4.5 Article

Total sleep deprivation alters cardiovascular reactivity to acute stressors in humans

Journal

JOURNAL OF APPLIED PHYSIOLOGY
Volume 113, Issue 6, Pages 903-908

Publisher

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.00561.2012

Keywords

autonomic activity; blood pressure; cold pressor test; mental stress; tachycardia

Funding

  1. National Heart, Lung, and Blood Institute [HL-098676]

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Yang H, Durocher JJ, Larson RA, DellaValla JP, Carter JR. Total sleep deprivation alters cardiovascular reactivity to acute stressors in humans. J Appl Physiol 113: 903-908, 2012. First published July 19, 2012; doi:10.1152/japplphysiol.00561.2012.-Exaggerated cardiovascular reactivity to mental stress (MS) and cold pressor test (CPT) has been linked to increased risk of cardiovascular disease. Recent epidemiological studies identify sleep deprivation as an important risk factor for hypertension, yet the relations between sleep deprivation and cardiovascular reactivity remain equivocal. We hypothesized that 24-h total sleep deprivation (TSD) would augment cardiovascular reactivity to MS and CPT and blunt the MS-induced forearm vasodilation. Because the associations between TSD and hypertension appear to be stronger in women, a secondary aim was to probe for sex differences. Mean arterial pressure (MAP), heart rate (HR), and muscle sympathetic nerve activity (MSNA) were recorded during MS and CPT in 28 young, healthy subjects (14 men and 14 women) after normal sleep (NS) and 24-h TSD (randomized, crossover design). Forearm vascular conductance (FVC) was recorded during MS. MAP, FVC, and MSNA (n = 10) responses to MS were not different between NS and TSD (condition x time, P > 0.05). Likewise, MAP and MSNA (n = 6) responses to CPT were not different between NS and TSD (condition x time, P > 0.05). In contrast, increases in HR during both MS and CPT were augmented after TSD (condition x time, P <= 0.05), and these augmented HR responses persisted during both recoveries. When analyzed for sex differences, cardiovascular reactivity to MS and CPT was not different between sexes (condition x time x sex, P > 0.05). We conclude that TSD does not significantly alter MAP, MSNA, or forearm vascular responses to MS and CPT. The augmented tachycardia responses during and after both acute stressors provide new insight regarding the emerging links among sleep deprivation, stress, and cardiovascular risk.

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