Exercise Training Protects Against Acute Myocardial Infarction via Improving Myocardial Energy Metabolism and Mitochondrial Biogenesis
Background/Aims: Acute myocardial infarction (AMI) represents a major cause of morbidity and mortality worldwide. Exercise has been proved to reduce myocardial ischemia-reperfusion (I/R) injury However it remains unclear whether, and (if so) how, exercise could protect against AMI. Methods: Mice wer...
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| Veröffentlicht in: | Cellular Physiology and Biochemistry 2015-01, Vol.37 (1), p.162-175 |
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| creator | Tao, Lichan Bei, Yihua Lin, Shenghui Zhang, Haifeng Zhou, Yanli Jiang, Jingfa Chen, Ping Shen, Shutong Xiao, Junjie Li, Xinli |
| description | Background/Aims: Acute myocardial infarction (AMI) represents a major cause of morbidity and mortality worldwide. Exercise has been proved to reduce myocardial ischemia-reperfusion (I/R) injury However it remains unclear whether, and (if so) how, exercise could protect against AMI. Methods: Mice were trained using a 3-week swimming protocol, and then subjected to left coronary artery (LCA) ligation, and finally sacrificed 24 h after AMI. Myocardial infarct size was examined with triphenyltetrazolium chloride staining. Cardiac apoptosis was determined by TUNEL staining. Mitochondria density was checked by Mito-Tracker immunofluorescent staining. Quantitative reverse transcription polymerase chain reactions and Western blotting were used to determine genes related to apoptosis, autophagy and myocardial energy metabolism. Results: Exercise training reduces myocardial infarct size and abolishes AMI-induced autophagy and apoptosis. AMI leads to a shift from fatty acid to glucose metabolism in the myocardium with a downregulation of PPAR-α and PPAR-γ. Also, AMI induces an adaptive increase of mitochondrial DNA replication and transcription in the acute phase of MI, accompanied by an activation of PGC-1α signaling. Exercise abolishes the derangement of myocardial glucose and lipid metabolism and further enhances the adaptive increase of mitochondrial biogenesis. Conclusion: Exercise training protects against AMI-induced acute cardiac injury through improving myocardial energy metabolism and enhancing the early adaptive change of mitochondrial biogenesis. |
| doi_str_mv | 10.1159/000430342 |
| format | Article |
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Exercise has been proved to reduce myocardial ischemia-reperfusion (I/R) injury However it remains unclear whether, and (if so) how, exercise could protect against AMI. Methods: Mice were trained using a 3-week swimming protocol, and then subjected to left coronary artery (LCA) ligation, and finally sacrificed 24 h after AMI. Myocardial infarct size was examined with triphenyltetrazolium chloride staining. Cardiac apoptosis was determined by TUNEL staining. Mitochondria density was checked by Mito-Tracker immunofluorescent staining. Quantitative reverse transcription polymerase chain reactions and Western blotting were used to determine genes related to apoptosis, autophagy and myocardial energy metabolism. Results: Exercise training reduces myocardial infarct size and abolishes AMI-induced autophagy and apoptosis. AMI leads to a shift from fatty acid to glucose metabolism in the myocardium with a downregulation of PPAR-α and PPAR-γ. Also, AMI induces an adaptive increase of mitochondrial DNA replication and transcription in the acute phase of MI, accompanied by an activation of PGC-1α signaling. Exercise abolishes the derangement of myocardial glucose and lipid metabolism and further enhances the adaptive increase of mitochondrial biogenesis. Conclusion: Exercise training protects against AMI-induced acute cardiac injury through improving myocardial energy metabolism and enhancing the early adaptive change of mitochondrial biogenesis.