) but not placebo and acute trials (P = 0.70), and total CHO oxidation was greater following chronic supplementation vs. placebo (mean ± standard deviation) of 93.8 (17.3) g/hr and 78.2 (23.3) g/h, respectively). In females, no difference in rate of, or total, CHO oxidation was observed between trials. No effects on fat oxidation or hematological responses were noted in either gender group. Under these experimental conditions, chronic LCLT supplementation increased CHO oxidation in males during exercise but this was not observed in females

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Elizabeth M. Broad, Ronald J. Maughan and Stuart D.R. Galloway

The effects of 15 d of supplementation with L-carnitine L-tartrate (LC) on metabolic responses to gradedintensity exercise under conditions of altered substrate availability were examined. Fifteen endurance-trained male athletes undertook exercise trials after a 2-d high-carbohydrate diet (60% CHO, 25% fat) at baseline (D0), on Day 14 (D14), and after a single day of high fat intake (15% CHO, 70% fat) on Day 15 (D15) in a double-blind, placebo-controlled, pair-matched design. Treatment consisted of 3 g LC (2 g L-carnitine/d; n = 8) or placebo (P, n = 7) for 15 d. Exercise trials consisted of 80 min of continuous cycling comprising 20-min periods at each of 20%, 40%, 60%, and 80% VO2peak. There was no significant difference between whole-body rates of CHO and fat oxidation at any workload between D0 and D14 trials for either the P or LC group. Both groups displayed increased fat and reduced carbohydrate oxidation between the D14 and D15 trials (p < .05). During the D15 trial, heart rate (p < .05 for 20%, 40%, and 60% workloads) and blood glucose concentration (p < .05 for 40% and 60% workloads) were lower during exercise in the LC group than in P. These responses suggest that LC may induce subtle changes in substrate handling in metabolically active tissues when fattyacid availability is increased, but it does not affect whole-body substrate utilization during short-duration exercise at the intensities studied.

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Elizabeth M. Broad, Ronald J. Maughan and Stuart D.R Galloway

Twenty nonvegetarian active males were pair-matched and randomly assigned to receive 2 g of L-carnitine L-tartrate (LC) or placebo per day for 2 wk. Participants exercised for 90 min at 70% VO2max after 2 days of a prescribed diet (M ±SD: 13.6 ± 1.6 MJ, 57% carbohydrate, 15% protein, 26% fat, 2% alcohol) before and after supplementation. Results indicated no change in carbohydrate oxidation, nitrogen excretion, branched-chain amino acid oxidation, or plasma urea during exercise between the beginning and end of supplementation in either group. After 2 wk of LC supplementation the plasma ammonia response to exercise tended to be suppressed (0 vs. 2 wk at 60 min exercise, 97 ± 26 vs. 80 ± 9, and 90 min exercise, 116 ± 47 vs. 87 ± 25 μmol/L), with no change in the placebo group. The data indicate that 2 wk of LC supplementation does not affect fat, carbohydrate, and protein contribution to metabolism during prolonged moderate-intensity cycling exercise. The tendency toward suppressed ammonia accumulation, however, indicates that oral LC supplementation might have the potential to reduce the metabolic stress of exercise or alter ammonia production or removal, which warrants further investigation.