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Defining cardiac adaptations and safety of endurance training in patients with m.3243A>G-related mitochondrial disease
Abstract Background Cardiac hypertrophic remodelling and systolic dysfunction are common in patients with mitochondrial disease and independent predictors of morbidity and early mortality. Endurance exercise training improves symptoms and skeletal muscle function, yet cardiac adaptations are unknown...
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Published in: | International journal of cardiology 2013-10, Vol.168 (4), p.3599-3608 |
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creator | Bates, Matthew G.D Newman, Jane H Jakovljevic, Djordje G Hollingsworth, Kieren G Alston, Charlotte L Zalewski, Pawel Klawe, Jacek J Blamire, Andrew M MacGowan, Guy A Keavney, Bernard D Bourke, John P Schaefer, Andrew McFarland, Robert Newton, Julia L Turnbull, Douglass M Taylor, Robert W Trenell, Michael I Gorman, Gráinne S |
description | Abstract Background Cardiac hypertrophic remodelling and systolic dysfunction are common in patients with mitochondrial disease and independent predictors of morbidity and early mortality. Endurance exercise training improves symptoms and skeletal muscle function, yet cardiac adaptations are unknown. Methods and results Before and after 16-weeks of training, exercise capacity, cardiac magnetic resonance imaging and phosphorus-31 spectroscopy, disease burden, fatigue, quality of life, heart rate variability (HRV) and blood pressure variability (BPV) were assessed in 10 adult patients with m.3243A>G-related mitochondrial disease, and compared to age- and gender-matched sedentary control subjects. At baseline, patients had increased left ventricular mass index (LVMI, p < 0.05) and LV mass to end-diastolic volume ratio, and decreased longitudinal shortening and myocardial phosphocreatine/adenosine triphosphate ratio (all p < 0.01). Peak arterial–venous oxygen difference ( p < 0.05), oxygen uptake (VO2 ) and power were decreased in patients (both p < 0.01) with no significant difference in cardiac power output. All patients remained stable and completed ≥ 80% sessions. With training, there were similar proportional increases in peak VO2 , anaerobic threshold and work capacity in patients and controls. LVMI increased in both groups ( p < 0.01), with no significant effect on myocardial function or bioenergetics. Pre- and post-exercise training, HRV and BPV demonstrated increased low frequency and decreased high frequency components in patients compared to controls (all p < 0.05). Conclusion Patients with mitochondrial disease and controls achieved similar proportional benefits of exercise training, without evidence of disease progression, or deleterious effects on cardiac function. Reduced exercise capacity is largely mediated through skeletal muscle dysfunction at baseline and sympathetic over-activation may be important in pathogenesis. |
doi_str_mv | 10.1016/j.ijcard.2013.05.062 |
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Endurance exercise training improves symptoms and skeletal muscle function, yet cardiac adaptations are unknown. Methods and results Before and after 16-weeks of training, exercise capacity, cardiac magnetic resonance imaging and phosphorus-31 spectroscopy, disease burden, fatigue, quality of life, heart rate variability (HRV) and blood pressure variability (BPV) were assessed in 10 adult patients with m.3243A>G-related mitochondrial disease, and compared to age- and gender-matched sedentary control subjects. At baseline, patients had increased left ventricular mass index (LVMI, p < 0.05) and LV mass to end-diastolic volume ratio, and decreased longitudinal shortening and myocardial phosphocreatine/adenosine triphosphate ratio (all p < 0.01). Peak