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000430342</identifier><identifier>PMID: 26303678</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Acute Disease ; Acute myocardial infarction ; Analysis ; Animals ; Apoptosis - genetics ; Apoptosis - physiology ; Autophagy - genetics ; Autophagy - physiology ; Bioenergetics ; DNA Replication - genetics ; DNA, Mitochondrial - genetics ; Down-Regulation - genetics ; Down-Regulation - physiology ; Energy metabolism ; Energy Metabolism - genetics ; Energy Metabolism - physiology ; Exercise therapy ; Exercise training ; Heart - physiopathology ; Heart attack ; In Situ Nick-End Labeling - methods ; Male ; Metabolism ; Mice ; Mice, Inbred C57BL ; Mitochondria ; Mitochondria - genetics ; Mitochondria - physiology ; Mitochondrial biogenesis ; Myocardial Infarction - genetics ; Myocardial Infarction - physiopathology ; Organelle Biogenesis ; Original Paper ; PGC-1α ; Physical Conditioning, Animal - physiology ; Physiological aspects ; Prevention ; Signal Transduction - genetics ; Transcription, Genetic - genetics</subject><ispartof>Cellular Physiology and Biochemistry, 2015-01, Vol.37 (1), p.162-175</ispartof><rights>2015 S. Karger AG, Basel</rights><rights>2015 S. Karger AG, Basel.</rights><rights>COPYRIGHT 2015 S. Karger AG</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c568t-52bc4664c9f34816f69cabf6526268e9b43e0db8fcc136891937cc75d71f74533</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,860,2095,27614,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26303678$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tao, Lichan</creatorcontrib><creatorcontrib>Bei, Yihua</creatorcontrib><creatorcontrib>Lin, Shenghui</creatorcontrib><creatorcontrib>Zhang, Haifeng</creatorcontrib><creatorcontrib>Zhou, Yanli</creatorcontrib><creatorcontrib>Jiang, Jingfa</creatorcontrib><creatorcontrib>Chen, Ping</creatorcontrib><creatorcontrib>Shen, Shutong</creatorcontrib><creatorcontrib>Xiao, Junjie</creatorcontrib><creatorcontrib>Li, Xinli</creatorcontrib><title>Exercise Training Protects Against Acute Myocardial Infarction via Improving Myocardial Energy Metabolism and Mitochondrial Biogenesis</title><title>Cellular Physiology and Biochemistry</title><addtitle>Cell Physiol Biochem</addtitle><description>Background/Aims: Acute myocardial infarction (AMI) represents a major cause of morbidity and mortality worldwide. Exercise has been proved to reduce myocardial ischemia-reperfusion (I/R) injury However it remains unclear whether, and (if so) how, exercise could protect against AMI. Methods: Mice were trained using a 3-week swimming protocol, and then subjected to left coronary artery (LCA) ligation, and finally sacrificed 24 h after AMI. Myocardial infarct size was examined with triphenyltetrazolium chloride staining. Cardiac apoptosis was determined by TUNEL staining. Mitochondria density was checked by Mito-Tracker immunofluorescent staining. Quantitative reverse transcription polymerase chain reactions and Western blotting were used to determine genes related to apoptosis, autophagy and myocardial energy metabolism. Results: Exercise training reduces myocardial infarct size and abolishes AMI-induced autophagy and apoptosis. AMI leads to a shift from fatty acid to glucose metabolism in the myocardium with a downregulation of PPAR-α and PPAR-γ. Also, AMI induces an adaptive increase of mitochondrial DNA replication and transcription in the acute phase of MI, accompanied by an activation of PGC-1α signaling. Exercise abolishes the derangement of myocardial glucose and lipid metabolism and further enhances the adaptive increase of mitochondrial biogenesis. Conclusion: Exercise training protects against AMI-induced acute cardiac injury through improving myocardial energy metabolism and enhancing the early adaptive change of mitochondrial biogenesis.