2016 Participants
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NAME: Amber Bryant

The Na/K-ATPase creates transmembrane ion gradients and is important to cell function and survival. The Na/K-ATPase is also the specific receptor for cardiac glycosides (CG) such as ouabain and digoxin. At high concentration, CG specifically inhibit the ion-pumping function of Na/K-ATPase, which is the molecular basis of their use to increase cardiac contractility in the management of congestive heart failure. At low concentrations that do not alter intracellular ion concentrations, CG also activate the newly recognized receptor function of Na/K-ATPase α1 and modulate intracellular signaling proteins. Evidence for endogenous forms of CG and their increased levels during exercise have been reported.
The aim of this research is to test the hypothesis that endogenous CG act on Na/K-ATPase α1 to increase exercise performance
To test this hypothesis, exercise performance of mice genetically engineered to be sensitive to endogenous CG (Na/K-ATPase α1 s/s) will be compared to control littermate mice that are naturally resistant to endogenous CG (α1 r/r) before and after 5 weeks of endurance training on a treadmill.

 

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