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CPT1 activity is based on adequate muscle levels of carnitine, which progressively declines with increased production of acetylcarnitines as exercise intensity and/or duration increases

It transports long-chain fatty acids, which are oxidized and broken down to produce energy, into the mitochondria

Reversible weakness and encephalopathy while on long-term valproate treatment due to carnitine deficiency

More recent reports have demonstrated that L-carnitine supplementation as adjuvant therapy contributes to the amelioration of blood markers of oxidative damage in patients affected by phenylketonuria [76], maple syrup urine disease [77], and disorders of propionate metabolism [78]

It is possible to establish a plausible mechanistic explanation using 1) the performance outcomes of the present investigation in combination with 2) previously established mechanisms of the underlying carnitine molecules, and 3) recent reports of increased muscle carnitine levels via insulin infusion