Hepatic fuel metabolism during exercise

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Bibliographic Details
Title translated into German:Funktion der Leber im Energiestoffwechsel
Author:Kjaer, M.
Editor:Hargreaves, Mark
Published in:Exercise metabolism
Published:Champaign: Human Kinetics (Verlag), 1995, 1995. S. 73-97, Lit., Lit.
Format: Publications (Database SPOLIT)
Publication Type: Compilation article
Media type: Print resource
Language:English
ISBN:0873224531
Keywords:
Online Access:
Identification number:PU199810305187
Source:BISp

Abstract

The role of the liver as a metabolic organ during exercise primarily involves the increase in production and mobilization of glucose into the bloodstream, but also includes chemical pathways for amino acid and fat metabolism that are accelerated during muscular work. Liver glucose production increases during exercise in a curvilinear fashion with work intensity. During light to moderate exercise glucose output rises two- to threefold, and during intense exercise it rises seven- to tenfold above resting values. The magnitude of liver glucose output during exercise is dependent on the liver glycogen content, which varies with the degree of fasting, the intake of food prior to exercise, and the degree of training in the individual. During exercise the glucose production is derived mainly from breakdown of liver glycogen (glycogenolysis), and only a small part (10-20%) is accounted for by gluconeogenesis. With increasing exercise duration (several hours) the contribution of gluconeogenesis rises to about 50% of the total liver glucose production. This rise occurs in parallel with a decline in liver glycogen stores and an increase in supply of gluconeogenic precursors to the liver. During light and prolonged exercise, feedback signals from contracting muscles, mediated both neurally and via the bloodstream, adjust the stimulus for glucose production to maintain euglycemia in the blood. A rise in blood glucose directly inhibits glucose production during exercise, whereas a drop in blood glucose via stimulation of counterregulatory hormones (e.g., glucagon) indirectly enhances liver glucose production during physical activity. In contrast, during intense exercise and at the onset of exercise, central mechanisms coupled to the degree of motor center activity, leading to a very pronounced hormonal response (e.g., rise in plasma epinephrine), are responsible for an increase in glucose mobilization that exceeds the peripheral glucose uptake, resulting in a rise in blood glucose level during intense exercise. Hormonal mechanisms can so far only partially explain the stimulation of glucose production during exercise in humans. Factors other than the ones currently identified must contribute to the exercise-induced rise in liver glucose production in humans. Amino acid uptake in the liver is accelerated during exercise to meet increased supply from muscle and gut proteolysis. Besides an increased gluconeogenic activity, urea formation, and probably formation of acute-phase proteins, is also intensified during exercise. Splanchnic fat depots may be mobilized by sympathetic nerve activity during exercise, and they probably reflect release of free fatty acids and glycerol from the gut that is taken up by the liver which not only accelerates gluconeogenesis, but also increases the ketogenesis during physical activity. Verf.-Referat (gekuerzt)