1. The effect of two-week L-carnitine supplementation on exercise -induced oxidative stress and muscle damage.
Parandak K1, Arazi H2, Khoshkhahesh F3, Nakhostin-Roohi B1.
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This study was conducted to assess the effect of Two-week L-carnitine supplementation on known markers of oxidative stress and muscle damage following acute bouts of exercise in active healthy young men.
METHODS:
Twenty-one active healthy men volunteered for this study. Participants were randomized in a double-blind placebo-controlled fashion into two groups: L-carnitine (C group; n=10) and placebo group (P group; n=11). They arrived at the laboratory after overnight fasting. A baseline blood sample was taken. Afterwards, subjects consumed either L-carnitine (2 capsules containing totally 2000 mg L-carnitine) or placebo (2 capsules containing totally 2000 mg lactose) daily for 14 days. On the day of the test, participants attended the athletics arena after overnight fasting. Then, participants were asked to run 14 km on the track at their highest ability. Blood samples were taken immediately, 2, and 24 hours after exercise. Plasma total antioxidant capacity (TAC), malondialdehyde (MDA) as thiobarbituric acid-reactive substance (TBARS) as a marker of lipid peroxidation, creatine kinase (CK) and lactate dehydrogenase (LDH) as markers of muscle damage were measured.
RESULTS:
TAC increased significantly 14 days after supplementation and 24h after exercise in C group compared with P group (P<0.05). Serum MDA-TBARS, CK, and LDH were significantly lower 24h after exercise in C group compared with P group (P<0.05).
CONCLUSION:
These results suggest that two-week daily oral supplementation of L-carnitine has alleviating effects on lipid peroxidation and muscle damage markers following an acute bout of exercise in active healthy young men.
2. L-Carnitine enhances exercise endurance capacity by promoting muscle oxidative metabolism in mice.
Kim JH1, Pan JH1, Lee ES1, Kim YJ2.
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Abstract
L-Carnitine (LC), the bioactive form of carnitine, has been shown to play a key role in muscle fuel metabolism during exercise, resulting in increased fatty acid oxidation and energy expenditure. However, whether LC contributes to improved endurance exercise performance remains controversial. This study was designed to investigate the effects of LC administration on endurance capacity and energy metabolism in mice during treadmill exercise. Male C57BL/6 mice were divided into two groups (sedentary and exercise) and received daily oral administration of LC (150 mg/kg) or vehicle with a high-fat diet for 3 weeks. During the experimental period, all animals were trained three times a week on a motorized treadmill, and the total running time until exhaustion was used as the index of endurance capacity. LC administration induced a significant increase in maximum running time with a reduction of body fat compared with the control group when mice were subjected to programmed exercise. The serum levels of triglyceride, non-esterified fatty acid, and urea nitrogen were significantly lower in the LC group than the corresponding levels in the control group, while serum ketone body levels were higher in the LC group. Muscle glycogen content of LC administered-mice was higher than that of control mice, concomitant with reduced triglyceride content. Importantly, muscle mRNA and protein expressions revealed enhanced fatty acid uptake and oxidative metabolism and increased mitochondrial biogenesis by LC administration. These results suggest that LC administration promotes fat oxidation and mitochondrial biogenesis while sparing stored glycogen in skeletal muscle during prolonged exercise, resulting in enhanced endurance capacity.
Copyright © 2015 Elsevier Inc. All rights reserved.
3. Responses of criterion variables to different supplemental doses of L-carnitine L-tartrate.
Spiering BA1, Kraemer WJ, Vingren JL, Hatfield DL, Fragala MS, Ho JY, Maresh CM, Anderson JM, Volek JS.
