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Effects of propionyl-L-carnitine on walking performance and plasma acetylcarnitine in peripheral arterial disease
Abstract   Peer reviewed

Effects of propionyl-L-carnitine on walking performance and plasma acetylcarnitine in peripheral arterial disease

G Barker, S Green, Christopher D Askew and P J Walker
IOC World Congress on Sport Sciences, 5th (Sydney, Australia, 31-Oct-1999–05-Nov-1999)
1999

Abstract

Human Movement and Sports Science
Oral supplementation with propionyl-L-carnitine (PLC) improves exercise performance in some, but not all people with PAD . In the present study we have further explored this ergogenic effect in seven subjects with PAD (age=59±13.6 y). Over 12 weeks each subject completed three, four-week phases; baseline (B), supplementation (S) and placebo (P) conditions. During S subjects consumed 2g of PLC per day; whereas during P they consumed galactose/cellulose tablets. Subjects were blinded to the order of supplementation. Walking performance was measured using an incremental walking test at the end of each condition. Pre- and post exercise blood sample were taken, and lactate and acetylcarnitine were measured. The final baseline walking performance averaged 584±191 s which was not different from prior baseline values. The individual coefficients of variation (CV) for walking during this phase averaged 17.4 %. Relative to baseline, walking performance failed to significantly increase during S (584 vs 634s, p = 0.30); however, five of the seven subjects increased their performance by an average of 19.5% which exceeded the corresponding CV for these subjects. Resting lactate was 1.92±0.51 mM at baseline and did not differ significantly between conditions. Neither resting, post exercise, or the pre to post difference in [lactate] was predictive of exercise performance. Resting acetylcarnitine was 3.00±0.68 m M at baseline and was not significantly different following supplementation, or placebo (3.419±1.677 and 3.122±0.763m M). Post-exercise plasma acetylcarnitine was not significantly higher than resting (B=3.533±1.381, S=4.370±1.956, W=3.108±0.433m M). Only at baseline were resting acetylcarnitine and lactate concentration related (r = 0.779, p=0.039). There was no relationship between resting plasma acetylcarnitine, change in acetylcarnitine with exercise and exercise performance under baseline conditions. Following supplementation, the magnitude of change in the plasma acetylcarnitine content was correlated with the patients walking performance (r = 0.747, p = 0.053). This suggests the ability to accumulate acetyl groups is important to exercise performance, and along with our previous data, reinforces the view that PLC supplementation improves flux through the pyruvate dehydrogenase complex. In contrast to previous workers , we found no value in using pre-supplemental acetylcarnitine levels to predict the response of a patient to supplementation.

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