Abstract
AMP-activated protein kinase (AMPK) plays a critical role in maintaining energy homeostasis and cardiac function during ischemia in the heart. However, the functional role of AMPK in the heart during exercise is unknown. We examined whether acute exercise increases AMPK activity in mouse hearts and determined the significance of these increases by studying transgenic (TG) mice expressing a cardiac-specific dominant-negative (inactivating) AMPKα2 subunit. Exercise increased cardiac AMPKα2 activity in the wild type mice but not in TG. We found that inactivation of AMPK did not result in abnormal ATP and glycogen consumption during exercise, cardiac function assessed by heart rhythm telemetry and stress echocardiography, or in maximal exercise capacity.
Original language | English (US) |
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Pages (from-to) | 2045-2050 |
Number of pages | 6 |
Journal | FEBS Letters |
Volume | 579 |
Issue number | 10 |
DOIs | |
State | Published - Apr 11 2005 |
Externally published | Yes |
Keywords
- AMP-activated protein kinase
- Acetyl CoA carboxylase
- Exercise
- Heart
- p38
ASJC Scopus subject areas
- Biophysics
- Structural Biology
- Biochemistry
- Molecular Biology
- Genetics
- Cell Biology