An objective look at L-carnitine supplementation for fat-loss and enhanced performance

Pill

Opening Comments

Over the past 25-plus years carnitine has received a lot of attention, both from researchers and supplement companies alike. Indeed, both camps are interested in carnitine’s role in fat metabolism; however, it is for two very different reasons. Researchers are primarily interested in the ergogenic capacity that carnitine may have to offer endurance athletes – namely carnitine’s glycogen sparing effect via increased fat oxidation – while supplement companies (and consumers) are mostly interested in carnitine for increased fat oxidation to enhance fat-loss and improve body composition. Being the skeptic that I am, today I will evaluate both sides of the aisle and make some final comments and conclusions about whether or not it’s practical to take carnitine supplements, be it for performance purposes or weight loss endeavors. As always, I will begin with some background information (with a little biochemistry thrown in there), follow it up with the pertinent research, and then end with some closing remarks and applications. Let’s get to it!

Rationale behind carnitine supplementation to improve performance

Before I actually get into the potential benefits of carnitine supplementation, I think it would be best to first cover the rationale behind taking carnitine for performance. In doing so, I will try to keep this as short as possible.

It has been well established that the body can use both carbohydrate and fat (in the form of free fatty acids) for muscular contraction [1]. However, the latter only remains true at low to moderate intensities. Indeed, as exercise intensity is increased (>75-85% VO2 max), the proportion of fat that is and can be used to fuel muscle contraction is decreased – if not completely inhibited – such that carbohydrate oxidation increases (see figure below) [2].

FFA ox

However, as moderate to intense exercise continues (as in a marathon or other endurance-type events) the reliance on FFAs is increased due to lowered glycogen stores and therefore less available glucose to fuel muscle contraction. This is important, because during the final leg of a race, runners, cyclists, etc. tend to speed up and may even sprint to the finish line. This would require additional glucose to fuel the high-intensity (>75% VO2 max) sprint. Depleting ones glycogen stores prior to the final stretch of the race could hinder the racer’s finish and (potentially) placement. It is from this paradigm that the theory of fat adaptation came about. Fat adaptation-ists believe that if one can shift their metabolism during moderate intensity exercise to exclusively rely on FFAs, then that person could potentially conserve glycogen stores for when they are needed most, like during the final stretch of a race (>75% VO2 max). Many dietary manipulations have been undertaken in order to help aid in this adaptation, however I will not cover those here as another entire article could be written on the subject. Rather, we will look at how carnitine may be able to facilitate this need (i.e. increase fat oxidation and spare glycogen) by first looking at some basic biochemistry behind fat metabolism (and thus carnitine’s role therein) that will lay the foundation for our discussion on whether or not carnitine can be used as an effective ergogenic and/or fat-loss aid.

Fat metabolism and carnitine’s role therein   

When talking about fat metabolism, it is important to note that there are various control points at which fat metabolism (in skeletal muscle) can be regulated. A recent review by Lawrence Spriet [3] eloquently states that fat metabolism can be regulated during exercise at six different ‘control points,’ one of which is FFA transport across the mitochondrial membrane (think back to high school biology class). It is at this point that carnitine is almost exclusively involved and where I will pick up the conversation.

Carnitine – named after the Latin word carnis, meaning ‘flesh’ – is a vitamin-like, water-soluble amine that can be obtained through dietary intake (for example: meat and milk) or by endogenous synthesis via S-adenosyl-methionine (SAM) and lysine in both the liver and kidneys. Almost all (~95-98%) of the bodily stores of carnitine are present in skeletal muscle and in the heart (with the remaining 2-5% in the liver, kidneys and plasma). Carnitine plays a pivotal role in both fat metabolism as well as carbohydrate metabolism (the latter I will briefly mention when needed) [4]. Throughout most of the day (assuming you don’t sprint everywhere) the human body runs on a mixture of glucose, amino acids, and free fatty acids, with the majority of ATP coming from FFAs. However, in order to oxidize these FFAs (and yield energy in the form of ATP) each fatty acid must undergo a process called beta-oxidation. Beta-oxidation takes place within the matrix of the mitochondria of the cell. In order for the fatty acid to even make it into the matrix, it must rely on the help of carnitine to facilitate its transport in. Once inside, the fatty acids can undergo beta-oxidation and proceed to the Tricarboxylic acid (TCA) cycle and produce ATP.

