Abstract
Greater cerebral pulsatility has been shown to cause cerebral microvascular damage, leading to structural damage within the brain. Recently, studies have demonstrated that cerebral pulsatility is influenced by a complex interplay between multiple hemodynamic variables including heart rate (HR), cerebral perfusion pressure, arterial blood pressure, arterial compliance, and cerebrovascular resistance. The sympathetic nervous system is an important regulator of blood pressure and blood flow; however, it is unknown if the sympathetic nervous system influences cerebral pulsatility at rest. The purpose of this study was to explore the influence of muscle sympathetic nerve activity (MSNA) on cerebral pulsatility index (PI) in young and older healthy adults. Further, we sought to explore the effects of age and sex on these relationships. Seventy-one healthy adults were evaluated including 33 young adults (M/F = 19/14; age = 24 ± 4 years; BMI = 24 ± 2 kg/m 2 ), and 38 older adults (M/F = 17/21; age = 60 ± 6 years; BMI = 24 ± 3 kg/m 2 ). Beat-to-beat mean arterial pressure (MAP) using finger photoplethysmography, HR using a 3-lead ECG, middle cerebral artery (MCA) blood velocity using transcranial doppler ultrasound, and MSNA using microneurography from the peroneal nerve were simultaneously recorded throughout the protocol. MCA PI, MSNA burst frequency (BF) and burst incidence (BI) were analyzed offline. Linear regression was used to assess the influence of MSNA and MAP on PI. As expected, older adults had a greater PI (Older: 0.79 ± 0.11 a.u. vs. Young: 0.69 ± 0.15 a.u.), MAP (Older: 100 ± 12 mmHg vs. Young: 95 ± 14 mmHg), MSNA BF (Older: 31 ± 10 bursts/min vs. Young: 17 ± 7 bursts/min), and MSNA BI compared with young adults (Older: 55 ± 16 bursts/100hb vs. Young: 33 ± 13 bursts/100hb; P < 0.05 for all). When assessed as a whole group, MSNA BI was positively associated with PI (r = 0.313, P < 0.05) and there was a trend towards a positive association between MSNA BF and PI (r = 0.214, P = 0.07); however, when adjusting for age and sex, these associations were abolished. MAP was not significantly associated with PI in the whole group. Interestingly, when assessed by age and sex, older females MSNA BF and BI were negatively associated with PI, such that greater MSNA BF and BI were associated with a lower PI (MSNA BF: r = -0.431, P < 0.05; MSNA BI: r = -0.431, P < 0.05). There were no significant associations between MSNA and PI for any other group. To further explore these age and sex differences, the influence of MAP on PI was also assessed. There was a positive association between MAP and PI in older males (r = 0.610, P < 0.05), such that a greater MAP was associated with a greater PI. Conversely, there was a trend for a negative association between MAP and PI in young females (r = -0.523, P = 0.055). There were no significant associations between MAP and PI in young males or older females. Sympathetic nerve activity and MAP influence cerebral pulsatility at rest; however, this may vary by age and sex. Older females resting MSNA was significantly but negatively associated with PI. Additionally, MAP was only significantly and positively associated with PI in older males. Future studies could explore the effects of a sympathoexcitatory stimuli on these relationships. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.