Effect of prolonged sleep restriction on the cardiovascular response to mental arithmetic

Objective Inadequate sleep is associated with an increased risk of hypertension. Exaggerated blood pressure (BP) reactivity to psychological stress is predictive of the development of hypertension. Following 24‐hours of total sleep deprivation, individuals exhibit an exaggerated BP response to mental stress (MS). The mechanisms contributing to this response and the generalizability to more prolonged exposure to restricted sleep are not clear. Thus we sought to examine the early hemodynamic response to MS in individuals before and during prolonged sleep restriction. We hypothesized the early rise in BP during MS would occur more slowly and would achieve a higher peak following 9 nights of restricted sleep when compared to control. We further hypothesized the contribution of total peripheral resistance (TPR) to the rise in BP would be greater following restricted sleep when compared to control. Methods Individuals completed two visits randomized to control sleep or experimental sleep restriction. Ten young (23±1 yrs) healthy, non‐obese (24±1 kg/m 2 ) men and women (5M/5F) completed the restriction visit and seven of the same individuals (23±1 yrs; 5M/2F; 24±1 kg/m 2 ) completed the control visit. Each visit consisted of 4 days of acclimation (9 hours of sleep per night) followed by 9 days of control (9 hours/night) or restricted (4 hours/night) sleep. For the purpose of this investigation, individuals were studied on days 2 and 13. Beat‐by‐beat heart rate (HR, electrocardiography) and BP (finger plethysmography) were measured continuously during 2 min of quiet rest followed by 5 min of mental arithmetic. Stroke volume (SV) was estimated from the pressure waveform and cardiac output (CO) and TPR were calculated. Peak change, time to peak, and rate of rise in BP were assessed during the initiation of mental stress (first 30‐s). Results BP increased during MS ( P <0.05) and the early peak BP did not differ between conditions ( P =0.35–0.84). However, following prolonged experimental sleep restriction, individuals achieved peak systolic BP earlier (Time to peak: 19±4 vs 9±3 s, P =0.04) and the rate of rise in diastolic BP at the onset of MS was significantly greater (0.7± 0.3 vs 2.3±0.7 mmHg/s, P =0.01) when compared to the acclimation period. No differences in time to peak BP or rate of rise at the onset of MS were observed on the control visit ( P =0.16–0.97). The peak change in SV (0.5±1.4 vs 6.3±2.1, P =0.03) and CO (1.1±0.2 vs 1.7±0.2 L/min, p=0.01) at the onset of MS were greater following prolonged sleep restriction when compared to the acclimation period. No differences in the change in SV or CO were observed on the control visit ( P =0.39–0.41) and no differences in the change in TPR were observed on either visit ( P =0.36–0.86). Conclusions Prolonged (9‐day) experimental sleep restriction (4 hours/night) results in a faster increase in BP in response to mental arithmetic. This rapid increase in BP at the onset of MS is achieved primarily via a greater increase in SV and CO when compared to the acclimation period. These data highlight an important role for CO in the BP response to stress in sleep restricted individuals and provide important insight into potential mechanisms which may contribute to the development of hypertension following inadequate sleep. Support or Funding Information NIH HL130339, NIH HL114676, NIH HL114024, NIH HL083947, APS UGSRF This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .