In the last article, we looked at the potential for a supplement called carnitine-l-tartrate (CLT) to improve muscle growth, strength, and recovery. In this article, we’ll take a look at the theoretical basis for CLT to improve something even more elusive—neural performance and recovery.

CLT is the most bioavailable form of the common fat loss supplement carnitine. Although it’s generally not marketed for performance and strength, recent data have emerged to suggest that it may play a positive role in these processes. Information on neural stress and recovery is limited, but a tenuous connection can be made between our applied physiology and supplementation.

Recall that CLT use results in both improved muscular performance and an increase in muscle testosterone receptors. The implications of the former are clear, but it is the latter effect that may be neurally ergogenic. That is because the more docking sites we have available for the anabolic hormone testosterone, the greater its ability to deliver its powerful message.

Getting neural

For the most part, exercise physiology has a decent understanding of muscle stress and recovery, which means that we have a few good ideas about how to improve or even optimize them. However, strength athletes are often more concerned about nervous system stresses, the details of which are far more obscure. After all, it’s easy enough to perform some kind of exercise intervention and take a muscle biopsy to see what’s going on. However, you can’t just cut out someone’s nerves for a study.

This lack of information is unfortunate considering that it is these nerve cells (a.k.a. neurons) that transmit all of the signals from our brain to our limbs (among other things). More specifically, it is our motor neurons that are in contact with our muscles, which deliver the message to contract. As we adapt in our training, our neurons are better able to transmit these signals, which is one of the more important mechanisms of becoming stronger, and we are better able to resist fatigue.

Androgenic adaptation

There are plenty of data to show the relation between testosterone and our neural development, protection, and adaptation. That is to say that androgens acting directly on our nerve cells are largely responsible for the changes that occur, and this can ultimately lead to performance. For example, during exogenous anabolic use, neurons grow in size. This size increase can lead to greater signal transmission to our working muscle as well as a resistance to neural fatigue (i.e. improved strength and strength endurance).

Interestingly, it is this specific “connection” or signaling area that ends up receiving much of the benefit from androgen use because this is where androgen receptor up-regulation occurs during androgen use. Again, more androgen receptors mean that more growth and recovery signals can be delivered to the cell.

Up-regulation: An ideal mechanism

If we consider the effect of increasing androgen uptake due to an increase in receptors, we can begin to see why this is such a powerful mechanism of action. In traditional hormonal manipulation schemes, it is our goal to increase the quantity of hormone in the blood. This transient effect usually has some kind of backlash in which the hormonal concentration is ultimately reduced, thus largely negating any positive outcome. However, by simply increasing the number of docking sites for the hormone, we’re actually increasing the clearance of the hormone from the blood. This signals the brain that we’re running low on that hormone after which more of it will be produced.

It’s clear that this latter mechanism is not only far more elegant but also more effective for our purposes.

Putting it all together

The point of all of this is that an increase in androgen receptor content in our working nerve cells would ultimately result in positive adaptations for strength and performance. If you’ll recall that CLT has the ability to elevate muscle androgen receptor content in response to training, the picture will become clearer.

If CLT can exert its protective effect on our working nerve cells, particularly at the level of the nerve-muscle connection, we’ll reap the benefit of increased androgenic adaptation. In fact, if such an adaptation exists, this could be the first supplement available to improve neural functioning and recovery.

Because neural recovery is far more limiting to performance and training than muscle recovery, the implications are quite powerful.

Summary

Although direct evidence for the performance enhancing effect of CLT exists, there is a theoretical basis for this supplement to positively interact with our nerve cells. Such an interaction would entail an increase in androgen receptor content, which would lead to greater anabolic signal delivery. In turn, this would ultimately increase strength, performance, and recovery at the neural level.

Where do you get CLT? I’ve been asked this quite a bit lately so it’s worth discussing here. CLT is a ubiquitous product. You simply have to read the actual label to ensure that the “l-carnitine” you’re looking at is actually CLT.

How much do you use? I recommend starting with 1.5 grams per 200 lbs with a minimum of 1 gram for lighter athletes. Moving up from 200 lbs would involve non-linear scaling, depending on numerous factors. The optimization of such a protocol is currently in development, and I’ll report on it shortly.

References

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Jones KJ, Brown TJ, Damaser M (2001) Neuroprotective effects of gonadal steroids on regenerating peripheral motoneurons. Brain Res Brain Res Rev 37(1–3):372–82.

Jordan CL, Price RH Jr, Handa RJ (2002) Androgen receptor messenger RNA and protein in adult rat sciatic nerve: Implications for site of androgen action. J Neurosci Res 69(4):509–18.

Kraemer WJ, Volek JS, French DN, Rubin MR, Sharman MJ, Gómez AL, Ratamess NA, Newton RU, Jemiolo B, Craig BW, Häkkinen K (2003) The effects of L-carnitine L-tartrate supplementation on hormonal responses to resistance exercise and recovery. J Strength Cond Res 17(3):455–62.

Kraemer WJ, Spiering BA, Volek JS, Ratamess NA, Sharman MJ, Rubin MR, French DN, Silvestre R, Hatfield DL, Van Heest JL, Vingren JL, Judelson DA, Deschenes MR, Maresh CM (2006) Androgenic responses to resistance exercise: Effects of feeding and l-carnitine. Med Sci Sports Exerc 38(7):1288–96.

Kujawa KA, Jacob JM, Jones KJ (1993) Testosterone regulation of the regenerative properties of injured rat sciatic motor neurons. J Neurosci Res 35(3):268–73.

Monks DA, O’Bryant EL, Jordan CL (2004) Androgen receptor immunoreactivity in skeletal muscle: enrichment at the neuromuscular junction. J Comp Neurol 473(1):59–72.

O’Bryant EL, Jordan CL (2005) Expression of nuclear receptor coactivators in androgen-responsive and -unresponsive motoneurons. Horm Behav 47(1):29–38.

Spiering BA, Kraemer WJ, Vingren JL, Hatfield DL, Fragala MS, Ho JY, Maresh CM, Anderson JM, Volek JS (2007) Responses of criterion variables to different supplemental doses of L-carnitine L-tartrate. J Strength Cond Res 21(1):259–64.