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Nutrition: Section Article

L-Carnitine Supplementation

Influence upon Physiological Function

Kraemer, William J.; Volek, Jeff S.; Dunn-Lewis, Courtenay

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Current Sports Medicine Reports: July 2008 - Volume 7 - Issue 4 - p 218-223
doi: 10.1249/JSR.0b013e318180735c
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Carnitine (L-3-hydroxytrimethylamminobutanoate) is a naturally occurring compound that can be synthesized in mammals from the essential amino acids lysine and methionine or ingested through diet. Primary sources of dietary carnitine are red meat and dairy products (Table), but commercially produced supplements also are available. Carnitine is stored primarily in skeletal muscle, but also is found in plasma (although in much lower concentrations). Biologically, carnitine is essential for the transport of long-chain (carbon chain length = 10) fatty acids across the outer- and inner-mitochondrial membranes (carnitine palmitoyltransferanse I and II, respectively). However, its physiological roles in human physiology may be much more diverse than previously thought (1).

L-carnitine in various foods.

Research into carnitine has shown that it is a safe supplement for human consumption (2,3). A study performed in our laboratory with 2 g·d−1 of L-carnitine examined complete blood chemistry panels in healthy young men along with symptom questionnaires. There were no observed negative effects or changes in any of the blood markers, including liver and renal function (4). Thus, side effects have been minimal across almost all studies using the 1 to 3 g range of supplementation.

Based on carnitine's function as a transporter of fatty acids, early work investigating the effects of carnitine focused on the experimental paradigm that carnitine supplementation would enhance skeletal muscle carnitine concentrations and increase transport (and thus oxidation) of fatty acids. This led to the belief that it should improve endurance exercise performance or maximum oxygen consumption. Studies investigating this mechanism of action have yielded conflicting results (5-7). This is primarily due to the fact that oral supplementation of L-carnitine typically has not been shown to increase skeletal muscle concentrations of L-carnitine nor its oxidative potential or lactate production (8-13). This resulted in less enthusiasm from athletes to use L-carnitine supplementation to enhance exercise performances as the muscle concentrations did not appear to be a limiting factor.


Owing to the fact that the role of L-carnitine was not obvious in the enhancement of metabolic support for endurance or even higher intensity exercises, a new line of inquiry in the area of L-carnitine and exercise evolved. Studies have indicated that a novel role for L-carnitine may reside in its ability to optimize recovery from the hypoxic effects of exercise (1). Recovery appears to be an important factor in exercise training. Well known to exercise physiologists, exercise places physiological stress on the body derived from primarily two different stimuli: 1) immediately, the mechanical forces, especially high eccentric forces, associated with exercise cause cellular structural damage to both skeletal muscle and their associated capillary beds, and 2) subsequently, chemical responses (e.g., oxygen reactive species) related to skeletal muscle damage and inflammation related to the tissue repair process cause tissue breakdown that can be observed for up to 10 d post-exercise.

The eccentric mechanical stress to skeletal muscle tissue is primarily mediated by the intensity of the eccentric muscle actions (muscle lengthening under force). Loading that is greater than concentric (muscle shortening) maximal strength (e.g., lowering weights with 105%-120% of the weight that can be raised) can lead to significant damage to contractile units. The mechanical stress of such overload can create muscle tissue damage and produce dramatic deformation in the geometrical organization of muscle fiber sarcomeres (14). Such damage can be significant, if not injurious, because of the loss of the structural integrity and contractile function (15). Under such conditions, the structure of the circulatory vessels is altered by changes in capillary luminal shapes and areas (16). Such conditions may limit the role of oxygen delivery, thereby obviating some of L-carnitine's potential role to mitigate chemical damage by allowing capillary sphincters to open (rather than close due to inadequate carnitine concentrations).

Again, while almost all exercise results in some disruption of muscle fibers due to mechanical stress, chemical factors associated with exercise stress can result in more long-term dysfunction due to free radical scavenging, which can continue to degrade tissue structures over the recovery period of 5 to 10 d (17,18). This problem is exacerbated by the increased release of cortisol, which has negative effects upon immune cell activation. These chemical responses to the mechanical stress of exercises cause physical performance decrements and delayed-onset muscle soreness (DOMS) (19a,19b). The paradigm shift for L-carnitine resides in its potential to reduce chemical damage to tissues and help the process of muscle tissue repair and remodeling. It only addresses this one partial phase of recovery in that oxygen delivery is vital to repair and hypoxia can create many negative effects. Potentially, L-carnitine may improve blood flow during and after exercise and optimize the signals supporting tissue repair processes, but intact capillary function would appear to be a necessity. Over the past several years, we have investigated this theoretical potential for L-Carnitine's role with exercise by examining outcome variables in this cascade of post-exercise events.

