The prior R29 award underwrote the first independent investigations, helped establish our research, and led to innovative findings on baroreflex control with aging and habitual exercise. We fully addressed the aims of the prior award by devising and perfecting our baroreflex methodology and by demonstrating the importance of vagal neural control in the age-related decrement and activity -related maintenance of baroreflex function. In addition, we found an important reciprocal relation between decreased cardiac vagal function and elevated vascular sympathetic outflow with age. A reciprocity suggests cardiovagal function determines the resting level of and baroreflex control of vascular sympathetic outflow. Since high sympathetic outflow relates to cardiovascular risk, this is germane to aging in the presence of coronary disease. If increased vagal control reduces sympathetic outflow, strategies that increase cardiovagal baroreflex function would be doubly beneficial. We seek renewed funding to: determine if reciprocity between baroreflex cardiac vagal and vascular sympathetic function is evident in older trained individuals and if altering the vagal state modifies sympathetic outflow and control in young and older healthy volunteers and in older trained individuals; determine the effects of coronary disease on the reciprocity between vagal and sympathetic baroreflex control; and, determine the effects of 6 months of aerobic exercise training on vagal and baroreflex function in older individuals and in coronary patients. Young (20-30 yrs) healthy volunteers, older (55-75 yrs) masters athletes (whom we have successfully studied in the past), older healthy individuals (who have been thoroughly screened for cardiovascular disease), and stable, revascularized coronary disease patients (based on previous MI or coronary angiography, and screened for heart failure) will be recruited to achieve these aims. Based on our previous work, we hypothesize that healthy older individuals with high vagal capacity (i.e., masters athletes) will have sympathetic outflow and control comparable to young individuals. Further, this reciprocal relation will allow manipulation of sympathetic outflow and control by enhancing (via drug or exercise) or depressing (via drug) vagal tone. Based on preliminary findings, we hypothesize greater vascular stiffness in coronary patients will relate to higher resting sympathetic outflow, but that increasing cardiovagal function with exercise will decrease sympathetic outflow in both coronary patients and healthy older individuals. This work will inform the striking incongruence between increased resting sympathetic outflow and apparently, maintained sympathetic baroreflex gain with age. Moreover, if increased vagal function results in reduced sympathetic outflow, exercise should result in an autonomic profile more favorable to cardiovascular health. We seek renewed funding to examine fully sympatho-vagal interactions with age and disease and prospectively assess the effects of exercise.