Indeed, L-carnitine is responsible for the increased use of long-chain fatty acids as an energy source, but studies on its weight-loss effects have produced mixed results. A meta-analysis of 37 studies published in concludes that taking L-carnitine as a supplement results in a mild weight loss, by an average of 1.

Carnitine can support weight loss due to its increased use of fat as an energy source on a low-calorie diet and its improved carbohydrate metabolism. However, the results of its use are seen primarily in people with excessive body weight and such effects help with weight loss, not fat burning.

L-carnitine is mainly found in meat, fish and dairy products. Vegetables provide small amounts. People on a balanced diet of meat and regular physical activity have no problem meeting their carnitine requirements through diet alone, but vegans and endurance athletes should consider supplementation.

The average diet containing meat and dairy provides between 60 and mg of carnitine per day, while a vegan diet provides only mg. How much L-carnitine do foods provide? L-carnitine supplements are recommended especially for endurance athletes and people who train professionally.

It can also be considered by vegans, the elderly and people suffering from PCOS, male infertility, heart disease or neurodegenerative diseases. An effective dose of L-carnitine is considered to be 2g per day.

This amount is most commonly used in scientific studies. Supplements are available as L-carnitine capsules and L-carnitine powder, which can be added to e. a milkshake with protein. L-Carnitine should not be used by people taking hormone medications for hypothyroidism, as L-Carnitine reduces the body's ability to utilise these hormones.

L-carnitine - not only for athletes. Effects and properties of L-carnitine Blog L-carnitine - not only for athletes. Effects and properties of L-carnitine.

Supplementation Health Workout Diet Weight loss. Since LC concentration in skeletal muscles is higher than that of blood plasma, active uptake of carnitine must take place [ 23 ]. Stephens et al. Moreover, higher serum insulin maintained by the consumption of simple sugars resulted in augmented LC retention in healthy human subjects supplemented by LC for 2 weeks [ 26 ].

This assumption has been confirmed in later studies [ 5 , 6 , 7 ]. Neither exercise metabolism nor muscle metabolites were modified by augmented TC in vegetarian [ 12 ]. Skeletal muscle mass depends on the rates of protein synthesis and degradation. Elevated protein synthesis and attenuated proteolysis are observed during muscle hypertrophy.

Both of these processes are mainly regulated by the signaling pathway: insulin-like growth factor-1 IGF-1 — phosphoinositidekinase PI3K — protein kinase B Akt — mammalian target of rapamycin mTOR. The activation of mTOR leads to phosphorylation and activation of S6 kinases S6Ks and hyperphosphorylation of 4E-binding proteins 4E-BPs , resulting in the acceleration of protein synthesis.

At the same time, Akt phosphorylates and inactivates forkhead box O FoxO , thereby inhibit the responsible for proteolysis ubiquitin ligases: muscle-specific RING finger-1 MuRF-1 and muscle atrophy F-box protein atrogin-1 , for review see [ 27 , 28 , 29 ].

The association between LC supplementation and the regulation of metabolic pathways involved in muscle protein balance have been shown in several animal studies Fig.

Four weeks of LC supplementation in rats increased plasma IGF-1 concentration [ 33 ]. FoxO inactivation attenuated MURF-1 expression in quadriceps fem oris muscle of supplemented rats compared to control [ 33 ]. All these findings together might suggest that LC supplementation protect muscle from atrophy, especially in pathophysiological conditions.

The association between LC supplementation and the regulation of metabolic pathways involved in muscle protein balance. L-carnitine LC ; insulin-like growth factor-1 IGF-1 ; phosphoinositidekinase PI3K ; protein kinase B Akt ; mammalian target of rapamycin mTOR ; forkhead box O FoxO ; muscle-specific RING finger-1 MuRF-1 ; muscle atrophy F-box atrogin-1 ; increase ; decrease ; activation ; inactivation.

Various effects might be due to different IGF-1 levels; significantly lower in the HIV-seropositive patients than in healthy subjects [ 38 ]. These findings altogether suggest that prolonged LC supplementation might affect body composition in specific conditions. Therefore, authors suggested that LC supplementation may be effective in obese and overweight subjects.

