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 Dietary Supplements: Supplemental Carnitine and Exercise  
 
Eric Brass P. MD, PhD ©
Introduction
Carnitine (L-3-hydroxytrimethylammoniobutanoate) is an endogenous molecule with several established roles in mammalian cellular metabolism.1 All of carnitine's known biochemical functions are mediated via the reversible transfer of activated carboxylic acids ("acyl" moieties) from coenzyme A to carnitine. In this way, the formation of acylcarnitines is critical for the mitochondrial oxidation of long-chain fatty acids, and formation of short-chain acylcarnitines protects the cell from potentially toxic acyl-CoA accretion.2 Thus, cells contain both carnitine and acylcarnitines, with the acylcarnitines composed of a spectrum of specific acylcarnitines (i.e., acetylcarnitine). Total carnitine refers to carnitine plus all acylcarnitines.

In humans, carnitine is derived from a variety of dietary sources, particularly dairy and meat products. Carnitine can also be synthesized in humans with lysine providing the carbon backbone of the molecule. Available evidence indicates that the biosynthetic capacity of carnitine is adequate to meet the needs of most people, and dietary intake is not required. In contrast, pathophysiologic conditions exist in which carnitine supplementation is of clear therapeutic value.

Carnitine metabolism is highly compartmentalized in humans. Tissues contain widely varied amounts of total carnitine, ranging from 60 mmol/L in plasma to 4,000 mmol/kg in skeletal muscle. Additionally, the distribution of the carnitine pool between carnitine and acylcarnitines can vary among tissues,3 and tissues have distinct turnover rates for carnitine.4

Carnitine Metabolism During Exercise
The bioenergetics of exercise require an enormous increase in muscle adenosine triphosphate (ATP) production and related changes in substrate fluxes. Carnitine, because of its intimate relationship with the coenzyme A pool, reflects many of these metabolic changes. As the ATP demands increase with increasing exercise workloads, a metabolic transition workload, termed the lactate threshold, is reached.5 At workloads below the lactate threshold, lactate does not accumulate in plasma or muscle, the respiratory exchange ratio (RER) remains approximately 0.80, and the exercise can be sustained. At workloads above the lactate threshold, lactate accumulates, the RER reaches 1.00, and performance at the workload cannot be sustained. At rest, the skeletal muscle carnitine pool contains a distribution of 80-90 percent carnitine and 10-20 percent acylcarnitines (primarily short-chain acylcarnitines). At workloads below the lactate threshold, the distribution of the muscle carnitine pool is not altered. However, as workloads exceed the lactate threshold, the muscle carnitine pool is redistributed into acylcarnitines so that 50-70 percent of the pool is in the form of acylcarnitines.6,7 This redistribution is not normalized 60 minutes after a 30-minute exercise session above the lactate threshold. It is now clear that this increase in acylcarnitine content is the result of acetyl-CoA accumulation, leading to acetylcarnitine generation.8 Importantly, the dramatic changes in the muscle carnitine pool during exercise are not reflected in the plasma or urine compartments.

Rationale for use of Carnitine to Enhance Exercise Performance
The relationship of the carnitine pool to the critical metabolic processes of bioenergetics has led to much speculation about the potential benefits in normal humans of supraphysiologic carnitine levels. The possible mechanisms by which carnitine could have an effect are varied and include the following:

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