L-Carnitine promotes energy production in cells by transporting fatty acids into the mitochondrion. Its primary function is to transfer long-chain fatty acids across the inner mitochondrial membrane. Fatty acid molecules are activated to coenzyme A (CoA) esters in the cytoplasm of the cell, and then esterified to L-Carnitine. The combination of a fatty acid molecule and L-Carnitine is called “acyl-carnitine.” Much of the body's L-Carnitine content is stored in the form of acyl-carnitine.1

The mitochondrion is the cell’s energy-generating furnace. Called an “organelle,” the mitochondrion is a self-contained structure inside the cell. Like all cellular structures, the mitochondrion is surrounded by a membrane. This membrane is an impenetrable barrier to acyl-CoA esters; passage across the membrane requires L-Carnitine as a transporter. On the inside of the mitochondrial membrane, the acyl-CoA esters are made available to be metabolized through the process of beta oxidation. One of the key metabolic byproducts of this process is acetyl-CoA, also called “active acetate,” which enters the Krebs cycle (also known as the “citric acid cycle”) to supply fuel for production of ATP, the cell’s primary energy “currency.” L-Carnitine shuttles excess fatty acid residues out of the mitochondrion, and in this role is essential for preventing toxic buildup of fatty acids inside the mitochondrion.

Evidence suggests that L-Carnitine and short chain acyl-carnitine esters can protect the mitochondrion from adverse effects of drugs and toxic chemicals. L-Carnitine has been shown to protect animals form cardiotoxins and decrease mortality rate in animals with diphtheria, due to this cardioprotective effect.2

Helps maintain a healthy heart and cardiovascular system*

Muscle tissue contains a high concentration of L-Carnitine. With its constant energy needs, heart muscle tissue is especially rich in L-Carnitine. If the body’s ability to biosynthesize L-Carnitine is compromised, energy production in muscle tissue is impaired, and a toxic buildup of fatty acids can occur.3 Defective production of L-Carnitine by the body can result from a variety of factors, including kidney or liver malfunction, increased catabolism or the inability of tissues to extract and retain L-Carnitine from the blood.

Along with glucose and lactate, fatty acids are the primary oxidation fuel for the heart. A considerable amount of scientific data from animal experiments indicates that L-Carnitine protects the heart under conditions of hypoxia, or low oxygen. In addition to the oxidation of fat for energy in the cell, L-Carnitine is involved in the metabolism of glucose.4 Evidence of L-Carnitine’s role in glucose metabolism was uncovered in a small trial on 9 diabetic individuals. Given intravenously, L-Carnitine improved insulin-mediated glucose utilization and insulin sensitivity.5

Depletion of the body’s L-Carnitine supply is linked to various abnormal states, especially of the heart muscle. The effect of L-Carnitine on hypoxic (oxygen-starved) isolated heart muscle tissue has been studied.6 At high concentrations, L-Carnitine demonstrates a clear-cut ability to potentiate the contractility of isolated heart muscle tissue, indicating the L-Carnitine has a strengthening effect on the heart. L-Carnitine has been shown to improve the performance of rats subjected to fatigue test.

Research has revealed that in animals and humans with defective heart muscle, the amount of free L-Carnitine (not bound to fatty acids) is reduced. Administration of L-Carnitine to hamsters prevents damage to the heart muscle. Given to humans with angina, L-Carnitine was found to improve exercise tolerance. In a small study, patients with congestive heart failure showed gains in heart function with oral consumption of L-Carnitine, reportedly by restoring normal oxidation of fatty acids.7 In heart valve replacement patients, L-Carnitine has been shown to increase the valve tissue levels of ATP, pyruvate and creatine phosphate, which are key cellular energy substrates. In a controlled study, L-Carnitine was administered to 38 patients prior to open heart surgery. Prior to surgery, heart circulatory function, as assessed by measurements of hemodynamics, was “good” in all 38. While there was evidence of a “preserving” effect of L-Carnitine on heart cells, no differences in cardiac performance were observed. These results suggest that noticeable improvements in heart muscle performance with L-Carnitine are most likely to occur in people with compromised hearts.8

It has been suggested that L-Carnitine favorably influences blood lipids. Preliminary evidence of this was seen in a small open trial on 26 patients who took 3 grams of L-Carnitine daily for 40 days. Blood levels of cholesterol and triglycerides dropped substantially, while the ratio of total to HDL cholesterol–– a known marker of cardiovascular health––markedly improved.9

While L-Carnitine is not a treatment for heart disease, (nor should it be used as a substitute for medical treatment) the results of these and other studies suggest that oral consumption of L-Carnitine has a beneficial influence on maintaining a healthy heart and cardiovascular system.