arterial–venous oxygen difference ( p < 0.05), oxygen uptake (VO2 ) and power were decreased in patients (both p < 0.01) with no significant difference in cardiac power output. All patients remained stable and completed ≥ 80% sessions. With training, there were similar proportional increases in peak VO2 , anaerobic threshold and work capacity in patients and controls. LVMI increased in both groups ( p < 0.01), with no significant effect on myocardial function or bioenergetics. Pre- and post-exercise training, HRV and BPV demonstrated increased low frequency and decreased high frequency components in patients compared to controls (all p < 0.05). Conclusion Patients with mitochondrial disease and controls achieved similar proportional benefits of exercise training, without evidence of disease progression, or deleterious effects on cardiac function. Reduced exercise capacity is largely mediated through skeletal muscle dysfunction at baseline and sympathetic over-activation may be important in pathogenesis.]]></description><identifier>ISSN: 0167-5273</identifier><identifier>EISSN: 1874-1754</identifier><identifier>DOI: 10.1016/j.ijcard.2013.05.062</identifier><identifier>PMID: 23742928</identifier><identifier>CODEN: IJCDD5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Adaptation, Physiological - physiology ; Adult ; Autonomic function ; Biological and medical sciences ; Cardiac magnetic resonance imaging ; Cardiac magnetic resonance spectroscopy ; Cardiac Output - physiology ; Cardio-pulmonary exercise testing ; Cardiology. Vascular system ; Cardiovascular ; Cohort Studies ; Endurance exercise ; Errors of metabolism ; Exercise Test - methods ; Exercise Tolerance - physiology ; Female ; Follow-Up Studies ; Heart ; Humans ; Male ; Medical sciences ; Metabolic diseases ; Middle Aged ; Miscellaneous hereditary metabolic disorders ; Mitochondrial Diseases - genetics ; Mitochondrial Diseases - physiopathology ; Mitochondrial Diseases - therapy ; Mitochondrial DNA ; Physical Endurance - physiology ; Point Mutation - genetics</subject><ispartof>International journal of cardiology, 2013-10, Vol.168 (4), p.3599-3608</ispartof><rights>The Authors</rights><rights>2013 The Authors</rights><rights>2014 INIST-CNRS</rights><rights>Copyright © 2013 The Authors. Published by Elsevier Ireland Ltd.. All rights reserved.</rights><rights>2013 The Authors 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c581t-c3f8c4c477a9f341a2b2012db770d9be58c9b1d0d9c939f24c7a3193a90c1de03</citedby><cites>FETCH-LOGICAL-c581t-c3f8c4c477a9f341a2b2012db770d9be58c9b1d0d9c939f24c7a3193a90c1de03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27909459$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23742928$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bates, Matthew G.D</creatorcontrib><creatorcontrib>Newman, Jane H</creatorcontrib><creatorcontrib>Jakovljevic, Djordje G</creatorcontrib><creatorcontrib>Hollingsworth, Kieren G</creatorcontrib><creatorcontrib>Alston, Charlotte L</creatorcontrib><creatorcontrib>Zalewski, Pawel</creatorcontrib><creatorcontrib>Klawe, Jacek J</creatorcontrib><creatorcontrib>Blamire, Andrew M</creatorcontrib><creatorcontrib>MacGowan, Guy A</creatorcontrib><creatorcontrib>Keavney, Bernard D</creatorcontrib><creatorcontrib>Bourke, John P</creatorcontrib><creatorcontrib>Schaefer, Andrew</creatorcontrib><creatorcontrib>McFarland, Robert</creatorcontrib><creatorcontrib>Newton, Julia L</creatorcontrib><creatorcontrib>Turnbull, Douglass M</creatorcontrib><creatorcontrib>Taylor, Robert W</creatorcontrib><creatorcontrib>Trenell, Michael I</creatorcontrib><creatorcontrib>Gorman, Gráinne S</creatorcontrib><title>Defining cardiac adaptations and safety of endurance training in patients with m.3243A>G-related mitochondrial disease</title><title>International journal of