Cardiovascular effects of partial sleep deprivation in healthy volunteers

• Published in: Journal of applied physiology (1985) Vol. 113; no. 2; pp. 232 - 236
• Main Authors: Dettoni, Josilene L, Consolim-Colombo, Fernanda Marciano, Drager, Luciano F, Rubira, Marcelo C, Souza, Silvia Beatriz P Cavasin de, Irigoyen, Maria Claudia, Mostarda, Cristiano, Borile, Suellen, Krieger, Eduardo M, Moreno, Jr, Heitor, Lorenzi-Filho, Geraldo
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 15.07.2012
• Subjects: Adult; Blood Pressure; Cardiovascular system; Endothelium, Vascular - physiopathology; Epidemiology; Heart Rate; Humans; Male; Morbidity; Mortality; Motor Activity; Risk assessment; Sleep; Sleep Deprivation - physiopathology; Sympathetic Nervous System - physiopathology; Vasodilation
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/japplphysiol.01604.2011

Sleep deprivation is common in Western societies and is associated with increased cardiovascular morbidity and mortality in epidemiological studies. However, the effects of partial sleep deprivation on the cardiovascular system are poorly understood. In the present study, we evaluated 13 healthy male volunteers (age: 31 ± 2 yr) monitoring sleep diary and wrist actigraphy during their daily routine for 12 nights. The subjects were randomized and crossover to 5 nights of control sleep (>7 h) or 5 nights of partial sleep deprivation (<5 h), interposed by 2 nights of unrestricted sleep. At the end of control and partial sleep deprivation periods, heart rate variability (HRV), blood pressure variability (BPV), serum norepinephrine, and venous endothelial function (dorsal hand vein technique) were measured at rest in a supine position. The subjects slept 8.0 ± 0.5 and 4.5 ± 0.3 h during control and partial sleep deprivation periods, respectively (P < 0.01). Compared with control, sleep deprivation caused significant increase in sympathetic activity as evidenced by increase in percent low-frequency (50 ± 15 vs. 59 ± 8) and a decrease in percent high-frequency (50 ± 10 vs. 41 ± 8) components of HRV, increase in low-frequency band of BPV, and increase in serum norepinephrine (119 ± 46 vs. 162 ± 58 ng/ml), as well as a reduction in maximum endothelial dependent venodilatation (100 ± 22 vs. 41 ± 20%; P < 0.05 for all comparisons). In conclusion, 5 nights of partial sleep deprivation is sufficient to cause significant increase in sympathetic activity and venous endothelial dysfunction. These results may help to explain the association between short sleep and increased cardiovascular risk in epidemiological studies.