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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #272031
Title: Lack of Nrf2 reduces voluntary exercise in mice: influences of sex and diet

Author
item Dekrey, Emilie
item Picklo, Matthew

Submitted to: Free Radicals in Biology and Medicine
Publication Type: Abstract Only
Publication Acceptance Date: 9/9/2011
Publication Date: 11/1/2011
Citation: Dekrey, E.E., Picklo, M.J. 2011. Lack of Nrf2 reduces voluntary exercise in mice: influences of sex and diet. Free Radicals in Biology and Medicine. SFRBM's 18th Annual Meeting: Program and Abstracts; 51(Supplement); S58.

Interpretive Summary:

Technical Abstract: Exercise is generally accepted to increase the generation of reactive oxygen species (ROS). However, the regulatory mechanisms that are involved in the adaptations occurring during exercise are not well understood. The Nrf2/antioxidant response element pathway adapts cells to elevated ROS. We tested the hypothesis that lack of Nrf2 transcription factor would decrease exercise capacity. We used wild type (WT) and Nrf2 knockout (KO) mice in a voluntary exercise model in which chow fed mice were maintained in a cage with a computer monitored, free-moving exercise wheel for 4 weeks. The average distance ran per day by male, Nrf2KO mice was 51% less than WT (2000 vs. 4100 meters). However, female WT and Nrf2KO mice ran similar distances, indicating a relationship between Nrf2 and sex. There was no difference in protein carbonyls, thiols, or total glutathione levels between male Nrf2KO and WT mice, suggesting that the reduced exercise capacity of male Nrf2KO mice was not due to elevated oxidative damage. While data indicate a relationship between Nrf2 and energy metabolism, we found no difference in activities of fructose 1,6-bisphosphate dehydrogenase and pyruvate kinase (main regulators of glycolysis) or in mitochondrial complex 1 protein content in liver or quadriceps of chow fed male WT or Nrf2KO mice. We did note a relationship between the distance run and the quadricep content of complex 1 protein in male Nrf2KO, but not WT mice. To determine if the dietary energy source altered exercise capacity we fed mice a high fat (45% fat calorie) diet prior to and during this exercise paradigm. In this case, running distances of the male WT and Nrf2KO mice were normalized. These data indicate an interaction of calorie sources and Nrf2. Our data demonstrate that Nrf2 influences voluntary exercise capacity through diet/energy metabolism and as yet unidentified sex-related mechanisms.