cardiology</title><addtitle>Int J Cardiol</addtitle><description><![CDATA[Abstract Background Cardiac hypertrophic remodelling and systolic dysfunction are common in patients with mitochondrial disease and independent predictors of morbidity and early mortality. Endurance exercise training improves symptoms and skeletal muscle function, yet cardiac adaptations are unknown. Methods and results Before and after 16-weeks of training, exercise capacity, cardiac magnetic resonance imaging and phosphorus-31 spectroscopy, disease burden, fatigue, quality of life, heart rate variability (HRV) and blood pressure variability (BPV) were assessed in 10 adult patients with m.3243A>G-related mitochondrial disease, and compared to age- and gender-matched sedentary control subjects. At baseline, patients had increased left ventricular mass index (LVMI, p < 0.05) and LV mass to end-diastolic volume ratio, and decreased longitudinal shortening and myocardial phosphocreatine/adenosine triphosphate ratio (all p < 0.01). Peak arterial–venous oxygen difference ( p < 0.05), oxygen uptake (VO2 ) and power were decreased in patients (both p < 0.01) with no significant difference in cardiac power output. All patients remained stable and completed ≥ 80% sessions. With training, there were similar proportional increases in peak VO2 , anaerobic threshold and work capacity in patients and controls. LVMI increased in both groups ( p < 0.01), with no significant effect on myocardial function or bioenergetics. Pre- and post-exercise training, HRV and BPV demonstrated increased low frequency and decreased high frequency components in patients compared to controls (all p < 0.05). Conclusion Patients with mitochondrial disease and controls achieved similar proportional benefits of exercise training, without evidence of disease progression, or deleterious effects on cardiac function. Reduced exercise capacity is largely mediated through skeletal muscle dysfunction at baseline and sympathetic over-activation may be important in pathogenesis.]]></description><subject>Adaptation, Physiological - physiology</subject><subject>Adult</subject><subject>Autonomic function</subject><subject>Biological and medical sciences</subject><subject>Cardiac magnetic resonance imaging</subject><subject>Cardiac magnetic resonance spectroscopy</subject><subject>Cardiac Output - physiology</subject><subject>Cardio-pulmonary exercise testing</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular</subject><subject>Cohort Studies</subject><subject>Endurance exercise</subject><subject>Errors of metabolism</subject><subject>Exercise Test - methods</subject><subject>Exercise Tolerance - physiology</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Heart</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Middle Aged</subject><subject>Miscellaneous hereditary metabolic disorders</subject><subject>Mitochondrial Diseases - genetics</subject><subject>Mitochondrial Diseases - physiopathology</subject><subject>Mitochondrial Diseases - therapy</subject><subject>Mitochondrial DNA</subject><subject>Physical Endurance - physiology</subject><subject>Point Mutation - genetics</subject><issn>0167-5273</issn><issn>1874-1754</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNqFkk1v1DAQhiMEokvhHyDkCxKXBH9u4kulqkBBqsQBkLhZE3vS9ZK1Fzu7aP89jnZpgUtPsZRnXo_nmap6yWjDKFu-XTd-bSG5hlMmGqoauuSPqgXrWlmzVsnH1aJgba14K86qZzmvKaVS6-5pdcZFK7nm3aLav8PBBx9uyZzlwRJwsJ1g8jFkAsGRDANOBxIHgsHtEgSLZEpwLPKBbAuLYcrkl59WZNMILsXlxXWdcIQJHdn4KdpVDC55GInzGSHj8-rJAGPGF6fvefXtw_uvVx_rm8_Xn64ub2qrOjbVVgydlVa2LehBSAa8L6_lrm9b6nSPqrO6Z66crRZ64NK2IJgWoKllDqk4ry6Oudtdv0FnS6MJRrNNfgPpYCJ48--f4FfmNu6N6JheclYC3pwCUvy5wzyZjc8WxxECxl02TAnZCcWEehiVUpTxK74sqDyiNsWcEw53HTFqZrtmbY52zWzXUGWK3VL26u_X3BX90VmA1ycAsoVxmG35fM-1mmqp9P1YsMx-7zGZbItEi84ntJNx0T_Uyf8BdiwbUe78gQfM67hLoXg1zGRuqPkyb-K8iExQqjX9Ln4DM1PbVA</recordid><startdate>20131009</startdate><enddate>20131009</enddate><creator>Bates, Matthew