It has been assumed that a combination of LC supplementation with increased energy expenditure may positively affect body composition. However, either with aerobic [ 41 , 42 ] or resistance [ 43 ] training, LC supplementation has not achieved successful endpoint.

Similarly, lack of LC effect has been reported in obese women [ 42 ]. Body composition, determined by dual energy X-ray absorptiometry, indicated no significant effect in fat mass and fat-free mass due to supplementation.

Moreover, LC administration did not influence bench press results. The number of leg press repetitions and the leg press third set lifting volume increased in the LC group compared to the placebo group [ 43 ].

Different LC effect in the limbs may be associated with the higher rates of glycogenolysis during arm exercise at the same relative intensity as leg exercise [ 44 ].

Aged people have accelerated protein catabolism, which is associated with muscle wasting [ 45 ]. LC could increase the amount of protein retention by inhibition of the proteolytic pathway. Six months of LC supplementation augmented fat free mass and reduced total body fat mass in centenarians [ 14 ].

Such effect was not observed in elder women age range 65—70 y. after a similar period of supplementation [ 15 ]. The effectiveness of LC supplementation may result from the age-wise distribution of sarcopenia. The prevalence of sarcopenia increased steeply with age, reaching Muscle damage may occur during exercise, especially eccentric exercise.

In the clearance of damaged tissues assist free radicals produced by neutrophils. Therefore, among other responses to exercise, neutrophils are released into the circulation.

While neutrophil-derived reactive oxygen species ROS play an important role in breaking down damaged fragments of the muscle tissue, ROS produced in excess may also contribute to oxidative stress for review see [ 47 , 48 ].

Based on the assumption that LC may provide cell membranes protection against oxidative stress [ 49 ], it has been hypothesized that LC supplementation would mitigate exercise-induced muscle damage and improve post-exercise recovery.

Since plasma LC elevates following 2 weeks of supplementation [ 21 , 22 ], short protocols of supplementation may be considered as effective in attenuating post-exercise muscle soreness. It has been shown, through magnetic resonance imaging technique that muscle disruption after strenuous exercise was reduced by LC supplementation [ 37 , 51 ].

This effect was accompanied by a significant reduction in released cytosolic proteins such as myoglobin and creatine kinase [ 50 , 52 , 53 ] as well as attenuation in plasma marker of oxidative stress - malondialdehyde [ 51 , 53 , 54 ]. Furthermore, 9 weeks of LC supplementation in conjunction with resistance training revealed a significant increase of circulating total antioxidant capacity and glutathione peroxidase activity and decrease in malondialdehyde concentration [ 43 ].

In Rebouche et al. Similar observations were noted in later human studies [ 56 , 57 ], with the peak serum TMAO observed within hours following oral administration of the tracer [ 56 ]. Prolonged LC treatment elevates fasting plasma TMAO [ 16 , 17 , 18 , 58 , 59 ].

Three months of oral LC supplementation in healthy aged women induced ten-fold increase of fasting plasma TMAO, and this level remained elevated for the further 3 months of supplementation [ 16 ].

Four months after cessation of LC supplementation, plasma TMAO reached a pre-supplementation concentration, which was stable for the following 8 months [ 60 ].

In Wang et al. Since diets high in red meat have been strongly related to heart disease and mortality [ 62 ], LC has been proposed as the red meat nutrient responsible for atherosclerosis promotion [ 8 ]. As a potential link between red meat consumption and the increasing risk of cardiovascular disease, TMAO has been indicated [ 8 ].

Numerous later studies have shown the association between increased plasma TMAO levels with a higher risk of cardiovascular events [ 63 , 64 , 65 , 66 ]. The recent meta-analyses indicated that in patients with high TMAO plasma level, the incidence of major adverse cardiovascular events was significantly higher compared with patients with low TMAO levels [ 67 ], and that all-cause mortality increased by 7.

The rise of plasma TMAO was on average three-fold compared with white meat and non-meat diets [ 70 ]. Conversely, habitual consumption of red, processed or white meat did not affect plasma TMAO in German adult population [ 71 ].

Similarly, a minor increase in plasma TMAO was observed following red meat and processed meat consumption in European multi-center study [ 72 ]. In the previous century, the underlined function of TMAO was the stabilization of proteins against various environmental stress factors, including high hydrostatic pressure [ 73 ].

