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24‐Hour Total Sleep Deprivation Alters Cardiovagal Baroreflex Sensitivity and Blood Pressure Reactivity in Mid‐Life Adults
Author(s) -
Colling Morgan E.,
Greenlund Ian M.,
Gonzalez Joshua E.,
Carter Jason R.
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.06308
Subject(s) - medicine , supine position , blood pressure , sphygmomanometer , heart rate , sleep deprivation , crossover study , valsalva maneuver , cold pressor test , baroreflex , sleep (system call) , cardiology , anesthesia , microneurography , circadian rhythm , physical therapy , operating system , alternative medicine , pathology , computer science , placebo
Nearly 1 in 3 American adults fail to get recommended levels hours of sleep, and epidemiological studies report a significant relationship between chronic sleep deprivation and hypertension. A number of studies from our laboratory and others have focused on neural and cardiovascular responses to a 24‐hour total sleep deprivation (TSD) model. However, these prior studies have primarily been conducted in young or older populations, with a gap in mid‐life adults. This is relevant because mid‐life can often be when chronic sleep levels reach a lifetime nadir. The purpose of this study was to determine the cardiovascular effects of 24‐h TSD on mid‐life adults. Nine participants (6 men and 3 women, BMI: 28 ± 5 vs. 22 ± 3 kg/m 2 ) between the ages of 40 and 55 yr were tested twice, once after 24‐h TSD and once after normal sleep (randomized, crossover design). In both tests, participants were equipped with an automated sphygmomanometer (Omron HEM‐907XL, Omron Health Care) to assess mean arterial pressure (MAP), finger plethysmography to measure beat‐to‐beat arterial pressure (NOVA, Finapres), and a three‐lead electrocardiogram to record heart rate. Following a 10‐minute supine baseline, participants performed three 15‐s Valsalva maneuvers (VM) with 1‐minute recovery periods. Following another 3‐minute post‐VM baseline, a 2‐minute cold pressor test (CPT) was performed by submersing each participant’s hand in ice water. Data were analyzed using WinCPRS software (Absolute Aliens, Turku, Finland). R‐waves were detected and marked in the time series. R‐R interval (ms) vs. systolic arterial pressure (SAP, mmHg) were plotted for Phase IV of each VM, which was defined as the interval between the first SAP that exceeded the mean supine resting baseline SAP to peak SAP during Phase IV “overshoot.” Cardiovagal baroreflex sensitivity (cBRS) was determined from the slope of the regression line. The cardiovascular responses to each VM were included if the correlation coefficient exceeded 0.7 and the SAP increase was at least 15 mmHg (n=7). Irregular “square waves” were excluded from analysis. Statistical analysis included repeated measures ANOVA (p<0.05). TSD did not alter baseline MAP (84±3 vs. 85±4 mmHg) or heart rate (62±4 vs. 58±3 beats/min, p>0.05 for both). Cardiovagal baroreflex sensitivity (cBRS) was significantly reduced after 24‐h TSD (21.9 ± 10.3 vs. 14.7 ± 6.47 ms/mmHg, p<0.05). SAP reactivity was augmented following TSD during CPT (Δ16±7 vs. Δ25±6 mmHg, p=0.05), and DAP reactivity trended higher following TSD during CPT (Δ14±3 vs. Δ19±4 mmHg, p=0.09). In summary, TSD impacts baroreflex sensitivity and blood pressure reactivity in mid‐life adults. Support or Funding Information Support was provided by the American Physiological Society’s (APS) Summer Undergraduate Research Fellowship, Michigan Space Grant Consortium, and the Portage Health Foundation.