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Abstract
L-carnitine L-tartrate (LCLT) supplementation beneficially affects markers of postexercise metabolic stress and muscle damage. However, to date, no study has determined the dose response of LCLT to elicit such responses. Therefore, the purpose of this study was to determine the effects of different doses of LCLT on criterion variables previously shown to be responsive to LCLT supplementation. Eight healthy men (22 +/- 3 y, 174 +/- 5 cm, 83.0 +/- 15.3 kg) were supplemented with 0 g, 1 g, and 2 g of LCLT for 3 weeks and then performed a bout of resistance exercise (5 sets of 15-20 repetition maximum with a 2-min rest between sets) with associated blood draws. This procedure was performed in a balanced, randomized, repeated measures design. Serum carnitine concentrations increased (p < or = 0.05) following the 1 g and 2 g doses, with the 2-g dose providing the highest carnitine concentrations. The 1- and 2-g doses reduced postexercise serum hypoxanthine, serum xanthine oxidase, serum myoglobin, and perceived muscle soreness. In conclusion, both the 1- and 2-g doses were effective in mediating various markers of metabolic stress and of muscle soreness. Use of LCLT appears to attenuate metabolic stress and the hypoxic chain of events leading to muscle damage after exercise.
4. The effects of L-carnitine L-tartrate supplementation on hormonal responses to resistance exercise and recovery.
Kraemer WJ1, Volek JS, French DN, Rubin MR, Sharman MJ, Gómez AL, Ratamess NA, Newton RU, Jemiolo B, Craig BW, Häkkinen K.
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Abstract
The purpose of this investigation was to examine the influence of L-carnitine L-tartrate (LCLT) supplementation using a balanced, cross-over, placebo-controlled research design on the anabolic hormone response (i.e., testosterone [T], insulin-like growth factor-I, insulin-like growth factor-binding protein-3 [IGFBP-3], and immunofunctional and immunoreactive growth hormone [GHif and GHir]) to acute resistance exercise. Ten healthy, recreationally weight-trained men (mean +/- SD age 23.7 +/- 2.3 years, weight 78.7 +/- 8.5 kg, and height 179.2 +/- 4.6 cm) volunteered and were matched, and after 3 weeks of supplementation (2 g LCLT per day), fasting morning blood samples were obtained on six consecutive days (D1-D6). Subjects performed a squat protocol (5 sets of 15-20 repetitions) on D2. During the squat protocol, blood samples were obtained before exercise and 0, 15, 30, 120, and 180 minutes postexercise. After a 1-week washout period, subjects consumed the other supplement for a 3-week period, and the same experimental protocol was repeated using the exact same procedures. Expected exercise-induced increases in all of the hormones were observed for GHir, GHif, IGFBP-3, and T. Over the recovery period, LCLT reduced the amount of exercise-induced muscle tissue damage, which was assessed via magnetic resonance imaging scans of the thigh. LCLT supplementation significantly (p < 0.05) increased IGFBP-3 concentrations prior to and at 30, 120, and 180 minutes after acute exercise. No other direct effects of LCLT supplementation were observed on the absolute concentrations of the hormones examined, but with more undamaged tissue, a greater number of intact receptors would be available for hormonal interactions. These data support the use of LCLT as a recovery supplement for hypoxic exercise and lend further insights into the hormonal mechanisms that may help to mediate quicker recovery.
5. Supplementation of L-carnitine in athletes: does it make sense?
Karlic H1, Lohninger A.
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Abstract
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 aggregation, and 3) the prevention of programmed cell death in immune cells. As recently shown, carnitine has direct effects in regulation of gene expression (i.e., carnitine-acyltransferases) and may also exert effects via modulating intracellular fatty acid concentration. Thus there is evidence for a beneficial effect of L-carnitine supplementation in training, competition, and recovery from strenuous exercise and in regenerative athletics.
6. L-carnitine supplementation as a potential antioxidant therapy for inherited neurometabolic disorders.
Ribas GS1, Vargas CR, Wajner M.
