Tolérance à l'effort après réduction de sommeil et après prise d'un hypnotique: Le Zolpidem

The aim of the present study was to investigate the effects of a delayed bedtime (3 a.m.), an advanced rising (3 a.m.), a sleep under placebo and under a hypnotic compound, i.e. 10 mg of Zolpidem (Stilnox®) on sleep structure and on the adaptations to a subsequent exercise in 8 male athletes. The chronology of these nights was randomized and each treatment administered in a double blind fashion. During each experimental night, subjects were monitored with conventional EEG/EOG/EMG polygraphic recordings. The next day, athletic performance was tested using a bicycle ergometer. A codified exercise was performed and consisted to a 10 min warm up followed by a 30 min steady state cycling corresponding to 75% of predetermined V˙O2 max. Then the work load increased progressively by steps of 10 W every minute until exhaustion. The recovery lasted 30 min. Heart rate, ventilation, V˙O2, ERO2 were monitored during all exercise and recovery. Plasma lactates and catecholamines were also measured at the same time. The data concerning sleep recordings showed that both nights with partial sleep deprivation resulted in a drop of time spent in slow wave sleep II (decrease of 55%) and in rapid eye movement sleep (decrease of 45%) while the amount of slow wave sleep III and IV were identical to that observed after the reference night. The sleep onset latency and the amount of sleep in stage I was reduced only after the delayed bedtime. Sleep data under Zolpidem did not show any significantly difference in the amount of different sleep stages. At subsequent exercise conducted after both reduced-sleep nights, lactate levels and minute ventilation were significantly higher during the constant load cycling whereas heart rate, V˙O2 and catecholamines were not altered. At maximal exercise, neither lactate nor V˙E were impaired while peak V˙O2 decreased and the V˙E/V˙O2 increased. The other parameters were not modified. The maximal sustained work load had a tendency to be lower after the late bedtime (294 ± 31 W) and after the early rising (292 ± 37 W) compared to control (308 ± 28.9 W). At recovery, no difference was observed in the studied parameters. After nights induced by Zolpidem or placebo, no alteration in cardiorespiratory and metabolic values was noted. These findings show that physiological adaptations and the ability to perform maximal exercise are affected by a partial sleep loss but not by a single ingestion of Zolpidem prior to sleep.