Is Carnitine Useless?
For years, carnitine has been touted as a top supplement for improving performance, fat loss and muscle recovery.
However, if you’re making this common mistake, your carnitine supplementation is likely not doing anything for you and completely going to waste.
Admittedly, it’s hard to find an avid supplement consumer to say anything bad about carnitine. It’s a common ingredient in most fat-burners, pre-workouts or standalone products, and has been loved by many athletes for the past 30 years. Some people are quick to point out scientific evidence for its effectiveness, but what has been coming abundantly clear is the inconsistency of the scientific literature, because for every manuscript that shows a benefit, there are several more that disprove it’s usefulness at all. It makes you wonder if there is any explanation for this discrepancy.
The Role of Carnitine in Muscle
There is no question that carnitine is a molecule for muscle. Coming from the Greek word ‘carnus’, that literally means ‘flesh’, carnitine was discovered in muscle over one hundred years ago and it hardly exists in any other tissue. In fact, more than 95% of the body’s total carnitine store exists within skeletal muscle tissue alone, providing empirical evidence of its necessity to muscle specifically. Truth be told, carnitine is required in skeletal muscle for at least two distinct purposes. The first of which is related to fat burning and the second is related to engaging in high-intensity exercise.
Background on Fat Burning
In order to shed unwanted fat, a long series of reactions needs to take place. The first step is breaking down the fat being stored as triglycerides in adipocytes, into free-fatty acids (FFA). As the FFA are released from the triglycerides they are free to exit the adipocyte and enter the bloodstream en route to an active muscle where it can be burned (oxidized). Fat oxidation is a long and complex process that occurs inside mitochondria of muscles, but this is where the problem lies. The problem that carnitine elegantly solves, is that the mitochondria membrane is absolutely impermeable to fatty acids. Using a series of enzymes (CPT1, CPT2) and transporters (CACT, CD36) carnitine is an indispensible carrier of FFA, transporting them across the mitochondrial membranes to allow for oxidation and the subsequent release of energy. The critical point is that the transport of FFAs into the mitochondria is considered to be the rate-limiting step of fat oxidation. This means that if the transport could occur faster, then more fat would be burned. Thus, it would be reasonable to assume that more carnitine would then lead to more fat transport and ultimately more fat oxidation.
Carnitine and High-Intensity Exercise
As mentioned earlier, muscle-carnitine has a second vital function independent from fat burning, and that is allowing high-intensity exercise to occur. This means that carnitine has its hands in carbohydrate metabolism as well. Studies from the early 80s and 90s reveal that muscle-carnitine levels disappear during high-intensity exercise, but the investigators couldn’t understand why. It was later discovered that carnitine is consumed by a reaction that buffers the rapid production of acetyl-CoA by producing acetyl-carnitine and freeing up coenzyme-A (CoA). The rapid production of Acetyl-CoA is the result of high-intensity exercise, since anaerobic carbohydrate metabolism (glycolysis) is the fastest process to produce energy (ATP).
Without the buffering of Acetyl-CoA and the liberation of free CoA, pyruvate levels would accumulate, forcing the production of lactate, which ultimately leads to muscle fatigue. In a hypothetical scenario without carnitine, exercise would become fatiguing within the one second of the initiation of muscle contraction. In other words, carnitine extends the timeframe in which high-intensity exercise can occur before lactic acid builds up and causes muscle failure.
The Tale of Two Mechanisms
It’s interesting that one molecule such as carnitine has such unrelated functions within the same cell. On one hand, it’s responsible for enhancing fat oxidation, then during exercise it becomes consumed with anaerobic metabolism (involving carbohydrates). What’s really interesting is that both of the carnitine functions cannot occur to their full potential at the same time. If free carnitine is being consumed during maximal exercise, then less is available for FFA transport into the mitochondria. This is partially responsible to why fat metabolism is reduced during high-intensity exercise. It has been determined that muscle-carnitine availability is the limiting factor for fat-oxidation to occur especially during exercise. This provides additional evidence that augmenting carnitine availability would not only lead to enhanced fat burning capabilities, but functional performance benefits as well.
Manipulating the Carnitine Pool of Skeletal Muscle
With the assumption that carnitine is the limiting factor for fat oxidation, it’s an easy inference that increasing muscle carnitine levels would benefit fat oxidation rates during high-intensity exercise. The additional benefit during exercise would be the sparing of carbohydrates leading to enhanced exercise capacities.
The good news is that a study in 1993 demonstrated that increasing skeletal muscle carnitine content in rat muscle does delay fatigue development by up to 25%. This observation was the foundation of the carnitine supplement industry that perpetuates the notion that carnitine feeding can increase fat oxidation at rest and promote weight loss. This would be great, however, if there was evidence that supplemental carnitine can actually get into human muscle cells.
Unfortunately, the majority of the pertinent studies in healthy humans have, however, failed to increase skeletal muscle carnitine content via neither oral ingestion nor intravenous injection of carnitine. Several studies have tried over and over each one becoming more elaborate than the last. Yet, after several studies running for as long as 3 months of daily carnitine ingestion or up to 5 straight hours of constant carnitine infusion, there is still no evidence of increased intramuscular carnitine content. Furthermore, none of the supplementation methods had any effects on perceived exertion, exercise performance, VO2, blood lactate or even glycogen content.
