Research has postulated that there are a few interrelated pathways that can utilize carnitine to enhance the use of long-chain FAs while manipulating acetyl-CoA and pyruvate dehydrogenase (PDH). This would allow for the increased burning of fat as a fuel and the sparing of muscle glycogen during exercise. The rationale behind these assumptions is that in vitro experiments have shown that the activation of the pyruvate dehydrogenase complex (PDC) is inhibited by high ratios of acetyl-CoA:free CoA and NADH:NAD+.41 Since carnitine is a known regulator of acetyl-CoA:free CoA via the formation of acylcarni tines, it is plausible to assume that carnitine may control the activity of the PDC.
This interaction can be illustrated during exercise when acetyl-CoA produced via the PDC and ^-oxidation can be delivered to the Krebs cycle or accumulate in an acetyl-CoA and acylcarnitine pool. Carnitine can then accept the acetyl-CoA groups that continue to accumulate, directly affecting acetyl-CoA and carnitine status during exercise.
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