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The mechanisms of both subacute and idiosyncratic VHT remain incompletely understood, but it has been believed since the early 1980s based on limited experimental and clinical evidence [5356] that hypocarnitinaemia, subsequent imbalance between -oxidation and -oxidation, and accumulation of 4-en-VPA are involved

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The vasodilatory effects are certainly directly related to NO levels while the increased power output may be related to increased cellular supply of the propionate unit which when converted to succinate provides an anaplerotic energy substrate

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