Sympathetic neural responses to 24-hour sleep deprivation in humans: sex differences

• Published in: American journal of physiology. Heart and circulatory physiology Vol. 302; no. 10; pp. H1991 - H1997
• Main Authors: Carter, Jason R, Durocher, John J, Larson, Robert A, DellaValla, Joseph P, Yang, Huan
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 15.05.2012
• Subjects: Baroreflex - physiology; Blood Pressure - physiology; Cardiovascular Neurohormonal Regulation; Correlation analysis; Estradiol - blood; Female; Gender differences; Heart Rate - physiology; Hormones; Humans; Hypertension; Hypertension - physiopathology; Male; Nervous system; Sex Characteristics; Sleep deprivation; Sleep Deprivation - blood; Sleep Deprivation - physiopathology; Sympathetic Nervous System - physiology; Testosterone - blood; Young Adult
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.01132.2011

Sleep deprivation has been linked to hypertension, and recent evidence suggests that associations between short sleep duration and hypertension are stronger in women. In the present study we hypothesized that 24 h of total sleep deprivation (TSD) would elicit an augmented pressor and sympathetic neural response in women compared with men. Resting heart rate (HR), blood pressure (BP), and muscle sympathetic nerve activity (MSNA) were measured in 30 healthy subjects (age, 22 ± 1; 15 men and 15 women). Relations between spontaneous fluctuations of diastolic arterial pressure and MSNA were used to assess sympathetic baroreflex function. Subjects were studied twice, once after normal sleep and once after TSD (randomized, crossover design). TSD elicited similar increases in systolic, diastolic, and mean BP in men and women (time, P < 0.05; time × sex, P > 0.05). TSD reduced MSNA in men (25 ± 2 to 16 ± 3 bursts/100 heart beats; P = 0.02), but not women. TSD did not alter spontaneous sympathetic or cardiovagal baroreflex sensitivities in either sex. However, TSD shifted the spontaneous sympathetic baroreflex operating point downward and rightward in men only. TSD reduced testosterone in men, and these changes were correlated to changes in resting MSNA (r = 0.59; P = 0.04). Resting HR, respiratory rate, and estradiol were not altered by TSD in either sex. In conclusion, TSD-induced hypertension occurs in both sexes, but only men demonstrate altered resting MSNA. The sex differences in MSNA are associated with sex differences in sympathetic baroreflex function (i.e., operating point) and testosterone. These findings may help explain why associations between sleep deprivation and hypertension appear to be sex dependent.