L-carnitine supplementation: influence upon physiological function (original) (raw)
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Carnitine in Human Muscle Bioenergetics: Can Carnitine Supplementation Improve Physical Exercise?
Molecules, 2020
l-Carnitine is an amino acid derivative widely known for its involvement in the transport of long-chain fatty acids into the mitochondrial matrix, where fatty acid oxidation occurs. Moreover, l-Carnitine protects the cell from acyl-CoA accretion through the generation of acylcarnitines. Circulating carnitine is mainly supplied by animal-based food products and to a lesser extent by endogenous biosynthesis in the liver and kidney. Human muscle contains high amounts of carnitine but it depends on the uptake of this compound from the bloodstream, due to muscle inability to synthesize carnitine. Mitochondrial fatty acid oxidation represents an important energy source for muscle metabolism particularly during physical exercise. However, especially during high-intensity exercise, this process seems to be limited by the mitochondrial availability of free l-carnitine. Hence, fatty acid oxidation rapidly declines, increasing exercise intensity from moderate to high. Considering the important role of fatty acids in muscle bioenergetics, and the limiting effect of free carnitine in fatty acid oxidation during endurance exercise, l-carnitine supplementation has been hypothesized to improve exercise performance. So far, the question of the role of l-carnitine supplementation on muscle performance has not definitively been clarified. Differences in exercise intensity, training or conditioning of the subjects, amount of l-carnitine administered, route and timing of administration relative to the exercise led to different experimental results. In this review, we will describe the role of l-carnitine in muscle energetics and the main causes that led to conflicting data on the use of l-carnitine as a supplement.
Clinica Chimica Acta, 2002
Background: Long-term administration of high oral doses of L-carnitine on the skeletal muscle composition and the physical performance has not been studied in humans. Methods: Eight healthy male adults were treated with 2 Â 2 g of L-carnitine per day for 3 months. Muscle biopsies and exercise tests were performed before, immediately after, and 2 months after the treatment. Exercise tests were performed using a bicycle ergometer for 10 min at 20%, 40%, and 60% of the individual maximal workload (P max), respectively, until exhaustion. Results: There were no significant differences between V O 2 max, RER max , and P max between the three time points investigated. At submaximal intensities, the only difference to the pretreatment values was a 5% increase in V O 2 at 20% and 40% of P max 2 months after the cessation of the treatment. The total carnitine content in the skeletal muscle was 4.10 F 0.82 mmol/g before, 4.79 F 1.19 mmol/g immediately after, and 4.19 F 0.61 mmol/g wet weight 2 months after the treatment (no significant difference). Activities of the two mitochondrial enzymes citrate synthase and cytochrome oxidase, as well as the skeletal muscle fiber composition also remained unaffected by the administration of Lcarnitine. Conclusions: Long-term oral treatment of healthy adults with L-carnitine is not associated with a significant increase in the muscle carnitine content, mitochondrial proliferation, or physical performance. Beneficial effects of the long-term treatment with L-carnitine on the physical performance of healthy adults cannot be explained by an increase in the carnitine muscle stores.
L-Carnitine Supplementation: A New Paradigm for its Role in Exercise
Monatshefte für Chemie - Chemical Monthly, 2005
Early research investigating the effects of L-carnitine supplementation has examined its role in substrate metabolism and in acute exercise performance. These studies have yielded equivocal findings, partially due to difficulties in increasing muscle carnitine concentrations. However, recent studies have proposed that L-carnitine may play a different role in exercise physiology, and preliminary results have been encouraging. Current investigations have theorized that L-carnitine supplementation facilitates exercise recovery. Proposed mechanism is as follows: 1) increased serum carnitine concentration enhances capillary endothelial function; 2) increased blood flow and reduced hypoxia mitigate the cascade of ensuing, destructive chemical events following exercise; 3) thus allowing reduced structural damage of skeletal muscle mediated by more intact receptors in muscle needed for improved protein signaling. This paradigm explains decreased markers of purine catabolism, free radical formation, and muscle tissue disruption after resistance exercise and the increased repair of muscle proteins following long-term L-carnitine supplementation.
European Journal of Applied Physiology and Occupational Physiology, 1992
Carnitine has a potential effect on exercise capacity due to its role in the transport of long-chain fatty acids into the mitochondria for p-oxidation, the export of acyl-coenzyme A compounds from mitochondria and the activation of branched-chain amino acid oxidation in the muscle. We studied the effect of carnitine supplementation on palmitate oxidation, maximal exercise capacity and nitrogen balance in rats. Daily carnitine supplementation (500 mg. kg-1 body mass for 6 weeks) was given to 30 rats, 15 of which were on an otherwise carnitine-free diet (group I) and 15 pair-fed with a conventional pellet diet (group II). A control group (group III, n = 6) was fed ad libitum the pellet diet. Palmitate oxidation was measured by collecting 14CO2 after an intraperitoneal injection of [1-14C]palmitate and exercise capacity by swimming to exhaustion. After carnitine supplementation carnitine concentrations in serum were supranormal [group I, total 150.8 (SD 48.5), free 78.9 (SD 18.4); group II, total 170.9 (SD 27.9), free 115.8 (SD 24.6) gmol. 1 -l] and liver carnitine concentrations were normal in both groups [group I, total 1.6 (SD 0.3), free 1.2 (SD 0.2); group II, total 1.3 (SD 0.3), free 0.9 (SD 0.2) gmol.g-1 dry mass]. In muscle carnitine concentrations were normal in group I [total 3.8 (SD 1.2), free 3.2 (SD 1.0) gmol.g -1 dry mass] and increased in group II [total 6.6 (SD 0.5), free 4.9 (SD 0.9) gmol.g-i dry mass]. Despite the difference in muscle carnitine concentrations there were no differences among the groups in cumulative palmitate oxidation after 3 h [group I, 39.7 (SD 11.6)%; group II, 29.6 (SD 14.0)%; group III, 36.5 (SD 10.8)% of injected activity] or swimming time to exhaustion [group I, 9.7 (SD 2.9); group II, 8.4 (SD 3.6); group III, 7.1 (SD 2.8) h]. A borderline increase in nitrogen balance was observed in group II. We concluded that increasing carnitine tissue concentrations by carnitine supplementation had no effect on palmitate oxidation and maximal exercise capacity in the rats studied.
Significance ofl-carnitine for human health
IUBMB Life, 2017
Carnitine acyltransferases catalyze the reversible transfer of acyl groups from acyl-coenzyme A esters to L-carnitine, forming acyl-carnitine esters that may be transported across cell membranes. L-Carnitine is a w ater-soluble compound that humans may obtain both by food ingestion and endogenous synthesis from trimethyl-lysine. Most L-carnitine is intracellular, being present predominantly in liver, skeletal muscle, heart and kidney. The organic cation transporter-2 facilitates Lcarnitine uptake inside cells. Congenital dysfunction of this transporter causes primary L-carnitine deficiency. Carnitine acetyltransferase is involved in the export of excess acetyl groups from the mitochondria and in acetylation reactions that regulate gene transcription and enzyme activity. Carnitine octanoyltransferase is a peroxysomal enzyme required for the complete oxidation of very long-chain fatty acids and phytanic acid, a branched-chain fatty acid. Carnitine palmitoyltransferase-1 is a transmembrane protein located on the outer mitochondrial membrane where it catalyzes the conversion of acyl-coenzyme A esters to acyl-carnitine esters. Carnitine acyl-carnitine translocase transports acyl-carnitine esters across the inner mitochondrial membrane in exchange for free L-carnitine that exits the mitochondrial matrix. Carnitine palmitoyltransferase-2 is anchored on the matrix side of the inner mitochondrial membrane, where it converts acyl-carnitine esters back to acyl-coenzyme A esters, which may be used in metabolic pathways, such as mitochondrial b-oxidation. L-Carnitine enhances nonoxidative glucose disposal under euglycemic hyperinsulinemic conditions in both healthy individuals and patients with type 2 diabetes, suggesting that L-carnitine strengthens insulin effect on glycogen storage. The plasma level of acyl-carnitine esters, primarily acetylcarnitine, increases during diabetic ketoacidosis, fasting, and physical activity, particularly high-intensity exercise. Plasma concentration of free L-carnitine decreases simultaneously under these conditions.
Supplementation of L-carnitine in athletes: does it make sense?
Nutrition (Burbank, Los Angeles County, Calif.)
Studies in athletes have shown that carnitine supplementation may foster exercise performance. As reported in the majority of studies, an increase in maximal oxygen consumption and a lowering of the respiratory quotient indicate that dietary carnitine has the potential to stimulate lipid metabolism. Treatment with L-carnitine also has been shown to induce a significant postexercise decrease in plasma lactate, which is formed and used continuously under fully aerobic conditions. Data from preliminary studies have indicated that L-carnitine supplementation can attenuate the deleterious effects of hypoxic training and speed up recovery from exercise stress. Recent data have indicated that L-carnitine plays a decisive role in the prevention of cellular damage and favorably affects recovery from exercise stress. Uptake of L-carnitine by blood cells may induce at least three mechanisms: 1) stimulation of hematopoiesis, 2) a dose-dependent inhibition of collagen-induced platelet aggregatio...