In recent years increasing evidence has emerged suggesting that oxidative stress is involved in the pathophysiology of a number of inherited metabolic disorders. However the clinical use of classical antioxidants in these diseases has been poorly evaluated and so far no benefit has been demonstrated. l-Carnitine is an endogenous substance that acts as a carrier for fatty acids across the inner mitochondrial membrane necessary for subsequent beta-oxidation and ATP production. Besides its important role in the metabolism of lipids, l-carnitine is also a potent antioxidant (free radical scavenger) and thus may protect tissues from oxidative damage. This review addresses recent findings obtained from patients with some inherited neurometabolic diseases showing that l-carnitine may be involved in the reduction of oxidative damage observed in these disorders. For some of these diseases, reduced concentrations of l-carnitine may occur due to the combination of this compound to the accumulating toxic metabolites, especially organic acids, or as a result of protein restricted diets. Thus, l-carnitine supplementation may be useful not only to prevent tissue deficiency of this element, but also to avoid oxidative damage secondary to increased production of reactive species in these diseases. Considering the ability of l-carnitine to easily cross the blood-brain barrier, l-carnitine supplementation may also be beneficial in preventing neurological damage derived from oxidative injury. However further studies are required to better explore this potential.
© 2013 Elsevier B.V. All rights reserved.
7. Plasma and urine carnitine concentrations in well-trained athletes at rest and after exercise. Influence of L-carnitine intake.
Nüesch R1, Rossetto M, Martina B.
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Abstract
L-carnitine is essential to cellular energy production mainly because of its acyl- and acetyl-carrier properties. Athletes commonly take L-carnitine, which is thought to improve exercise performance. There are no reports on carnitine plasma concentrations and carnitine excretion in short-duration maximal exercise in well-trained athletes taking this substance. We measured plasma and urine carnitine concentrations before and 10 min after maximal treadmill ergometry in nine well-trained sportsmen with and without oral supplementation with 1 g L-carnitine. In athletes without L-carnitine intake, plasma free carnitine concentration decreased significantly from 45.2 +/- 5.3 to 41.6 +/- 5.0 mumol/l (mean +/- SD, p < 0.001) 10 min after exercise compared with baseline. In athletes with oral L-carnitine supplementation, plasma free carnitine concentration at baseline was 71.3 +/- 10.2 mumol/l and did not change after maximal exercise (71.8 mumol/l +/- 10.7 mumol/l). The elevated plasma concentration of free carnitine without decrease after maximal exercise in well-trained athletes taking L-carnitine could be important in view of the newly postulated direct vascular effects of L-carnitine in improving skeletal muscle performance.
8. The effect of (L-)carnitine on weight loss in adults: a systematic review and meta-analysis of randomized controlled trials.
Pooyandjoo M1, Nouhi M2, Shab-Bidar S3, Djafarian K4, Olyaeemanesh A5.
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Abstract
This study provides a systematic review and meta-analysis of randomized controlled trials, which have examined the effect of the carnitine on adult weight loss. Relevant studies were identified by systematic search of PubMed, Embase, Cochrane Central Register of Controlled Trials and reference lists of relevant marker studies. Nine studies (total n = 911) of adequate methodological quality were included in the review. Trials with mean difference (MD) of 95% confidence interval (CI) were pooled using random effect model. Results from meta-analysis of eligible trials revealed that subjects who received carnitine lost significantly more weight (MD: -1.33 kg; 95% CI: -2.09 to -0.57) and showed a decrease in body mass index (MD: -0.47 kg m(-2) ; 95% CI: -0.88 to -0.05) compared with the control group. The results of meta-regression analysis of duration of consumption revealed that the magnitude of weight loss resulted by carnitine supplementation significantly decreased over time (p = 0.002). We conclude that receiving the carnitine resulted in weight loss. Using multiple-treatments meta-analysis of the drugs and non-pharmacotherapy options seem to be insightful areas for research. © 2016 World Obesity.
© 2016 World Obesity.
9. Effects of L-carnitine supplementation on lipid profiles in patients with coronary artery disease.
Lee BJ1, Lin JS2, Lin YC3, Lin PT4,5.
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Abstract
BACKGROUND:
L-carnitine (LC) plays an important physiologic role in lipid metabolism. To date, no clinical study has been performed to examine the effect of LC supplementation on the lipid status of coronary artery disease (CAD) patients. The aim of this study was to investigate the lipid lowering effects of LC supplementation (1000 mg/d) in CAD patients.
