The influence of ethanol on human splanchnic and skeletal muscle metabolism during exercise

Abstract

Arterial concentrations and splanchnic and leg exchange of ethanol, acetate, glucose, pyruvate, lactate, glycerol, free fatty acids and ketone bodies were determined in sixteen healthy male volunteers after administration of small doses of ethanol. Measurements were made at rest and during 40 min work (50% of max V·_o2). Two doses of ethanol were administered, giving blood concentrations at which the ethanol elimination capacity was not saturated (2·5 mmol/l) and where ethanol was eliminated with maximal velocity (8·5 mmol/l).

Splanchnic blood flow and oxygen uptake were not influenced by ethanol during exercise. Ethanol uptake in the liver was restricted by the arterial inflow during exercise when the smaller dose was administered but when the larger dose was infused, hepatic uptake was not influenced by exercise. Most of the acetate released from the liver after ethanol treatment was taken up by skeletal muscle. Splanchnic output of glucose was reduced by ethanol but the leg uptake was not influenced during exercise, resulting in lower arterial glucose concentrations after ethanol treatment. The normal uptake of lactate in the splanchnic area was converted into a release, when the larger dose of ethanol was administered; in spite of this, arterial lactate concentration did not rise significantly during exercise, since release of lactate from the leg was inhibited after only 10 min exercise. The splanchnic uptake of glycerol was not influenced per se by ethanol but correlated highly to the splanchnic inflow. The smaller dose of ethanol induced a decrease in arterial free fatty acids of 30–40%, while no obvious effect was observed with the larger dose.

It is concluded that: (a) most of the acetate released from the liver after ethanol treatment is taken up in skeletal muscle but is of minor importance as an energy substrate during exercise; (b) even moderate doses of ethanol inhibit liver gluconeogenesis and reduce the splanchnic glucose release; (c) the Cori cycle is inhibited without any significant increase in arterial lactate concentration; (d) oxygen supply during exercise is not a limiting factor for the ability of the liver to reoxidate cytoplasmatic NADH₂.

Key Words:

• acetate
• alcohol
• gluconeogenesis
• liver
• skeletal muscle