No abstract

It is well‐documented that feedforward cardiovascular responses occur at the onset of exercise, but it is unclear if such responses are associated with other types of movements. In this study, we tested the hypothesis that feedforward cardiovascular responses occur when a passive (imposed) 60° head‐up tilt is anticipated, such that changes in heart rate and carotid artery blood flow (CBF) commence prior to the onset of the rotation. A light cue preceded head‐up tilts by 10 sec, and heart rate and CBF were determined for 5‐sec time periods prior to and during tilts. Even after these stimuli were provided for thousands of trials spanning several months, no systematic changes in CBF and heart rate occurred prior to tilts, and variability in cardiovascular adjustments during tilt remained substantial over time. We also hypothesized that substitution of 20° for 60° tilts in a subset of trials would result in exaggerated cardiovascular responses (as animals expected 60° tilts), which were not observed. These data suggest that cardiovascular adjustments during passive changes in posture are mainly elicited by feedback mechanisms, and that anticipation of passive head‐up tilts does not diminish the likelihood that a decrease in carotid blood flow will occur during the movements.

Background Psychological stress and insufficient sleep are both associated with an increased risk of developing hypertension. While the underlying mechanisms are not well defined, it has been postulated that this may be facilitated by modulation of baroreflex control of sympathetic activity. Short periods (<5 min) of mental stress attenuate sympathetic baroreflex sensitivity (sBRS), but it is currently unclear whether this holds true for longer bouts of stress. As such, we sought to examine the effect of 10 min of mental stress on sBRS. Additionally, we evaluated the impact of experimental sleep restriction on baroreflex control of blood pressure during mental stress. We hypothesized that mental stress would attenuate sBRS, and that prolonged exposure to restricted sleep would result in a greater reduction in sBRS during mental stress. Methods Fourteen healthy adults (10M/4F, 25±1 yrs) underwent 10 min of mental stress consisting of a 5‐min mental arithmetic task, followed immediately by a 5‐min Stroop color‐word conflict test. Heart rate (electrocardiography), blood pressure (finger photoplethysmography), and muscle sympathetic nerve activity (microneurography of the common peroneal nerve) were continuously measured to determine sBRS at baseline and during mental stress. A subset of participants (n=9) completed the mental stress protocol under both experimental sleep restriction (4 hr/night) and control sleep conditions (8–9 hr/night) while inpatient at a hospital‐based clinical research unit. Subjects underwent a 3‐night acclimation period, followed by 9 or 14 nights of either sleep restriction or control sleep. Data from Day 2/1 or Day 13/15 (during control sleep only) were used to assess the effect of mental stress alone, and data from Day 13/15 (under both conditions) were used to assess the effect of sleep restriction. Results Acute mental stress resulted in a marked blunting of sBRS from baseline (−2.7±0.5 to −1.5±0.4 bursts·100hb−1·mmHg−1, p=0.04). Examining the mental stress interventions individually revealed a significant decrease in sBRS during the initial 5 min of stress (mental arithmetic, p=0.03), but not during the subsequent 5 min of testing (Stroop test, p=0.75). Mental stress also reduced baroreflex function following sleep restriction (main effect of condition, p<0.01); however, the reduction in sBRS was not significantly different in restricted sleep compared to control (main effect of visit, p=0.78). There was no significant interaction effect between sleep restriction and mental stress (p=0.81). Conclusions These data provide further support that, in young healthy individuals, sBRS is attenuated early in mental stress but quickly returns to baseline values. In contrast, prolonged sleep restriction does not appear to alter sympathetic control of blood pressure. Support or Funding Information NIH HL114024 (VKS), NIH HL114676 (VKS), NIH HL083947 (MJJ), FAER Medical Student Anesthesia Research Fellowship (NMP)