Abstract

Increased muscle sympathetic nerve activity (MSNA) during heat stress in young humans likely reflects the sympathetic drive responsible for the cardiovascular adjustments that facilitate an increase in skin blood flow. In contrast, cardiovascular adjustments during heat stress are attenuated in the aged, and could therefore be due to a lower sympathetic drive. We compared plasma epinephrine ([E]) and norepinephrine ([NE]), as well as MSNA in 11 young (Y: 28 ± 4 y) and 8 aged (A: 71 ± 5 y) subjects prior to and during passive heat stress. A cold pressor test (CPT) was superimposed upon heating to assess if a ceiling in MSNA was attained. Baseline MSNA burst frequency (15 ± 7 vs. 29 ± 4 bursts/min, p=0.01) and burst incidence (26 ± 13 vs. 46 ± 8 bursts/100 c.c., p<0.01) were greater in the aged. Heat stress increased core temperature to a similar extent in both groups (Y: +1.2 ± 0.1 vs. A: +1.2 ± 0.1°C, p=0.99). Changes in plasma [E] (Y: +21 ± 38 vs. A: ‐2 ± 37 pg/mL, p=0.24) and [NE] (Y: +182 ± 127 vs. A: +113 ± 156 pg/mL, p=0.32) with heating did not differ between groups. MSNA burst frequency (47 ± 10 vs. 61 ± 16 bursts/min, p<0.01) and burst incidence (48 ± 14 vs. 65 ± 12 bursts/100 c.c., p=0.01) remained greater in the aged during heating, although both increased similarly between groups (p>0.1). The CPT further increased MSNA burst frequency (Y: +11 ± 11 vs. A: +8 ± 5 bursts/min) and burst incidence (Y: +9 ± 11 vs. A: +10 ± 9 bursts/100 c.c), to a similar extent between groups (p>0.1). These data suggest that the aged do not have a lower sympathetic drive during whole‐body passive heat stress. Funded by NIH HL61388.

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