It is at this point that I would like to stop and regroup. The above paragraph is extremely important because it really lays out the basis (theoretically) for carnitine improving both performance and body composition. This however, operates under a couple of assumptions: 1) that carnitine translocation is the rate limiting step in fatty acid oxidation, meaning that; 2) increasing carnitine levels will equate to greater transport of fatty acids into the matrix and greater levels of oxidation; and lastly that, 3) you can indeed increase muscle levels of carnitine in the first place. Granted that all three of these factors are true, than yes, there may be a reasonable case for carnitine supplementation. The real question here is whether or not they hold up under scientific scrutiny.

Research against carnitine supplementation

Above, we just saw that carnitine helps “ship” FFAs into the mitochondria so that they can be oxidized to produce ATP. Therefore, potentially having more carnitine may mean more FFA oxidation and therefore a “sparing effect” on muscle glycogen stores which may lead to increased performance. Indeed, muscle carnitine levels decrease as exercise intensity increases [3]. It would make sense that low muscle carnitine levels would therefore lead to a decrease in FFA usage, given that this effect does hold true under high intensities. However, and counter intuitively, the highest FFA oxidation rates actually occur when carnitine levels are well below resting levels [3]. Furthermore, when fat availability in the blood is artificially increased during exercise (at 80% VO2 max), with no concomitant increases in carnitine, the muscle does indeed oxidize more fat [5]. This suggests that carnitine isn’t the rate limiting step during fat metabolism. Therefore, theoretically increasing muscle carnitine levels may not even amount to further increases in fat oxidation given that maximal rates are already being achieved with reduced levels of muscle carnitine and that artificially high levels of FFA are easily handled in the absence of additional carnitine as it is. Lastly, and most importantly, increasing muscular levels of carnitine has been shown time and time again to be quite futile.

In 1994, Barnett and colleagues showed that 14 days of carnitine supplementation (at 4g/day) did not significantly affect muscle levels of carnitine [6]. Similarly, in the same year, Vukovich et al. investigated the effects of carnitine supplementation on muscle carnitine concentrations and glycogen content during submaximal exercise [7]. Here, subjects ingested 6g/day of carnitine and still did not show any increases in muscular levels of carnitine. And if two weeks isn’t long enough to convince you, Wächter and co. [8] gave subjects 4g of carnitine per day for three months and still saw no increase in muscle levels of carnitine. Moreover, had you even thought about hooking up your at-home IV kit and mainlining your carnitine, you’d still be wasting your time as direct infusion has been shown to be unsuccessful [9, 10]. What’s more is that performance parameters such as perceived exertion, exercise performance, VO2 max, or markers of muscle substrate such as RER, VO2, blood lactate levels, leg FFA turnover, and post-exercise muscle glycogen content were all unaffected by the ingestion of 2-5g of carnitine per day (anywhere from one week up to three months) [11]. Thus, the majority of relevant data looking at the oral ingestion and infusion of carnitine has failed to increase muscular levels leading to a lack of improved performance. Therefore, if we still buy into the hypothesis that fat metabolism can be increased via an increase in muscle levels of carnitine we are sadly left with the realization that this is just not possible. Or is it…

Research supporting carnitine supplementation

Although we just saw that the vast majority of research shows that carnitine supplementation (of up to 3 months) has very little impact – if any – on muscle levels of carnitine, it doesn’t leave out the fact there are some studies that do show an impact of oral ingestion and infusion of carnitine on muscle concentrations. First we will examine the infusion studies.

Effective means of carnitine infusion

As noted earlier, straight infusion of carnitine has little impact on muscle levels of carnitine [9, 10]. However, infusion of carnitine alongside an infusion of insulin actually does have an impact on muscle levels [10]. What researchers saw was ~15% increase in muscle levels of carnitine. Although significant, this is not truly representative of the population taking carnitine because I don’t know about you, but I’m not willing to start injecting myself with physiologically high levels of insulin just to increase my muscle carnitine stores. Nevertheless, for those of you who may be considering this option, there may be an easier way.

