ArticleAmerican journal of physiology. Cell physiology2009
Conditional knockout of Mn-SOD targeted to type IIB skeletal muscle fibers increases oxidative stress and is sufficient to alter aerobic exercise capacity.
Article in American journal of physiology. Cell physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 78 citations in OpenAlex.
- Trial
- Mitochondrial oxidative stress in skeletal muscle alters metabolic signaling responses to acute muscle contraction.Free radical biology & medicine · 2026Article
- Unacylated Ghrelin Protects Against Age-Related Loss of Muscle Mass and Contractile Dysfunction in Skeletal Muscle.Aging cell · 2024Article
- Mouse models used to test the role of reactive oxygen species in aging and age-related chronic diseases.Free radical biology & medicine · 2024Review
- Axonal mitochondria regulate gentle touch response through control of axonal actin dynamics.bioRxiv : the preprint server for biology · 2024Article
- Impact of a Whole-Food, High-Soluble Fiber Diet on the Gut-Muscle Axis in Aged Mice.Nutrients · 2024Article
- The persistence of stress-induced physical inactivity in rats: an investigation of central monoamine neurotransmitters and skeletal muscle oxidative stress.Frontiers in behavioral neuroscience · 2023Article
- Acylated Ghrelin Receptor Agonist HM01 Decreases Lean Body and Muscle Mass, but Unacylated Ghrelin Protects against Redox-Dependent Sarcopenia.Antioxidants (Basel, Switzerland) · 2022Article
- Article
- Selective Ablation ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Cytosolic adaptation to mitochondria-induced proteostatic stress causes progressive muscle wasting.iScience · 2022Article
- Sestrins are evolutionarily conserved mediators of exercise benefits.Nature communications · 2020Article
- Mitochondrial-targeted methionine sulfoxide reductase overexpression increases the production of oxidative stress in mitochondria from skeletal muscle.Aging pathobiology and therapeutics · 2020Article
- Genome-Wide Identification and Characterization ofMarine drugs · 2019Article
- Muscle strength is increased in mice that are colonized with microbiota from high-functioning older adults.Experimental gerontology · 2019Article
- Mitochondrial oxidative stress impairs contractile function but paradoxically increases muscle mass via fibre branching.Journal of cachexia, sarcopenia and muscle · 2019Article
- Juzentaihoto hot water extract alleviates muscle atrophy and improves motor function in streptozotocin-induced diabetic oxidative stress mice.Journal of natural medicines · 2019Article
- Base-excision repair deficiency alone or combined with increased oxidative stress does not increase mtDNA point mutations in mice.Nucleic acids research · 2018Article
- Redox homeostasis and age-related deficits in neuromuscular integrity and function.Journal of cachexia, sarcopenia and muscle · 2017Review
- On the Origin of Superoxide Dismutase: An Evolutionary Perspective of Superoxide-Mediated Redox Signaling.Antioxidants (Basel, Switzerland) · 2017Review
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Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
Abstract
In vitro studies of isolated skeletal muscle have shown that oxidative stress is limiting with respect to contractile function. Mitochondria are a potential source of muscle function-limiting oxidants. To test the hypothesis that skeletal muscle-specific mitochondrial oxidative stress is sufficient to limit muscle function, we bred mice expressing Cre recombinase driven by the promoter for the inhibitory subunit of troponin (TnIFast-iCre) with mice containing a floxed Sod2 (Sod2(fl/fl)) allele. Mn-SOD activity was reduced by 82% in glycolytic (mainly type II) muscle fiber homogenates from young TnIFastCreSod2(fl/fl) mice. Furthermore, Mn-SOD content was reduced by 70% only in type IIB muscle fibers. Aconitase activity was decreased by 56%, which suggests an increase in mitochondrial matrix superoxide. Mitochondrial superoxide release was elevated more than twofold by mitochondria isolated from glycolytic skeletal muscle in TnIFastCreSod2(fl/fl) mice. In contrast, the rate of mitochondrial H(2)O(2) production was reduced by 33%, and only during respiration with complex II substrate. F(2)-isoprostanes were increased by 36% in tibialis anterior muscles isolated from TnIFastCreSod2(fl/fl) mice. Elevated glycolytic muscle-specific mitochondrial oxidative stress and damage in TnIFastCreSod2(fl/fl) mice were associated with a decreased ability of the extensor digitorum longus and gastrocnemius muscles to produce contractile force as a function of time, whereas force production by the soleus muscle was unaffected. TnIFastCreSod2(fl/fl) mice ran 55% less distance on a treadmill than wild-type mice. Collectively, these data suggest that elevated mitochondrial oxidative stress and damage in glycolytic muscle fibers are sufficient to reduce contractile muscle function and aerobic exercise capacity.
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