Though conventional wisdom suggests that a rise in blood pressure is a reality of advancing age, in fact, it appears that progressive elevation in sympathetic activity, not necessarily accompanied by increased blood pressure, is intrinsic to cardiovascular aging in humans. The mechanism behind this elevation would seem to reside in homeostatic cardiovascular regulation; nonetheless, the balance of factors that result in elevated sympathetic outflow with age remains elusive. Age-related increases in sympathetic nervous outflow cannot be fully explained by increases in body mass, body adiposity, or other metabolic factors; interrelations among cardiac output, peripheral resistance, and blood pressure may not reflect a determinative hemodynamic interrelation but rather parallel phenomena; and there is no simple linear relationship between baroreflex control and resting levels of sympathetic activity. In contrast to systemic relationships, available data suggest that elevated sympathetic outflow may derive from the inter-relationship between centrally driven sympathoexcitation and a decline in the ability of sympathetic outflow to effect peripheral vascular responses. This review aims to integrate the current knowledge of mechanisms underlying elevated sympathetic outflow with age. It seeks to synthesize these data in the context of proposing that an age-related decline in the ability of sympathetic outflow to effect regional vascular responses incites a compensatory elevation in resting sympathetic activity to maintain homeostatic balance, presumably to maintain adequate control of blood pressure.