Journal article
Exercise training improves vascular mitochondrial function
American journal of physiology. Heart and circulatory physiology, Vol.310(7), pp.H821-H829
04/01/2016
DOI: 10.1152/ajpheart.00751.2015
PMCID: PMC4867356
PMID: 26825520
Abstract
Exercise training is recognized to improve cardiac and skeletal muscle mitochondrial respiratory capacity; however, the impact of chronic exercise on vascular mitochondrial respiratory function is unknown. We hypothesized that exercise training concomitantly increases both vascular mitochondrial respiratory capacity and vascular function. Arteries from both sedentary (SED) and swim-trained (EX, 5 wk) mice were compared in terms of mitochondrial respiratory function, mitochondrial content, markers of mitochondrial biogenesis, redox balance, nitric oxide (NO) signaling, and vessel function. Mitochondrial complex I and complex I + II state 3 respiration and the respiratory control ratio (complex I + II state 3 respiration/complex I state 2 respiration) were greater in vessels from EX relative to SED mice, despite similar levels of arterial citrate synthase activity and mitochondrial DNA content. Furthermore, compared with the SED mice, arteries from EX mice displayed elevated transcript levels of peroxisome proliferative activated receptor-γ coactivator-1α and the downstream targets cytochrome c oxidase subunit IV isoform 1,isocitrate dehydrogenase(Idh)2, and Idh3a, increased manganese superoxide dismutase protein expression, increased endothelial NO synthase phosphorylation (Ser(1177)), and suppressed reactive oxygen species generation (all P< 0.05). Although there were no differences in EX and SED mice concerning endothelium-dependent and endothelium-independent vasorelaxation, phenylephrine-induced vasocontraction was blunted in vessels from EX compared with SED mice, and this effect was normalized by NOS inhibition. These training-induced increases in vascular mitochondrial respiratory capacity and evidence of improved redox balance, which may, at least in part, be attributable to elevated NO bioavailability, have the potential to protect against age- and disease-related challenges to arterial function.
Details
- Title: Subtitle
- Exercise training improves vascular mitochondrial function
- Creators
- Song-Young Park - Geriatric Research, Education, and Clinical Center, George E. Whalen Veterans Affairs Medical Center, Salt Lake City, Utah; Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UtahMatthew J Rossman - Geriatric Research, Education, and Clinical Center, George E. Whalen Veterans Affairs Medical Center, Salt Lake City, Utah; Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UtahJayson R Gifford - Geriatric Research, Education, and Clinical Center, George E. Whalen Veterans Affairs Medical Center, Salt Lake City, Utah; Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UtahLeena P Bharath - Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, Utah; Division of Endocrinology, Metabolism and Diabetes, and Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, Utah; andJohann Bauersachs - Department of Cardiology and Angiology, Hannover Medical School, Hannover, GermanyRussell S Richardson - Geriatric Research, Education, and Clinical Center, George E. Whalen Veterans Affairs Medical Center, Salt Lake City, Utah; Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, Utah; Division of Geriatrics, Department of Internal Medicine, University of Utah, Salt Lake City, UtahE Dale Abel - Division of Endocrinology, Metabolism and Diabetes, and Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, Utah; and Fraternal Order of Eagles Diabetes Research Center and Division of Endocrinology and Metabolism, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IowaJ David Symons - Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, Utah; Division of Endocrinology, Metabolism and Diabetes, and Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, Utah; andChristian Riehle - Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany; Division of Endocrinology, Metabolism and Diabetes, and Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, Utah; and Fraternal Order of Eagles Diabetes Research Center and Division of Endocrinology and Metabolism, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, Iowa riehle.christian@mh-hannover.de
- Resource Type
- Journal article
- Publication Details
- American journal of physiology. Heart and circulatory physiology, Vol.310(7), pp.H821-H829
- Publisher
- United States
- DOI
- 10.1152/ajpheart.00751.2015
- PMID
- 26825520
- PMCID
- PMC4867356
- ISSN
- 0363-6135
- eISSN
- 1522-1539
- Grant note
- R01-DK-092065 / NIDDK NIH HHS P01-HL-091830 / NHLBI NIH HHS 2R15-HL-091493 / NHLBI NIH HHS
- Language
- English
- Date published
- 04/01/2016
- Academic Unit
- Roy J. Carver Department of Biomedical Engineering; Biochemistry and Molecular Biology; Endocrinology and Metabolism; Internal Medicine
- Record Identifier
- 9984024523402771
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