Abstract
The link between short sleep duration and cardiovascular disease may be related to exaggerated neurocardiovascular reactivity. We examined the association of actigraphy-measured habitual sleep duration (HSD) with muscle sympathetic nerve activity (MSNA) and blood pressure (BP) at rest and in response to a cold pressor test (CPT). Thirteen adults (5 males/8 females; 30 ± 9 yr; 26.9 ± 5.8 kg/m(2), 117 ± 13/76 ± 6 mmHg) were instrumented for measurement of beat-to-beat BP, forearm vascular resistance, and MSNA at rest and during a 2-min CPT. HSD was measured using wrist actigraphy across 6-7 days. Partial correlations (r(XY·Z)) described the relation between HSD with sympathetic and cardiovascular activity at rest and in response to the CPT (Δ), accounting for sex, age, and relative body fat. The CPT induced increases in systolic (+8.1 ± 7 mmHg; P = 0.002), diastolic (+6.4 ± 4; P < 0.001), and mean BP (+7.0 ± 4; P < 0.001), as well as in MSNA burst frequency (+9.1 ± 8 bursts/min; P = 0.001), burst incidence (+11.5 ± 11 bursts/100 heartbeats; P = 0.003), and total MSNA (+1,296.6 ± 1,329 total normalized burst area/min; P = 0.004). HSD was not associated with resting MSNA or BP (all P > 0.14). However, HSD was strongly associated with the CPT-induced changes in MSNA burst frequency (r(XY·Z) = -0.69; P = 0.028), diastolic (r(XY·Z) = -0.69; P = 0.028), and mean BP (r(XY·Z) = -0.77; P = 0.009). Although HSD is not strongly associated with resting sympathetic neural activity or BP, it is associated with sympathetic and BP reactivity to physiological stress. These findings support an important role for MSNA and BP reactivity in the described association of sleep duration with CVD risk.NEW & NOTEWORTHY Recent evidence has suggested that habitual sleep duration is not strongly associated with resting sympathetic neural activity. However, the present findings suggest that habitual sleep duration is inversely associated with muscle sympathetic nerve activation and blood pressure responses to sympathoexcitatory stress. Therefore, enhanced neurocardiovascular reactivity-rather than tonic sympathetic activation-may be a more relevant pathway by which chronic insufficient sleep contributes to cardiovascular disease pathophysiology.