Aerobic Exercise Training Induces the Mitonuclear Imbalance and UPRmt in the Skeletal Muscle of Aged Mice
Abstract The impairment of the mitochondrial functions is a hallmark of aging. During aging, there is a downregulation of two mechanisms strictly associated with mitochondrial integrity, including the mitonuclear imbalance (eg, imbalance in mitochondrial- versus nuclear-encoded mitochondrial protein...
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| creator | Cordeiro, André V Brícola, Rafael S Braga, Renata R Lenhare, Luciene Silva, Vagner R R Anaruma, Chadi P Katashima, Carlos K Crisol, Barbara M Simabuco, Fernando M Silva, Adelino S R Cintra, Dennys E Moura, Leandro P Pauli, José R Ropelle, Eduardo R |
| description | Abstract
The impairment of the mitochondrial functions is a hallmark of aging. During aging, there is a downregulation of two mechanisms strictly associated with mitochondrial integrity, including the mitonuclear imbalance (eg, imbalance in mitochondrial- versus nuclear-encoded mitochondrial proteins) and the mitochondrial unfolded protein response (UPRmt). Here, we evaluated the effects of aerobic exercise in the mitonuclear imbalance and UPRmt markers in the skeletal muscle of old mice. We combined the physiological tests, molecular and bioinformatic analyzes to evaluate the effects of 4 weeks of aerobic exercise training on mitonuclear imbalance and UPRmt markers in the skeletal muscle of young (2 months) and aged (24 months) C57BL/6J mice. Initially, we found that aging reduced several mitochondrial genes in the gastrocnemius muscle, and it was accompanied by the low levels of UPRmt markers, including Yme1l1 and Clpp mRNA. As expected, physical training improved the whole-body metabolism and physical performance of aged mice. The aerobic exercise increased key proteins involved in the mitochondrial biogenesis/functions (VDAC and SIRT1) along with mitochondrial-encoded genes (mtNd1, mtCytB, and mtD-Loop) in the skeletal muscle of old mice. Interestingly, aerobic exercise induced the mitonuclear imbalance, increasing MTCO1/ATP5a ratio and UPRmt markers in the skeletal muscle, including HSP60, Lonp1, and Yme1L1 protein levels in the gastrocnemius muscle of aged mice. These data demonstrate that aerobic exercise training induced mitonuclear imbalance and UPRmt in the skeletal muscle during aging. These phenomena could be involved in the improvement of the mitochondrial metabolism and oxidative capacity in aged individuals. |
| doi_str_mv | 10.1093/gerona/glaa059 |
| format | Article |
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The impairment of the mitochondrial functions is a hallmark of aging. During aging, there is a downregulation of two mechanisms strictly associated with mitochondrial integrity, including the mitonuclear imbalance (eg, imbalance in mitochondrial- versus nuclear-encoded mitochondrial proteins) and the mitochondrial unfolded protein response (UPRmt). Here, we evaluated the effects of aerobic exercise in the mitonuclear imbalance and UPRmt markers in the skeletal muscle of old mice. We combined the physiological tests, molecular and bioinformatic analyzes to evaluate the effects of 4 weeks of aerobic exercise training on mitonuclear imbalance and UPRmt markers in the skeletal muscle of young (2 months) and aged (24 months) C57BL/6J mice. Initially, we found that aging reduced several mitochondrial genes in the gastrocnemius muscle, and it was accompanied by the low levels of UPRmt markers, including Yme1l1 and Clpp mRNA. As expected, physical training improved the whole-body metabolism and physical performance of aged mice. The aerobic exercise increased key proteins involved in the mitochondrial biogenesis/functions (VDAC and SIRT1) along with mitochondrial-encoded genes (mtNd1, mtCytB, and mtD-Loop) in the skeletal muscle of old mice. Interestingly, aerobic exercise induced the mitonuclear imbalance, increasing MTCO1/ATP5a ratio and UPRmt markers in the skeletal muscle, including HSP60, Lonp1, and Yme1L1 protein levels in the gastrocnemius muscle of aged mice. These data demonstrate that aerobic exercise training induced mitonuclear imbalance and UPRmt in the skeletal muscle during aging. These phenomena could be involved in the improvement of the mitochondrial metabolism and oxidative capacity in aged individuals.