Lincoln, Zoe R.

Insufficiency or irregularity in sleep is associated with high blood pressure (BP) and aortic stiffness, both of which are independent predictors of all‐cause and cardiovascular mortality. The cardiovascular ramifications of short and irregular sleep are well documented in shift workers, but the health implications of possible differences between sleep duration on workdays (WD) and free days (FD) in non‐shift workers is less clear. PURPOSE We sought to examine associations between WD and FD sleep duration, and then to inspect for relationships between WD and FD sleep duration, as well as the difference between WD and FD sleep duration (i.e., sleep irregularity), with BP and indices of arterial stiffness in apparently healthy young adults. We hypothesized 1) participants would sleep less on WD than FD, and 2) that participants with short WD sleep duration would exhibit higher BP and arterial stiffness, and 3) those with greater sleep irregularity would exhibit higher BP and arterial stiffness. METHODS 16 apparently healthy young adults (21.8±4.0 yrs; 24.4±2.9 kg/m 2 ; Mean±SD) participated in this study. All participants completed the Munich ChronoType Questionnaire to assess self‐described WD and FD sleep‐wake behavior. WD and FD sleep duration were determined, and sleep irregularity was quantified as the absolute value of the difference between WD and FD sleep duration. Following 10‐min of supine rest, we used an automated oscillometric device (SphygmoCor XCEL) to measure BP and augmentation index (AIx), an indirect measure of arterial stiffness. Aortic stiffness was then assessed using carotid‐femoral pulse wave velocity (cf‐PWV). WD and FD sleep duration were compared using a paired t‐test and associations between sleep with BP and indices of arterial stiffness were assessed using Pearson correlations, or the non‐parametric equivalent for sleep irregularity. RESULTS WD sleep duration was 492±85 min, FD sleep duration was 480±83 min, and sleep irregularity was 53±49 min. Systolic BP was 120±10 mmHg, diastolic BP was 68±7 mmHg, AIx was 10.9±9.8 %, and cf‐PWV was 5.8±0.7 m/s. WD sleep duration was significantly greater (P<0.01) than FD sleep duration, and WD sleep duration was not associated (P>0.05) with systolic BP (r=0.10), diastolic BP (r=0.10), AIx (r=0.07), or cf‐PWV (r=‐0.18). FD sleep duration was inversely correlated with cf‐PWV (r=‐0.65; P=0.01), but was not associated (P>0.05) with systolic BP (r=‐0.12), diastolic BP (r =‐0.08), or AIx (r=0.25). Sleep irregularity was not associated (P>0.05) with systolic BP (r=0.37), diastolic BP (r=0.45), AIx (r=0.08), or cf‐PWV (r=0.14). CONCLUSIONS Contrary to our hypothesis, FD, but not WD, sleep duration was associated with aortic stiffness in apparently healthy young adults. Average sleep duration of our cohort exceeded the recommended minimum of 7 hours per night and sleep irregularity was small (i.e., <60 min on average), thus potentially masking elevations in BP and arterial stiffness seen with short and/or irregular sleep such as in shift workers.

Stimuli that evoke pain stimulate the sympathetic nervous system leading to downstream vascular and hemodynamic adjustments. In clinical populations and older individuals, the perception of pain is associated with cardiovascular responses (e.g., heart rate, blood pressure, and arterial stiffness). However, there are extensive inter‐individual differences in the perception of pain, pain perception may be influenced by age, and it’s unclear if pain is associated with cardiovascular responses in younger adults. PURPOSE Therefore, we sought to determine whether heart rate, blood pressure, and arterial stiffness responses to sympathoexcitatory stimuli were associated with perceived pain, in apparently healthy young adults METHODS 17 young adults (21.6±3.9 yrs; BMI: 24.4±2.8 kg/m 2 ;Mean±SD) participated in this investigation. Following 10‐min of supine rest, we measured heart rate (HR) and mean arterial pressure (MAP), via pulse wave analysis (PWA), and arterial stiffness via carotid‐femoral pulse wave velocity (cf‐PWV). Measures were obtained in duplicate then averaged for analysis. Participants then performed a 3‐min isometric handgrip exercise (HG) at 30% of maximum voluntary contraction, which was immediately followed by 3‐min of brachial cuff‐occlusion at 240mmHg. Perceived pain was assessed via visual analog scale (0‐10; 0=no pain, 10=most pain) at the first minute of each stimulus. HR and MAP were assessed at minute two and arterial stiffness was acquired in the final minute of each stimulus. Associations between perceived pain scores during HG and cuff‐occlusion with percent change in cardiovascular responses were assessed using Spearman’s correlations (α=0.05) RESULTS During HG, significant (P<0.01) increases in HR (pre: 63±6 vs. post: 78±11 bpm; 23±15 %), MAP (pre: 86±9 vs. post: 105±14 mmHg; 22±10 %), and cf‐PWV (pre: 6.5±1.7 vs. post: 7.2±1.0 m/s; 13±26 %) were observed. During cuff‐occlusion, relative to pre, significant (P<0.05) increases in MAP (post: 100±13 mmHg; 18±15%) and cf‐PWV (post: 7.2±1.4 m/s; 14±13%), but not (P>0.05) HR (post: 64±7 bpm; 7±6%) were observed. Perceived pain during cuff‐occlusion (3.73±1.79 A.U.) was significantly greater (P=0.01) than during HG (1.88±1.20 A.U.). While no relationships were observed between perceived pain and cardiovascular responsiveness during HG (P>0.05) with HR (r=0.28; P=0.28), BP (r=0.45; P=0.07), or cf‐PVW (r=0.28; P=0.28), perceived pain was associated with increases in BP (r=0.57; P=0.02) and cf‐PWV (r=0.55; P=0.02;), but not HR (r=0.19; P=0.47), during cuff‐occlusion. CONCLUSIONS While pain during HG was not associated with cardiovascular responses, significantly greater cuff‐occlusion evoked pain was associated with cardiovascular responsiveness. Our data suggests that the relation between perceived pain and cardiovascular responsiveness to sympathoexcitatory stimuli exists in younger adults, although additional data in larger cohorts and using varied stimuli are warranted.