Christophe Rault1,2, Aude Sangaré3, Véronique Diaz1,2, Stéphanie Ragot1,4, Jean-Pierre Frat1,5, Mathieu Raux6,7, Thomas Similowski6,8, René Robert1,5, Arnaud W Thille1,5, Xavier Drouot1,2,3,9. 1. INSERM, CIC 1402, Equipe Alive, Faculté de Médecine et de Pharmacie, Université de Poitiers, Poitiers, France. 2. Service d'Explorations fonctionnelles, Physiologie respiratoire et de l'exercice. 3. Service de Neurophysiologie Clinique. 4. Centre d'Investigation Clinique, Unité de méthodologie biostatistique, and. 5. Réanimation Médicale, CHU de Poitiers, Poitiers, France. 6. Sorbonne Universités, INSERM, UMRS1158 Neurophysiologie Respiratoire Expérimentale et Clinique, Paris, France. 7. AP-HP, Groupe Hospitalier Pitié-Salpêtrière Charles Foix, SSIAP, Département d'Anesthésie-Réanimation, Paris, France. 8. AP-HP, Groupe Hospitalier Pitié-Salpêtrière Charles Foix, SSIAP, Service de Pneumologie, Medecine Intensive et Réanimation, Département R3S, Paris, France; and. 9. INSERM U-1084, Experimental and Clinical Neurosciences Laboratory, Neurobiology and Neuroplasticity and Neuro-development Group, Poitiers, France.
Abstract
Rationale: Sleep deprivation can alter endurance of skeletal muscles, but its impact on respiratory command is unknown. Objectives: We aimed to assess the effect of sleep deprivation on respiratory motor output and inspiratory endurance. Methods:Inspiratory endurance was investigated twice in random order, following a normal sleep night and a sleepless night. Healthy participants were asked to breathe as long as possible until task failure against a moderate inspiratory threshold constraint. Transdiaphragmatic pressure and diaphragm electrical activity were measured throughout the trial to assess pressure output of the diaphragm and overall respiratory motor output. Cortical contribution to respiratory motor output was assessed by measurement of preinspiratory motor potential amplitude and by cervical magnetic simulation.Measurements and Main Results:Twenty healthy male participants were studied. Time to task failure was significantly shorter after sleep deprivation than after normal sleep: (30 min [interquartile range [IQR], 17-41] vs. 60 min [IQR, 45-60], P = 0.002). At the beginning of the trial, preinspiratory motor potential amplitude was significantly lower in the sleep-deprivation condition (4.5 μV [IQR, 2.5-6.4] vs. 7.3 μV [IQR, 4.3-10.4], P = 0.02) and correlated significantly with the duration of the endurance trial. In the sleep-deprivation condition, preinspiratory motor potential amplitude, electrical activity of the diaphragm, pressure output of the diaphragm, and Vt decreased and the respiratory rate increased significantly from the beginning to the end of the trial. Such decreases did not occur in the normal-sleep condition.Conclusions: One night of sleep deprivation reduces respiratory motor output by altering its cortical component with subsequent reduction of inspiratory endurance by half. These results suggest that altered sleep triggers severe brain dysfunctions that could precipitate respiratory failure.
RCT Entities:
Rationale: Sleep deprivation can alter endurance of skeletal muscles, but its impact on respiratory command is unknown. Objectives: We aimed to assess the effect of sleep deprivation on respiratory motor output and inspiratory endurance. Methods: Inspiratory endurance was investigated twice in random order, following a normal sleep night and a sleepless night. Healthy participants were asked to breathe as long as possible until task failure against a moderate inspiratory threshold constraint. Transdiaphragmatic pressure and diaphragm electrical activity were measured throughout the trial to assess pressure output of the diaphragm and overall respiratory motor output. Cortical contribution to respiratory motor output was assessed by measurement of preinspiratory motor potential amplitude and by cervical magnetic simulation.Measurements and Main Results: Twenty healthy male participants were studied. Time to task failure was significantly shorter after sleep deprivation than after normal sleep: (30 min [interquartile range [IQR], 17-41] vs. 60 min [IQR, 45-60], P = 0.002). At the beginning of the trial, preinspiratory motor potential amplitude was significantly lower in the sleep-deprivation condition (4.5 μV [IQR, 2.5-6.4] vs. 7.3 μV [IQR, 4.3-10.4], P = 0.02) and correlated significantly with the duration of the endurance trial. In the sleep-deprivation condition, preinspiratory motor potential amplitude, electrical activity of the diaphragm, pressure output of the diaphragm, and Vt decreased and the respiratory rate increased significantly from the beginning to the end of the trial. Such decreases did not occur in the normal-sleep condition.Conclusions: One night of sleep deprivation reduces respiratory motor output by altering its cortical component with subsequent reduction of inspiratory endurance by half. These results suggest that altered sleep triggers severe brain dysfunctions that could precipitate respiratory failure.