</description><identifier>ISSN: 1079-5006</identifier><identifier>EISSN: 1758-535X</identifier><identifier>DOI: 10.1093/gerona/glaa059</identifier><identifier>PMID: 32173728</identifier><language>eng</language><publisher>US: OXFORD UNIVERSITY PRESS</publisher><subject>Aerobics ; Aging ; Aging - physiology ; Animals ; Endopeptidase Clp - metabolism ; Exercise ; Gastrocnemius muscle ; Hsp60 protein ; Male ; Metalloendopeptidases - metabolism ; Mice ; Mice, Inbred C57BL ; Mitochondria ; Mitochondria, Muscle - metabolism ; Mitochondrial DNA ; mRNA ; Muscle, Skeletal - metabolism ; Muscular system ; Musculoskeletal system ; Oxidative metabolism ; Physical Conditioning, Animal - physiology ; Physical training ; Protein folding ; SIRT1 protein ; Sirtuin 1 - metabolism ; Skeletal muscle ; Unfolded Protein Response - physiology ; Voltage-Dependent Anion Channel 1 - metabolism</subject><ispartof>The journals of gerontology. Series A, Biological sciences and medical sciences, 2020-12, Vol.75 (12), p.2258-2261</ispartof><rights>The Author(s) 2020. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com. 2020</rights><rights>The Author(s) 2020. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.</rights><rights>Copyright Oxford University Press Dec 2020</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c385t-92c9581e4c26ddaaccf63d8890ea6d60fd928f6d8faf4f93e68a2ef4c6ee7e873</citedby><cites>FETCH-LOGICAL-c385t-92c9581e4c26ddaaccf63d8890ea6d60fd928f6d8faf4f93e68a2ef4c6ee7e873</cites><orcidid>0000-0003-4202-429X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1578,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32173728$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cordeiro, André V</creatorcontrib><creatorcontrib>Brícola, Rafael S</creatorcontrib><creatorcontrib>Braga, Renata R</creatorcontrib><creatorcontrib>Lenhare, Luciene</creatorcontrib><creatorcontrib>Silva, Vagner R R</creatorcontrib><creatorcontrib>Anaruma, Chadi P</creatorcontrib><creatorcontrib>Katashima, Carlos K</creatorcontrib><creatorcontrib>Crisol, Barbara M</creatorcontrib><creatorcontrib>Simabuco, Fernando M</creatorcontrib><creatorcontrib>Silva, Adelino S R</creatorcontrib><creatorcontrib>Cintra, Dennys E</creatorcontrib><creatorcontrib>Moura, Leandro P</creatorcontrib><creatorcontrib>Pauli, José R</creatorcontrib><creatorcontrib>Ropelle, Eduardo R</creatorcontrib><title>Aerobic Exercise Training Induces the Mitonuclear Imbalance and UPRmt in the Skeletal Muscle of Aged Mice</title><title>The journals of gerontology. Series A, Biological sciences and medical sciences</title><addtitle>J Gerontol A Biol Sci Med Sci</addtitle><description>Abstract
The impairment of the mitochondrial functions is a hallmark of aging. During aging, there is a downregulation of two mechanisms strictly associated with mitochondrial integrity, including the mitonuclear imbalance (eg, imbalance in mitochondrial- versus nuclear-encoded mitochondrial proteins) and the mitochondrial unfolded protein response (UPRmt). Here, we evaluated the effects of aerobic exercise in the mitonuclear imbalance and UPRmt markers in the skeletal muscle of old mice. We combined the physiological tests, molecular and bioinformatic analyzes to evaluate the effects of 4 weeks of aerobic exercise training on mitonuclear imbalance and UPRmt markers in the skeletal muscle of young (2 months) and aged (24 months) C57BL/6J mice. Initially, we found that aging reduced several mitochondrial genes in the gastrocnemius muscle, and it was accompanied by the low levels of UPRmt markers, including Yme1l1 and Clpp mRNA. As expected, physical training improved the whole-body metabolism and physical performance of aged mice. The aerobic exercise increased key proteins involved in the mitochondrial biogenesis/functions (VDAC and SIRT1) along with mitochondrial-encoded genes (mtNd1, mtCytB, and mtD-Loop) in the skeletal muscle of old mice. Interestingly, aerobic exercise induced the mitonuclear imbalance, increasing MTCO1/ATP5a ratio and UPRmt markers in the skeletal muscle, including HSP60, Lonp1, and Yme1L1 protein levels in the gastrocnemius muscle of aged mice. These data demonstrate that aerobic exercise training induced mitonuclear imbalance and UPRmt in the skeletal muscle during aging. These phenomena could be involved in the improvement of the mitochondrial metabolism and oxidative capacity in aged individuals.</description><subject>Aerobics</subject><subject>Aging</subject><subject>Aging - physiology</subject><subject>Animals</subject><subject>Endopeptidase Clp - metabolism</subject><subject>Exercise</subject><subject>Gastrocnemius muscle</subject><subject>Hsp60 protein</subject><subject>Male</subject><subject>Metalloendopeptidases - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mitochondria</subject><subject>Mitochondria, Muscle - metabolism</subject><subject>Mitochondrial DNA</subject><subject>mRNA</subject><subject>Muscle, Skeletal - metabolism</subject><subject>Muscular system</subject><subject>Musculoskeletal system</subject><subject>Oxidative metabolism</subject><subject>Physical Conditioning, Animal - physiology</subject><subject>Physical training</subject><subject>Protein folding</subject><subject>SIRT1 protein</subject><subject>Sirtuin 1 - metabolism</subject><subject>Skeletal muscle</subject><subject>Unfolded Protein Response - physiology</subject><subject>Voltage-Dependent Anion Channel 1 - metabolism</subject><issn>1079-5006</issn><issn>1758-535X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0c1PFDEYBvDGaATRK0fThIseBvox_TpuCMImEI1C4m3Sbd8uxZnO2s4k8t9T2MWDB-zl7eH3PnmTB6FDSo4pMfxkDXlM9mTdW0uEeYX2qRK6EVz8fF3_RJlGECL30LtS7sjjE-wt2uOMKq6Y3kdxUQNW0eGzP5BdLICvs40ppjVeJj87KHi6BXwVpzHNrgeb8XJY2d4mB9gmj2--fR8mHNMT-_ELephsj6_mUjEeA16swdd1B-_Rm2D7Ah928wDdfDm7Pr1oLr-eL08Xl43jWkyNYc4ITaF1THpvrXNBcq-1IWCllyR4w3SQXgcb2mA4SG0ZhNZJAAVa8QP0aZu7yePvGcrUDbE46OvJMM6lY1wpqZQRtNKjf-jdOOdUr-tYq7lsqaHqZaUo4UQJUdXxVrk8lpIhdJscB5vvO0q6x6q6bVXdrqq68HEXO68G8H_5czcVfN6Ccd78L-wBF2ae_Q</recordid><startdate>20201201</startdate><enddate>20201201</enddate><creator>Cordeiro, André V</creator><creator>Brícola, Rafael S</creator><creator>Braga, Renata R</creator><creator>Lenhare, Luciene</creator><creator>Silva, Vagner R R</creator><creator>Anaruma, Chadi P</creator><creator>Katashima, Carlos K</creator><creator>Crisol, Barbara M</creator><creator>Simabuco, Fernando M</creator><creator>Silva, Adelino S R</creator><creator>Cintra, Dennys E</creator><creator>Moura, Leandro P</creator><creator>Pauli, José R</creator><creator>Ropelle, Eduardo R</creator><general>OXFORD UNIVERSITY PRESS</general><general>Oxford University Press</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-4202-429X</orcidid></search><sort><creationdate>20201201</creationdate><title>Aerobic Exercise Training Induces the Mitonuclear Imbalance and UPRmt in the Skeletal Muscle of Aged Mice</title><author>Cordeiro, André V ; Brícola, Rafael S ; Braga, Renata R ; Lenhare, Luciene ; Silva, Vagner R R ; Anaruma, Chadi P ; Katashima, Carlos K ; Crisol, Barbara M ; Simabuco, Fernando M ; Silva, Adelino S R ; Cintra, Dennys E ; Moura, Leandro P ; Pauli, José R ; Ropelle, Eduardo R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c385t-92c9581e4c26ddaaccf63d8890ea6d60fd928f6d8faf4f93e68a2ef4c6ee7e873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Aerobics</topic><topic>Aging</topic><topic>Aging - physiology</topic><topic>Animals</topic><topic>Endopeptidase Clp - metabolism</topic><topic>Exercise</topic><topic>Gastrocnemius muscle</topic><topic>Hsp60 protein</topic><topic>Male</topic><topic>Metalloendopeptidases - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mitochondria</topic><topic>Mitochondria, Muscle - metabolism</topic><topic>Mitochondrial DNA</topic><topic>mRNA</topic><topic>Muscle, Skeletal - metabolism</topic><topic>Muscular