METHODS:
CAD patients were identified by cardiac catheterization as having at least 50 % stenosis of one major coronary artery. Forty-seven subjects were recruited and randomly assigned to the placebo (n = 24) and to the LC (n = 23) groups. The intervention was administered for 12 weeks. The levels of LC, lipid profiles, and antioxidant enzyme activity (superoxide dismutase, SOD) were measured.
RESULTS:
The subjects in the LC group had significantly higher SOD activity (20.7 ± 4.2 versus 13.1 ± 2.9 U/mg of protein, P < 0.01), high density lipoprotein-cholesterol (1.34 ± 0.42 vs. 1.16 ± 0.24 mmol/L, HDL-C, P = 0.03), and apolipoprotein-A1 (Apo-A1, 1.24 ± 0.18 vs. 1.12 ± 0.13 g/L, P = 0.02) than those in the placebo group at week 12. Triglyceride (TG) level was slightly significantly reduced (1.40 ± 0.74 vs. 1.35 ± 0.62 mmol/L, P = 0.06) and the level of LC was negatively correlated with TG and apolipoprotein-B (Apo-B), and positively correlated with HDL-C and Apo-A1 after LC supplementation. Additionally, SOD activity was significantly negatively correlated with lipid profiles (total cholesterol, TG, and Apo-B) after supplementation.
CONCLUSION:
LC supplementation at a dose of 1000 mg/d showed significantly increased in HDL-C and Apo-A1 levels and a slight decrease in TG levels but no other changes in other lipids in CAD patients, and this lipid-lowering effect may be related to its antioxidant ability. Further studies should be conducted to define an optimal dose of LC for lipid-lowering in patients with CAD.
10. Effects of L-carnitine supplementation on oxidative stress and antioxidant enzymes activities in patients with coronary artery disease: a randomized, placebo-controlled trial.
Lee BJ, Lin JS, Lin YC, Lin PT1.
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Abstract
BACKGROUND:
Cardiovascular disease is the leading cause of death worldwide. Higher oxidative stress may contribute to the pathogenesis of coronary artery disease (CAD). The purpose of this study was to investigate the effect of L-carnitine (LC, 1000 mg/d) on the markers of oxidative stress and antioxidant enzymes activities in CAD patients.
METHODS:
We enrolled 47 CAD patients in the study. The CAD patients were identified by cardiac catheterization as having at least 50% stenosis of one major coronary artery. The subjects were randomly assigned to the placebo (n = 24) and LC (n = 23) groups. The intervention was administered for 12 weeks. The levels of serum LC, plasma malondialdehyde (MDA), and erythrocyte antioxidant enzymes activities [catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx)] were measured before and after intervention.
RESULTS:
Thirty-nine subjects completed the study (placebo, n = 19; LC, n = 20). After 12 weeks of LC supplementation, the level of MDA was significantly reduced (2.0 ± 0.3 to 1.8 ± 0.3 μmol/L, P = 0.02) and the level of LC (33.6 ± 13.6 to 40.0 ± 12.0 μmol/L, P = 0.04) and antioxidant enzymes activities [CAT (12.7 ± 5.5 to 13.1 ± 5.8 U/mg of protein, P = 0.02), SOD (14.8 ± 2.9 to 20.7 ± 5.8 U/mg of protein, P < 0.01), and GPx (20.3 ± 3.4 to 23.0 ± 3.1 U/mg of protein, P = 0.01)] were significantly increased. The level of LC was significantly positively correlated with the antioxidant enzymes activities (CAT, β = 0.87, P = 0.02; SOD, β = 0.72, P < 0.01).
CONCLUSION:
LC supplementation at a dose of 1000 mg/d was associated with a significant reduction in oxidative stress and an increase in antioxidant enzymes activities in CAD patients. CAD patients might benefit from using LC supplements to increase their anti-oxidation capacity.
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