G.D</creator><creator>Newman, Jane H</creator><creator>Jakovljevic, Djordje G</creator><creator>Hollingsworth, Kieren G</creator><creator>Alston, Charlotte L</creator><creator>Zalewski, Pawel</creator><creator>Klawe, Jacek J</creator><creator>Blamire, Andrew M</creator><creator>MacGowan, Guy A</creator><creator>Keavney, Bernard D</creator><creator>Bourke, John P</creator><creator>Schaefer, Andrew</creator><creator>McFarland, Robert</creator><creator>Newton, Julia L</creator><creator>Turnbull, Douglass M</creator><creator>Taylor, Robert W</creator><creator>Trenell, Michael I</creator><creator>Gorman, Gráinne S</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>6I.</scope><scope>AAFTH</scope><scope>IQODW</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>7X8</scope><scope>7TS</scope><scope>5PM</scope></search><sort><creationdate>20131009</creationdate><title>Defining cardiac adaptations and safety of endurance training in patients with m.3243A>G-related mitochondrial disease</title><author>Bates, Matthew G.D ; Newman, Jane H ; Jakovljevic, Djordje G ; Hollingsworth, Kieren G ; Alston, Charlotte L ; Zalewski, Pawel ; Klawe, Jacek J ; Blamire, Andrew M ; MacGowan, Guy A ; Keavney, Bernard D ; Bourke, John P ; Schaefer, Andrew ; McFarland, Robert ; Newton, Julia L ; Turnbull, Douglass M ; Taylor, Robert W ; Trenell, Michael I ; Gorman, Gráinne S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c581t-c3f8c4c477a9f341a2b2012db770d9be58c9b1d0d9c939f24c7a3193a90c1de03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adaptation, Physiological - physiology</topic><topic>Adult</topic><topic>Autonomic function</topic><topic>Biological and medical sciences</topic><topic>Cardiac magnetic resonance imaging</topic><topic>Cardiac magnetic resonance spectroscopy</topic><topic>Cardiac Output - physiology</topic><topic>Cardio-pulmonary exercise testing</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular</topic><topic>Cohort Studies</topic><topic>Endurance exercise</topic><topic>Errors of metabolism</topic><topic>Exercise Test - methods</topic><topic>Exercise Tolerance - physiology</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Heart</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Middle Aged</topic><topic>Miscellaneous hereditary metabolic disorders</topic><topic>Mitochondrial Diseases - genetics</topic><topic>Mitochondrial Diseases - physiopathology</topic><topic>Mitochondrial Diseases - therapy</topic><topic>Mitochondrial DNA</topic><topic>Physical Endurance - physiology</topic><topic>Point Mutation - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bates, Matthew G.D</creatorcontrib><creatorcontrib>Newman, Jane H</creatorcontrib><creatorcontrib>Jakovljevic, Djordje G</creatorcontrib><creatorcontrib>Hollingsworth, Kieren G</creatorcontrib><creatorcontrib>Alston, Charlotte L</creatorcontrib><creatorcontrib>Zalewski, Pawel</creatorcontrib><creatorcontrib>Klawe, Jacek J</creatorcontrib><creatorcontrib>Blamire, Andrew M</creatorcontrib><creatorcontrib>MacGowan, Guy A</creatorcontrib><creatorcontrib>Keavney, Bernard D</creatorcontrib><creatorcontrib>Bourke, John P</creatorcontrib><creatorcontrib>Schaefer, Andrew</creatorcontrib><creatorcontrib>McFarland, Robert</creatorcontrib><creatorcontrib>Newton, Julia L</creatorcontrib><creatorcontrib>Turnbull, Douglass M</creatorcontrib><creatorcontrib>Taylor, Robert W</creatorcontrib><creatorcontrib>Trenell, Michael I</creatorcontrib><creatorcontrib>Gorman, Gráinne S</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Physical Education Index</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bates, Matthew G.D</au><au>Newman, Jane H</au><au>Jakovljevic, Djordje G</au><au>Hollingsworth, Kieren G</au><au>Alston, Charlotte