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Updated: Mar 8, 2026

Establishing a Device for Sleep Deprivation in Mice
Published on: September 22, 2023
Protective effects of exercise training on endothelial dysfunction induced by total sleep deprivation in healthy
Fabien Sauvet1, Pierrick J Arnal2, Pierre Emmanuel Tardo-Dino3
1Institut de recherche biomédicale des armées (IRBA), Brétigny-sur-Orge, France; Equipe VIFASOM (EA7330), Université Paris Descartes, Hôtel Dieu, France.
Background:
Sleep loss is a risk factor for cardiovascular events mediated through endothelial dysfunction.
Aims:
To determine if 7weeks 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 7weeks 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).
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