OBJECTIVE: Arousal (AR) from sleep is associated with an autonomic reflex activation raising blood pressure and heart rate (HR). Recent studies indicate that sleep deprivation may affect the autonomic system, contributing to high vascular risk. Since in sleep disorders a sleep fragmentation and a partial sleep deprivation occurs, it could be suggested that the cardiovascular effects observed at AR from sleep might be physiologically affected when associated with sleep deprivation. The aim of the study was to examine the effect of sleep deprivation on cardiac arousal response in healthy subjects. METHODS: Seven healthy male subjects participated in a 64 h sleep deprivation protocol. Arousals were classified into four groups, i.e. >3<6 s, >6<10 s, >10<15 s and >15 s, according to their duration. Pre-AR HR values were measured during 10 beats preceding the AR onset, and the event-related HR fluctuations were calculated during the 20 beats following AR onset. As an index of cardiac activation, the ratio of highest HR in the post-AR period over the lowest recorded before AR (HR ratio) was calculated. RESULTS: For AR lasting less than 10 s, the occurrence of AR induces typical HR oscillations in a bimodal pattern, tachycardia followed by bradycardia. For AR lasting more than 10 s, i.e. awakenings, the pattern was unimodal with a more marked and sustained HR rise. The HR response was consistently similar across nights, during NREM and REM sleep, without difference between conditions. CONCLUSIONS: Overall, total sleep deprivation appeared to have no substantial effect on cardiac response to spontaneous arousals and awakenings from sleep in healthy subjects. Further studies are needed to clarify the role of chronic sleep deprivation on cardiovascular risk in patients with sleep disorders. SIGNIFICANCE: In healthy subjects acute prolonged sleep deprivation does not affect the cardiac response to arousal.
OBJECTIVE: Arousal (AR) from sleep is associated with an autonomic reflex activation raising blood pressure and heart rate (HR). Recent studies indicate that sleep deprivation may affect the autonomic system, contributing to high vascular risk. Since in sleep disorders a sleep fragmentation and a partial sleep deprivation occurs, it could be suggested that the cardiovascular effects observed at AR from sleep might be physiologically affected when associated with sleep deprivation. The aim of the study was to examine the effect of sleep deprivation on cardiac arousal response in healthy subjects. METHODS: Seven healthy male subjects participated in a 64 h sleep deprivation protocol. Arousals were classified into four groups, i.e. >3<6 s, >6<10 s, >10<15 s and >15 s, according to their duration. Pre-AR HR values were measured during 10 beats preceding the AR onset, and the event-related HR fluctuations were calculated during the 20 beats following AR onset. As an index of cardiac activation, the ratio of highest HR in the post-AR period over the lowest recorded before AR (HR ratio) was calculated. RESULTS: For AR lasting less than 10 s, the occurrence of AR induces typical HR oscillations in a bimodal pattern, tachycardia followed by bradycardia. For AR lasting more than 10 s, i.e. awakenings, the pattern was unimodal with a more marked and sustained HR rise. The HR response was consistently similar across nights, during NREM and REM sleep, without difference between conditions. CONCLUSIONS: Overall, total sleep deprivation appeared to have no substantial effect on cardiac response to spontaneous arousals and awakenings from sleep in healthy subjects. Further studies are needed to clarify the role of chronic sleep deprivation on cardiovascular risk in patients with sleep disorders. SIGNIFICANCE: In healthy subjects acute prolonged sleep deprivation does not affect the cardiac response to arousal.
Authors: M O Mendez; A M Bianchi; N Montano; V Patruno; E Gil; C Mantaras; S Aiolfi; S Cerutti Journal: Med Biol Eng Comput Date: 2008-02-12 Impact factor: 2.602
Authors: Jeremy A Bigalke; Ian M Greenlund; Jennifer R Nicevski; Carl A Smoot; Benjamin Oosterhoff; Neha A John-Henderson; Jason R Carter Journal: Am J Physiol Heart Circ Physiol Date: 2021-07-30 Impact factor: 5.125