title: Fuel selection, muscle fibre.
abstract: The fuel selection of muscle fibres at rest is dependent on substrate availability. Increased lipid availability results in an increase citrate concentration with inhibition of glycolysis. Fat utilization also increases the concentration ratio acetyl-CoA:CoASH, with inhibition of PDH transformation to the active form. The result is an inhibition of carbohydrate utilization in conformity with the classical glucose-fatty acid style. During exercise fuel selection is dependent on the intensity of exercise, the recruitment pattern of fibre type and the availability of fuels. During exercise at maximum intensity the main fuels are PCr and muscle glycogen, the highest energy release occurring with type II fibres. At exercise intensities between 70 and 100% VO2max carbohydrate is the main fuel after the intake of normal mixed or carbohydrate-rich diets. No inhibition of PDHa formation was observed by increased concentration ratio acetyl-CoA:CoASH during the exercise, but the activation and transport of fatty-acyl groups from NEFA may be inhibited by a decrease in the concentration of CoASH. This mechanism may limit the contribution of fat to metabolism during exercise at intensities above 60% VO2max, after an intake of carbohydrate-rich diets. After carbohydrate starvation or an infusion of a fat emulsion, there was a substantial increase in the utilization of fat which, after the infusion, was concomitant with a high PDHa and a high lactate production. This is thought to be due to a decrease in glycolysis and in the catalytic activity of PDHa, especially in type I fibres, while lactate production continues in type II fibres. When exercise intensities fall below 60% VO2max, fat becomes the dominant fuel during prolonged exercise. At the same time the recruitment pattern is shifted toward type I fibres which have the lowest activation threshold and the highest oxidative capacity.
authors.affiliation: Department of Medical Laboratory Sciences and Technology, Huddinge University Hospital, Karolinska Institute, Sweden.
authors.forename: E
authors.initials: E
authors.lastname: Hultman
mesh_terms: D000105:Acetyl Coenzyme A / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D004734:Energy Metabolism / Q000502:physiology*; D015444:Exercise / Q000502:physiology; D005227:Fatty Acids / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism; D006801:Humans; D018485:Muscle Fibers, Skeletal / Q000378:metabolism* / Q000502:physiology; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000502:physiology; D011768:Pyruvate Dehydrogenase Complex / Q000378:metabolism
chemical_list: D005227:Fatty Acids; D011768:Pyruvate Dehydrogenase Complex; D000105:Acetyl Coenzyme A; D000255:Adenosine Triphosphate; D006003:Glycogen; D005947:Glucose