This paper gives an overview of oxidative fuel metabolism in swimming fish, and known or potential modifications occurring in high-performance species are explored. Carbohydrate catabolism is the only source of ATP for sprint swimming where locomotory muscles operate as closed systems. In contrast, this substrate only plays a very minor role in prolonged swimming. Glucose fluxes have been measured in vivo in several species, but mainly at rest and with somewhat questionable methodologies. High-performance species may be able to sustain higher maximal glucose fluxes that their sedentary counterparts by: a) upregulating gluconeogenesis, b) increasing glucose transporter density or V max of individual transporters, c) storing larger amounts of glycogen in liver and muscle, and d) increasing muscle hexokinase activity. Even though lipids represent a much more important source of energy for sustained swimming, their fluxes have not been measured in vivo , even at rest, probably because of their diversity and complex chemistry. Except for elasmobranchs who do not possess plasma proteins for lipid transport, high-performance fish should be able to sustain high maximal lipid fluxes by: a) elevating lipolytic capacity, b) increasing rates of circulatory lipid transport through modified plasma proteins, c) augmenting intramuscular lipid reserves, and d) upregulating capacity for lipid oxidation in locomotory muscle mitochondria. The quantitative assessment of amino acid oxidation in swimming fish is a priority for future research because protein is probably a dominant metabolic fuel in most swimming fish. Finally, we predict that high-performance species should use proportionately more proteins/lipids and less carbohydrates than low-aerobic fish. Also, and similarly to endurance-adapted mammals, high-performance fish should increase their relative reliance on intramuscular fuel reserves and decrease their relative use of circulatory fuels.
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