L</au><au>Zalewski, Pawel</au><au>Klawe, Jacek J</au><au>Blamire, Andrew M</au><au>MacGowan, Guy A</au><au>Keavney, Bernard D</au><au>Bourke, John P</au><au>Schaefer, Andrew</au><au>McFarland, Robert</au><au>Newton, Julia L</au><au>Turnbull, Douglass M</au><au>Taylor, Robert W</au><au>Trenell, Michael I</au><au>Gorman, Gráinne S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Defining cardiac adaptations and safety of endurance training in patients with m.3243A>G-related mitochondrial disease</atitle><jtitle>International journal of cardiology</jtitle><addtitle>Int J Cardiol</addtitle><date>2013-10-09</date><risdate>2013</risdate><volume>168</volume><issue>4</issue><spage>3599</spage><epage>3608</epage><pages>3599-3608</pages><issn>0167-5273</issn><eissn>1874-1754</eissn><coden>IJCDD5</coden><abstract><![CDATA[Abstract Background Cardiac hypertrophic remodelling and systolic dysfunction are common in patients with mitochondrial disease and independent predictors of morbidity and early mortality. Endurance exercise training improves symptoms and skeletal muscle function, yet cardiac adaptations are unknown. Methods and results Before and after 16-weeks of training, exercise capacity, cardiac magnetic resonance imaging and phosphorus-31 spectroscopy, disease burden, fatigue, quality of life, heart rate variability (HRV) and blood pressure variability (BPV) were assessed in 10 adult patients with m.3243A>G-related mitochondrial disease, and compared to age- and gender-matched sedentary control subjects. At baseline, patients had increased left ventricular mass index (LVMI, p < 0.05) and LV mass to end-diastolic volume ratio, and decreased longitudinal shortening and myocardial phosphocreatine/adenosine triphosphate ratio (all p < 0.01). Peak arterial–venous oxygen difference ( p < 0.05), oxygen uptake (VO2 ) and power were decreased in patients (both p < 0.01) with no significant difference in cardiac power output. All patients remained stable and completed ≥ 80% sessions. With training, there were similar proportional increases in peak VO2 , anaerobic threshold and work capacity in patients and controls. LVMI increased in both groups ( p < 0.01), with no significant effect on myocardial function or bioenergetics. Pre- and post-exercise training, HRV and BPV demonstrated increased low frequency and decreased high frequency components in patients compared to controls (all p < 0.05). Conclusion Patients with mitochondrial disease and controls achieved similar proportional benefits of exercise training, without evidence of disease progression, or deleterious effects on cardiac function. Reduced exercise capacity is largely mediated through skeletal muscle dysfunction at baseline and sympathetic over-activation may be important in pathogenesis.]]></abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>23742928</pmid><doi>10.1016/j.ijcard.2013.05.062</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adaptation, Physiological - physiology Adult Autonomic function Biological and medical sciences Cardiac magnetic resonance imaging Cardiac magnetic resonance spectroscopy Cardiac Output - physiology Cardio-pulmonary exercise testing Cardiology. Vascular system Cardiovascular Cohort Studies Endurance exercise Errors of metabolism Exercise Test - methods Exercise Tolerance - physiology Female Follow-Up Studies Heart Humans Male Medical sciences Metabolic diseases Middle Aged Miscellaneous hereditary metabolic disorders Mitochondrial Diseases - genetics Mitochondrial Diseases - physiopathology Mitochondrial Diseases - therapy Mitochondrial DNA Physical Endurance - physiology Point Mutation - genetics |
title | Defining cardiac adaptations and safety of endurance training in patients with m.3243A>G-related mitochondrial disease |
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