ArticleScientific reports2018
Swimming Exercise and Transient Food Deprivation in Caenorhabditis elegans Promote Mitochondrial Maintenance and Protect Against Chemical-Induced Mitotoxicity.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 49 citations in OpenAlex.
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- Seminar: Functional Exposomics and Mechanisms of Toxicity-Insights from Model Systems and NAMs.Environmental health perspectives · 2024Review
- Comprehensive characterization of mitochondrial bioenergetics at different larval stages reveals novel insights about the developmental metabolism ofbioRxiv : the preprint server for biology · 2024Article
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- The consequences of tetraploidy on Caenorhabditis elegans physiology and sensitivity to chemotherapeutics.Scientific reports · 2023Article
- 3'sialyllactose and 6'sialyllactose enhance performance in endurance-type exercise through metabolic adaptation.Food science & nutrition · 2023Article
- Mitochondria in the Spotlight:Cells · 2023Review
- Twenty-four hour rhythmicity in mitochondrial network connectivity and mitochondrial respiration; a study in human skeletal muscle biopsies of young lean and older individuals with obesity.Molecular metabolism · 2023Article
- Acoustic streaming enabled moderate swimming exercise reduces neurodegeneration inScience advances · 2023Article
- Exercise preserves physical fitness during aging through AMPK and mitochondrial dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
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- Long-Term Culture and Monitoring of Isolated Caenorhabditis elegans on Solid Media in Multi-Well Devices.Journal of visualized experiments : JoVE · 2022Article
- A hierarchical process model links behavioral aging and lifespan in C. elegans.PLoS computational biology · 2022Article
- Exercise and the Brain: Lessons From Invertebrate Studies.Frontiers in behavioral neuroscience · 2022Review
- Exercise/Resistance Training and Muscle Stem Cells.Endocrinology and metabolism (Seoul, Korea) · 2021Article
- GWAS reveal a role for the central nervous system in regulating weight and weight change in response to exercise.Scientific reports · 2021Article
- Spaceflight affects neuronal morphology and alters transcellular degradation of neuronal debris in adultiScience · 2021Article
- Multiple metabolic changes mediate the response of Caenorhabditis elegans to the complex I inhibitor rotenone.Toxicology · 2021Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Exercise and caloric restriction improve health, including reducing risk of cardiovascular disease, neurological disease, and cancer. However, molecular mechanisms underlying these protections are poorly understood, partly due to the cost and time investment of mammalian long-term diet and exercise intervention studies. We subjected Caenorhabditis elegans nematodes to a 6-day, twice daily swimming exercise regimen, during which time the animals also experienced brief, transient food deprivation. Accordingly, we included a non-exercise group with the same transient food deprivation, a non-exercise control with ad libitum access to food, and a group that exercised in food-containing medium. Following these regimens, we assessed mitochondrial health and sensitivity to mitochondrial toxicants. Exercise protected against age-related decline in mitochondrial morphology in body-wall muscle. Food deprivation increased organismal basal respiration; however, exercise was the sole intervention that increased spare respiratory capacity and proton leak. We observed increased lifespan in exercised animals compared to both control and transiently food-deprived nematodes. Finally, exercised animals (and to a lesser extent, transiently food-deprived animals) were markedly protected against lethality from acute exposures to the mitotoxicants rotenone and arsenic. Thus, swimming exercise and brief food deprivation provide effective intervention in C. elegans, protecting from age-associated mitochondrial decline and providing resistance to mitotoxicant exposures.
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