Insomnia and cardiovascular autonomic control

Abstract

Insomnia is the most prevalent sleep disorder, particularly among middle and older aged adults, and is associated with a variety of negative health consequences, including higher risk for cardiovascular disease. Unfortunately, the mechanisms linking insomnia with cardiovascular risk remain largely unknown, thus limiting targeted therapeutic interventions. The hyperarousal hypothesis has attracted the most support, positing that insomnia is a result of multisystem over-activation, including sympathetic hyperactivity, which promotes wakefulness and blocks the occurrence of sleep at the desired time. The results from literature in support of this hypothesis are inconclusive and mainly relay on studies that used methods to assess sympathetic activity lacking in specificity and reproducibility. The present review aims at summarizing the primary findings on autonomic nervous system regulation in insomnia while highlighting the advantages and limitations of the methods mainly used to support the increase in sympathetic function in insomnia. Collectively, this review aims to provide novel perspectives on conceptualizing insomnia and suggest innovative approaches to help elucidate the relationship between insomnia and autonomic nervous system activity.