TMAO was shown as widely distributed in sea animals [ 74 ], with concentration in the tissue increasing proportionally to the depth of the fishes natural environment [ 75 ]. Consequently, fish and seafood nutritional intake has a great impact on TMAO level in the human body [ 76 ], significantly elevating also plasma TMAO concentration [ 72 ].

Therefore, link between plasma TMAO and the risk of cardiovascular disease [ 8 ] seems like a paradox, since more fish in the diet reduces this risk [ 77 ]. Not only dietary modification may affect TMAO plasma levels.

Due to TMAO excretion in urine [ 56 , 57 ], in chronic renal disease patients, TMAO elimination from the body fails, causing elevation of its plasma concentration [ 78 ]. Therefore, higher plasma TMAO in humans was suggested as a marker of kidney damage [ 79 ]. It is worthy to note that cardiovascular disease and kidney disease are closely interrelated [ 80 ] and diminished renal function is strongly associated with morbidity and mortality in heart failure patients [ 81 ].

Moreover, decreased TMAO urine excretion is associated with high salt dietary intake, increasing plasma TMAO concentration [ 82 ]. The relation between TMAO and chronic disease can be ambiguous, involving kidney function [ 79 ], disturbed gut-blood barrier [ 83 ], or flavin-containing monooxygenase 3 genotype [ 84 ].

Thus, whether TMAO is an atherogenic factor responsible for the development and progression of cardiovascular disease, or simply a marker of an underlined pathology, remains unclear [ 85 ].

Carnitine preparations administered orally can occasionally cause heart-burn or dyspepsia [ 86 ]. It is worthy to mention that Bakalov et al. The strength of this review is a focus on the period of LC treatment, very important aspect often missed in many articles dealing with this supplement.

This limitation is also magnified by the varied design of the studies available including different supplementation protocols and outcome measures.

There is also a high degree of heterogeneity among participants of the analyzed studies. Therefore, the results should be taken with caution, and more research is required before definitive recommendations. Lasting for several years opinion that LC supplementation does not change metabolism, especially exercise metabolism, is based mostly on short-term supplementation protocols.

Nevertheless, LC is still used by elite [ 9 ] and sub-elite [ 10 ] athletes. Recent studies suggest that LC supplementation may elevate muscle TC content; therefore, modify muscle fuel metabolism and performance during the exercise. Due to insulin-mediated LC transport to the muscle, oral administration regimen should be combined with CHO.

Because of LC poor bioavailability, it is likely that the supplementation protocol would take at least 3 months. Shorter period of supplementation may be effective in prevention of exercise-induced muscle damage, but not metabolic changes. On the other hand, it is also clear that prolonged LC supplementation elevates fasting plasma TMAO [ 16 , 17 , 18 , 58 , 59 ], compound supposed to be pro-atherogenic [ 61 ].

Therefore, additional studies focusing on long-term supplementation and its longitudinal effect on the TMAO metabolism and cardiovascular system are needed.

Bremer J. Carnitine--metabolism and functions. Physiol Rev. Article CAS PubMed Google Scholar. Arenas J, Huertas R, Campos Y, Diaz AE, Villalon JM, Vilas E.

Effects of L-carnitine on the pyruvate dehydrogenase complex and carnitine palmitoyl transferase activities in muscle of endurance athletes. FEBS Lett. Ringseis R, Keller J, Eder K. Mechanisms underlying the anti-wasting effect of L-carnitine supplementation under pathologic conditions: evidence from experimental and clinical studies.

Eur J Nutr. Brass EP. Supplemental carnitine and exercise. Am J Clin Nutr. Wall BT, Stephens FB, Constantin-Teodosiu D, Marimuthu K, Macdonald IA, Greenhaff PL. Chronic oral ingestion of L-carnitine and carbohydrate increases muscle carnitine content and alters muscle fuel metabolism during exercise in humans.

J Physiol. Article CAS PubMed PubMed Central Google Scholar. Stephens FB, Wall BT, Marimuthu K, Shannon CE, Constantin-Teodosiu D, Macdonald IA, Greenhaff PL. Skeletal muscle carnitine loading increases energy expenditure, modulates fuel metabolism gene networks and prevents body fat accumulation in humans.

