Decreased cutaneous vasodilation in aged skin: Mechanisms, consequences and interventions

(1) Aged men and women respond to both local heating of the skin and to increased body core temperature (T_c) with an attenuated rise in skin blood flow (SkBF). While aerobic capacity (Vo_2max), acclimation status, hydration, diseases and medications all influence SkBF, the relative inability of aged skin to vasodilate appears to be a primary consequence of advanced age. (2) Prolonged local heating elicits a lower maximal SkBF in older individuals, presumably reflecting structural changes in the cutaneous vessels. The decline in maximal SkBF is relatively linear from age 10 to 85 yr. Mechanistic changes underlying this decrement (e.g., the role of nitric oxide and sensory nerves) have not been elucidated. (3) Reflex increases in SkBF in response to increasing T_c are likewise attenuated in aged skin. Augmented noradrenergic vasoconstriction plays little or no role in this response; rather decreased active vasodilator sensitivity coupled with the aforementioned structural changes combine to limit the SkBF at a given T_c. (4) In addition to aerobic training, heat acclimation, and other countermeasures, unopposed exogenous estrogen has been shown to increase SkBF at a given T_c in postmenopausal women. Estrogen increases the SkBF at a given T_c by shifting the threshold for onset of vasodilation to a lower T_c, i.e., by directly affecting hypothalamic control. Peripheral effects are minimal. (5) While the primary purpose of increasing human SkBF in hyperthermic conditions is heat transfer and dissipation, the principle challenge of aged individuals exposed to passive heat stress is not to thermal homeostasis, but rather to cardiovascular homeostasis.