Sleep Duration is Associated with Heightened Sympathetic Nerve Activation in Response to the Cold Pressor Test, but not at Rest

Short sleep is associated with cardiovascular disease (CVD), likely by influencing sympathetic neural control. Recent evidence suggests that sleep duration is not associated with resting blood pressure (BP) or muscle sympathetic nerve activity (MSNA) in healthy young adults, but it is unclear whether sleep duration is associated with cardiovascular or sympathetic reactivity to physiologic stress. Purpose: The purpose of this study was to examine associations between actigraphy measured sleep duration and indices of cardiovascular and sympathetic regulation at rest and in response to a cold pressor test (CPT). We hypothesized that sleep duration would be inversely associated with BP and MSNA in response to the CPT, but not at rest. Methods: Fourteenadults(7 males, 7 females; age = 27±2 y; 31.6±2.3% body fat) underwent autonomic testing that included simultaneous measurement of beat-to-beat BP, heart rate, and MSNA during 5 minutes of quiet supine rest immediately prior to and during a 2-min CPT. Systolic, diastolic, and mean BP, heart rate, and MSNA were averaged across the 5-minute rest period and during the second minute of the CPT. Prior to the experimental visit, sleep duration was assessed as the total sleep time measured using wrist actigraphy across 3.7 (±0.8) nights. Cardiovascular and sympathetic reactivity to the CPT were examined using paired t-tests. Partial Spearman correlation coefficients (ρ XY·Z ) were calculated to describe the relation of sleep duration with cardiovascular and sympathetic neural activity at rest and in response to the CPT, accounting for the effects of age, sex, and relative body fat. Results: The CPT induced significant increases in systolic (+9±2 mmHg; p < 0.001), diastolic (+7±1; p < 0.001) and mean BP (+8±1; p < 0.001), heart rate (+5±2 bpm; p = 0.039), as well as in MSNA burst frequency (+11±2 bursts/min; p < 0.001), MSNA burst incidence (+15±3 bursts/100 heartbeats; p < 0.001), and total MSNA (+1606±397 total normalized burst areas/min; p = 0.001) from rest. Sleep duration was not associated with resting cardiovascular activity or MSNA (all p > 0.18), nor with the change in heart rate induced by the CPT ( p = 0.79). However, sleep duration was moderately, but not significantly associated with the changes in systolic (ρ XY·Z =-0.49, p = 0.13), diastolic (ρ XY·Z =-0.56, p = 0.08), and mean BP (ρ XY·Z = -0.51, p = 0.11) and was strongly associated with changes in MSNA burst frequency (ρ XY·Z = -0.79; p = 0.004), burst incidence (ρ XY·Z = -0.63; p = 0.04), and total normalized activity (ρ XY·Z = -0.73; p = 0.01) induced by the CPT. Conclusions: Our findings build on recent evidence and suggest that while sleep duration is not associated with resting cardiovascular or sympathetic neural activity, it is associated with cardiovascular and sympathetic reactivity to physiologic stress. These findings support an important role for the sympathetic nervous system, particularly BP and MSNA reactivity, in the described association of short sleep with increased CVD risk. Supported by a John Perkins, Jr. Research Career Enhancement Award, and NIH and AHA funding to NDMJ (R01HL167788, L30HL149066, & 24TPA1290435) and JKL (R01HL153523). 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.