ArticleActa physiologica (Oxford, England)2025
A 12-Week Strength Training Improves Mitochondrial Respiration, H
Article in Acta physiologica (Oxford, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed.
- Multilevel impairment of mitochondrial respiration with sex-specific signatures in inclusion body myositis.bioRxiv : the preprint server for biology · 2026Article
- A 12-Week Strength Training Improves Mitochondrial Respiration, HActa physiologica (Oxford, England) · 2025Article
- Effects of postoperative electrical stimulation on quadriceps muscular atrophy in patients with incomplete cervical spinal cord injury. A retrospective study.Frontiers in neurologyArticle
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Authors and funding
14 authors.
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Abstract
backgroundMyotonic 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.
objectivesWe 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.
methodsVastus lateralis muscle biopsies were collected pre- and post-training in participants with DM1 and once in unaffected/untrained individuals. Mitochondrial respiration and hydrogen peroxide emission (marker of ROS production) were assessed in permeabilized myofibers, while OXPHOS protein contents were quantified by immunoblotting and immunofluorescence. Markers of myofiber denervation (NCAM+) and integrity (centrally located myonuclei, damaged laminin, nuclear clumps) were assessed on histological sections.
resultsAt baseline, DM1 participants exhibited lower mitochondrial respiration compared to unaffected individuals. Strength training significantly improved mitochondrial respiration and content in DM1 participants. At baseline, absolute ROS production was lower, while ROS production normalized to oxygen consumption (free radical leak) was higher, in DM1. Histological signs of denervation and altered muscle integrity were observed. Strength training partially normalized mitochondrial free radical leak and restored some markers of myofiber integrity.
conclusionCollectively, our results indicate that strength training enhances mitochondrial health and improves myofiber integrity in women with DM1.
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