Carnitine Supplementation and Performance

Up to this point we have examined the influence of acute and chronic exercise on carnitine levels in the muscle, plasma, and urine. The literature is fairly consistent in that there does not seem to be a depletion of total muscle carnitine and that an acute bout or chronic training does not change these levels. It is important to now focus on the performance aspect of these and other studies. The intent is to ascertain whether carnitine supplementation enhances performance as measured by such variables as VO2 max, RQ, exercise duration, blood lactate concentrations, substrate metabolism, and glycogen sparing. There have been several studies that measured all or some combination of these markers, and they will be presented in chronological order to help follow the progression of carnitine research.

An early study by Marconi et al.62 used six competitive racewalkers and measured VO2 max, blood lactate, and RQ. Subjects were supplemented with 4 g of oral carnitine for 2 weeks after which VO2 max was found to be significantly increased from 54.5 ± 3.7 ml-kg-min1 to 57.8 ± 4.7 ml-kg-min1. In addition, there were no significant changes in blood lactate accumulation or RQ at a fixed workload. The authors62 speculated that this slight but significant increase in VO2 max was due to the activation of substrate flow through the Krebs cycle. This simply means that with an increase in substrate flow through the Krebs cycle, there is a postulated increase in ATP production that allowed the subjects to increase VO2 max. Subsequent studies69 could not reproduce these results and found that 2 g of oral carnitine administered to separate groups for either 14 or 28 days produced no significant effects on either VO2 max or lactate. It is important to note that the training statuses of the two groups were different, one being trained62 and the other untrained.69 However, neither study was able to alter blood lactate, RQ, heart rate (HR), or ventilation (VE), suggesting that the increases in VO2 max found in the Marconi study62 may not be physiologically significant.

Angelini et al.70 used a double-blind protocol to examine untrained subjects who were given either a placebo or carnitine supplementation (50 mg/kg/day) for 1 month during an exercise regiment. VO2 max increased after the supplementation period, but it was not possible to determine whether the affect was due to the carnitine supplementation or the training regimen since untrained individuals can show significant improvements in VO2 max within 30 days of aerobic training. Furthermore, Cooper et al.65 showed that there was no significant improvement in marathon race time despite a daily supplementation of 4 g of oral carnitine for 10 days.

Oyono-Enguelle et al.71 and Soop et al.51 found no effect of carnitine supplementation for VO2, volume of carbon dioxide (VCO2), lactate, blood glucose at a fixed workload, or FA turnover. These studies used untrained71 and moderately trained51 individuals and supplemented 5 g orally for 10 days71 and 2 g orally for 28 days,51 respectively. Both studies concluded that in healthy subjects carnitine supplementation does not influence FA utilization, suggesting that the endogenous production of carnitine is sufficient to support exercise.

Gorostiaga et al.55 utilized 10 endurance-trained subjects (8 marathoners, 1 cyclist, 1 jogger) and supplemented 2 g of oral carnitine for 28 days. Subjects exercised for 45 min at 66% of VO2 max. Significant differences were observed between supplemented and nonsupplemented groups with respect to RQ during the 38- to 45-min interval (0.95 ± 0.01 vs. 0.98 ± 0.02, respectively), but not any of the earlier time intervals. There were no other changes reported in any of the other variables measured, which included VO2 max, HR, blood glycerol, and resting blood FA concentrations. These results seem insignificant since other physiological parameters do not help to substantiate the reduction in RQ at one time interval.

In 1990, Siliprandi et al.53 and Vecchiet et al.54 examined the effects of 2 g of oral carnitine in a single dose approximately 1 h prior to cycle ergometer exercise. Carnitine supplementation was reported to reduce blood lactate and increase VO2 max post-exercise. The authors claim that during this high-intensity exercise the PDC is stimulated, thereby reducing lactate production due to the alteration of the acetyl-CoA:free CoA ratio. These findings, however, were not supported, as Con-stantin-Teodosiu42-44 showed that full activity of the PDC was reached within a minute of activation and is independent of carnitine supplementation.

Subsequent studies4572-77 have tried to extend carnitine research to cover varying lengths of time (7 to 14 days), utilize different exercise modalities, including swimming, and alter administration via either oral or intravenous doses. The variables measured included performance times, VO2 max, VCO2, substrate utilization, glycogen storage, blood lactate, and FA turnover. Findings from these experiments exhibit no support for the ergogenic benefits of carnitine on performance (Table 11.1). These physiological parameters are what govern our performance, and if a supplement is not successful in consistently altering these parameters, then the efficacy of carnitine as an ergogenic aid is diminished. It is important to note here that there have also been studies trying to elucidate carnitine as a weight-loss supplement due to its association with FA metabolism. The fact remains that these studies78,79 show that carnitine is not a contributing factor to weight loss since many supplements are given with calorie-restricted diets and exercise programs that are in themselves effective tools in reducing weight and increasing muscle mass. Supplement companies then mask their results behind the truly effective tools in weight management.

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