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Updated: May 31, 2026

Activating Autophagy by Aerobic Exercise in Mice
Published on: February 3, 2017
Acute exercise activates AMPK and eNOS in the mouse aorta.
José M Cacicedo1, Marie-Soleil Gauthier, Nathan K Lebrasseur
1Diabetes and Metabolism Research Unit, Department of Medicine and Section of Endocrinology, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
An acute bout of exercise activates AMP-activated protein kinase (AMPK) and endothelial nitric oxide synthase (eNOS) in mouse aortas. This study suggests AMPK is the principal activator of eNOS, potentially mediated by SIRT1-LKB1 and CaMKKβ.
Area of Science:
- Cardiovascular physiology
- Molecular biology
- Exercise science
Background:
- Exercise confers protection against endothelial cell (EC) dysfunction and atherosclerosis.
- The underlying molecular mechanisms remain incompletely understood.
Purpose of the Study:
- To investigate whether acute exercise activates key enzymes like AMP-activated protein kinase (AMPK) and endothelial nitric oxide synthase (eNOS) in ECs.
- To determine if exercise modulates known regulators of these enzymes.
Main Methods:
- C57BL/6 mice subjected to a single bout of exhaustive treadmill exercise.
- Analysis of aortas for activation of AMPK, its regulatory proteins, eNOS, and other eNOS-activating kinases.
- Immunohistochemical analysis of ECs within the aorta.
Main Results:
- Acute exercise activated both AMPK and eNOS in the entire aorta.
- Activation levels correlated with exercise duration and the activation of AMPK regulators silent information regulator-1 (SIRT1)-LKB1 and CaMKKβ.
- Other eNOS-activating kinases (Akt, PKA, PKG, Src) remained unaffected; AMPK and eNOS activation was confirmed in aortic ECs.
Conclusions:
- This study provides the first evidence of acute exercise-induced activation of AMPK and eNOS in aortic endothelium.
- AMPK appears to be the primary activator of eNOS following exercise.
- SIRT1-LKB1 and CaMKKβ may mediate AMPK activation in this context.
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