A shift in the paradigm started with an examination of the recovery process and some of the known concepts related to carnitine's role in myocardial vasculature. Thus, recent research in our laboratory has centered around an evolving hypothesis: that carnitine supplementation may facilitate recovery post-exercise by replenishing carnitine that is depleted in endothelial tissue of vascular smooth muscle, thereby mitigating some of the hypoxia associated with exercise and its subsequent chemical damage due to oxygen reactive species. Inherent to this postulation was an intact capillary bed and circulatory viability obviating its effect with such exercises with extreme eccentric mechanical forces that produce marked tissue damage. This supplementation allowed the blood to perfuse the tissues, increasing the delivery of oxygen and decreasing oxidative stress markers and muscle damage (19a,19b).

Bloomer (20) proposed a possible role for L-carnitine in ameliorating signs and symptoms of injury. Our lab has investigated various mechanisms for L-carnitine's role in recovery from light to moderate intensity resistance exercise. There are several aspects of carnitine that could influence recovery. Our laboratory has shown that carnitine reduces chemical tissue damage caused by exercise-induced hypoxia and causes an increase in IGFBP-3 concentrations post-exercise. In addition, the preserved tissue theoretically allows for a higher number of intact receptors that are able to interact with anabolic hormones. This supports the importance of carnitine in promoting recovery in response to hypoxic exercise that can result in chemical damage to tissues (21).

Carnitine also has shown a smaller increase, as compared with placebo, in several markers of hypoxic damage. In particular, we found that markers of purine catabolism, including hypoxanthine, xanthineoxidase, and serum uric acid, were attenuated. The same pattern followed with circulating cytosolic proteins, namely myoglobin, creatine kinase, and fatty acid-binding protein. Malondialdehyde, which increased in response to the resistance training, decreased more swiftly in carnitine-supplemented subjects. Magnetic resonance image (MRI) scans showed a significant difference in the area of skeletal muscle disruption after the exercise stress, as the area of damage in subjects supplemented with carnitine was only 41%-45% of the area of damage in placebo (19a,19b).

In an effort to elucidate the impact of dose upon the effects of carnitine, a study was performed to compare 1- versus 2-g doses. Both doses were found to be equally effective, once again verifying the ability of L-carnitine L-tartrate to mediate markers of metabolic stress, diminish the degree of the hypoxic chain of events, and reduce muscle soreness (22). In a separate investigation, our laboratory found that L-carnitine L-tartrate, in conjunction with post-exercise feeding, upregulates androgen receptors in men in response to resistance exercise, thereby suggesting one mechanism for improved recovery from resistance exercise previously postulated to be caused by more intact tissue and circulatory perfusion (23).

Building upon the data we have collected, our laboratory has presented a new hypothesis. Vascular endothelial cells rely on carnitine to promote the oxidation of fatty acids. Our current working hypothesis is that supplementation of carnitine acts to protect vascular endothelial cells from carnitine deficiency. In doing so, supplementation helps to improve the regulation of blood flow to deliver oxygen directly to affected tissues. An increase in oxygen to the affected tissue reduces the hypoxia generated by physical activity. This helps to reduce membrane disruption, muscle soreness, purine catabolism, and the formation of free radicals (Figure).

The underlying components of our paradigm. Independent of mechanical damage, exercise results in breakdown of adenosine triphosphate (ATP), accumulation of adenosine diphosphate (ADP) within the smooth muscle of the pre-capillary sphincter (#1a), and activation of the enzyme adenylate kinase (#1b). Adenylate kinase then catalyzes the formation of ATP and adenosine monophosphate (AMP) from two molecules of ADP (#1c). Accumulation of AMP leads to the formation of hypoxanthine that diffuses out of the capillary endothelial cell. Hypoxia induced by exercise (#2a) also causes a mismatch between ATP supply and demand resulting in the malfunction of ATP-dependent calcium pumps (#2b) and intracellular accumulation of calcium. The increase in intracellular calcium activates calcium-dependent proteases (#2c) that lead to the proteolytic cleavage of a portion of xanthine dehydrogenase, converting it to xanthine oxidase (#2d). Recent work by Hellsten et al. provides evidence for an increase in xanthine oxidase in human vascular cells of skeletal muscle after exercise. Xanthine oxidase then catalyzes the formation of xanthine from hypoxanthine (#3a) and converts it to uric acid (#3b). These reactions use molecular oxygen as an electron acceptor and form a superoxide radical (#3c). The superoxide radical can combine with iron and form reactive hydroxy radicals that attack polyunsaturated fatty acids in cell membranes (#4). This attack initiates a chain of lipid peroxidation reactions. Lipid peroxidation results in the formation of numerous aldehydes of different chain lengths, such as the 3-carbon product malondialdehyde (MDA) (#5). MDA is thus used as a plasma marker of free radical damage. The disruption to the cell membrane results in leakage of cytosolic proteins such as creatine kinase (CK) (#6). Finally, superoxide radicals also form intermediate (#7a) that attract neutrophils (#7b), furthering membrane disruption.


Based in part upon carnitine's role in transporting fatty acids into mitochondria, much of the compound's research has focused upon the effects of carnitine supplementation on fat oxidation. Some studies also have suggested that carnitine supplementation increased maximal oxygen uptake and decreased respiratory quotient. As a result, investigators have postulated that L-carnitine could increase lipid metabolism (24).

Despite its theoretical underpinnings, research into L-carnitine and lipid oxidation has failed to provide convincing evidence that increases in oral supplementation of L-carnitine has any effect upon lipid oxidation. The majority of the research has shown no effect on fatty acid oxidation or muscle concentrations of carnitine despite increases in plasma carnitine (9). Some studies indicate that endogenous carnitine is sufficient for fatty acid oxidation (10,25). Other studies have shown declines in fatty acid oxidation. Healthy young men exhibited a decrease in fatty acid oxidization with increased concentrations of plasma carnitine; the authors believe that more carnitine was being converted to acetylcarnitine (26). In women, lipid peroxidation decreased while retinol and alpha-tocopherol were conserved with supplementation of choline and carnitine (27).

A study examining fatty acid-binding protein content and beta-hydroxyacyl CoA dehydrogenase activity showed no additive stimulation of their activity when carnitine supplementation was coupled with exercise. The authors suggest that the prescription of carnitine and exercise together did not have an impact of fatty acid oxidation and therefore would have little impact on performance (28). While hypothetically carnitine supplementation could increase fatty acid oxidation, there is no strong evidence in support of the theory (29). It is of interest that men but not women have been shown to increase carbohydrate oxidation during exercise when supplementing with carnitine (30).

There has been no strong set of research data to indicate that carnitine supplementation increases fatty acid oxidation. It is therefore assumed that endurance performance improvements witnessed in healthy subjects supplementing with carnitine cannot be wholly attributed to increased fatty acid oxidation. Theoretically it was thought that lipid oxidation could not be affected by L-carnitine without increases in muscle concentrations of carnitine, which has not been shown to occur. Thus the conundrum that has evolved with this line of research related to the understanding in muscle of temporal kinetic and turnover dynamics remains unknown.


Several studies have shown marked benefits for those people with specific disorders taking L-carnitine. Most of the research has shown specific improvements in exercise performance in patient populations while supplementing with L-carnitine. Patients with congestive heart failure are typically deficient in L-carnitine. When given L-carnitine, exercise time and peak oxygen consumption increases with a corresponding decrease in cardiac dimension (31). The ability for L-carnitine to prevent apoptosis has also been hypothesized to have relevance for those with congestive heart failure (32). Subjects with peripheral arterial disease (PAD) increase performance on a treadmill when supplementing with 2 g of L-carnitine twice daily (33). Patients with PAD also experience a significant increase in strength and ability to walk when supplemented for 4 wk with propionyl-L-carnitine (34). Patients with chronic stable angina were able to exercise longer and recover sooner from exercise when supplemented with carnitine (35). In bicycle ergometry, supplemented patients with advanced cardiac insufficiency exhibit higher maximum performance than their placebo counterparts. In addition, these performance results last beyond the supplementation period (36).

