Racial differences in cardiovascular responses following an acute bout of aerobic exercise

African-Americans (AA) are at greater risk than Caucasians (CA) for developing hypertension, cardiovascular disease, stroke and renal disease. An acute bout of moderate aerobic exercise causes a sustained reduction in blood pressure (BP), termed post-exercise hypotension (PEH) in CA. Histamine receptors 1 and 2 (H1R and H2R) have been shown to be responsible for post exercise vasodilation and associated PEH in Caucasians. It appears that AA women may not exhibit PEH following aerobic exercise. Hence, this study sought to determine the extent to which AA develop PEH, and the contribution of histamine receptors to PEH (or lack thereof) in this population. Forty-nine (9 AA men, 13 AA women, 14 CA men and 13 CA women) young and healthy subjects completed the study. Subjects were randomly assigned to take either a combined H1R and H2R antagonist (fexofenadine and ranitidine) or a control placebo followed by the other condition on the second visit between 3 pm to 8 pm. During study visits, subjects rested in the supine position for baseline BP, cardiac output, peripheral resistance and arterial stiffness measurements and 30 min, 60 min and 90 min after 45 min of treadmill exercise at 70% HRreserve. An acute bout of aerobic exercise increases DBP in young AA but not in CA. The underlying mechanism for the BP increases may be related to increases in brachial artery stiffness and sympathetic activation and but not to changes in cardiac output. Moreover, DBP is also elevated in AA after exercise with histamine receptor blockade. Additionally, H1R and H2R blockade elicited differential responses in cardiac function and carotid artery between AA and CA following exercise, suggesting a potential role of histamine receptors in mediating post exercise BP in AA. Our study also indicates that central BP may better reflect the level of vascular burden in young AA than Brachial BP. The heightened BP and vascular responses to exercise stimulus may play a role in the pathogenesis of hypertension in AA