title: Impact of various exercise modalities on hepatic mitochondrial function.
abstract: OBJECTIVE
  Hepatic mitochondrial adaptations to exercise are largely unknown. In this study, we sought to determine the effects of various exercise modalities on measures of hepatic mitochondrial function and metabolism.
  
  
  METHODS
  Male Sprague-Dawley rats were randomly assigned (n = 8-10 per group) into sedentary (SED), voluntary wheel running (VWR), VWR with food pulled during the dark cycle (VMR-OF), treadmill endurance exercise (TM-END; 30 m·min, 12% gradient, 60 min·d, 5 d·wk), or treadmill interval sprint training (TM-IST; 50 m·min, 12% gradient, 6 × 2.5 min bouts, 5 d·wk) groups for a 4-wk intervention.
  
  
  RESULTS
  Hepatic mitochondrial state 3 and maximal uncoupled respiration were significantly (P < 0.05) increased in all four exercise groups compared with SED animals. In addition, hepatic mitochondrial [1-C] pyruvate oxidation to CO2, an index of pyruvate dehydrogenase (PDH) activity, was significantly increased in VWR-OF, TM-END, and TM-IST rats (P < 0.05), whereas exercise-induced increases in [2-C] pyruvate oxidation and [1-C] palmitate oxidation to CO2 did not reach statistical significance. Hepatic mitochondrial sirtuin 3 protein content, which putatively increases activity of mitochondrial proteins, was elevated in the VWR, VWR-OF, and TM-END groups (P < 0.05). In addition, only VWR-OF animals experienced increases in hepatic cytochrome c protein content and phosphoenolpyruvate carboxykinase mRNA, whereas PGC-1α mRNA expression and phospho-CREB protein content was increased in VWR-OF and TM-END groups.
  
  
  CONCLUSIONS
  Four weeks of exercise training, regardless of exercise modality, significantly increased hepatic mitochondrial respiration and evoked other unique improvements in mitochondrial metabolism that do not appear to be dependent on increases in mitochondrial content.
authors.affiliation: 1Harry S. Truman Memorial Veterans' Hospital, Columbia, MO; 2Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO; and 3Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Missouri, Columbia, MO.
authors.forename: Justin A
authors.initials: JA
authors.lastname: Fletcher
authors.forename: Grace M
authors.initials: GM
authors.lastname: Meers
authors.forename: Melissa A
authors.initials: MA
authors.lastname: Linden
authors.forename: Monica L
authors.initials: ML
authors.lastname: Kearney
authors.forename: E Matthew
authors.initials: EM
authors.lastname: Morris
authors.forename: John P
authors.initials: JP
authors.lastname: Thyfault
authors.forename: R Scott
authors.initials: RS
authors.lastname: Rector
mesh_terms: D000818:Animals; D005215:Fasting; D005943:Gluconeogenesis; D008297:Male; D008930:Mitochondria, Liver / Q000201:enzymology / Q000378:metabolism*; D024101:Mitochondrial Proteins / Q000378:metabolism; D009043:Motor Activity / Q000502:physiology; D001678:Organelle Biogenesis; D010084:Oxidation-Reduction; D010168:Palmitates / Q000378:metabolism; D010805:Physical Conditioning, Animal / Q000379:methods* / Q000502:physiology*; D010807:Physical Endurance / Q000502:physiology; D019289:Pyruvic Acid / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D017207:Rats, Sprague-Dawley
chemical_list: D024101:Mitochondrial Proteins; D010168:Palmitates; D012333:RNA, Messenger; D019289:Pyruvic Acid