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There is a sustained reduction in arterial blood pressure that occurs in aged adults following acute exposure to leg heating. Concurrent with this blood pressure response is an increase in systemic vascular conductance that is not fully offset by an increase in cardiac output, which suggests that acute leg heating may alter neurovascular control. Therefore, the purpose of this study was to test the hypothesis that acute leg heating reduces sympathetic neurovascular transduction in aged humans. Six healthy young adults (3 females; age 25 ± 4 yrs; height 175 ± 9 cm; weight 74 ± 17 kg; mean ± SD) and 4 healthy aged adults (3 females; age 69 ± 4 yrs; height 163 ± 3 cm; weight 66 ± 7 kg) were exposed to 45 min of acute leg heating. Subjects wore a tube‐lined water‐circulating garment that allowed leg skin temperature to be clamped at ~40 °C during heating. Intestinal temperature was measured throughout via a telemetric pill. Systemic vascular conductance was calculated as cardiac output (Modelflow) divided by mean arterial pressure. Femoral vascular conductance was calculated as blood flow (Doppler ultrasound) divided by mean arterial pressure. Neurovascular transduction was estimated before and 30 min after leg heating by measuring the percent reduction in femoral vascular conductance (ΔFVC) during isometric handgrip exercise performed to fatigue. Compared to pre‐heat, intestinal temperature was increased for both groups at 45 min of leg heating (young adults, Δ0.5 ± 0.1 °C; aged adults, Δ0.9 ± 0.2 °C; both P < 0.05 vs. 0 change) and remained elevated 30 min after heating (young adults, Δ0.3 ± 0.1 °C; aged adults, Δ0.5 ± 0.2 °C; both P < 0.05 vs. 0 change). Thirty min after heating, mean arterial pressure did not differ from pre‐heat in young adults (pre 86 ± 3 mmHg vs. post 87 ± 3 mmHg; P = 0.9) but was decreased in aged adults (pre 102 ± 3 mmHg vs. post 96 ± 2 mmHg; P = 0.06). Resting systemic vascular conductance (pre 65.8 ± 3.6 ml min −1 mmHg −1 vs. post 66.4 ± 4.5 ml min −1 mmHg −1 ; P = 1.0) and femoral vascular conductance (pre 3.1 ± 0.4 ml min −1 mmHg −1 vs. post 3.3 ± 0.6 ml min −1 mmHg −1 ; P = 0.5) did not differ from pre‐heat in young adults. However, in aged adults, both resting systemic vascular conductance (pre 46.5 ± 3.7 ml min −1 mmHg −1 vs. post 59.2 ± 8.8 ml min −1 mmHg −1 ; P = 0.03) and femoral vascular conductance (pre 2.6 ± 0.6 ml min −1 mmHg −1 vs. post 3.4 ± 0.6 ml min −1 mmHg −1 ; P = 0.07) remained elevated 30 min after heating. Neurovascular transduction was reduced after heating in both groups (young adults, pre ΔFVC −28 ± 8 % vs. post ΔFVC −13 ± 10 %; aged adults, pre ΔFVC −30 ± 6 % vs. post ΔFVC −23 ± 7 %; P = 0.03). Taken together, it appears that the reduction in arterial blood pressure that occurs in aged adults after acute leg heating is mediated by a persistent vasodilation that is due, at least in part, to reduced neurovascular transduction. In young adults, blood pressure is well maintained after leg heating despite reduced neurovascular transduction, which may be related to an increase in basal sympathetic vasoconstrictor outflow. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .