title: Exercise-induced AMPK and pyruvate dehydrogenase regulation is maintained during short-term low-grade inflammation.
abstract: 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.
authors.affiliation: 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.
authors.forename: Rasmus Sjørup
authors.initials: RS
authors.lastname: Biensø
authors.forename: Jesper
authors.initials: J
authors.lastname: Olesen
authors.forename: Line
authors.initials: L
authors.lastname: van Hauen
authors.forename: Simon
authors.initials: S
authors.lastname: Meinertz
authors.forename: Jens Frey
authors.initials: JF
authors.lastname: Halling
authors.forename: Lasse
authors.initials: L
authors.lastname: Gliemann
authors.forename: Peter
authors.initials: P
authors.lastname: Plomgaard
authors.forename: Henriette
authors.initials: H
authors.lastname: Pilegaard
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000378:metabolism*; D000103:Acetyl-CoA Carboxylase / Q000378:metabolism; D000328:Adult; D015444:Exercise; D006003:Glycogen / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000378:metabolism; D019344:Lactic Acid / Q000378:metabolism; D008070:Lipopolysaccharides / Q000633:toxicity; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000502:physiology; D010766:Phosphorylation; D011768:Pyruvate Dehydrogenase Complex / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D008070:Lipopolysaccharides; D011768:Pyruvate Dehydrogenase Complex; D014409:Tumor Necrosis Factor-alpha; D019344:Lactic Acid; D006003:Glycogen; D055372:AMP-Activated Protein Kinases; D000103:Acetyl-CoA Carboxylase