Sympathetic and cardiovagal baroreflex resetting during apnea in humans

In humans, the mechanisms governing the large pressor response to apnea remain unclear. We hypothesized that the pressor response to apnea is supported by sympathetic action potential (AP) and cardiovagal baroreflex resetting. Muscle sympathetic APs (peroneal microneurography, continuous wavelet transform), blood pressure (Finometer), and R-R interval (ECG) were recorded in 12 healthy adults (22 ± 2 years; 4 females) during baseline rest (BSL) and a maximal voluntary end-inspiratory apnea (APN). Sympathetic AP baroreflex threshold gain was quantified as the linear function between AP discharge probability and diastolic pressure. Sympathetic AP baroreflex sensitivity gain was quantified as the linear function between AP clusters/burst and diastolic pressure. Cardiovagal baroreflex gain was quantified as the linear function between R-R interval and systolic pressure (sequence technique). Statistical analyses included paired t-tests and repeated-measures ANOVA. Data are presented as the mean ± SD. Apnea reset baroreflex threshold functions for all sympathetic APs rightwards to higher diastolic pressures (BSL: 76 ± 6 mmHg, APN: 84 ± 8 mmHg; p = 0.004) and upwards to higher discharge probabilities for medium-sized APs only (BSL Cluster 3: 35 ± 13 %, APN Cluster 3: 89 ± 54 %; p < 0.001). Apnea did not affect the discharge of small- (BSL Cluster 1: 12 ± 9 %, APN Cluster 1: 11 ± 8 %; p = 0.323) or large-sized APs (BSL Cluster 8: 1 ± 1 %, APN Cluster 8: 4 ± 2 %; p = 0.685). Baroreflex threshold gains were reduced during apnea for medium-sized APs (BSL Cluster 3: -5.2 ± 3.4 %/mmHg, APN Cluster 3: -1.6 ± 3.7 %/mmHg; p < 0.001) but not small- (BSL Cluster 1: -2.1 ± 2.1 %/mmHg, APN Cluster 1: -1.4 ± 1.2 %/mmHg; p = 0.680) or large-sized APs (BSL Cluster 8: -0.4 ± 0.1 %/mmHg, APN Cluster 8: -0.8 ± 1.0 %/mmHg; p = 0.735). Apnea reset sympathetic AP baroreflex sensitivity functions rightwards to higher diastolic pressures and trended towards upwards resetting to a greater number of AP clusters per burst (BSL: 4 ± 2 AP clusters/burst, APN: 5 ± 2 AP clusters/burst; p = 0.084). Sympathetic AP baroreflex sensitivity gain was reduced during apnea (BSL: -0.09 ± 0.08 AP clusters/burst/mmHg, APN: -0.01 ± 0.10 AP clusters/burst/mmHg; p = 0.031). Apnea reset cardiovagal baroreflex functions rightwards to higher systolic pressures (BSL: 125 ± 10 mmHg, APN: 133 ± 15 mmHg; p = 0.018) but did not affect R-R interval (BSL: 987 ± 185 ms, APN: 1012 ± 151 ms; p = 0.532). Cardiovagal baroreflex gain was reduced during apnea (BSL: 35 ± 16 ms/mmHg, APN: 26 ± 9 ms/mmHg; p = 0.038). In summary, sympathetic AP and cardiovagal baroreflex functions operate with reduced gain and are reset to higher blood pressures during apnea. For medium-sized sympathetic APs only, baroreflex functions are reset to higher discharge probabilities. These findings suggest that the large pressor response to apnea is supported by sympathetic AP and cardiovagal baroreflex resetting. 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 2026 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.