1 Integrated Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, Københavns Universitet2 Molecular Integrative Physiology, Department of Biology, Faculty of Science, Københavns Universitet3 Centre of Inflammation and Metabolism, The Center for Physical Activity Research and August Krogh Centre, Department of Biology, University of Copenhagen, Universitesparken 13, 2100, Copenhagen Ø, Denmark.4 Centre of Inflammation and Metabolism and The Centre for Physical Activity Research, Department of Clinical Biochemistry, Rigshospitalet, Copenhagen5 Cell Biology and Physiology, Department of Biology, Faculty of Science, Københavns Universitet6 Molecular Integrative Physiology, Department of Biology, Faculty of Science, Københavns Universitet7 Integrated Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, Københavns Universitet8 Cell Biology and Physiology, Department of Biology, Faculty of Science, Københavns Universitet
The aim of the present study was to examine the effect of lipopolysaccharide (LPS)-induced inflammation on AMP-activated protein kinase (AMPK) and pyruvate dehydrogenase (PDH) regulation in human skeletal muscle at rest and during exercise. Nine young healthy physically inactive male subjects completed two trials. In an LPS trial, the subjects received a single LPS injection (0.3 ng/kg body weight) and blood samples and vastus lateralis muscle biopsies were obtained before and 2 h after the LPS injection and immediately after a 10-min one-legged knee extensor exercise bout performed approximately 2½ h after the LPS injection. The exercise bout with muscle samples obtained before and immediately after was repeated in a control trial without LPS injection. The plasma tumor necrosis factor α concentration increased 17-fold 2 h after LPS relative to before. Muscle lactate and muscle glycogen were unchanged from before to 2 h after LPS and exercise increased muscle lactate and decreased muscle glycogen in the control (P < 0.05) and the LPS (0.05 ≤ P < 0.1) trial with no differences between the trials. AMPK, acetyl-CoA carboxylase (ACC) and PDH phosphorylation as well as PDHa activity were unaffected 2 h after LPS relative to before. Exercise decreased (P < 0.05) PDH and increased (P < 0.05) AMPK and ACC phosphorylation as well as increased (P < 0.05) PDHa activity similarly in the LPS and control trial. In conclusion, LPS-induced inflammation does not affect resting or exercise-induced AMPK and PDH regulation in human skeletal muscle. This suggests that metabolic flexibility during exercise is maintained during short-term low-grade inflammation in humans.
Pfluegers Archiv, 2015, Vol 467, Issue 2, p. 341-350