Journal
FEBS LETTERS
Volume 579, Issue 10, Pages 2045-2050Publisher
WILEY
DOI: 10.1016/j.febslet.2005.02.052
Keywords
AMP-activated protein kinase; acetyl CoA carboxylase; p38; heart; exercise
Funding
- NHLBI NIH HHS [HL67970] Funding Source: Medline
- NIAMS NIH HHS [AR45670] Funding Source: Medline
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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) AMPK alpha 2 subunit. Exercise increased cardiac AMPK alpha 2 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. (c) 2605 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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