title: Female rats selectively bred for high intrinsic aerobic fitness are protected from ovariectomy-associated metabolic dysfunction.
abstract: Ovariectomized rodents model human menopause in that they rapidly gain weight, reduce spontaneous physical activity (SPA), and develop metabolic dysfunction, including insulin resistance. How contrasting aerobic fitness levels impacts ovariectomy (OVX)-associated metabolic dysfunction is not known. Female rats selectively bred for high and low intrinsic aerobic fitness [high-capacity runners (HCR) and low-capacity runners (LCR), respectively] were maintained under sedentary conditions for 39 wk. Midway through the observation period, OVX or sham (SHM) operations were performed providing HCR-SHM, HCR-OVX, LCR-SHM, and LCR-OVX groups. Glucose tolerance, energy expenditure, and SPA were measured before and 4 wk after surgery, while body composition via dual-energy X-ray absorptiometry and adipose tissue distribution, brown adipose tissue (BAT), and skeletal muscle phenotype, hepatic lipid content, insulin resistance via homeostatic assessment model of insulin resistance and AdipoIR, and blood lipids were assessed at death. Remarkably, HCR were protected from OVX-associated increases in adiposity and insulin resistance, observed only in LCR. HCR rats were ∼30% smaller, had ∼70% greater spontaneous physical activity (SPA), consumed ∼10% more relative energy, had greater skeletal muscle proliferator-activated receptor coactivator 1-alpha, and ∼40% more BAT. OVX did not increase energy intake and reduced SPA to the same extent in both HCR and LCR. LCR were particularly affected by an OVX-associated reduction in resting energy expenditure and experienced a reduction in relative BAT; resting energy expenditure correlated positively with BAT across all animals (r = 0.6; P < 0.001). In conclusion, despite reduced SPA following OVX, high intrinsic aerobic fitness protects against OVX-associated increases in adiposity and insulin resistance. The mechanism may involve preservation of resting energy expenditure.
authors.affiliation: Nutrition and Exercise Physiology, University of Missouri, Columbia, Missouri; vieirapotterv@missouri.edu.
authors.forename: Victoria J
authors.initials: VJ
authors.lastname: Vieira-Potter
authors.affiliation: Nutrition and Exercise Physiology, University of Missouri, Columbia, Missouri; Child Health, University of Missouri, Columbia, Missouri; Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri;
authors.forename: Jaume
authors.initials: J
authors.lastname: Padilla
authors.affiliation: Nutrition and Exercise Physiology, University of Missouri, Columbia, Missouri;
authors.forename: Young-Min
authors.initials: YM
authors.lastname: Park
authors.affiliation: Nutrition and Exercise Physiology, University of Missouri, Columbia, Missouri;
authors.forename: Rebecca J
authors.initials: RJ
authors.lastname: Welly
authors.affiliation: Nutrition and Exercise Physiology, University of Missouri, Columbia, Missouri;
authors.forename: Rebecca J
authors.initials: RJ
authors.lastname: Scroggins
authors.affiliation: Department of Anesthesiology, University of Michigan Medical School, Ann Arbor, Michigan;
authors.forename: Steven L
authors.initials: SL
authors.lastname: Britton
authors.affiliation: Department of Anesthesiology, University of Michigan Medical School, Ann Arbor, Michigan;
authors.forename: Lauren G
authors.initials: LG
authors.lastname: Koch
authors.affiliation: Department of Kinesiology, University of Georgia, Athens, Georgia;
authors.forename: Nathan T
authors.initials: NT
authors.lastname: Jenkins
authors.affiliation: Nutrition and Exercise Physiology, University of Missouri, Columbia, Missouri; Department of Nutritional Sciences, University of Texas, Austin, Texas;
authors.forename: Jacqueline M
authors.initials: JM
authors.lastname: Crissey
authors.affiliation: Nutrition and Exercise Physiology, University of Missouri, Columbia, Missouri;
authors.forename: Terese
authors.initials: T
authors.lastname: Zidon
authors.affiliation: Nutrition and Exercise Physiology, University of Missouri, Columbia, Missouri; Medicine Division of GI and Hepatology, University of Missouri, Columbia, Missouri; and.
authors.forename: E Matthew
authors.initials: EM
authors.lastname: Morris
authors.affiliation: Nutrition and Exercise Physiology, University of Missouri, Columbia, Missouri; Medicine Division of GI and Hepatology, University of Missouri, Columbia, Missouri; and.
authors.forename: Grace M E
authors.initials: GM
authors.lastname: Meers
authors.affiliation: Nutrition and Exercise Physiology, University of Missouri, Columbia, Missouri; Medicine Division of GI and Hepatology, University of Missouri, Columbia, Missouri; and Research Service, Harry S. Truman Memorial VA Hospital, Columbia, Missouri.
authors.forename: John P
authors.initials: JP
authors.lastname: Thyfault
mesh_terms: D002001:Adipose Tissue, Brown / Q000378:metabolism / Q000503:physiopathology; D052436:Adipose Tissue, White / Q000378:metabolism / Q000503:physiopathology; D050154:Adiposity; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D004195:Disease Models, Animal; D004734:Energy Metabolism; D017079:Exercise Tolerance; D005260:Female; D005838:Genotype; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008055:Lipids / Q000097:blood; D008099:Liver / Q000378:metabolism; D008659:Metabolic Diseases / Q000097:blood / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D009043:Motor Activity; D018482:Muscle, Skeletal / Q000378:metabolism / Q000503:physiopathology; D010052:Ovariectomy; D010084:Oxidation-Reduction; D010641:Phenotype; D010807:Physical Endurance / Q000235:genetics; D011919:Rats, Inbred Strains; D012420:Running; D057185:Sedentary Behavior; D013997:Time Factors; D015430:Weight Gain
chemical_list: D001786:Blood Glucose; D007328:Insulin; D008055:Lipids
keywords: brown adipose tissue; energy expenditure; fitness; menopause; ovarian hormones