African Americans have the highest incidence of essential hypertension (HT) than any racial group in the United States. The cause of this high prevalence of HIV in this population is not known. There is an undeniable genetic component to HT; however, this account for only a portion of the variance in blood pressure (BP) leading many researchers to emphasize the additional importance of environmental factors such as stress and physical inactivity. Studies have indicated that physically inactive individuals and offspring of hypertensive parents have an exaggerated BP response to stress. Demonstrations of abnormal increases in BP responsiveness to stress among normotensive individuals is of clinical importance in that such pressor reactivity is associated with the cause of or a marker for future development of HT. This abnormal increase in BP reactivity to stress in both sedentary individuals and offspring of hypertensive parents is attributed to an elevated sympathetic neural activity (SNA) which alters the cardiac output and or systemic vascular resistance. Aerobic physical activity intervention has been shown to decrease the SNA and thus may alter the pressor reactivity to stress. Whether a familial history of HT interact with physical activity to affect BP responses to stress in African Americans is not known. We hypothesize that aerobic physical activity intervention will attenuate the BP response to stress in sedentary normotensive young adult African Americans with a familial history of HIT. We further hypothesize that aerobic physical activity will attenuate the BP response to groups of sedentary normotensive young adult African Americans with a familial history of HT (n= 12 females and 12 males) and without a familial history of HT (n= 12 females and 12 males) will undergo a 12 week aerobic physical activity intervention program. Similar size sedentary groups with familial HT (12 females and 12 males) and without familial HT (12 females and 12 males) will not undergo the physical activity intervention and will serve as the control. Systolic Bp, diastolic BP, and mean arterial BP responses at baseline and during conditions of provocative mental and physical stress will be determined and analyzed for between-group differences. Maximal oxygen uptake, cardiac output, stroke volume, systemic vascular resistance, heart rate, cardiac autonomic outflow, and skeletal muscle blood flow will be measured to determine the possible mechanism(s) of observed effects. The pattern of responses observed will increase our understanding of the interaction of genetics, physical activity interventions, and stress in the control of BP, and the cardiovascular factors involved in BP control.
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