Effective means of oral carnitine ingestion  

Indeed, it has been shown that oral ingestion of carnitine, alongside a rather large dose of carbohydrate (~80-94g), is able to effectively stimulate the “uptake” of carnitine as measured indirectly via plasma levels and urinary excretion [12, 13]. This is undoubtedly due to carbohydrates’ insulin stimulatory effect. Although 80-94g of carbohydrate is not unusual for a bodybuilder or weightlifter to consume in one sitting in the offseason or even in the earlier stages of dieting, the dosage may come into conflict during the later stages of prep (when carbs are being reduced) or for those who have lower CHO requirements by default (like the average American). Therefore, some practical limitations may come into play, especially when it means eating relatively high amounts of carbohydrate in order to gain what may be a trivial fat-burning effect from carnitine. What’s more is that although muscle levels of carnitine were indirectly seen to increase, there was absolutely no measure of improved body composition during the studies. However, what they did see was a reduction in glycogen breakdown at low intensity exercise (50% VO2 max), but this was effectively eliminated at intensities around 80% VO2 max. Either way, this does not reveal any convincing evidence that carnitine is a potent fat-burner or ergogenic aid even though major shifts in fuel metabolism can be seen; essentially showing a greater reliance on FFAs as a fuel source. These findings, nevertheless, are limited to conjectures about fat-loss in the long-term and are confounded by methodological issues that do not apply to the normal bodybuilder/fitness population or the endurance athlete – or anyone for that matter.

Conclusions

Although it may be physically possible to increase muscle levels of carnitine using relatively large amounts of carbohydrate repeatedly throughout the day, the fact still remains that there is limited convincing data that shows that carnitine is a potent fat-burner or ergogenic aid. Furthermore, when practical limitations come into play, the usefulness of carnitine as a fat-burner is undoubtedly overshadowed by the well-known effects of a solid caloric deficit in combination with increased physical activity (usually in the form of cardio). I should also note that carnitine has been implicated in aiding recovery from resistance exercise in both young and middle-aged populations [14-16] as well as increasing androgen receptor (AR) synthesis and therefore increasing cellular uptake up testosterone following weight training. This potentially leads to the activation various muscle synthetic pathways [17]. However, despite the potential beneficial basis of carnitine supplementation for muscle recovery and hypertrophy there just isn’t enough convincing data that shows supplemental carnitine will do jack-diddly in terms of sizeable gains in muscle mass accretion. We just don’t have the long-term studies necessary to make that conclusion. Conversely, there is some convincing evidence that transient elevations in anabolic hormones (due to exercise) such as testosterone and growth hormone are not closely associated with increases in muscle mass [18-20]. Therefore, increasing AR synthesis and testosterone uptake may be trivial in the larger scope of things.

The bottom line is that the beneficial role of carnitine for either exercise (be it endurance or resistance) or fat burning in young, healthy populations (especially the athlete) are, at this stage, completely theoretical and, most likely, trivial at best.

References

1. Asmussen E. Muscle metabolism during exercise in man. A historical survey; in Pernow B, Saltin B (eds): Muscle Metabolism during Exercise. New York, Plenum Press, 1971, pp. 1-11.

2. van Loon LJ, Greenhaff PL, Constantin-Teodosiu D, Saris WH, Wagenmakers AJ. The effects of increasing exercise intensity on muscle fuel utilisation in humans. J Physiol. 2001;536(Pt. 1):295-304.

3. Spriet LL. Metabolic regulation of fat use during exercise and recovery. Nestlé Nutr Inst Workshop Ser. 2011;69:39-53;discussion 53-8.

4. Constantin-Teodosiu D, Carlin JI, Cederblad G, Harris RC, Hultman E. Acetyl group accumulation and pyruvate dehydrogenase activity in human muscle during incremental exercise. Acta Physiol Scand. 1991;143:367-372.

5. Romjin JA, Coyle EF, Sidossis LS, et al. Relationship between fatty acid delivery and fatty acid oxidation during strenuous exercise. J Appl Physiol. 1995;79:1939-1945.

6. 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. 1994;4(3):280-8.

7. Vukovich MD, Costill DL, Fink WJ. Carnitine supplementation: effect on muscle carnitine and glycogen content during exercise. Med Sci Sports Exerc. 1994;26(9):1122-9.

8. Wächter S, Vogt M, Kreis R, Boesch C, Bigler P, Hoppeler H, Krähenbühl S. Long-term administration of L-carnitine to humans: effect on skeletal muscle carnitine content and physical performance. Clin Chim Acta. 2002;318(1-2):51-61.

9. Brass EP, Hoppel CL, Hiatt WR. Effect of intravenous L-carnitine on carnitine homeostasis and fuel metabolism during exercise in humans. Clin Pharmacol Ther. 1994;55(6):681-92.

10. Stephens FB, Constantin-Teodosiu D, Laithwaithe D, Simpson EJ, Greenhaff PL. Insulin stimulates L-carnitine accumulation in human skeletal muscle. FASEB J. 2006; 20:377-379.