Shannon CE, Ghasemi R, Greenhaff PL, Stephens FB. Increasing skeletal muscle carnitine availability does not alter the adaptations to high-intensity interval training. Scand J Med Sci Sports. Article PubMed Google Scholar. Koeth RA, Wang Z, Levison BS, Buffa JA, Org E, Sheehy BT, Britt EB, Fu X, Wu Y, Li L, et al.

Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis. Nat Med. Baltazar-Martins G, Brito de Souza D, Aguilar-Navarro M, Munoz-Guerra J, MDM P, Del Coso J.

Prevalence and patterns of dietary supplement use in elite Spanish athletes. J Int Soc Sports Nutr. Wardenaar FC, Ceelen IJ, Van Dijk JW, Hangelbroek RW, Van Roy L, Van der Pouw B, De Vries JH, Mensink M, Witkamp RF.

Nutritional supplement use by Dutch elite and sub-elite athletes: does receiving dietary counseling make a difference? Int J Sport Nutr Exerc Metab.

Wachter S, Vogt M, Kreis R, Boesch C, Bigler P, Hoppeler H, Krahenbuhl S. Long-term administration of L-carnitine to humans: effect on skeletal muscle carnitine content and physical performance. Clin Chim Acta. Novakova K, Kummer O, Bouitbir J, Stoffel SD, Hoerler-Koerner U, Bodmer M, Roberts P, Urwyler A, Ehrsam R, Krahenbuhl S.

Effect of L-carnitine supplementation on the body carnitine pool, skeletal muscle energy metabolism and physical performance in male vegetarians. Lohninger A, Sendic A, Litzlbauer E, Hofbauer R, Staniek H, Blesky D, Schwieglhofer C, Eder M, Bergmuller H, Mascher D, et al.

Endurance exercise training and L-carnitine supplementation stimulates gene expression in the blood and muscle cells in young athletes and middle aged subjects.

Monatshefte Fur Chemie. Article CAS Google Scholar. Malaguarnera M, Cammalleri L, Gargante MP, Vacante M, Colonna V, Motta M. L-Carnitine treatment reduces severity of physical and mental fatigue and increases cognitive functions in centenarians: a randomized and controlled clinical trial.

Sawicka AK, Hartmane D, Lipinska P, Wojtowicz E, Lysiak-Szydlowska W, Olek RA. l-Carnitine Supplementation in Older Women. A Pilot Study on Aging Skeletal Muscle Mass and Function. Samulak JJ, Sawicka AK, Hartmane D, Grinberga S, Pugovics O, Lysiak-Szydlowska W, Olek RA.

L-Carnitine supplementation increases Trimethylamine-N-oxide but not markers of atherosclerosis in healthy aged women. Ann Nutr Metab. Olek RA, Samulak JJ, Sawicka AK, Hartmane D, Grinberga S, Pugovics O, Lysiak-Szydlowska W.

Increased Trimethylamine N-oxide is not associated with oxidative stress markers in healthy aged women. Oxidative Med Cell Longev. Bordoni L, Sawicka AK, Szarmach A, Winklewski PJ, Olek RA, Gabbianelli R. A pilot study on the effects of l-Carnitine and Trimethylamine-N-oxide on platelet mitochondrial DNA methylation and CVD biomarkers in aged women.

Int J Mol Sci. Grunewald KK, Bailey RS. Commercially marketed supplements for bodybuilding athletes. Sports Med. Hawley JA, Brouns F, Jeukendrup A. Strategies to enhance fat utilisation during exercise.

Barnett C, Costill DL, Vukovich MD, Cole KJ, Goodpaster BH, Trappe SW, Fink WJ. Effect of L-carnitine supplementation on muscle and blood carnitine content and lactate accumulation during high-intensity sprint cycling. Int J Sport Nutr. Vukovich MD, Costill DL, Fink WJ. Carnitine supplementation: effect on muscle carnitine and glycogen content during exercise.

Med Sci Sports Exerc. Rebouche CJ. Carnitine movement across muscle cell membranes. Studies in isolated rat muscle.

