Please Scroll Down to See Forums Below AlphamaleStS
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Anyone take this alone in high dosages, aside from IN a fat burner such as ripped fuel?
L- Carnatine
- Thread starter AlphamaleStS
- Start date
stringfellow
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Ya I take one 500mg tablet every day but I haven't noticed anything so I think I am going to save my money and stop taking it. I'm on way too many supps right now anyways. 500mg isn't that much so maybe I need to take higher doses to know but it cost me about $12 for 30-500mg tabs at wal-mart which is pretty expensive so instead of taking more each day I think that I am just going to stop using it altogether. If anybody has had any results from this supplement I would be interested to know what they were. L-carnitine is suppose to aid in weight loss by making the fat cells more redily available to the muscles to use as energy. This is what is says on my bottle:AlphamaleStS said:
Carnitine assists in fat metabolism and plays an essential role in making fatty acids available for muscle tissue.
JustJacked
New member
most of these fat burners work. but they only work well when taken together. thats why these companies have like 3-4 diferent ingredients inside there product. its like a chain reaction. they all assist eachother.
macrophage69alpha
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macrophage69alpha
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SPORT SCIENTIST
Banned
Carnite has a sound theoretical mechanism for its actions, however most clinical trials have not seen substantiated effects. However I did find the following 2 studies SEE BELOW "STUDIES": p.s. The really interesting bit is headed "L-CARNITE-L-TARTRATE"
- This is without doubt, the form of carnite that you should try to get - although not primarily for the purpose of fatty acid metabolism.
Carnitine is a vitamin like nutrient essential for energy production and fat metabolism. Theoretically, L-Carnitine helps transport long chain fatty acids across the mitochondrial membrane for subsequent fat breakdown and energy production. A special form of L carnitine (L-carnitine L-tartrate) has been shown in newer research to reduce muscle breakdown secondary to weight training. Taking 1-2 grams daily may be effective.
STUDIES
Effects of oral L-carnitine supplementation on in vivo long-chain fatty acid oxidation in healthy adults.
Muller DM, Seim H, Kiess W, Loster H, Richter T.
University of Leipzig, Children's Hospital, Germany.
Despite an abundance of literature describing the basic mechanisms of action of L-carnitine metabolism, there remains some uncertainty regarding the effects of oral L-carnitine supplementation on in vivo fatty acid oxidation in normal subjects under normal conditions. It is well known that L-carnitine normalizes the metabolism of long-chain fatty acids in cases of carnitine deficiency. However, it has not yet been shown that L-carnitine influences the metabolism of long-chain fatty acids in subjects without disturbances in fatty acid metabolism. Therefore, we investigated the effects of oral L-carnitine supplementation on in vivo long-chain fatty acid oxidation by measuring 1-[(13)C] palmitic acid oxidation in healthy subjects before and after L-carnitine supplementation (3 x 1 g/d for 10 days). We observed a significant increase in (13)CO(2) exhalation. This is the first investigation to conclusively demonstrate that oral L-carnitine supplementation results in an increase in long-chain fatty acid oxidation in vivo in subjects without L-carnitine deficiency or without prolonged fatty acid metabolism. Copyright 2002, Elsevier Science (USA). All rights reserved.
L-Carnitine: therapeutic applications of a conditionally-essential amino acid.
Kelly GS.
A trimethylated amino acid roughly similar in structure to choline, carnitine is a cofactor required for transformation of free long-chain fatty acids into acylcarnitines, and for their subsequent transport into the mitochondrial matrix, where they undergo beta-oxidation for cellular energy production. Mitochondrial fatty acid oxidation is the primary fuel source in heart and skeletal muscle, pointing to the relative importance of this nutrient for proper function in these tissues. Although L-carnitine deficiency is an infrequent problem in a healthy, well-nourished population consuming adequate protein, many individuals within the population appear to be somewhere along a continuum, characterized by mild deficiency at one extreme, and tissue pathology at the other. Conditions which seem to benefit from exogenous supplementation of L-carnitine include anorexia, chronic fatigue, coronary vascular disease, diphtheria, hypoglycemia, male infertility, muscular myopathies, and Rett syndrome. In addition, preterm infants, dialysis patients, and HIV+ individuals seem to be prone to a deficiency of L-carnitine, and benefit from supplementation. Although available data on L-carnitine as an ergogenic aid is not compelling, under some experimental conditions pretreatment has favored aerobic processes and resulted in improved endurance performance.
CARNITE IN MORE DEPTH:
Carnitine is critical for normal skeletal muscle bioenergetics. Carnitine has a dual role as it is required for long-chain fatty acid oxidation, and also shuttles accumulated acyl groups out of the mitochondria.
