Abstract

BACKGROUND: Cardiac output and cutaneous vasodilation are attenuated in healthy aged humans during heat stress. It is well established that changes in peripheral vascular control limit the extent of cutaneous vasodilation in the aged. However, it remains unknown if the attenuated increase in cardiac output seen in older individuals during heat stress also contributes to reduced cutaneous vasodilation. PURPOSE: We tested the hypothesis that an acute increase in cardiac output, via rapid saline infusion, would augment cutaneous vasodilation in healthy aged humans during heat stress. METHODS: Right heart catheterization was performed in 9 aged (A: 69 ± 3 yrs, 164 ± 9 cm, 67 ± 9 kg, 3 males/6 females) and 12 young (Y: 26 ± 5 yrs, 165 ± 6 cm, 64 ± 10 kg, 6 males/6 females) healthy individuals exposed to whole-body passive heat stress until pulmonary artery blood temperature increased by 1.5°C. At this increase in blood temperature, cardiac output (thermodilution), forearm vascular conductance (FVC, venous occlusion plethysmography) and cutaneous vascular conductance (CVC, laser-Doppler) were measured before and after rapid (~7 min) infusion of 15 mL/kg warm saline. RESULTS: Prior to saline infusion, cardiac output (A: 6.6 ± 0.6 vs. Y: 9.2 ± 1.2 L/min), FVC (A: 0.09 ± 0.02 vs. Y: 0.17 ± 0.04 mL/100 mL/min/mmHg), and CVC (A: 1.23 ± 0.50 vs. Y: 1.94 ± 0.50 units/mmHg) were each lower in the aged (all P<0.01). Saline infusion significantly increased cardiac output (A: +29 ± 9 vs. Y: +21 ± 12%, p=0.13), FVC (A: +17 ± 13 vs. Y: +29 ± 16%, p=0.09), and CVC (A: +21 ± 8 vs. Y: +15 ± 12%, p=0.22) to a similar extent in both groups. Pulmonary artery blood temperature increased slightly during saline infusion (A: 38.1 ± 0.2 to 38.2 ± 0.2°C vs. Y: 38.4 ± 0.3 to 38.5 ± 0.2°C), but the increase not differ between groups (p=0.46). CONCLUSIONS: These data suggest that attenuated increases in cardiac output contribute to attenuated cutaneous vasodilation during passive heat stress in healthy aged humans. Funding support: National Institutes of Health (GM-068865), Department of Defense (W81XWH-12-1-0152), and ACSM Foundation Research Endowment.

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