Baynard, Tracy

Exaggerated SBP responses to exercise testing are more frequent in Black than in White male adults. Such responses, if translatable to females, may detect early racial disparities arriving during menopause. Because the endothelium regulates BP and fibrinolytic responses, these could be linked during exercise. At peak exercise, Black but not White postmenopausal females had more exaggerated SPB responses regardless of reduced fibrinolytic potential. Maximal exercise unmasked risk factors for cardiovascular disease in Black postmenopausal females.

Acute exercise appears to have positive influence on arterial function during the recovery period, yet the effect of obesity is poorly understood in recovery. We examined the effects of an acute bout of exercise on arterial function in obese versus healthy weight individuals. Young (23 yr), lean (n=38, BMI=22.3 kg/m 2 ) and obese (n=20, BMI=34.0 kg/m 2 ) individuals had arterial measurements obtained at rest, and 15 and 30 min following a maximal bout of aerobic exercise. Arterial tonometry and ultrasound were used to obtain central BP, arterial compliance and stiffness (beta stiffness, elastic modulus (Ep), and central pulse wave velocity (PWV)). Despite similar central mean BP, the obese group had higher cPWV following exercise. Beta stiffness and Ep responded similarly to exercise between groups. Arterial compliance was higher in obese but the response in recovery was similar between groups. Lean Obese Pre 15‐min post 30‐min post Pre 15‐min post 30‐min post Mean aortic BP 82 83 82 87 86 87 Central PWV 5.67 5.46 5.35 5.84 6.11 6.16 Beta Stiffness 5.89 6.34 5.78 4.88 6.04 5.31 Elastic Modulus 69 75 67 67 78 66 In this young cohort, obesity was associated with increased central arterial stiffness, independent of BP, but higher arterial compliance. This suggests that measures of arterial stiffness provide differential information potentially associated with where in the arterial tree measures were made.

We examined the role of sympathetic activation in restraining vasodilatory responses to hyperinsulinemia and sustaining blood pressure in healthy adults. Data are reported from two separate experimental protocols in humans and one experimental protocol in isolated arteries from mice. Contrary to our hypothesis, the present findings support the idea that during hyperinsulinemia, a sympathetically mediated increase in cardiac output, rather than restraint of peripheral vasodilation, is the principal contributor to the maintenance of systemic blood pressure.