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Supramaximal Intensity Hypoxic Exercise and Vascular Function Assessment in Mice
Published on: March 15, 2019
Strain differences in response to acute hypoxia: CD-1 versus C57BL/6J mice
Charles F Zwemer1, Michael Y Song, Katari A Carello
1Department of Biology, Dickinson College, Carlisle, Pennsylvania, USA.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|August 19, 2006
Summary
Mice strains show different responses to low oxygen. C57BL/6J mice enhance survival by switching fuel sources, while CD-1 mice reduce metabolic demand, demonstrating distinct hypoxic tolerance strategies.
Area of Science:
- Physiology
- Comparative Biology
- Metabolic Science
Background:
- Mammalian hypoxia response varies, with reduced metabolic demand or increased oxygen efficiency.
- The relative effectiveness of these strategies for hypoxic tolerance remains debated.
Purpose of the Study:
- To compare hypoxic tolerance strategies in two mouse strains: CD-1 (lowers demand) and C57BL/6J (maximizes efficiency).
- To investigate the physiological mechanisms underlying differential hypoxic tolerance.
Main Methods:
- Used unanesthetized adult male CD-1 and C57BL/6J mice.
- Assessed hypoxic tolerance through survival times under severe hypoxia (4.5% O2).
- Utilized indirect calorimetry and plasma ketone assays to analyze metabolic responses to hypoxic conditioning.
Main Results:
- C57BL/6J mice exhibited significantly longer survival under hypoxia than CD-1 mice, both naturally and after hypoxic conditioning.
- Hypoxic conditioning increased hypoxic tolerance 10-fold in C57BL/6J mice, compared to a smaller increase in CD-1 mice.
- C57BL/6J mice maintained oxygen consumption by switching to ketone metabolism, while CD-1 mice reduced metabolic rate.
Conclusions:
- Maximizing oxygen efficiency through fuel switching (ketones) while maintaining oxygen consumption provides a greater survival advantage during severe hypoxia than reducing metabolic demand.
- C57BL/6J mice demonstrate a superior adaptive strategy for severe hypoxia tolerance compared to CD-1 mice.
