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April 27, 2012Journal of Applied Physiology242 citations

Cardiovascular effects of partial sleep deprivation in healthy volunteers

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JDJosilene Lopes DettoniFCFernanda Marciano Consolim‐ColomboLDLuciano F. Drager

Key Result

Five nights of partial sleep deprivation significantly increased sympathetic activity and reduced maximum endothelial dependent venodilatation (41% vs 100%; P<0.05) compared to control sleep.

Study Design

Type

RCT (n=13)

Randomization

crossover

Structured PICO

Does partial sleep deprivation increase sympathetic activity and impair venous endothelial function in healthy volunteers?

P
Population
13 healthy male volunteers, age 31 ± 2 years
I
Intervention
5 nights of partial sleep deprivation (<5 h)
C
Comparator
5 nights of control sleep (>7 h)
O
Outcome
Heart rate variability (HRV), blood pressure variability (BPV), serum norepinephrine, and venous endothelial function measured at rest in a supine positionsurrogate

Partial sleep deprivation over 5 nights significantly increases sympathetic activity and impairs venous endothelial function in healthy young men, providing a potential mechanism for the epidemiological association between short sleep and increased cardiovascular risk.

Main Result

p-value: p=<0.05

Abstract

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.

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Cite This Study

Dettoni et al. (2012) conducted an RCT in Healthy volunteers (n=13). Partial sleep deprivation (<5 h) vs. Control sleep (>7 h) was evaluated on Heart rate variability, blood pressure variability, serum norepinephrine, and venous endothelial function (p=<0.05). Five nights of partial sleep deprivation significantly increased sympathetic activity and reduced maximum endothelial dependent venodilatation (41% vs 100%; P<0.05) compared to control sleep.

synapsesocial.com/papers/6a1109491457680e71f336fahttps://doi.org/10.1152/japplphysiol.01604.2011
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