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Review
. 2014 Oct 29;3:17.
doi: 10.1186/2046-7648-3-17. eCollection 2014.

Acute Nutritional Ketosis: Implications for Exercise Performance and Metabolism

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Free PMC article
Review

Acute Nutritional Ketosis: Implications for Exercise Performance and Metabolism

Pete J Cox et al. Extrem Physiol Med. .
Free PMC article

Abstract

Ketone bodies acetoacetate (AcAc) and D-β-hydroxybutyrate (βHB) may provide an alternative carbon source to fuel exercise when delivered acutely in nutritional form. The metabolic actions of ketone bodies are based on sound evolutionary principles to prolong survival during caloric deprivation. By harnessing the potential of these metabolic actions during exercise, athletic performance could be influenced, providing a useful model for the application of ketosis in therapeutic conditions. This article examines the energetic implications of ketone body utilisation with particular reference to exercise metabolism and substrate energetics.

Keywords: Exercise performance; Ketone body; Ketone ester; Ketosis; Nutrition.

Figures

Figure 1
Figure 1
Endogenous and exogenous ketosis. Contrast between ketosis induced by starvation or high-fat diet (endogenous ketosis) and that generated by nutritional ketone ester ingestion (exogenous ketosis). Ketone bodies are endogenously produced in the liver from high circulating free fatty acids (FFA) from adipolysis. In contrast, nutritional ketone esters are cleaved in the gut and are absorbed through the gut epithelium and monocarboxylate transporters (MCT) into the circulation or undergo first-pass metabolism to ketone bodies in the liver. High concentrations of ketone bodies inhibit the nicotinic acid receptor (PUMA-G)-controlling adipolysis. Once released into the bloodstream, the ketones are metabolised by extrahepatic tissues in an identical fashion and being transported across the plasma and mitochondrial membranes by MCTs. D-β-Hydroxybutyrate (D-βHB) is converted to acetoacetate by D-β-hydroxybutyrate dehydrogenase (D-βHB DH) before entering the tricarboxylic acid (TCA) cycle as acetyl-CoA.

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