Jeffrey J Hsu1, Felicia Fong1, Radha Patel1, Rong Qiao1, Karen Lo1, Akrivoula Soundia2, Chih-Chiang Chang3, Victoria Le1, Chi-Hong Tseng1, Linda L Demer1,3,4, Yin Tintut5,6,7,8. 1. Department of Medicine, University of California, Los Angeles, Los Angeles, CA, USA. 2. School of Dentistry, University of California, Los Angeles, Los Angeles, CA, USA. 3. Department of Bioengineering, University of California, Los Angeles, Los Angeles, CA, USA. 4. Department of Physiology, University of California, Los Angeles, Los Angeles, CA, USA. 5. Department of Medicine, University of California, Los Angeles, Los Angeles, CA, USA. ytintut@mednet.ucla.edu. 6. Department of Physiology, University of California, Los Angeles, Los Angeles, CA, USA. ytintut@mednet.ucla.edu. 7. Department of Orthopaedic Surgery, University of California, Los Angeles, Los Angeles, CA, USA. ytintut@mednet.ucla.edu. 8. Center for the Health Sciences A2-237, David Geffen School of Medicine, University of California, Los Angeles, 10833 Le Conte Ave, Los Angeles, CA, 90095-1679, USA. ytintut@mednet.ucla.edu.
Abstract
BACKGROUND: Despite the association of physical activity with improved cardiovascular outcomes and the association of high coronary artery calcification (CAC) scores with poor prognosis, elite endurance athletes have increased CAC. Yet, they nevertheless have better cardiovascular survival. We hypothesized that exercise may transform vascular calcium deposits to a more stable morphology. METHODS: To test this, hyperlipidemic mice (Apoe-/-) with baseline aortic calcification were separated into 2 groups (n = 9/group) with control mice allowed to move ad-lib while the exercise group underwent a progressive treadmill regimen for 9 weeks. All mice underwent blood collections and in vivo 18F-NaF μPET/μCT imaging both at the start and end of the exercise regimen. At euthanasia, aortic root specimens were obtained for histomorphometry. RESULTS: Results showed that, while aortic calcification progressed similarly in both groups based on µCT, the fold change in 18F-NaF density was significantly less in the exercise group. Histomorphometric analysis of the aortic root calcium deposits showed that the exercised mice had a lower mineral surface area index than the control group. The exercise regimen also raised serum PTH levels twofold. CONCLUSION: These findings suggest that weeks-long progressive exercise alters the microarchitecture of atherosclerotic calcium deposits by reducing mineral surface growth, potentially favoring plaque stability.
BACKGROUND: Despite the association of physical activity with improved cardiovascular outcomes and the association of high coronary artery calcification (CAC) scores with poor prognosis, elite endurance athletes have increased CAC. Yet, they nevertheless have better cardiovascular survival. We hypothesized that exercise may transform vascular calcium deposits to a more stable morphology. METHODS: To test this, hyperlipidemic mice (Apoe-/-) with baseline aortic calcification were separated into 2 groups (n = 9/group) with control mice allowed to move ad-lib while the exercise group underwent a progressive treadmill regimen for 9 weeks. All mice underwent blood collections and in vivo 18F-NaF μPET/μCT imaging both at the start and end of the exercise regimen. At euthanasia, aortic root specimens were obtained for histomorphometry. RESULTS: Results showed that, while aortic calcification progressed similarly in both groups based on µCT, the fold change in 18F-NaF density was significantly less in the exercise group. Histomorphometric analysis of the aortic root calcium deposits showed that the exercised mice had a lower mineral surface area index than the control group. The exercise regimen also raised serum PTH levels twofold. CONCLUSION: These findings suggest that weeks-long progressive exercise alters the microarchitecture of atherosclerotic calcium deposits by reducing mineral surface growth, potentially favoring plaque stability.
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