New Study Shows Sleep Deprivation Causes Endothelial Dysfunction, and Exercise Reverses the Effect

New Study Shows Sleep Deprivation Causes Endothelial Dysfunction, and Exercise Reverses the Effect

New Study Protective effects of exercise training on endothelial dysfunction induced by total sleep deprivation in healthy subjects Sauvet F1, Arnal PJ2, Tardo-Dino PE3, Drogou C4, Van Beers P4, Bougard C4, Rabat A4, Dispersyn G4, Malgoyre A3, Leger D5, Gomez-Merino D4, Chennaoui M4.

• 1Institut de recherche biomédicale des armées (IRBA), Brétigny-sur-Orge, France; Equipe VIFASOM (EA7330), Université Paris Descartes, Hôtel Dieu, France. Electronic address: Fabien.sauvet@gmail.com.

• 2Institut de recherche biomédicale des armées (IRBA), Brétigny-sur-Orge, France; Equipe VIFASOM (EA7330), Université Paris Descartes, Hôtel Dieu, France; Laboratoire de Physiologie de l’Exercice, Université de Lyon, Saint Etienne, France.

• 3Institut de recherche biomédicale des armées (IRBA), Brétigny-sur-Orge, France.

• 4Institut de recherche biomédicale des armées (IRBA), Brétigny-sur-Orge, France; Equipe VIFASOM (EA7330), Université Paris Descartes, Hôtel Dieu, France.

• 5Equipe VIFASOM (EA7330), Université Paris Descartes, Hôtel Dieu, France; APHP, Hôtel Dieu, Centre du Sommeil et de la Vigilance, Paris, France

Highlights

• •Sleep deprivation triggers endothelial dysfunction and inflammatory response.

• •Exercise training prevents endothelial dysfunction induced by sleep deprivation.

• •Exercise training could be considered as a relevant countermeasure to sleep deprivation.

• •Protective effect of exercise training is linked to inflammatory responses.

Background Sleep loss is a risk factor for cardiovascular events mediated through endothelial dysfunction. Aims To determine if 7 weeks of exercise training can limit cardiovascular dysfunction induced by total sleep deprivation (TSD) in healthy young men.

Methods 16 subjects were examined during 40-h TSD, both before and after 7 weeks of interval exercise training. Vasodilatation induced by ACh, insulin and heat (42 °C) and pulse wave velocity (PWV), blood pressure and heart rate (HR) were assessed before TSD (controlday), during TSD, and after one night of sleep recovery. Biomarkers of endothelial activation, inflammation, and hormones were measured from morning blood samples.

Results Before training, ACh-, insulin- and heat-induced vasodilatations were significantly decreased during TSD and recovery as compared with the control day, with no difference after training. Training prevented the decrease of ACh-induced vasodilation related to TSD after sleep recovery, as well as the PWV increase after TSD. A global lowering effect of training was found on HR values during TSD, but not on blood pressure. Training induces the decrease of TNF-α concentration after TSD and prevents the increase of MCP-1 after sleep recovery. Before training, IL-6 concentrations increased. Cortisol and testosterone decreased after TSD as compared with the control day, while insulin and E-selectin increased after sleep recovery. No effect of TSD or training was found on CRP and sICAM-1.

Conclusions In healthy young men, a moderate to high-intensity interval training is effective at improving aerobic fitness and limiting vascular dysfunction induced by TSD, possibly through pro-inflammatory cytokine responses.(ClinicalTrial:NCT02820649)