system</topic><topic>Musculoskeletal system</topic><topic>Oxidative metabolism</topic><topic>Physical Conditioning, Animal - physiology</topic><topic>Physical training</topic><topic>Protein folding</topic><topic>SIRT1 protein</topic><topic>Sirtuin 1 - metabolism</topic><topic>Skeletal muscle</topic><topic>Unfolded Protein Response - physiology</topic><topic>Voltage-Dependent Anion Channel 1 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cordeiro, André V</creatorcontrib><creatorcontrib>Brícola, Rafael S</creatorcontrib><creatorcontrib>Braga, Renata R</creatorcontrib><creatorcontrib>Lenhare, Luciene</creatorcontrib><creatorcontrib>Silva, Vagner R R</creatorcontrib><creatorcontrib>Anaruma, Chadi P</creatorcontrib><creatorcontrib>Katashima, Carlos K</creatorcontrib><creatorcontrib>Crisol, Barbara M</creatorcontrib><creatorcontrib>Simabuco, Fernando M</creatorcontrib><creatorcontrib>Silva, Adelino S R</creatorcontrib><creatorcontrib>Cintra, Dennys E</creatorcontrib><creatorcontrib>Moura, Leandro P</creatorcontrib><creatorcontrib>Pauli, José R</creatorcontrib><creatorcontrib>Ropelle, Eduardo R</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>The journals of gerontology. 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The impairment of the mitochondrial functions is a hallmark of aging. During aging, there is a downregulation of two mechanisms strictly associated with mitochondrial integrity, including the mitonuclear imbalance (eg, imbalance in mitochondrial- versus nuclear-encoded mitochondrial proteins) and the mitochondrial unfolded protein response (UPRmt). Here, we evaluated the effects of aerobic exercise in the mitonuclear imbalance and UPRmt markers in the skeletal muscle of old mice. We combined the physiological tests, molecular and bioinformatic analyzes to evaluate the effects of 4 weeks of aerobic exercise training on mitonuclear imbalance and UPRmt markers in the skeletal muscle of young (2 months) and aged (24 months) C57BL/6J mice. Initially, we found that aging reduced several mitochondrial genes in the gastrocnemius muscle, and it was accompanied by the low levels of UPRmt markers, including Yme1l1 and Clpp mRNA. As expected, physical training improved the whole-body metabolism and physical performance of aged mice. The aerobic exercise increased key proteins involved in the mitochondrial biogenesis/functions (VDAC and SIRT1) along with mitochondrial-encoded genes (mtNd1, mtCytB, and mtD-Loop) in the skeletal muscle of old mice. Interestingly, aerobic exercise induced the mitonuclear imbalance, increasing MTCO1/ATP5a ratio and UPRmt markers in the skeletal muscle, including HSP60, Lonp1, and Yme1L1 protein levels in the gastrocnemius muscle of aged mice. These data demonstrate that aerobic exercise training induced mitonuclear imbalance and UPRmt in the skeletal muscle during aging. These phenomena could be involved in the improvement of the mitochondrial metabolism and oxidative capacity in aged individuals.</abstract><cop>US</cop><pub>OXFORD UNIVERSITY PRESS</pub><pmid>32173728</pmid><doi>10.1093/gerona/glaa059</doi><tpages>4</tpages><orcidid>https://orcid.org/0000-0003-4202-429X</orcidid></addata></record> |
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| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; Alma/SFX Local Collection |
| subjects | Aerobics Aging Aging - physiology Animals Endopeptidase Clp - metabolism Exercise Gastrocnemius muscle Hsp60 protein Male Metalloendopeptidases - metabolism Mice Mice, Inbred C57BL Mitochondria Mitochondria, Muscle - metabolism Mitochondrial DNA mRNA Muscle, Skeletal - metabolism Muscular system Musculoskeletal system Oxidative metabolism Physical Conditioning, Animal - physiology Physical training Protein folding SIRT1 protein Sirtuin 1 - metabolism Skeletal muscle Unfolded Protein Response - physiology Voltage-Dependent Anion Channel 1 - metabolism |
| title | Aerobic Exercise Training Induces the Mitonuclear Imbalance and UPRmt in the Skeletal Muscle of Aged Mice |
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