Muscle requires optimization of both of these metabolic processes during peak exercise performance. Theoretically, carnitine availability may become limiting for either fatty acid oxidation or the removal of acyl-CoAs during exercise. Despite the theoretical basis for carnitine supplementation in otherwise healthy persons to improve exercise performance, clinical data have not demonstrated consistent benefits of carnitine administration. Additionally, most of the anticipated metabolic effects of carnitine supplementation have not been observed in healthy persons.
The failure to demonstrate clinical efficacy of carnitine may reflect the complex pharmacokinetics and pharmacodynamics of carnitine supplementation, the challenges of clinical trial design for performance endpoints, or the adequacy of endogenous carnitine content to meet even extreme metabolic demands in the healthy state. In patients with end stage renal disease there is evidence of impaired cellular metabolism, the accumulation of metabolic intermediates and increased carnitine demands to support acylcarnitine production. Years of nutritional changes and dialysis therapy may also lower skeletal muscle carnitine content in these patients. Preliminary data have demonstrated beneficial effects of carnitine supplementation to improve muscle function and exercise capacity in these patients. Peripheral arterial disease (PAD) is also associated with altered muscle metabolic function and endogenous acylcarnitine accumulation. Therapy with either carnitine or propionylcarnitine has been shown to increase claudication-limited exercise capacity in patients with PAD. Further clinical research is needed to define the optimal use of carnitine and acylcarnitines as therapeutic modalities to improve exercise performance in disease states, and any potential benefit in healthy individuals.
L-CARNITE-L-TARTRATE:
Am J Physiol Endocrinol Metab 2002 Feb;282(2):E474-82
L-Carnitine L-tartrate supplementation favorably affects markers of recovery from exercise stress.
Volek JS, Kraemer WJ, Rubin MR, Gomez AL, Ratamess NA, Gaynor P.
Human Performance Laboratory, Department of Kinesiology, University of Connecticut, Storrs, Connecticut 06269, USA. [email protected]
We examined the influence of L-carnitine L-tartrate (LCLT) on markers of purine catabolism, free radical formation, and muscle tissue disruption after squat exercise. With the use of a balanced, crossover design (1 wk washout), 10 resistance-trained men consumed a placebo or LCLT supplement (2 g L-carnitine/day) for 3 wk before obtaining blood samples on six consecutive days (D1 to D6). Blood was also sampled before and after a squat protocol (5 sets, 15-20 repetitions) on D2. Muscle tissue disruption at the midthigh was assessed using magnetic resonance imaging (MRI) before exercise and on D3 and D6. Exercise-induced increases in plasma markers of purine catabolism (hypoxanthine, xanthine oxidase, and serum uric acid) and circulating cytosolic proteins (myoglobin, fatty acid-binding protein, and creatine kinase) were significantly (P < or = 0.05) attenuated by LCLT. Exercise-induced increases in plasma malondialdehyde returned to resting values sooner during LCLT compared with placebo. The amount of muscle disruption from MRI scans during LCLT was 41-45% of the placebo area. These data indicate that LCLT supplementation is effective in assisting recovery from high-repetition squat exercise.
- This is without doubt, the form of carnite that you should try to get - although not primarily for the purpose of fatty acid metabolism.
Carnitine is a vitamin like nutrient essential for energy production and fat metabolism. Theoretically, L-Carnitine helps transport long chain fatty acids across the mitochondrial membrane for subsequent fat breakdown and energy production. A special form of L carnitine (L-carnitine L-tartrate) has been shown in newer research to reduce muscle breakdown secondary to weight training. Taking 1-2 grams daily may be effective.
STUDIES
Effects of oral L-carnitine supplementation on in vivo long-chain fatty acid oxidation in healthy adults.
Muller DM, Seim H, Kiess W, Loster H, Richter T.
University of Leipzig, Children's Hospital, Germany.
Despite an abundance of literature describing the basic mechanisms of action of L-carnitine metabolism, there remains some uncertainty regarding the effects of oral L-carnitine supplementation on in vivo fatty acid oxidation in normal subjects under normal conditions. It is well known that L-carnitine normalizes the metabolism of long-chain fatty acids in cases of carnitine deficiency. However, it has not yet been shown that L-carnitine influences the metabolism of long-chain fatty acids in subjects without disturbances in fatty acid metabolism. Therefore, we investigated the effects of oral L-carnitine supplementation on in vivo long-chain fatty acid oxidation by measuring 1-[(13)C] palmitic acid oxidation in healthy subjects before and after L-carnitine supplementation (3 x 1 g/d for 10 days). We observed a significant increase in (13)CO(2) exhalation. This is the first investigation to conclusively demonstrate that oral L-carnitine supplementation results in an increase in long-chain fatty acid oxidation in vivo in subjects without L-carnitine deficiency or without prolonged fatty acid metabolism. Copyright 2002, Elsevier Science (USA). All rights reserved.
