Swim Training Modulates Mouse Skeletal Muscle Energy Metabolism and Ameliorates Reduction in Grip Strength in a Mouse Model of Amyotrophic Lateral Sclerosis
| Autor: | Jedrzej Antosiewicz, Malgorzata Halon-Golabek, Karol Cieminski, Mariusz R. Wieckowski, Jan J. Kaczor, Katarzyna Patrycja Dzik, Wieslaw Ziolkowski, Damian Jozef Flis |
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| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
Bioenergetics
medicine.disease_cause bioenergetics lcsh:Chemistry Mice Superoxide Dismutase-1 Citrate synthase Amyotrophic lateral sclerosis lcsh:QH301-705.5 Spectroscopy biology exercise Chemistry Neurodegeneration neurodegeneration General Medicine Computer Science Applications Mitochondria medicine.anatomical_structure medicine.medical_specialty SOD1 Mice Transgenic Oxidative phosphorylation Catalysis Article Inorganic Chemistry Electron Transport Complex IV Internal medicine medicine Animals Humans Muscle Strength Physical and Theoretical Chemistry Muscle Skeletal Molecular Biology Swimming Organic Chemistry Amyotrophic Lateral Sclerosis Skeletal muscle medicine.disease Disease Models Animal Oxidative Stress Endocrinology lcsh:Biology (General) lcsh:QD1-999 biology.protein ALS Energy Metabolism Oxidative stress Biomarkers |
| Zdroj: | International Journal of Molecular Sciences Volume 20 Issue 2 International Journal of Molecular Sciences, Vol 20, Iss 2, p 233 (2019) |
| ISSN: | 1422-0067 |
| Popis: | Metabolic reprogramming in skeletal muscles in the human and animal models of amyotrophic lateral sclerosis (ALS) may be an important factor in the diseases progression. We hypothesized that swim training, a modulator of cellular metabolism via changes in muscle bioenergetics and oxidative stress, ameliorates the reduction in muscle strength in ALS mice. In this study, we used transgenic male mice with the G93A human SOD1 mutation B6SJL-Tg (SOD1G93A) 1Gur/J and wild type B6SJL (WT) mice. Mice were subjected to a grip strength test and isolated skeletal muscle mitochondria were used to perform high-resolution respirometry. Moreover, the activities of enzymes involved in the oxidative energy metabolism and total sulfhydryl groups (as an oxidative stress marker) were evaluated in skeletal muscle. ALS reduces muscle strength (&minus 70% between 11 and 15 weeks, p < 0.05), modulates muscle metabolism through lowering citrate synthase (CS) (&minus 30% vs. WT, p = 0.0007) and increasing cytochrome c oxidase and malate dehydrogenase activities, and elevates oxidative stress markers in skeletal muscle. Swim training slows the reduction in muscle strength (&minus 5% between 11 and 15 weeks) and increases CS activity (+26% vs. ALS I, p = 0.0048). Our findings indicate that swim training is a modulator of skeletal muscle energy metabolism with concomitant improvement of skeletal muscle function in ALS mice. |
| Databáze: | OpenAIRE |
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