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Randomized Controlled Trial
. 2011 Feb 15;589(Pt 4):963-73.
doi: 10.1113/jphysiol.2010.201343. Epub 2011 Jan 4.

Chronic Oral Ingestion of L-carnitine and Carbohydrate Increases Muscle Carnitine Content and Alters Muscle Fuel Metabolism During Exercise in Humans

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Free PMC article
Randomized Controlled Trial

Chronic Oral Ingestion of L-carnitine and Carbohydrate Increases Muscle Carnitine Content and Alters Muscle Fuel Metabolism During Exercise in Humans

Benjamin T Wall et al. J Physiol. .
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Abstract

We have previously shown that insulin increases muscle total carnitine (TC) content during acute i.v. l-carnitine infusion. Here we determined the effects of chronic l-carnitine and carbohydrate (CHO; to elevate serum insulin) ingestion on muscle TC content and exercise metabolism and performance in humans. On three visits, each separated by 12 weeks, 14 healthy male volunteers (age 25.9 ± 2.1 years, BMI 23.0 ± 0.8 kg m−2) performed an exercise test comprising 30 min cycling at 50% , 30 min at 80% , then a 30 min work output performance trial. Muscle biopsies were obtained at rest and after exercise at 50% and 80% on each occasion. Following visit one, volunteers ingested either 80 g of CHO (Control) or 2 g of l-carnitine-l-tartrate and 80 g of CHO (Carnitine) twice daily for 24 weeks in a randomised, double blind manner. All significant effects reported occurred after 24 weeks. Muscle TC increased from basal by 21% in Carnitine (P < 0.05), and was unchanged in Control. At 50% , the Carnitine group utilised 55% less muscle glycogen compared to Control (P < 0.05) and 31% less pyruvate dehydrogenase complex (PDC) activation compared to before supplementation (P < 0.05). Conversely, at 80% , muscle PDC activation was 38% higher (P < 0.05), acetylcarnitine content showed a trend to be 16% greater (P < 0.10), muscle lactate content was 44% lower (P < 0.05) and the muscle PCr/ATP ratio was better maintained (P < 0.05) in Carnitine compared to Control. The Carnitine group increased work output 11% from baseline in the performance trial, while Control showed no change. This is the first demonstration that human muscle TC can be increased by dietary means and results in muscle glycogen sparing during low intensity exercise (consistent with an increase in lipid utilisation) and a better matching of glycolytic, PDC and mitochondrial flux during high intensity exercise, thereby reducing muscle anaerobic ATP production. Furthermore, these changes were associated with an improvement in exercise performance.

Figures

Figure 1
Figure 1
Total skeletal muscle carnitine content (calculated as the mean of 3 biopsies taken from each individual during a given visit) before (0) and 12 and 24 weeks after twice daily oral ingestion of either 80 g of carbohydrate (Control; n= 7) or 80 g of carbohydrate containing 2 g l-carnitine tartrate (Carnitine; n= 7). All values are means ±s.e.m.). Significantly different from Control: *P < 0.05. Significantly different from before supplementation (0): †P < 0.05.
Figure 2
Figure 2
Skeletal muscle glycogen utilisation (A), lactate accumulation (B) and pyruvate dehydrogenase complex activation status (C) during 30 min of exercise at 50 and 80%formula image before (0) and 12 and 24 weeks after twice daily oral ingestion of either 80 g of carbohydrate (Control; n= 7) or 80 g of carbohydrate containing 2 g l-carnitine tartrate (Carnitine; n= 7). All values are means ±s.e.m. Significantly different from corresponding Control: *P < 0.05. Significantly different from before supplementation (0): †P < 0.05.
Figure 3
Figure 3
Work output generated during a 30 min ‘all-out’ exercise performance test performed immediately following 30 min of exercise at 50 and 80%formula image before (0) and 12 and 24 weeks after twice daily oral ingestion of either 80 g of carbohydrate (Control; n= 7) or 80 g of carbohydrate containing 2 g l-carnitine tartrate (Carnitine; n= 7). All values are means ±s.e.m. Significantly different from Control: *P < 0.05. Significantly different from before supplementation (0): †P < 0.05.

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