Vascular Dysfunction, Inflammation, and Exercise in Diabetes

Normal vascular function is characterized by a continuous interaction between the endothelium and vascular smooth muscle that maintains optimal vascular tone and organ perfusion via balanced vasodilatory and vasoconstrictive mechanisms. In an environment of chronic hyperglycemia, such as that occurring in diabetes mellitus, normal vascular function is disrupted most likely due to elevations in reactive oxygen species and the compounding effects of vascular inflammation. Such vascular dysfunctions represent key mechanisms for atherosclerotic changes and primary events in the pathogenesis of cardiovascular disease, which remains the single leading cause of mortality for those with type 1 or type 2 diabetes. Exercise has been described as a cornerstone in the management and treatment of diabetes due to its prominent role in improving both metabolic and cardiovascular health. Evidence suggests that habitual physical activity disrupts chronic hyperglycemic by improving glycemic control via enhanced GLUT protein activation and increased insulin sensitivity. Furthermore, exercise-mediated shear stress may enhance vasodilatory capacity by improving expression of endothelial nitric oxide synthase proteins and enhancing nitric oxide bioavailability. Although some specific precautions must be adhered to when prescribing exercise to diabetic populations, the benefits significantly outweigh the consequences of continuing a sedentary lifestyle. This chapter will present a non-exhaustive review focusing on changes in vascular function and inflammatory status from healthy to diabetic states, techniques that are often implemented to quantify such changes in vascular function, and the role of exercise in improving underlying mechanisms critical to maintaining normal vascular function and disrupting the pathogenesis of cardiovascular disease.