Long-Term Exercise Stabilizes Atherosclerotic Plaque in ApoE Knockout Mice

• 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
• ISSN: 0195-9131; 1530-0315
• DOI: 10.1249/mss.0b013e3181a8d530

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.