It is evident that changes occur within the plasma and muscle with regard to free carnitine and acylcarnitine, but not necessarily total carnitine. The next logical step is to analyze the effect of intensity on carnitine concentrations. High-intensity exercise will decrease the free carnitine levels because of the reaction with acetyl-CoA. Furthermore, at very high intensities free carnitine will decrease to very low levels. Brass and Hiatt52 have reported values as low as 0.5 to 1.0 mM/kg of wet muscle weight, which approach the concentration needed for half-maximal activity (0.25 to 0.45 mM/kg of wet muscle) of CAT. This decrease in free carnitine has been postulated to be the reason why exercise physiologists report a transition in substrate utilization between moderate- to high-intensity exercise.
Siliprandi et al.53 supplemented with 2 g of carnitine before high-intensity exercise and found that PDH activity was stimulated and there was a reduction in both plasma lactate and pyruvate. In a similar study, Vecchiet et al.54 administered L-carnitine or a placebo 1 h before cycle ergometer exercise. The exercise was a graded protocol designed to increase by 50 W every 3 min until exhaustion. Seventy-two hours later the subjects came in to repeat the trial; however, those who got carnitine first did their second trial with the placebo and vice versa. Results showed that VO2 max increased while carbon dioxide production, pulmonary ventilation, and lactate production decreased.
Several authors have reported a decreased respiratory quotient (RQ) with carnitine supplementation,55-57 suggesting that carnitine influences substrate utilization. In support of this hypothesis, both Gorostiaga et al.55 and Muller et al.57 reported an increase in lipid utilization, therefore sparing carbohydrates and prolonging exercise time.
High-intensity exercise has been implicated in muscle soreness. Giamberardino et al.58 examined the effects of carnitine on pain using the Visual Analog Scale, tenderness (pain thresholds), and creatine kinase (CK) release. Subjects were given 3 g/day of a placebo for 3 weeks, and then after a week, washout was given, 3 g/day of carnitine. Subjects performed a step test to stimulate eccentric muscular work during both supplementation periods. Results showed that carnitine supplementation reduced pain, tenderness, and CK release compared to placebo. These results are supported by Kraemer et al.,59 who also found decreased muscle tissue damage as assessed by magnetic resonance imaging (MRI). Both authors suggest that carnitine supplementation is beneficial for hypoxic (high-intensity) exercise, perhaps due to its vasodilatory properties, and will reduce sarcolemma disruption and perceived muscle soreness.
Despite several studies showing the benefits of carnitine supplementation, there are several that do not show significant results. Hiatt et al.46 set out to characterize carnitine at two different exercise intensities: 60 min at 50% lactate threshold (LT) and 30 min at a workload between LT and maximal work capacity for each individual. This was intended to reflect exercise intensities that primarily utilize FAs (50% LT) and carbohydrates (above LT to maximum) for energy production. Findings revealed that the lower-intensity exercise was not associated with changes in muscle carnitine metabolism as reflected by alterations in free carnitine and acylcarnitine.46 In contrast, within 10 min of the high-intensity exercise, muscle acylcarnitine increased by 5.5-fold and free carnitine decreased by 66%. These changes remained over the duration of the high-intensity exercise and persisted for 60 min into recovery. The changes were seen in both long- and short-chain acylcarnitines. In addition, plasma acylcarnitine levels were also increased, suggesting that there is a redistribution of the carnitine pool that may persist even after recovery.46 It is important to note that the authors did report that neither exercise bout was associated with changes in carnitine urinary excretion rates or plasma concentrations.
In support of this idea, Sahlin60 examined carnitine concentrations during several exercise intensities (40, 75, and 100% VO2 max). No changes were seen with cycling in total muscle carnitine concentration, acylcarnitine, or free carnitine during the low-intensity exercise (40% VO2 max), but the high-intensity (75 and 100% VO2 max) workout produced a significant increase in acylcarnitine from rest (6.9 ± 1.9 mmol/kg) to exercise (18.1 ± 1.0 mmol/kg). In addition, there was a concurrent decrease in free carnitine levels.60 Decombaz et al.47 took the next step and studied cross-country skiers who underwent prolonged strenuous exercise to determine if a carnitine deficiency developed. The exercise consisted of a ski race in the Swiss Alps with an average completion time of 13 hours 26 minutes. Carnitine intake was evaluated for 2 weeks prior to the race (average, 50 ± 4 mg/day) in these highly trained individuals. Again, there was no difference in total carnitine content from rest (17.9 ± 1.0 mmol/kg) to post-exercise (18.3 ± 0.8 mmol/kg). In addition, there was a 20% decline in free carnitine concentration that was offset by a 108% increase in acylcarnitine. The authors47 concluded that carnitine deficiency would not develop in trained athletes with a moderate carnitine dietary intake.
There are varying results when analyzing the effects of carnitine on high-intensity exercise. Karlic and Lohninger38 critically examined the effects of carnitine supplementation among athletes and reported that 305 subjects demonstrated improved exercise performance and maximum oxygen consumption while 70 did not. It is therefore important to evaluate the efficacy of supplementation on an individual basis, determining whether it will work for you.
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