European Journal of Applied Physiology and Occupational Physiology, 1996
A double-blind crossover field study was performed to investigate the effects of acute L-carnitine supplementation on metabolism and performance of endurance-trained athletes during and after a marathon run. Seven male subjects were given supplements of 2 g L-carnitine 2 h before the start of a marathon run and again after 20 km of the run. The plasma concentration of metabolites and hormones was analysed 1 h before, immediately after and 1 h after the run, as well as the next morning after the run. In addition, the respiratory exchange ratio (R) was determined before and at the end of the run, and a submaximal performance test was completed on a treadmill the morning after the run. The administration of L-carnitine was associated with a significant increase in the plasma concentration of all analysed carnitine fractions (i.e. free carnitine, short-chain acylcarnitine, long-chain acylcarnitine, total acid soluble carnitine, total carnitine) but caused no significant change in marathon running time, in R, in the plasma concentrations of carbohydrate metabolites (glucose, lactate, pyruvate), of fat metabolites (free fatty acids, glycerol, ]~-hydroxybutyrate), of hormones (insulin, glucagon, cortisol), and of enzyme activities (creatine kinase, lactate P. Colombani ([2~).
Croatica Chemica Acta, 2006
Because of its role in a transport of fatty acids from cytosol into mitochondrion, a consumption of L-carnitine became popular among athletes, and/or as a weight loss supplement. In an attempt to obtain more data on the effect of L-carnitine supplementation on some biochemical parameters in blood serum, a double-blind, placebo-controlled study was carried. Healthy volunteers with declared sedentary activities received 2 g/day of either L-carnitine or placebo for 2 weeks. L-carnitine administration induced no statistically significant changes in blood serum concentrations of glucose, triacylglycerols, total cholesterol, HDL-cholesterol and creatinine, neither affected the activity of analysed enzymes (AST, ALT, LDH, and CK). The only observed effect was a decline in the concentration of free fatty acids in serum from 0.439 mmol/L at the beginning to 0.279 mmol/L at the end of the experiment. Body mass reduction was not achieved. We conclude that L-carnitine supplementation cannot be ...
REVIEW ARTICLE Supplementation of L-Carnitine in Athletes: Does It Make Sense?
2013
Studies in athletes have shown that carnitine supplementation may foster exercise performance. As reported in the majority of studies, an increase in maximal oxygen consumption and a lowering of the respiratory quotient indicate that dietary carnitine has the potential to stimulate lipid metabolism. Treatment with L-carnitine also has been shown to induce a significant postexercise decrease in plasma lactate, which is formed and used continuously under fully aerobic conditions. Data from preliminary studies have indicated that L-carnitine supplementation can attenuate the deleterious effects of hypoxic training and speed up recovery from exercise stress. Recent data have indicated that L-carnitine plays a decisive role in the prevention of cellular damage and favorably affects recovery from exercise stress. Uptake of L-carnitine by blood cells may induce at least three mechanisms: 1) stimulation of hematopoiesis, 2) a dose-dependent inhibition of collagen-induced platelet aggregatio...
Asian Journal of Sports Medicine, 2016
Background: The effectiveness of L-carnitine supplementation has been met with conflicting findings when used by sedentary and athletic adults. Objectives: This study aimed to investigate the acute effects of L-carnitine supplementation on aerobic metabolic efficiency and lipid profiles in sedentary and athletic men. Methods: Fifteen sedentary (20.4 ± 1.5 years) and 15 athletic (21.5 ± 2.4 years) men were studied in durations of control, placebo intake and 2 g of L-carnitine supplementation. Lipid profiles, including triglyceride, cholesterol, high-density lipoprotein (HDL) and very-low density lipoprotein (VLDL), were determined before and 40 min after either the placebo or L-carnitine intake. Oxygen consumption (direct VO2), ventilatory threshold (VT), and running time (RT) were recorded after a submaximal treadmill exercise test. Results: Direct VO2 increased significantly at 80% of maximal heart rate after L-carnitine supplementation in both athletic and sedentary men, whereas, a statistical increase in VT and RT occurred only after L-carnitine use in athletes, when compared to the control and placebo subjects. The sedentary group showed no changes in lipid parameters, but triglyceride levels reduced significantly in the athletes after consuming L-carnitine. Conclusions: Acute L-carnitine supplementation possibly affects exercise performance and triglycerides in athletes rather than sedentary men.