Aging and sympathetic transduction to blood pressure in humans: methodological and physiological considerations

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Abstract

Recent reports suggest that quantification of signal-averaged sympathetic transduction is influenced by resting muscle sympathetic nerve activity (MSNA) and burst occurrence relative to the average mean arterial pressure (MAP). Herein, we asked how these findings may influence age-related reductions in sympathetic transduction. Beat-to-beat blood pressure and MSNA were recorded during 5 min of rest in 27 younger (13 females: age, 25 ± 5 yr; BMI, 25 ± 4 kg/m2) and 26 older (15 females: age, 59 ± 5 yr; BMI, 26 ± 4 kg/m2) healthy adults. All MSNA bursts were signal averaged together. Beat-to-beat MAP values were then split into low (T1), middle (T2), and high (T3) tertiles, and signal-averaged transduction was calculated within each tertile. Resting MSNA was higher in older adults and MAP was similar between groups. Older adults exhibited blunted overall MAP transduction (younger, D1.5 ± 0.6 vs. older, D0.9 ± 0.7 mmHg; P ¼ 0.005), which was irrespective of relation to prevailing MAP. A greater proportion of bursts occurred above the average MAP in older adults (P < 0.001), and a larger proportion of these bursts were associated with depressor responses (P ¼ 0.005). Nonetheless, assessment of bursts above the average MAP associated with pressor responses revealed similar age-associated reductions in transduction (younger, D2.6 ± 1.6 vs. older, D1.7 ± 0.8 mmHg; P ¼ 0.016). These findings indicate an age-related increase in burst occurrence above the average resting MAP, which alone does not explain blunted transduction, thereby supporting the physiological underpinnings of age-related decrements in sympathetic transduction to blood pressure.

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APA

Bigalke, J. A., Young, B. E., Cleveland, E. L., Fadel, P. J., & Carter, J. R. (2024). Aging and sympathetic transduction to blood pressure in humans: methodological and physiological considerations. American Journal of Physiology - Heart and Circulatory Physiology, 326(1), H148–H157. https://doi.org/10.1152/ajpheart.00359.2023

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