This raised the conundrum of how do our muscles actually maintain carnitine levels if it doesn’t appear to transportable into the muscle. The answer was discovered in 1998, when the sarcolemmal carnitine transporter was identified (OCTN2). It was discovered that carnitine transport into muscle just works slowly and that it is already operating at maximum capacity with only basal level of carnitine in the bloodstream. Therefore when carnitine is being supplemented, OCTN2 can’t work any faster to import any additional carnitine.
Although this information did not halt the supplement industry, it wasn’t until another eight years later when a significant breakthrough occurred. For the first time in 2006 an investigator decided to infuse carnitine simultaneously with insulin. This combination was the answer to the carnitine delivery problem, because this experiment was the first one to demonstrate an increase in muscle total carnitine content. As it turns out insulin augments the transport of carnitine into muscle just like it does for amino acids and creatine.
Since then it has been determined that 2-3g of L-carnitine when combined with enough carbohydrates to spike serum insulin results in a greater whole body retention of carnitine compared to the lack of retention from the ingestion of L-carnitine alone.
The Best of Both Worlds
In regards to fat burning capabilities, the increase in muscle-carnitine leads to an increase in fat oxidation, which ultimately results in greater fat loss. During exercise, this also accounts for decreased glycogen utilization, a reduction of fatigue and an increase in work output. Although, greatest of all is how carnitine switches functions when exercise switches from low or moderate intensity to high-intensity. Increased muscle carnitine levels spares carbohydrate use during low-intensity exercise. However, during exercise intensities above 80% maximum, increased muscle carnitine functions to optimize carbohydrate metabolism for maximal performance. This was demonstrated clinically when carnitine supplementation was associated with a 31% lower glycolytic flux, compared to control, during cycling at 50% maximum, while associated with a 38% higher glycolytic flux, compared to control, when cycling at 80% maximum. Here we see the two distinct functions of carnitine working together to get the best out of any stage of exercise.
There is no doubt that carnitine supplementation is popular amongst athletes. There just may be some confusion on what it does and how it works. Despite the last 30 years of research showing inconsistent results, the most recent data illustrate that carnitine supplementation by itself is completely ineffective.
However, when combined with other components that result in a spike in insulin, the benefits of carnitine come into play. Knowing of course that spiking your insulin more than necessary is not good for your health, combining 2g of carnitine daily with a post-workout meal, when your muscles are most sensitive to insulin, is an ideal way to maximize muscle carnitine levels. In time, your muscles will be maximum performing, fat burning machines.
This is exactly why Post-Factor™ is formulated to give you the full 2g of L-Carnitine-L-Tartate combined with the proper carbohydrate and protein ratios to maximize your muscle growth and recovery.
Post-Factor™ is the easiest way to ensure your carnitine isn't going to waste and you're getting the best results possible when it comes to post-workout recovery.
- Brass EP, Scarrow AM, Ruff LJ, Masterson KA & Van Lunteren E (1993). Carnitine delays rat skeletal muscle fatigue in vitro. J Appl Physiol 75, 1595–1600.
- Constantin-Teodosiu D, Tsintzas K,Williams C, Boobis L & Greenhaff PL (1996). Carnitine metabolism in human muscle fibre types at the onset of sub-maximal exercise. J Physiol 523.P.
- Coyle EF, Jeukendrup AE,Wagenmakers AJ & Saris WH (1997). Fatty acid oxidation is directly regulated by carbohydrate metabolism during exercise. Am J Physiol Endocrinol Metab 273, E268–E275.
- Fritz IB & McEwen B (1959). Effects of carnitine on fatty-acid oxidation by muscle. Science 129, 334–335.
- Fritz IB & Yue KTN (1963). Long-chain carnitine acyltransferase and the role of acylcarnitine derivatives in the catalytic increase of fatty acid oxidation induced by carnitine. J Lipid Res 4, 279–288.
- Harper P, Elwin CE & Cederblad G (1988). Pharmacokinetics of intravenous and oral bolus doses of L-carnitine in healthy subjects. Eur J Clin Pharmacol 35, 555–562.
- McGarry JD & Brown NF (1997). The mitochondrial carnitine palmitoyltransferase system. From concept to molecular analysis. Eur J Biochem 244, 1–14.
- Stephens FB, Constantin-Teodosiu D, Laithwaite D, Simpson EJ & Greenhaff PL (2006a). Insulin stimulates L-carnitine accumulation in human skeletal muscle. FASEB J 20, 377–379.
- Stephens FB, Constantin-Teodosiu D, Laithwaite D, Simpson EJ & Greenhaff PL (2006b). Skeletal muscle carnitine accumulation alters fuel metabolism in resting human skeletal muscle. J Clin Endocrinol Metab 91, 5013–5018.
- Stephens FB, Evans CE, Constantin-Teodosiu D & Greenhaff PL (2006d). Carbohydrate ingestion augments L-carnitine retention in humans. J Appl Physiol 102, 1065–1070.
- Tamai I, Ohashi R, Nezu J, Yabuuchi H, Oku A, Shimane M, Sai Y & Tsuji A (1998). Molecular and functional identification of sodium ion-dependent, high affinity human carnitine transporter OCTN2. J Biol Chem 273, 20378–20382.
- Timmons JA, Gustafsson T, Sundberg CJ, Jansson E & Greenhaff PL (1998a). Acetyl group availability is a major determinant of the oxygen deficit in human skeletal muscle during submaximal exercise. Am J Physiol Endocrinol Metab 274, E377–E380.
- van Loon LJ, Greenhaff PL, Constantin-Teodosiu D, Saris WH &Wagenmakers AJ (2001). The effects of increasing exercise intensity on muscle fuel utilisation in humans. J Physiol 536, 295–304.