<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Marcangeli V</submitter><funding>Natural Sciences and Engineering Research Council of Canada</funding><funding>Canadian Space Agency</funding><funding>Centre d'Excellence en Recherche sur les Maladies Orphelines-Fondation Courtois</funding><funding>Rare Disease Foundation</funding><funding>Fondation du Grand défi Pierre Lavoie</funding><funding>Canadian Frailty Network</funding><funding>Canadian Institute of Health Research</funding><funding>FRQS</funding><pagination>e70135</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12619986</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>241(12)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Myotonic dystrophy type 1 (DM1) is caused by expanded CTG repeats in the DMPK gene, causing the accumulation of toxic RNA that sequesters RNA-binding proteins. Clinically, DM1 is characterized by progressive muscle weakness and atrophy, resulting in reduced physical capacity and quality of life. Recent evidence implicates mitochondrial dysfunction in DM1 pathophysiology. While aerobic exercise has been shown to improve skeletal muscle and mitochondrial health in individuals with DM1, the benefits of strength training remain unexplored.&lt;h4>Objectives&lt;/h4>We investigated the effects of a 12-week strength training program on mitochondrial respiration, reactive oxygen species (ROS) production and muscle integrity in women with DM1.&lt;h4>Methods&lt;/h4>Vastus lateralis muscle biop</pubmed_abstract><journal>Acta physiologica (Oxford, England)</journal><pubmed_title>A 12-Week Strength Training Improves Mitochondrial Respiration, H&amp;lt;sub&amp;gt;2&amp;lt;/sub&amp;gt;O&amp;lt;sub&amp;gt;2&amp;lt;/sub&amp;gt; Emission and Skeletal Muscle Integrity in Women With Myotonic Dystrophy Type 1.</pubmed_title><pmcid>PMC12619986</pmcid><funding_grant_id>RGPIN-2021-03724</funding_grant_id><funding_grant_id>UH2-161692</funding_grant_id><funding_grant_id>31186</funding_grant_id><funding_grant_id>317693</funding_grant_id><funding_grant_id>35184</funding_grant_id><funding_grant_id>RGPIN-2024-05033</funding_grant_id><pubmed_authors>Hajj-Boutros G</pubmed_authors><pubmed_authors>Roussel MP</pubmed_authors><pubmed_authors>Dulac M</pubmed_authors><pubmed_authors>Marcangeli V</pubmed_authors><pubmed_authors>Di Leo V</pubmed_authors><pubmed_authors>Duchesne E</pubmed_authors><pubmed_authors>Lawless C</pubmed_authors><pubmed_authors>Gouspillou G</pubmed_authors><pubmed_authors>Charest O</pubmed_authors><pubmed_authors>Leduc-Gaudet JP</pubmed_authors><pubmed_authors>Argaw A</pubmed_authors><pubmed_authors>Morais JA</pubmed_authors><pubmed_authors>Vincent A</pubmed_authors><pubmed_authors>Girard-Cote L</pubmed_authors></additional><is_claimable>false</is_claimable><name>A 12-Week Strength Training Improves Mitochondrial Respiration, H&amp;lt;sub&amp;gt;2&amp;lt;/sub&amp;gt;O&amp;lt;sub&amp;gt;2&amp;lt;/sub&amp;gt; Emission and Skeletal Muscle Integrity in Women With Myotonic Dystrophy Type 1.</name><description>&lt;h4>Background&lt;/h4>Myotonic dystrophy type 1 (DM1) is caused by expanded CTG repeats in the DMPK gene, causing the accumulation of toxic RNA that sequesters RNA-binding proteins. Clinically, DM1 is characterized by progressive muscle weakness and atrophy, resulting in reduced physical capacity and quality of life. Recent evidence implicates mitochondrial dysfunction in DM1 pathophysiology. While aerobic exercise has been shown to improve skeletal muscle and mitochondrial health in individuals with DM1, the benefits of strength training remain unexplored.&lt;h4>Objectives&lt;/h4>We investigated the effects of a 12-week strength training program on mitochondrial respiration, reactive oxygen species (ROS) production and muscle integrity in women with DM1.&lt;h4>Methods&lt;/h4>Vastus lateralis muscle biop</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Dec</publication><modification>2026-06-05T16:24:12.125Z</modification><creation>2026-06-05T03:06:23.648Z</creation></dates><accession>S-EPMC12619986</accession><cross_references><pubmed>41241935</pubmed><doi>10.1111/apha.70135</doi></cross_references></HashMap>