When completing both respiratory training and total-body training programs, patients with chronic obstructive pulmonary disease (COPD) who are supplemented with L-carnitine experience greater improvements than placebo. These patients see greater improvement in muscular strength, walking tolerance, heart rate, blood pressure, oxygen saturation, and blood lactate (37). Patients with medium-chain acyl-CoAdehydrogenase (MCAD) deficiency who are supplemented with carnitine do not experience the typical fall in plasma carnitine concentrations during exertion. This hypothetically enables the subjects to improve their tolerance of exercise and leads to greater increases in acylcarnitine excretion (38). Also, patients with Thalassemia (a genetic blood disorder that affects the production of the hemoglobin, the oxygen-carrying component of red blood cells) have been shown to increase cardiac performance and their fitness level, including oxygen pulse, oxygen consumption, and cardiac output, to a higher degree when they supplement with L-carnitine (39).

Investigators found no difference in patients with end-stage renal disease (ESRD) in terms of muscle function or metabolism after 16 wk. The study revealed an expected increase in the plasma concentration of carnitine, but decreased blood flow to muscle in patients with ESRD (40). This relationship may be expected; patients with ESRD exhibit decreased mitochondrial function in muscle, and supplementation of carnitine has not been shown to increase muscle concentrations of carnitine.

In summary, carnitine supplementation has strong, positive impacts upon patients with specific pathologic conditions. These particular diseases, most notably cardiovascular diseases, have a tendency to show improvements in exercise performance and recovery capabilities. ESRD was an exception, possibly because of the inability of carnitine supplementation to mediate any of the mechanisms that impact this disease.


As previously noted, while some studies in healthy populations indicate improvements in aerobic exercise performance, most studies indicate very little difference in maximal oxygen uptake and other measures. Based upon studies indicating improvements in maximal oxygen uptake and respiratory ratio, one review suggests there could be aerobic benefits to supplementing with carnitine (41).

Among trained athletes, L-carnitine supplementation leads to overall increases in free carnitine that does not decrease during maximal exercise (42). Type I fibers appear less likely to fatigue when supplementing with carnitine (43). Maximal oxygen uptake slightly increases with supplementation, but lipid oxidation does not change (44). Supplementation with carnitine has led to improvements in measures of evoked muscular potential, free fatty acids, and triglycerides, leading early authors to suggest supplementation (6). The role of L-carnitine in oxidative function may be reflected it its ability to reduce hypoxic stress as observed in rats exposed to hypobaric/hypoxic conditions (45).

No differences were observed in muscle carnitine, aerobic performance, or anaerobic performance after 8 wk of supplementation with 3 g of glycinepropionyl-L-carnitine when accompanied with aerobic exercise (46). Additionally, after 4 wk of carnitine supplementation, there was no discernable change in either aerobic performance or substrate utilization during supplementation, indicating a potential highly contextual conditions that may need to be present for carnitine to have an effect (47). This again was shown when supplementing with 2 g of carnitine made no difference in the ability to perform a second bout of exercise within 3 h after the first (48). In highly trained swimmers, no differences in either blood markers or timed performance were observed (13). As previously mentioned, one major issue with the hypothesis that carnitine increases performance through increases in fatty acid oxidation is that supplementation with carnitine increases serum, not muscle, levels of carnitine. However, when insulin is also added, carnitine appears to accumulate readily in muscle. More research on this subject is needed to again understand the role of insulinand its many effects on metabolism as it relates to endurance performance (49).


While carnitine serves in the role of transporting fatty acids across the mitochondrial membrane, it does not appear that oral supplementation with carnitine has strong effects on facilitating the process at the level of skeletal muscle tissue. Carnitine does not appear to increase in concentration in muscle fibers in response to oral supplementation, but does appear to increase in concentration in plasma. Carnitine does appear to help populations with certain conditions achieve a higher level of exercise performance, particularly those with various dimensions of cardiovascular disease. However, it does not appear that carnitine has a major impact upon healthy populations in terms of exercise performance. Instead, a novel paradigm is emerging that places carnitine in the important role of facilitating the recovery process in response to hypoxic stimulus such as physical activity. In this role, supplemental carnitine helps to protect the endothelial cells from carnitine deficiency, mediate the markers of purine catabolism, reduce tissue damage and muscle soreness, and facilitate the overall process of recovery. This also was supported with its positive effects in the enhancement of exercise performance in animals in altitude-like conditions. Thus, L-carnitine is an emerging supplement that may well have targeted and specific roles to play in the exercise domain with both clinical populations and exercise recovery.


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