ArticlePloS one2017
Skeletal muscle metabolic adaptations to endurance exercise training are attainable in mice with simvastatin treatment.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- Structural basis for simvastatin-induced skeletal muscle weakness associated with type 1 ryanodine receptor T4709M mutation.The Journal of clinical investigation · 2025Article
- Brain-derived neurotrophic factor drives muscle adaptation similar to aerobic training in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Advancing β-adrenoreceptor agonism for recovery after volumetric muscle loss through regenerative rehabilitation and biomaterial delivery approaches.Regenerative biomaterials · 2025Article
- Relationships between endurance exercise training-induced muscle fiber-type shifting and autophagy in slow- and fast-twitch skeletal muscles of mice.Physical activity and nutrition · 2024Article
- Migration increases mitochondrial oxidative capacity without increasing reactive oxygen species emission in a songbird.The Journal of experimental biology · 2024Article
- Social jet lag impairs exercise volume and attenuates physiological and metabolic adaptations to voluntary exercise training.Journal of applied physiology (Bethesda, Md. : 1985) · 2024Article
- Resistance wheel running improves contractile strength, but not metabolic capacity, in a murine model of volumetric muscle loss injury.Experimental physiology · 2023Article
- Mitochondrial Fission as a Therapeutic Target for Metabolic Diseases: Insights into Antioxidant Strategies.Antioxidants (Basel, Switzerland) · 2023Review
- Pharmaceutical Agents for Contractile-Metabolic Dysfunction After Volumetric Muscle Loss.Tissue engineering. Part A · 2022Article
- Mitochondrial Dysfunctions and Potential Molecular Markers in Sport Horses.International journal of molecular sciences · 2022Review
- Impact of Atorvastatin on Skeletal Muscle Mitochondrial Activity, Locomotion and Axonal Excitability-Evidence fromInternational journal of molecular sciences · 2022Article
- Effect of statin treatment in obese selenium-supplemented mice lacking selenocysteine lyase.Molecular and cellular endocrinology · 2021Article
- The impact of statin therapy and aerobic exercise training on skeletal muscle and whole-body aerobic capacity.American heart journal plus : cardiology research and practice · 2021Article
- Optogenetic activation of muscle contractionConnective tissue research · 2021Article
- Skeletal muscle effects of two different 10-week exercise regimens, voluntary wheel running, and forced treadmill running, in mice: A pilot study.Physiological reports · 2020Article
- Mitochondrial dysfunction in skeletal muscle of fukutin-deficient mice is resistant to exercise- and 5-aminoimidazole-4-carboxamide ribonucleotide-induced rescue.Experimental physiology · 2020Article
- Impact of aerobic exercise type on blood flow, muscle energy metabolism, and mitochondrial biogenesis in experimental lower extremity artery disease.Scientific reports · 2020Article
- Exercise Training Protects against Atorvastatin-Induced Skeletal Muscle Dysfunction and Mitochondrial Dysfunction in the Skeletal Muscle of Rats.Journal of clinical medicine · 2020Article
- Mitochondrial-specific autophagy linked to mitochondrial dysfunction following traumatic freeze injury in mice.American journal of physiology. Cell physiology · 2020Article
- What and How Can Physical Activity Prevention Function on Parkinson's Disease?Oxidative medicine and cellular longevity · 2020Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We tested the hypothesis that a 6-week regimen of simvastatin would attenuate skeletal muscle adaptation to low-intensity exercise. Male C57BL/6J wildtype mice were subjected to 6-weeks of voluntary wheel running or normal cage activities with or without simvastatin treatment (20 mg/kg/d, n = 7-8 per group). Adaptations in in vivo fatigue resistance were determined by a treadmill running test, and by ankle plantarflexor contractile assessment. The tibialis anterior, gastrocnemius, and plantaris muscles were evaluated for exercised-induced mitochondrial adaptations (i.e., biogenesis, function, autophagy). There was no difference in weekly wheel running distance between control and simvastatin-treated mice (P = 0.51). Trained mice had greater treadmill running distance (296%, P<0.001), and ankle plantarflexor contractile fatigue resistance (9%, P<0.05) compared to sedentary mice, independent of simvastatin treatment. At the cellular level, trained mice had greater mitochondrial biogenesis (e.g., ~2-fold greater PGC1α expression, P<0.05) and mitochondrial content (e.g., 25% greater citrate synthase activity, P<0.05), independent of simvastatin treatment. Mitochondrial autophagy-related protein contents were greater in trained mice (e.g., 40% greater Bnip3, P<0.05), independent of simvastatin treatment. However, Drp1, a marker of mitochondrial fission, was less in simvastatin treated mice, independent of exercise training, and there was a significant interaction between training and statin treatment (P<0.022) for LC3-II protein content, a marker of autophagy flux. These data indicate that whole body and skeletal muscle adaptations to endurance exercise training are attainable with simvastatin treatment, but simvastatin may have side effects on muscle mitochondrial maintenance via autophagy, which could have long-term implications on muscle health.
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Registered trials
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