Biochim Biophys Acta. Stephens FB, Constantin-Teodosiu D, Laithwaite D, Simpson EJ, Greenhaff PL. Insulin stimulates L-carnitine accumulation in human skeletal muscle. FASEB J. An acute increase in skeletal muscle carnitine content alters fuel metabolism in resting human skeletal muscle.

J Clin Endocrinol Metab. Stephens FB, Evans CE, Constantin-Teodosiu D, Greenhaff PL. Carbohydrate ingestion augments L-carnitine retention in humans. J Appl Physiol Attaix D, Ventadour S, Codran A, Bechet D, Taillandier D, Combaret L. The ubiquitin-proteasome system and skeletal muscle wasting.

Essays Biochem. Schiaffino S, Dyar KA, Ciciliot S, Blaauw B, Sandri M. Mechanisms regulating skeletal muscle growth and atrophy. FEBS J. Sanchez AM, Candau RB, Bernardi H.

FoxO transcription factors: their roles in the maintenance of skeletal muscle homeostasis. Cell Mol Life Sci. Keller J, Ringseis R, Priebe S, Guthke R, Kluge H, Eder K. Dietary L-carnitine alters gene expression in skeletal muscle of piglets.

Mol Nutr Food Res. Keller J, Ringseis R, Koc A, Lukas I, Kluge H, Eder K. Supplementation with l-carnitine downregulates genes of the ubiquitin proteasome system in the skeletal muscle and liver of piglets. Busquets S, Serpe R, Toledo M, Betancourt A, Marmonti E, Orpi M, Pin F, Capdevila E, Madeddu C, Lopez-Soriano FJ, et al.

L-Carnitine: an adequate supplement for a multi-targeted anti-wasting therapy in cancer. Clin Nutr. That ingredient exists! L-Carnitine L-Tartrate LCLT is a specific type of L-Carnitine, which is a vitamin-like compound formed in the kidneys out of the amino acids methionine and lysine. The primary role of L-Carnitine is to deliver fuel fat to the mitochondria, the powerhouse of each cell.

L-Carnitine has many other secondary functions, which research has shown to be very important for both recovery and athletic performance. Let that sink in. That is a lot more work output!

It cannot just be the changes in muscle fuel metabolism that resulted in this amazing increase in work output from the LCLT supplementation group. Other studies have provided some insight into how LCLT supplementation can increase workout output, and therefore training volume, perhaps by decreasing muscle damage and muscle soreness.

The potential of the combined effect of all of these benefits is more work done with less recovery time between training bouts.

If you can increase your work output to get more training out of each session and accumulate more training sessions, you are doing things not only efficiently, but perhaps even optimally. You are not only taking your recovery and repair game to a whole new level, but your athletic performance, too!

That is the goal, after all. L-Carnitine is found naturally in animal protein, with the highest concentrations found in red meat. Real changes to athletic performance come from a well-developed training plan and program to progressively increase your training volume.

Trying to improve your skill and athleticism without having your macronutrients optimized for your goals will have its limitations. There must be an equal emphasis on applying the stress of training, and then the removal of the stress in conjunction with providing the body the nutrients it needs to buffer the stress, recover and repair from that stress, and then adapt to it.

L-Carnitine L-Tartrate has the potential to influence all of those things.

This process is known as beta-oxidation, and it is essential for energy production and maintaining healthy metabolism.

In addition to helping transport fatty acids, L-Carnitine also helps to remove waste products from the mitochondria, such as acetyl-CoA and coenzyme A. These waste products can inhibit energy production, so their removal can help to improve mitochondrial function and increase energy production.

Overall, L-Carnitine's ability to transport fatty acids into the mitochondria and remove waste products makes it an important player in energy production.

By increasing the availability of fatty acids for energy, L-Carnitine can help to improve endurance and reduce fatigue during exercise. Whether you're an elite athlete looking to improve your peak performance or a weekend warrior trying to reach your fitness goals and stay fit, L-Carnitine offers many amazing benefits that can help you optimize those goals.

By increasing fat metabolism and energy production, L-Carnitine can improve endurance, reduce fatigue, and enhance recovery. It can also help to support heart health, brain function, and immune function.

When choosing an L-Carnitine supplement, it's important to consider the different forms available and their respective benefits. L-Carnitine L-Tartrate is a popular form for athletes due to its ability to enhance recovery and reduce muscle damage.

