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1 Anesthesia, Rigshospitalet, Copenhagen, Copenhagen, Denmark
2 RMIT University, Cellular and Molecular Metabolism Laboratory, Bundoora, Victoria, Australia
3 Medical department V, Aarhus University Hospital, Aarhus, Aarhus, Denmark
4 Department of Human Physiology, Institute of Exercise and Sport Sciences - August Krogh Institute - University of Copenhagen, Copenhagen, Copenhagen, Denmark
* To whom correspondence should be addressed. E-mail: hbay{at}vip.cybercity.dk.
The exponential rise in blood lactate with exercise intensity may relate to a reduced hepatic lactate uptake. We compared muscle derived lactate to the hepatic elimination during 2 hr prolonged cycling (62 ± 4% of maximal O2 uptake, VO2max) followed by incremental exercise in seven healthy males. Hepatic blood flow was assessed by indocyanine green dye elimination and leg blood flow by thermo-dilution. During prolonged exercise, the hepatic glucose output was lower than the leg glucose uptake (3.8 ± 0.5 vs. 6.5 ± 0.6 mmol·min-1; mean ± SEM) and at an arterial lactate of 2.0 ± 0.2 mM, the leg lactate output of 3.0 ± 1.8 mmol·min-1 was about four-fold higher than the hepatic lactate uptake (0.7 ± 0.3 mmol·min-1). During incremental exercise, the hepatic glucose output was about one-third of the leg glucose uptake (2.0 ± 0.4 vs. 6.2 ± 1.3 mmol·min-1) and the arterial lactate reached 6.0 ± 1.1 mM because the leg lactate output of 8.9 ± 2.7 mmol·min-1 was markedly higher than the lactate taken up by the liver (1.1 ± 0.6 mmol·min-1). Compared to prolonged exercise, the hepatic lactate uptake increased during incremental exercise, but the relative hepatic lactate uptake decreased to about one-tenth of the lactate released by the legs. This drop in relative hepatic lactate extraction may contribute to the increase in arterial lactate during intense exercise.
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