</description><subject>Acute Disease</subject><subject>Acute myocardial infarction</subject><subject>Analysis</subject><subject>Animals</subject><subject>Apoptosis - genetics</subject><subject>Apoptosis - physiology</subject><subject>Autophagy - genetics</subject><subject>Autophagy - physiology</subject><subject>Bioenergetics</subject><subject>DNA Replication - genetics</subject><subject>DNA, Mitochondrial - genetics</subject><subject>Down-Regulation - genetics</subject><subject>Down-Regulation - physiology</subject><subject>Energy metabolism</subject><subject>Energy Metabolism - genetics</subject><subject>Energy Metabolism - physiology</subject><subject>Exercise therapy</subject><subject>Exercise training</subject><subject>Heart - physiopathology</subject><subject>Heart attack</subject><subject>In Situ Nick-End Labeling - methods</subject><subject>Male</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mitochondria</subject><subject>Mitochondria - genetics</subject><subject>Mitochondria - physiology</subject><subject>Mitochondrial biogenesis</subject><subject>Myocardial Infarction - genetics</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Organelle Biogenesis</subject><subject>Original Paper</subject><subject>PGC-1α</subject><subject>Physical Conditioning, Animal - physiology</subject><subject>Physiological aspects</subject><subject>Prevention</subject><subject>Signal Transduction - genetics</subject><subject>Transcription, Genetic - genetics</subject><issn>1015-8987</issn><issn>1421-9778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>DOA</sourceid><recordid>eNptkUtvEzEUhUcIREthwR6hkbqBRYpf48cyjQJEakQXZT3yeK4Hlxm72E5F_gC_G4cJEQvkhe2j7557rm5VvcboCuNGfUAIMYooI0-qc8wIXigh5NPyRrhZSCXFWfUipXtUvkKR59UZ4QXnQp5Xv9Y_IRqXoL6L2nnnh_o2hgwmp3o5FCXleml2GertPhgde6fHeuOtjia74OtHp-vN9BDD46H0H2btIQ77egtZd2F0aaq17-uty8F8C76PB-bahQE8JJdeVs-sHhO8Ot4X1deP67vV58XNl0-b1fJmYRou86IhnWGcM6MsZRJzy5XRneUN4YRLUB2jgPpOWmMw5VJhRYUxoukFtoI1lF5Um9m3D_q-fYhu0nHfBu3aP0KIQ6tjdmaEFqhWUoHuFOmZAS2bBpcunFDoiCW2eL2bvcr0P3aQcju5ZGActYewSy0WqERkCqmCXs3ooIuz8zbkqE05PUzOBA_WFX3JqWgQZuiQ8_1cYGJIKYI9ZcWoPey8Pe28sG-POXbdBP2J_LvkAlzOwHcdB4gnYHV7PVu0D_1hnDf_pY5dfgMSMrwi</recordid><startdate>20150101</startdate><enddate>20150101</enddate><creator>Tao, Lichan</creator><creator>Bei, Yihua</creator><creator>Lin, Shenghui</creator><creator>Zhang, Haifeng</creator><creator>Zhou, Yanli</creator><creator>Jiang, Jingfa</creator><creator>Chen, Ping</creator><creator>Shen, Shutong</creator><creator>Xiao, Junjie</creator><creator>Li, Xinli</creator><general>S. Karger AG</general><general>Cell Physiol Biochem Press GmbH & Co KG</general><scope>M--</scope><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>IAO</scope><scope>7X8</scope><scope>DOA</scope></search><sort><creationdate>20150101</creationdate><title>Exercise Training Protects Against Acute Myocardial Infarction via Improving Myocardial Energy Metabolism and Mitochondrial Biogenesis</title><author>Tao, Lichan ; Bei, Yihua ; Lin, Shenghui ; Zhang, Haifeng ; Zhou, Yanli ; Jiang, Jingfa ; Chen, Ping ; Shen, Shutong ; Xiao, Junjie ; Li, Xinli</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c568t-52bc4664c9f34816f69cabf6526268e9b43e0db8fcc136891937cc75d71f74533</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Acute Disease</topic><topic>Acute myocardial infarction</topic><topic>Analysis</topic><topic>Animals</topic><topic>Apoptosis - genetics</topic><topic>Apoptosis - physiology</topic><topic>Autophagy - genetics</topic><topic>Autophagy - physiology</topic><topic>Bioenergetics</topic><topic>DNA Replication - genetics</topic><topic>DNA, Mitochondrial - genetics</topic><topic>Down-Regulation - genetics</topic><topic>Down-Regulation - physiology</topic><topic>Energy metabolism</topic><topic>Energy Metabolism - genetics</topic><topic>Energy Metabolism - physiology</topic><topic>Exercise therapy</topic><topic>Exercise training</topic><topic>Heart - physiopathology</topic><topic>Heart attack</topic><topic>In Situ Nick-End Labeling - methods</topic><topic>Male</topic><topic>Metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mitochondria</topic><topic>Mitochondria - genetics</topic><topic>Mitochondria - physiology</topic><topic>Mitochondrial biogenesis</topic><topic>Myocardial Infarction - genetics</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Organelle Biogenesis</topic><topic>Original Paper</topic><topic>PGC-1α</topic><topic>Physical Conditioning, Animal - physiology</topic><topic>Physiological aspects</topic><topic>Prevention</topic><topic>Signal Transduction - genetics</topic><topic>Transcription, Genetic - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tao, Lichan</creatorcontrib><creatorcontrib>Bei, Yihua</creatorcontrib><creatorcontrib>Lin, Shenghui</creatorcontrib><creatorcontrib>Zhang, Haifeng</creatorcontrib><creatorcontrib>Zhou, Yanli</creatorcontrib><creatorcontrib>Jiang, Jingfa</creatorcontrib><creatorcontrib>Chen, Ping</creatorcontrib><creatorcontrib>Shen, Shutong</creatorcontrib><creatorcontrib>Xiao, Junjie</creatorcontrib><creatorcontrib>Li, Xinli</creatorcontrib><collection>Karger Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale Academic OneFile</collection><collection>MEDLINE - Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cellular Physiology and Biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tao, Lichan</au><au>Bei, Yihua</au><au>Lin, Shenghui</au><au>Zhang, Haifeng</au><au>Zhou, Yanli</au><au>Jiang, Jingfa</au><au>Chen, Ping</au><au>Shen, Shutong</au><au>Xiao, Junjie</au><au>Li, Xinli</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Exercise Training Protects Against Acute Myocardial Infarction via Improving Myocardial Energy Metabolism and Mitochondrial Biogenesis</atitle><jtitle>Cellular Physiology and Biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2015-01-01</date><risdate>2015</risdate><volume>37</volume><issue>1</issue><spage>162</spage><epage>175</epage><pages>162-175</pages><issn>1015-8987</issn><eissn>1421-9778</eissn><abstract>Background/Aims: Acute myocardial infarction (AMI) represents a major cause of morbidity and mortality worldwide. Exercise has been proved to reduce myocardial ischemia-reperfusion (I/R) injury However it remains unclear whether, and (if so) how, exercise could protect against AMI. Methods: Mice were trained using a 3-week swimming protocol, and then subjected to left coronary artery (LCA) ligation, and finally sacrificed 24 h after AMI. Myocardial infarct size was examined with triphenyltetrazolium chloride staining. Cardiac apoptosis was determined by TUNEL staining. Mitochondria density was checked by Mito-Tracker immunofluorescent staining. Quantitative reverse transcription polymerase chain reactions and Western blotting were used to determine genes related to apoptosis, autophagy and myocardial energy metabolism. Results: Exercise training reduces myocardial infarct size and abolishes AMI-induced autophagy and apoptosis. AMI leads to a shift from fatty acid to glucose metabolism in the myocardium with a downregulation of PPAR-α and PPAR-γ. Also, AMI induces an adaptive increase of mitochondrial DNA replication and transcription in the acute phase of MI, accompanied by an activation of PGC-1α signaling. Exercise abolishes the derangement of myocardial glucose and lipid metabolism and further enhances the adaptive increase of mitochondrial biogenesis. Conclusion: Exercise training protects against AMI-induced acute cardiac injury through improving myocardial energy metabolism and enhancing the early adaptive change of mitochondrial biogenesis.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>26303678</pmid><doi>10.1159/000430342</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acute Disease Acute myocardial infarction Analysis Animals Apoptosis - genetics Apoptosis - physiology Autophagy - genetics Autophagy - physiology Bioenergetics DNA Replication - genetics DNA, Mitochondrial - genetics Down-Regulation - genetics Down-Regulation - physiology Energy metabolism Energy Metabolism - genetics Energy Metabolism - physiology Exercise therapy Exercise training Heart - physiopathology Heart attack In Situ Nick-End Labeling - methods Male Metabolism Mice Mice, Inbred C57BL Mitochondria Mitochondria - genetics Mitochondria - physiology Mitochondrial biogenesis Myocardial Infarction - genetics Myocardial Infarction - physiopathology Organelle Biogenesis Original Paper PGC-1α Physical Conditioning, Animal - physiology Physiological aspects Prevention Signal Transduction - genetics Transcription, Genetic - genetics |
| title | Exercise Training Protects Against Acute Myocardial Infarction via Improving Myocardial Energy Metabolism and Mitochondrial Biogenesis |
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