Abstract

Objective Physical activity is associated with improved carotid atherosclerosis in spinal cord injury (SCI) subjects independent of variation in hemodynamic, metabolic and inflammatory variables. The present study investigated the role of oxidized low-density lipoprotein (Ox-LDL), matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs) in this regard. Design and Methods We studied 40 men with chronic (>1 year of injury) SCI and no voluntary motor activity [17 sedentary (47% tetraplegic) and 23 athletes (52% tetraplegic)] by clinical, anthropometric, laboratory (glucose, lipid profile and C-reactive protein), hemodynamic (blood pressure and cardiac output) and carotid ultrasound analysis. All enrolled subjects were normotensive, non-diabetics, non-smokers and normolipemic. Plasmatic Ox-LDL, MMP2, MMP8, MMP9, TIMP1 and TIMP2 were determined by ELISA. Data are presented as mean±SEM. A p-value <0.05 was considered significant. Results Sedentary SCI subjects and SCI athletes presented similar clinical, anthropometric, laboratory and hemodynamic features. Carotid intima-media thickness (IMT) of SCI athletes was lower than that of SCI sedentary individuals (0.54±0.01 vs 0.69±0.02 mm; p<0.001). SCI athletes presented lower Ox-LDL (38.4±2.1 vs 54.1±4.1 U/L; p<0.001) levels in comparison with SCI sedentary individuals. Conversely, MMPs and TIMPs levels as were as MMP8/TIMP1, MMP9/TIMP1 and MMP2/TIMP2 ratios were similar between the SCI groups. Bivariate correlation analysis including all SCI subjects showed that carotid IMT correlated with Ox-LDL (r=0.54; p<0.001), but not with any MMPs or MMP/TIMP ratios. Further linear regression analysis adjusted for the presence or not of physical activity showed that Ox-LDL was still associated with carotid IMT (beta=0.293±0.141; p=0.044) in the whole sample. Conclusions Plasmatic Ox-LDL levels are associated with increased carotid IMT in SCI subjects and are lower in physically active SCI individuals than in sedentary SCI ones. These findings may provide a potential mechanism by which physical activity attenuates SCI-induced atherosclerosis.

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