Meanwhile, Acetyl-L-Carnitine is known for its cognitive benefits and potential for improving brain function. Overall, L-Carnitine is a safe and very effective supplement that can help athletes reach their full potential.

Whether you're looking to improve your athletic performance, enhance your workouts, or enhance your overall health and wellness, L-Carnitine is a supplement worth considering. Pause slideshow Play slideshow Shop The App For Free Gifts.

What is L-Carnitine? What are the different variations of L-Carnitine? L-carnitine was first isolated from muscle at the beginning of the 20th century and its name comes exactly from it Latin: carnus. Carnitine exists in two forms - biologically active L-carnitine and inactive D-carnitine.

The names L-carnitine and carnitine are often used together because the "D" form of carnitine is not important for the human body and is often omitted. L-carnitine is necessary for the proper functioning of the heart and skeletal muscles. This compound is produced in the kidneys and liver from the amino acids - methionine and lysine.

In some physiological conditions, endogenous production does not fully cover the muscle requirement for this component. It is necessary to supply carnitine from food and sometimes from supplements. The body's requirement for L-carnitine is on average mg per day, but it increases significantly among physically active people.

It is estimated that athletes can consume up to mg of L-carnitine per day. L-carnitine takes part in the metabolism of fats - its role is to transport long-chain fatty acids from the cytosol, which fills the cell interior, to the mitochondria where energy is produced.

The presence of L-carnitine increases the beta-oxidation of fatty acids, which means that it enables much easier and more effective use of fats as an energy source. L-carnitine's role is also removing secondary metabolites of fatty acid combustion in the mitochondria.

From a medical point of view, it is crucial, as these metabolites are toxic in excess. Carnitine deficiencies lead to disrupted metabolic cycles and problems with the heart muscle. It appears that L-carnitine may have a preventive or healing effect in some diseases. Most researchers conclude that further, long-term studies on larger groups of people are needed to talk about L-carnitine therapy, but preliminary studies indicate that:.

The demand for carnitine increases with the amount of used energy. Naturally, physically active people should therefore take more L-carnitine to cover the demand related to the increased transport of fatty acids to the mitochondria. However, it turns out that L-carnitine can additionally increase athletic performance and improve the effects of long training sessions.

The facilitated oxidation of fats thanks to carnitine results in a better energy supply during endurance training. This indicates a key role for L-carnitine in maintaining healthy protein status and blood flow, including to the brain, while preventing age-associated muscle gradation.

In addition, L-carnitine preserves healthy homeostasis, or biochemical balance, within mitochondria, the powerhouse organelles in cells that generate energy. An interesting pilot study also in , compared the effects of L-carnitine on metabolic profiles of elite-level athletes. By searching for biomarkers with potential therapeutic implications, the data provided evidence that high-power and high-endurance athletes have a distinct metabolic profile, including: steroid biosynthesis, fatty acid metabolism, oxidative stress, and energy-related metabolites.

All of these characteristics are improved or encouraged by L-carnitine supplementation. In our clinic, our athletic patients have seen consistent long-term benefits with L-carnitine. People report improved performance and endurance, faster recovery, more efficient muscle building, and less fatigue and soreness after training.

These improvements can steadily increase with 3 to 6 or more months of taking L-carnitine. Recommendation: L-carnitine 1,mg, one to three times per day, with any meals, or as directed by your healthcare provider.

An overview of research examining the value of L-carnitine for athletes summarized the following key points: 1 The majority of studies report stimulation of lipid metabolism by carnitine with improved efficiency of oxygen consumption and better respiratory quotient.

This means that L-carnitine improves the uptake of oxygen from the blood into tissues and helps its actions there, while reducing the amount of carbon dioxide waste in proportion. L-carnitine significantly decreases post-exercise plasma lactate levels. Lactate is a waste product which is formed and cleared continuously under fully aerobic conditions.

Recent data from preliminary studies indicate that L-carnitine eases the deleterious effects on tissues of hypoxic training and can speed up recovery from exercise stress.

L-carnitine plays a decisive role in preventing cellular damage, and speeds cell repair and recovery from exercise stress.