11. Stephens FB, Constantin-Teodosiu D, Greenhaff PL. New insights concerning the role of carnitine in the regulation of fuel metabolism in skeletal muscle. J Physiol. 2007;581(2):431-444.

12. Wall BT, et al. Chronic oral ingestion of L-carnitine and carbohydrate increases muscle carnitine content and alters muscle fuel metabolism during exercise in humans. J Physiol. 2011;589(4):963-973.

13. Stephens FB, Evans CE, Constantin-Teodosiu D, Greenhaff PL. Carbohydrate ingestion augments L-carnitine retention in humans. J Appl Physiol.. 2007;102:1065-1070.

14. Volek JS, Kraemer WJ, Rubin MR, et al. L-carnitine L-tartrate supplementation favorably affects markers of recovery from exercise stress. Am J Physiol Endocrinol Metab. 2002;282:E474-E482.

15. Kraemer WJ, Volek JS, French DN, et al. The effects of L-carnitine L-tartrate supplementation on hormonal responses to resistance exercise and recovery. J Strength Cond Res. 2003;17(3):455-62.

16. Ho JY, Kraemer WJ, Volek JS, et al. L-carnitine L-tartrate supplementation favorably effects biochemical markers of recovery and from physical exertion in middle-aged men and women. Metabolism 2010;58(8):1190-9.

17. Kraemer WJ, Spiering BA, Volek JS, et al. Androgenic responses to resistance exercise: effects of feeding and L-carnitine. Med Sci Sports Exerc. 2006;38(7):1288-96.

18. West DW, Phillips SM. Anabolic processes in human skeletal muscle: restoring the identities of growth hormone and testosterone. Phys Sportsmed. 2010;38(3):97-104.

19. West DW, Phillips SM. Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training. Eur J Apply Physiol. 2012;112:2693-2702.

20. West DW, Burd NA, Staples AW, Phillips SM. Human exercise-mediated skeletal muscle hypertrophy in an intrinsic process. Int J Biochem Cell Biol. 2010;42:1371-1375.

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9 Responses to An objective look at L-carnitine supplementation for fat-loss and enhanced performance

  1. Great article Dylan. So even when muscle carnitine levels are “low,” it’s still more than enough for fat oxidation; any idea what all the excess carnitine is doing when muscle carnitine levels are high?

    • decline104 says:

      Sorry for the delayed response, I was in Brazil all last week and just returned this morning. To be honest, I am wondering the same thing. We know that increased muscle levels of carnitine leads to increases in FFA oxidation at low to moderate intensities, but the practicality of increasing one’s stores (i.e. insulin infusion and/or relatively large quantities of CHO) makes it essentially irrelevant for the average population. What’s more is that potential confounders may explain this happening. Indeed, increases in FFA ox with increased levels of muscle carnitine via insulin infusion/high-CHO feeding – as opposed to normal levels with substantial excess carnitine – may be the result of upregulation of various mitochondrial fat transport proteins (via insulin) that could lead to increased FFA ox (something, in hindsight, I should have mentioned above). So, to answer your question the long way; I have no idea. It appears that physiological levels of muscle carnitine are more than enough for normal levels of FFA and any excess proves to be just that; excess.

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  4. Maria says:

    Thank you! Great article! Such a good research..this is exactly what I was willing to read. Once again the supplement industry knows well how to make money out of people´s ingorance,( there are too many, sadly..)

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  6. S.Walsh says:

    The only issue I take with this summation is that my personal results after injecting LCar over the course of 6 weeks is already kind of unbelievable. Possibly due to androgen receptor up-regulation? Nothing else has changed aside from the addition of LCAR

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  8. Jakkie says:

    From other sources it seems that positive effects of supplementing carnitine are observed after 3 months. Read this http://www.nutritionexpress.com/article+index/vitamins+supplements+a-z/protein/showarticle.aspx?id=1487
    There is a few articles by the Poliquin group that states that L-carnitine is a extremely effective supplement. They also suggest that instead of 80g of carbs one must use Omega 3 to a ratio of 5:1. So if you take 4g of carnitine you must take 20g of Omega 3. (Which is not uncommon in the weight training world). This high amounts of Omega3 makes your cells more sensitive to insulin, which makes the need for high carbs less. The article can be found here: http://www.poliquingroup.com/ArticlesMultimedia/Articles/Article/767/Top_12_Reasons_to_Use_Carnitine.aspx

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