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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...

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Autores principales: Gioscia-Ryan, Rachel A., Battson, Micah L., Cuevas, Lauren M., Zigler, Melanie C., Sindler, Amy L., Seals, Douglas R.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2016
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.
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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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