ArticleThe Journal of physiology2013
Altered skeletal muscle mitochondrial biogenesis but improved endurance capacity in trained OPA1-deficient mice.
Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Quantitative assessment of efficacy and evaluation of feasibility of exercise training protocols in adult and pediatric primary mitochondrial disease.BMC medicine · 2026Pooled it
- Mitochondrial Quality Control.Advances in experimental medicine and biology · 2025Review
- Age and sex-specific changes in mitochondrial quality control in skeletal and cardiac muscle.Frontiers in aging · 2025Article
- Normobaric hypoxia accelerates high-intensity intermittent training-induced mitochondrial biogenesis (PGC-1α)- and dynamics (OPA1)-related protein expressions in rat gastrocnemius muscle.Journal of physiology and biochemistry · 2024Article
- Migration increases mitochondrial oxidative capacity without increasing reactive oxygen species emission in a songbird.The Journal of experimental biology · 2024Article
- Review
- Article
- Association of mitochondrial homeostasis and dynamic balance with malignant biological behaviors of gastrointestinal cancer.Journal of translational medicine · 2023Review
- Exercise: a molecular tool to boost muscle growth and mitochondrial performance in heart failure?European journal of heart failure · 2022Review
- Exercise and mitochondrial mechanisms in patients with sarcopenia.Frontiers in physiology · 2022Review
- Effects of voluntary wheel running on mitochondrial content and dynamics in rat skeletal muscle.Journal of muscle research and cell motility · 2021Article
- Cardiolipin content controls mitochondrial coupling and energetic efficiency in muscle.Science advances · 2021Article
- Article
- β-Hydroxybutyrate Increases Exercise Capacity Associated with Changes in Mitochondrial Function in Skeletal Muscle.Nutrients · 2020Article
- Article
- Adult skeletal muscle deletion of Mitofusin 1 and 2 impedes exercise performance and training capacity.Journal of applied physiology (Bethesda, Md. : 1985) · 2019Article
- Exercise and Mitochondrial Dynamics: Keeping in Shape with ROS and AMPK.Antioxidants (Basel, Switzerland) · 2018Review
- Chronic Exercise Improves Mitochondrial Function and Insulin Sensitivity in Brown Adipose Tissue.Frontiers in physiology · 2018Article
- Metabolic Syndrome and Antipsychotics: The Role of Mitochondrial Fission/Fusion Imbalance.Frontiers in endocrinology · 2018Article
- Age-Associated Loss of OPA1 in Muscle Impacts Muscle Mass, Metabolic Homeostasis, Systemic Inflammation, and Epithelial Senescence.Cell metabolism · 2017Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of OPA1, a GTPase dynamin protein mainly involved in the fusion of inner mitochondrial membranes, has been studied in many cell types, but only a few studies have been conducted on adult differentiated tissues such as cardiac or skeletal muscle cells. Yet OPA1 is highly expressed in these cells, and could play different roles, especially in response to an environmental stress like exercise. Endurance exercise increases energy demand in skeletal muscle and repeated activity induces mitochondrial biogenesis and activation of fusion-fission cycles for the synthesis of new mitochondria. But currently no study has clearly shown a link between mitochondrial dynamics and biogenesis. Using a mouse model of haploinsufficiency for the Opa1 gene (Opa1(+/-)), we therefore studied the impact of OPA1 deficiency on the adaptation ability of fast skeletal muscles to endurance exercise training. Our results show that, surprisingly, Opa1(+/-) mice were able to perform the same physical activity as control mice. However, the adaptation strategies of both strains after training differed: while in control mice mitochondrial biogenesis was increased as expected, in Opa1(+/-) mice this process was blunted. Instead, training in Opa1(+/-) mice led to an increase in endurance capacity, and a specific adaptive response involving a metabolic remodelling towards enhanced fatty acid utilization. In conclusion, OPA1 appears necessary for the normal adaptive response and mitochondrial biogenesis of skeletal muscle to training. This work opens new perspectives on the role of mitochondrial dynamics in skeletal muscle cells and during adaptation to stress.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.