Swimming Exercise and Transient Food Deprivation in Caenorhabditis elegans Promote Mitochondrial Maintenance and Protect Against Chemical-Induced Mitotoxicity.
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.
Type
Journal articlePermalink
https://hdl.handle.net/10161/17077Published Version (Please cite this version)
10.1038/s41598-018-26552-9Publication Info
Hartman, Jessica H; Smith, Latasha L; Gordon, Kacy L; Laranjeiro, Ricardo; Driscoll,
Monica; Sherwood, David R; & Meyer, Joel N (2018). Swimming Exercise and Transient Food Deprivation in Caenorhabditis elegans Promote
Mitochondrial Maintenance and Protect Against Chemical-Induced Mitotoxicity. Scientific reports, 8(1). 10.1038/s41598-018-26552-9. Retrieved from https://hdl.handle.net/10161/17077.This is constructed from limited available data and may be imprecise. To cite this
article, please review & use the official citation provided by the journal.
Collections
More Info
Show full item recordScholars@Duke
Joel Meyer
Professor of Environmental Genomics in the Division of Environmental Sciences and
Policy
Dr. Meyer studies the effects of toxic agents and stressors on human and wildlife
health. He is particularly interested in understanding the mechanisms by which environmental
agents cause DNA damage, the molecular processes that organisms employ to protect
prevent and repair DNA damage, and genetic differences that may lead to increased
or decreased sensitivity to DNA damage. Mitochondrial DNA damage and repair, as well
as mitochondrial function in general, are a particular focus. He studies
David R. Sherwood
Jerry G. and Patricia Crawford Hubbard Professor
The Sherwood lab is interested in understanding mechanisms that drive dynamic cellular
behaviors underlying normal development and human disease. We study 1) How cells invade
into tissues, 2) How stem cells interact with their niches, and 3) How cells control
and interact with extracellular matrix. Our lab primarily examines C. elegans development,
in which simple cellular complexity, amenability to geneti
Alphabetical list of authors with Scholars@Duke profiles.

Articles written by Duke faculty are made available through the campus open access policy. For more information see: Duke Open Access Policy
Rights for Collection: Scholarly Articles
Works are deposited here by their authors, and represent their research and opinions, not that of Duke University. Some materials and descriptions may include offensive content. More info