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Voluntary aerobic exercise increases arterial resilience and mitochondrial health with aging in mice
Mitochondrial dysregulation and associated excessive reactive oxygen species (mtROS) production is a key source of oxidative stress in aging arteries that reduces baseline function and may influence resilience (ability to withstand stress). We hypothesized that voluntary aerobic exercise would incre...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5191877/ https://www.ncbi.nlm.nih.gov/pubmed/27875805 http://dx.doi.org/10.18632/aging.101099 |
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author | Gioscia-Ryan, Rachel A. Battson, Micah L. Cuevas, Lauren M. Zigler, Melanie C. Sindler, Amy L. Seals, Douglas R. |
author_facet | Gioscia-Ryan, Rachel A. Battson, Micah L. Cuevas, Lauren M. Zigler, Melanie C. Sindler, Amy L. Seals, Douglas R. |
author_sort | Gioscia-Ryan, Rachel A. |
collection | PubMed |
description | Mitochondrial dysregulation and associated excessive reactive oxygen species (mtROS) production is a key source of oxidative stress in aging arteries that reduces baseline function and may influence resilience (ability to withstand stress). We hypothesized that voluntary aerobic exercise would increase arterial resilience in old mice. An acute mitochondrial stressor (rotenone) caused greater (further) impairment in peak carotid EDD in old (~27 mo., OC, n=12;−32.5±-10.5%) versus young (~7 mo., YC n=11;−5.4±- 3.7%) control male mice, whereas arteries from young and old exercising (YVR n=10 and OVR n=11, 10-wk voluntary running;−0.8±-2.1% and −8.0±4.9%, respectively) mice were protected. Ex-vivo simulated Western diet (WD, high glucose and palmitate) caused greater impairment in EDD in OC (-28.5±8.6%) versus YC (-16.9±5.2%) and YVR (-15.3±2.3%), whereas OVR (-8.9±3.9%) were more resilient (not different versus YC). Simultaneous ex-vivo treatment with mitochondria-specific antioxidant MitoQ attenuated WD-induced impairments in YC and OC, but not YVR or OVR, suggesting that exercise improved resilience to mtROS-mediated stress. Exercise normalized age-related alterations in aortic mitochondrial protein markers PGC-1α, SIRT-3 and Fis1 and augmented cellular antioxidant and stress response proteins. Our results indicate that arterial aging is accompanied by reduced resilience and mitochondrial health, which are restored by voluntary aerobic exercise. |
format | Online Article Text |
id | pubmed-5191877 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-51918772016-12-28 Voluntary aerobic exercise increases arterial resilience and mitochondrial health with aging in mice Gioscia-Ryan, Rachel A. Battson, Micah L. Cuevas, Lauren M. Zigler, Melanie C. Sindler, Amy L. Seals, Douglas R. Aging (Albany NY) Research Paper Mitochondrial dysregulation and associated excessive reactive oxygen species (mtROS) production is a key source of oxidative stress in aging arteries that reduces baseline function and may influence resilience (ability to withstand stress). We hypothesized that voluntary aerobic exercise would increase arterial resilience in old mice. An acute mitochondrial stressor (rotenone) caused greater (further) impairment in peak carotid EDD in old (~27 mo., OC, n=12;−32.5±-10.5%) versus young (~7 mo., YC n=11;−5.4±- 3.7%) control male mice, whereas arteries from young and old exercising (YVR n=10 and OVR n=11, 10-wk voluntary running;−0.8±-2.1% and −8.0±4.9%, respectively) mice were protected. Ex-vivo simulated Western diet (WD, high glucose and palmitate) caused greater impairment in EDD in OC (-28.5±8.6%) versus YC (-16.9±5.2%) and YVR (-15.3±2.3%), whereas OVR (-8.9±3.9%) were more resilient (not different versus YC). Simultaneous ex-vivo treatment with mitochondria-specific antioxidant MitoQ attenuated WD-induced impairments in YC and OC, but not YVR or OVR, suggesting that exercise improved resilience to mtROS-mediated stress. Exercise normalized age-related alterations in aortic mitochondrial protein markers PGC-1α, SIRT-3 and Fis1 and augmented cellular antioxidant and stress response proteins. Our results indicate that arterial aging is accompanied by reduced resilience and mitochondrial health, which are restored by voluntary aerobic exercise. Impact Journals LLC 2016-11-22 /pmc/articles/PMC5191877/ /pubmed/27875805 http://dx.doi.org/10.18632/aging.101099 Text en Copyright: © 2016 Gioscia-Ryan et al. http://creativecommons.org/licenses/by/3.0/ This article is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) (CC-BY), which permits unrestricted use and redistribution provided that the original author and source are credited. |
spellingShingle | Research Paper Gioscia-Ryan, Rachel A. Battson, Micah L. Cuevas, Lauren M. Zigler, Melanie C. Sindler, Amy L. Seals, Douglas R. Voluntary aerobic exercise increases arterial resilience and mitochondrial health with aging in mice |
title | Voluntary aerobic exercise increases arterial resilience and mitochondrial health with aging in mice |
title_full | Voluntary aerobic exercise increases arterial resilience and mitochondrial health with aging in mice |
title_fullStr | Voluntary aerobic exercise increases arterial resilience and mitochondrial health with aging in mice |
title_full_unstemmed | Voluntary aerobic exercise increases arterial resilience and mitochondrial health with aging in mice |
title_short | Voluntary aerobic exercise increases arterial resilience and mitochondrial health with aging in mice |
title_sort | voluntary aerobic exercise increases arterial resilience and mitochondrial health with aging in mice |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5191877/ https://www.ncbi.nlm.nih.gov/pubmed/27875805 http://dx.doi.org/10.18632/aging.101099 |
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