Long-Term Exercise Stabilizes Atherosclerotic Plaque in ApoE Knockout Mice

Exercise is known to reduce cardiovascular mortality. However, the precise mechanisms are still unknown. Because atherosclerotic plaque destabilization and rupture leads to dramatic cardiovascular events, stabilization of plaque might be regarded as an important goal of an exercise preventive therap...

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Published in:Medicine and science in sports and exercise 2009-12, Vol.41 (12), p.2128-2135
Main Authors: PELLEGRIN, Maxime, MIGUET-ALFONSI, Carole, BOUZOURENE, Karima, AUBERT, Jean-François, DECKERT, Valérie, BERTHELOT, Alain, MAZZOLAI, Lucia, LAURANT, Pascal
Format: Article
Language:English
Subjects:
Animals
Apolipoproteins E - physiology
Atherosclerosis - physiopathology
Atherosclerosis - prevention & control
Biological and medical sciences
Blotting, Western
Fundamental and applied biological sciences. Psychology
Immunochemistry
Lipids - blood
Male
Mice
Mice, Knockout
Muscle, Skeletal - metabolism
Oxidative Stress - physiology
Random Allocation
Sedentary Lifestyle
Space life sciences
Swimming - physiology
Vertebrates: body movement. Posture. Locomotion. Flight. Swimming. Physical exercise. Rest. Sports
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Summary:Exercise is known to reduce cardiovascular mortality. However, the precise mechanisms are still unknown. Because atherosclerotic plaque destabilization and rupture leads to dramatic cardiovascular events, stabilization of plaque might be regarded as an important goal of an exercise preventive therapy. The present study examined the plaque-stabilizing effect of long-term exercise in experimental atherosclerosis using apolipoprotein E-deficient mice (ApoE(-/-)). ApoE(-/-) mice were subjected to 6 months of swimming exercise. A group of sedentary animals were used as controls. Morphometry and characteristics of atherosclerotic plaque stability were assessed in aortic sinus by immunohistochemistry. Aortic levels of total protein kinase Akt (protein kinase B), phosphorylated Akt at Ser(473) (p-Akt), total endothelial nitric oxide synthase (eNOS), and phosphorylated eNOS at Ser(1177) (p-eNOS) were assessed by Western blotting. Exercised mice developed a more stable plaque phenotype as shown by decreased macrophage and increased smooth muscle cell content. Protein expressions of Akt, p-Akt, eNOS, and p-eNOS were not modulated by exercise. Long-term exercise promotes plaque stability in ApoE(-/-) mice. The Akt-mediated eNOS phosphorylation pathway seems not to be the primary molecular mechanism.
ISSN:0195-9131
1530-0315
DOI:10.1249/mss.0b013e3181a8d530