L-Carnitine: therapeutic applications of a conditionally-essential amino acid.
Kelly GS.
A trimethylated amino acid roughly similar in structure to choline, carnitine is a cofactor required for transformation of free long-chain fatty acids into acylcarnitines, and for their subsequent transport into the mitochondrial matrix, where they undergo beta-oxidation for cellular energy production. Mitochondrial fatty acid oxidation is the primary fuel source in heart and skeletal muscle, pointing to the relative importance of this nutrient for proper function in these tissues. Although L-carnitine deficiency is an infrequent problem in a healthy, well-nourished population consuming adequate protein, many individuals within the population appear to be somewhere along a continuum, characterized by mild deficiency at one extreme, and tissue pathology at the other. Conditions which seem to benefit from exogenous supplementation of L-carnitine include anorexia, chronic fatigue, coronary vascular disease, diphtheria, hypoglycemia, male infertility, muscular myopathies, and Rett syndrome. In addition, preterm infants, dialysis patients, and HIV+ individuals seem to be prone to a deficiency of L-carnitine, and benefit from supplementation. Although available data on L-carnitine as an ergogenic aid is not compelling, under some experimental conditions pretreatment has favored aerobic processes and resulted in improved endurance performance.
CARNITE IN MORE DEPTH:
Carnitine is critical for normal skeletal muscle bioenergetics. Carnitine has a dual role as it is required for long-chain fatty acid oxidation, and also shuttles accumulated acyl groups out of the mitochondria.
Muscle requires optimization of both of these metabolic processes during peak exercise performance. Theoretically, carnitine availability may become limiting for either fatty acid oxidation or the removal of acyl-CoAs during exercise. Despite the theoretical basis for carnitine supplementation in otherwise healthy persons to improve exercise performance, clinical data have not demonstrated consistent benefits of carnitine administration. Additionally, most of the anticipated metabolic effects of carnitine supplementation have not been observed in healthy persons.
The failure to demonstrate clinical efficacy of carnitine may reflect the complex pharmacokinetics and pharmacodynamics of carnitine supplementation, the challenges of clinical trial design for performance endpoints, or the adequacy of endogenous carnitine content to meet even extreme metabolic demands in the healthy state. In patients with end stage renal disease there is evidence of impaired cellular metabolism, the accumulation of metabolic intermediates and increased carnitine demands to support acylcarnitine production. Years of nutritional changes and dialysis therapy may also lower skeletal muscle carnitine content in these patients. Preliminary data have demonstrated beneficial effects of carnitine supplementation to improve muscle function and exercise capacity in these patients. Peripheral arterial disease (PAD) is also associated with altered muscle metabolic function and endogenous acylcarnitine accumulation. Therapy with either carnitine or propionylcarnitine has been shown to increase claudication-limited exercise capacity in patients with PAD. Further clinical research is needed to define the optimal use of carnitine and acylcarnitines as therapeutic modalities to improve exercise performance in disease states, and any potential benefit in healthy individuals.
L-CARNITE-L-TARTRATE:
Am J Physiol Endocrinol Metab 2002 Feb;282(2):E474-82
L-Carnitine L-tartrate supplementation favorably affects markers of recovery from exercise stress.
Volek JS, Kraemer WJ, Rubin MR, Gomez AL, Ratamess NA, Gaynor P.
Human Performance Laboratory, Department of Kinesiology, University of Connecticut, Storrs, Connecticut 06269, USA. [email protected]
We examined the influence of L-carnitine L-tartrate (LCLT) on markers of purine catabolism, free radical formation, and muscle tissue disruption after squat exercise. With the use of a balanced, crossover design (1 wk washout), 10 resistance-trained men consumed a placebo or LCLT supplement (2 g L-carnitine/day) for 3 wk before obtaining blood samples on six consecutive days (D1 to D6). Blood was also sampled before and after a squat protocol (5 sets, 15-20 repetitions) on D2. Muscle tissue disruption at the midthigh was assessed using magnetic resonance imaging (MRI) before exercise and on D3 and D6. Exercise-induced increases in plasma markers of purine catabolism (hypoxanthine, xanthine oxidase, and serum uric acid) and circulating cytosolic proteins (myoglobin, fatty acid-binding protein, and creatine kinase) were significantly (P < or = 0.05) attenuated by LCLT. Exercise-induced increases in plasma malondialdehyde returned to resting values sooner during LCLT compared with placebo. The amount of muscle disruption from MRI scans during LCLT was 41-45% of the placebo area. These data indicate that LCLT supplementation is effective in assisting recovery from high-repetition squat exercise.
