title: Maternal exercise upregulates mitochondrial gene expression and increases enzyme activity of fetal mouse hearts.
abstract: Maternal exercise during pregnancy has been shown to improve the long-term health of offspring in later life. Mitochondria are important organelles for maintaining adequate heart function, and mitochondrial dysfunction is linked to cardiovascular disease. However, the effects of maternal exercise during pregnancy on mitochondrial biogenesis in hearts are not well understood. Thus, the purpose of this study was to test the hypothesis that mitochondrial gene expression in fetal myocardium would be upregulated by maternal exercise. Twelve-week-old female C57BL/6 mice were divided into sedentary and exercise groups. Mice in the exercise group were exposed to a voluntary cage-wheel from gestational day 1 through 17. Litter size and individual fetal weights were taken when pregnant dams were sacrificed at 17 days of gestation. Three to four hearts from the same group were pooled to study gene expression, protein expression, and enzyme activity. There were no significant differences in litter size, sex distribution, and average fetal body weight per litter between sedentary and exercised dams. Genes encoding mitochondrial biogenesis and dynamics, including nuclear respiratory factor-1 (Nrf1),Nrf2, and dynamin-related GTPase termed mitofusin-2 (Mfn2) were significantly upregulated in the fetal hearts from exercised dams. Cytochrome c oxidase activity and ATP production were significantly increased, while the hydrogen peroxide level was significantly decreased in the fetal hearts by maternal exercise. Our results demonstrate that maternal exercise initiated at day 1 of gestation could transfer the positive mitochondrial phenotype to fetal hearts.
authors.affiliation: Department of Kinesiology, Health, and Nutrition, University of Texas at San Antonio, San Antonio, Texas eunhee.chung@utsa.edu.
authors.forename: Eunhee
authors.identifier: http://orcid.org/0000-0002-4501-9333
authors.initials: E
authors.lastname: Chung
authors.affiliation: Department of Kinesiology and Sport Management, Texas Tech University, Lubbock, Texas.
authors.forename: Hayli E
authors.initials: HE
authors.lastname: Joiner
authors.affiliation: Department of Kinesiology and Sport Management, Texas Tech University, Lubbock, Texas.
authors.forename: Tracer
authors.initials: T
authors.lastname: Skelton
authors.affiliation: Department of Kinesiology and Sport Management, Texas Tech University, Lubbock, Texas.
authors.forename: Kalli D
authors.initials: KD
authors.lastname: Looten
authors.affiliation: Cell Biology and Biochemistry and Garrison Institute on Aging, Texas Tech University Health Sciences Center, Lubbock, Texas.
authors.forename: Maria
authors.initials: M
authors.lastname: Manczak
authors.affiliation: Cell Biology and Biochemistry and Garrison Institute on Aging, Texas Tech University Health Sciences Center, Lubbock, Texas.
authors.forename: P Hemachandra
authors.initials: PH
authors.lastname: Reddy
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003576:Electron Transport Complex IV / Q000378:metabolism; D005260:Female; D005318:Fetal Heart / Q000201:enzymology*; D020558:GTP Phosphohydrolases / Q000235:genetics / Q000378:metabolism; D015870:Gene Expression; D050259:Genes, Mitochondrial; D006861:Hydrogen Peroxide / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008928:Mitochondria / Q000235:genetics* / Q000378:metabolism; D051267:NF-E2-Related Factor 2 / Q000235:genetics / Q000378:metabolism; D051266:Nuclear Respiratory Factor 1 / Q000235:genetics / Q000378:metabolism; D010805:Physical Conditioning, Animal / Q000502:physiology*; D015854:Up-Regulation
chemical_list: D051267:NF-E2-Related Factor 2; C495636:Nfe2l2 protein, mouse; C495634:Nrf1 protein, mouse; D051266:Nuclear Respiratory Factor 1; D000255:Adenosine Triphosphate; D006861:Hydrogen Peroxide; D003576:Electron Transport Complex IV; D020558:GTP Phosphohydrolases; C488751:Mfn2 protein, mouse
keywords: Cytochrome c oxidase; electron transport chain; fetal hearts; hydrogen peroxide; mitochondria