How long does l carnitine work

L-carnitine is an amino acid derivative that transports fatty acids into your cells to be processed for energy. It is made by your body and also available as a supplement. In theory, using L-carnitine as a weight loss supplement makes sense. Since L-carnitine helps move more fatty acids into your cells to be burned for energy, you might think this would increase your ability to burn fat and lose weight.

However, the human body is extremely complex, and the results of both human and animal studies are mixed 24 , 25 , 26 , Four weeks of taking supplements did not increase fat burning However, one analysis of nine studies — mostly in obese individuals or older adults — found that people lost an average of 2. More research is needed to confirm the benefits of L-carnitine in a younger, more active population. While it may aid in weight loss for obese individuals or older adults, a thorough diet and exercise regimen must be in place first.

Although the cellular mechanism of L-carnitine suggests it could benefit weight loss, its effects — if present at all — are small. Some animal studies suggest that the acetyl form, acetyl-L-carnitine ALCAR , may help prevent age-related mental decline and improve markers of learning 30 , In a day study, people with alcohol addictions who took 2 grams of acetyl-L-carnitine per day experienced significant improvements in all measures of brain function L-carnitine — specifically acetyl-L-carnitine — can have beneficial effects on brain function in various diseases.

Some studies demonstrate a potential for reducing blood pressure and the inflammatory process associated with heart disease 23 , In one study, 2 grams of acetyl-L-carnitine per day resulted in an almost point drop in systolic blood pressure — the top number of a blood pressure reading and an important indicator of heart health and disease risk L-carnitine is also linked to improvements in patients with severe heart disorders, such as coronary heart disease and chronic heart failure 40 , One month study observed a reduction in heart failure and deaths among participants who took L-carnitine supplements However, several studies note mild benefits associated with larger or more long-term doses 43 , 44 , This differs from supplements like caffeine or creatine , which can directly enhance sports performance.

L-carnitine may also reduce symptoms of type 2 diabetes and its associated risk factors 52 , 53 , One study of people with type 2 diabetes taking anti-diabetic medication indicated that carnitine supplements significantly reduced blood sugar levels , compared to a placebo Research suggests that L-carnitine may aid exercise performance and treat health conditions like heart disease and type 2 diabetes.

For most people, 2 grams or less per day is relatively safe and free from any serious side effects. Weight Loss Specials. San Diego Location. Contact Us. September 13, Lipotropic Injections. What is L-carnitine? L-carnitine burns fat With higher levels of L-carnitine, your body becomes more efficient at burning fat. L-carnitine boosts your metabolism to help you lose weight Taking that energy increase into your exercise routine will allow you to perform with more intensity, providing a boost to your metabolism.

Elevated protein synthesis and attenuated proteolysis are observed during muscle hypertrophy. 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. 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. 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. 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 ]. 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 ].

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. Effects of L-carnitine on the pyruvate dehydrogenase complex and carnitine palmitoyl transferase activities in muscle of endurance athletes.

FEBS Lett. 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. Chronic oral ingestion of L-carnitine and carbohydrate increases muscle carnitine content and alters muscle fuel metabolism during exercise in humans. As the kidneys and liver help create and use L-carnitine, disease in these organs or organ failure may lead to L-carnitine deficiency.

Doctors may recommend L-carnitine supplementation in these cases to support the function of the kidneys and liver and prevent deficiency. Most people tolerate L-carnitine well. However, some individuals may experience digestive side effects when taking L-carnitine. These include :. Some studies suggest that high levels of L-creatine may raise the long-term risks of cardiovascular diseases, such as atherosclerosis. L-carnitine supplements may interact with certain antibiotics or anticonvulsants.

Anyone considering taking L-carnitine should talk to their doctor to discuss any medications they are taking and the possible drug interactions. The liver and kidneys will create enough to meet their daily needs.

Even though the body produces it naturally, carnitine is widely available in a number of simple foods. Animal proteins, such as fish, red meat, and poultry, are some of the best sources. According to the NIH , adults who eat a mixed diet that includes red meat and other animal products get about 60— milligrams mg of carnitine per day. People who avoid animal products, such as those following a vegan diet, may get roughly 10—12 mg from their diet.

The kidneys also eliminate excess carnitine through urine to maintain healthful concentrations. Generally speaking, otherwise healthy adults do not need to take L-carnitine to support their health. Some athletes take extra L-carnitine, believing that it will boost their athletic performance. L-carnitine availability seems to limit muscle metabolism during very high intensity exercise.

So, in theory, supplementing carnitine during workouts may support exercise performance. However, a study in Molecules notes that the evidence for this practice is lacking. While many athletes take L-carnitine, years of research does not provide conclusive evidence to support these claims. As L-carnitine helps burn fatty acids for energy, many people assume that taking more of it may help them lose weight. More research is necessary, but some studies support this idea. In a review of nine different trials, researchers found some evidence to support this claim.