Rhythmicity and neurovascular integration of synchronous and asynchronous sympathetic action potential subpopulations in human muscle sympathetic nerve activity

This study investigated the time-varying discharge patterns and neurovascular integration of synchronous and asynchronous sympathetic action potential (AP) subpopulations. Muscle sympathetic APs (peroneal microneurography, continuous wavelet transform) and diastolic blood pressure (DBP; Finometer) were recorded in 9 healthy adults (3 female; 20-30 years) during baseline rest (5-min). Time-varying discharge patterns of different AP subpopulations were quantified as the mean firing frequency (hertz; Hz) of each AP subpopulation for falling and rising DBPs. Mixed-effects modeling and t -tests quantified differences in AP firing frequencies and neurovascular responses. When all DBPs were considered, the mean firing frequency of medium-sized APs was higher for synchronous APs compared to asynchronous APs (Cluster 3; synchronous: 0.29 ± 0.11 Hz, asynchronous: 0.16 ± 0.06 Hz; p < 0.001). The mean firing frequencies of small- and large-sized APs were not different for synchronous and asynchronous APs (all p > 0.16). For synchronous APs, the mean firing frequency of medium-sized APs was higher for DBP falls compared to rises (Cluster 3; DBP fall: 0.24 ± 0.10 Hz, DBP rise: 0.20 ± 0.10 Hz; p < 0.001). The mean firing frequencies of small- and large-sized synchronous APs were not different for DBP falls and rises (all p > 0.06). For asynchronous APs, no differences were observed in the mean firing frequency of any AP subpopulation for DBP falls and rises (all p > 0.26). Neurovascular integration of sympathetic AP discharge was quantified as the DBP response to synchronous and asynchronous AP discharge for falling and rising DBPs (signal averaging). Transduction gain was quantified as the slope of the linear relationship between the maximal DBP response and the time-to-maximal DBP response. When all DBPs were considered, synchronous APs produced DBP increases (synchronous: 2.20 ± 0.53 mmHg) whereas asynchronous APs attenuated DBP reductions (asynchronous: -1.23 ± 0.62 mmHg), compared to periods with no AP activity (no AP activity: -1.69 ± 0.76 mmHg; all p < 0.011). For synchronous APs that fired during DBP rises, the DBP transduction curve was reset upwards to larger peak responses compared to DBP falls (DBP rise: 3.45 ± 1.58 mmHg, DBP fall: 2.61 ± 1.25 mmHg; p = 0.015). The transduction gain for synchronous APs was not different for DBP rises and falls (DBP rise: 0.48 ± 0.38 mmHg/cardiac cycle, DBP fall: 0.43 ± 0.14 mmHg/cardiac cycle; p = 0.672). For asynchronous APs that fired during DBP falls, there was a larger nadir response compared to DBP rises (DBP fall: -1.79 ± 0.72 mmHg, DBP rise: -1.34 ± 0.88 mmHg; p = 0.011). However, the transduction gain for asynchronous APs was positive for DBP falls and negative for DBP rises (DBP fall: 0.05 ± 0.08 mmHg/cardiac cycle, DBP rise: -0.10 ± 0.05 mmHg/cardiac cycle; p < 0.001). These data suggest that: 1) synchronous but not asynchronous sympathetic APs express time-varying discharge patterns related to blood pressure oscillations, 2) asynchronous AP discharge supports homeostatic blood pressure regulation, and 3) neurovascular integration is affected by both the synchronization and rhythmicity of sympathetic AP discharge. This work was supported by Queen Elizabeth II and Ontario Graduate Scholarships and the Natural Sciences and Engineering Research Council of Canada (NSERC). 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.