title: Increased aerobic capacity reduces susceptibility to acute high-fat diet-induced weight gain.
abstract: Aerobic capacity is the most powerful predictor of all-cause mortality in humans; however, its role in the development of obesity and susceptibility for high-fat diet (HFD)-induced weight gain is not completely understood.
  
  
  
  Herein, a rodent model system of divergent intrinsic aerobic capacity [high capacity running (HCR) and low capacity running (LCR)] was utilized to evaluate the role of aerobic fitness on 1-week HFD-induced (45% and 60% kcal) weight gain. Food/energy intake, body composition analysis, and brown adipose tissue gene expression were assessed as important potential factors involved in modulating HFD-induced weight gain.
  
  
  
  HCR rats had reduced 1-week weight gain on both HFDs compared with LCR. Reduced HFD-induced weight gain was associated with greater adaptability to decrease food intake following initiation of the HFDs. Further, the HCR rats were observed to have reduced feeding efficiency and greater brown adipose mass and expression of genes involved in thermogenesis.
  
  
  
  Rats with high intrinsic aerobic capacity have reduced susceptibility to 1-week HFD-induced weight gain, which is associated with greater food intake adaptability to control intake of energy-dense HFDs, reduced weight gain per kcal consumed, and greater brown adipose tissue mass and thermogenic gene expression.
authors.affiliation: Department of Nutrition and Exercise Physiology, School of Medicine, University of Missouri, Columbia, Missouri, USA.|Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas, USA.
authors.forename: E
authors.initials: E
authors.lastname: Matthew Morris
authors.affiliation: Department of Nutrition and Exercise Physiology, School of Medicine, University of Missouri, Columbia, Missouri, USA.
authors.forename: Grace M E
authors.initials: GM
authors.lastname: Meers
authors.affiliation: Department of Anesthesiology, University of Michigan, Ann Arbor, Michigan, USA.
authors.forename: Lauren G
authors.initials: LG
authors.lastname: Koch
authors.affiliation: Department of Anesthesiology, University of Michigan, Ann Arbor, Michigan, USA.
authors.forename: Steven L
authors.initials: SL
authors.lastname: Britton
authors.affiliation: Departments of Physiology and Biophysics, Anschutz Health and Wellness Center, Aurora, Colorado, USA.|Division of Endocrinology, Metabolism, and Diabetes, University of Colorado School of Medicine, Aurora, Colorado, USA.
authors.forename: Paul S
authors.initials: PS
authors.lastname: MacLean
authors.affiliation: Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas, USA.|Kansas City VA Medical Center-Research Service, Kansas City, Missouri, USA.
authors.forename: John P
authors.initials: JP
authors.lastname: Thyfault
mesh_terms: D002001:Adipose Tissue, Brown / Q000378:metabolism; D000818:Animals; D059305:Diet, High-Fat; D004041:Dietary Fats / Q000378:metabolism*; D004198:Disease Susceptibility; D004435:Eating; D004734:Energy Metabolism; D017079:Exercise Tolerance; D008297:Male; D009765:Obesity / Q000378:metabolism; D010805:Physical Conditioning, Animal; D010809:Physical Fitness / Q000502:physiology*; D051381:Rats
chemical_list: D004041:Dietary Fats