On 2016 Nov 15, IRWIN FEINBERG commented:

Kurth et al base their study on a faulty premise, stated in the first sentence: “Brain networks respond to sleep deprivation or restriction (emphasis added) with increased sleep depth which is quantified as slow-wave activity (SWA) in the sleep electroencephalogram (EEG)…” In fact, there is now abundant evidence that sleep restriction does not increase SWA in subsequent sleep, although it produces strong increases in behavioral sleepiness. We first observed this result in a 1991 study of the effects of acute termination of the last 3.5 h of sleep. This decrease in sleep duration did not produce the expected increase in either visually scored or computer measured SWA Feinberg I, 1991. This result so surprised us that we immediately repeated the experiment in a new group of subjects and obtained the same result Travis F, 1991. Since it was well established that a night of total sleep deprivation increases SWA, we sought to determine how much sleep restriction is needed to increase SWA. We limited sleep to 100 min and found that this restriction increased SWA. However, the increased SWA after 100 min of sleep differed from that after a night of total sleep deprivation (TSD). Whereas TSD reduced both the amplitude and incidence of slow waves, restriction to 100 min of sleep increased SW incidence but not amplitude Feinberg I, 1988. Subsequently, an extensive study by van Dongen et al showed that sleep restriction to 4 h/night for 14 consecutive nights does not increase SWA although it produces intense sleepiness and impaired vigilance Van Dongen HP, 2003. The previous studies were done with young adults so that it remained possible that the young subjects Kurth et al studied might have a different SWA response to sleep restriction. This is not the case. Sleep restriction in late childhood also failed to increase SWA Campbell IG, 2016. An incidental but reliable observation in our previous studies was that TSD Feinberg I, 1979 and partial sleep deprivation by restricted sleep (studies cited above) both reduce eye movement density in REM sleep. None of this previous work is cited or discussed by Kurth et al. The omissions are especially regrettable for two reasons. First, the failure of sleep restriction to increase SWA illustrates one of the major predictive failures of recovery models of SWA (both our own Feinberg I, 1974 and the similar two-process model Borbély AA, 2016). Second, the suppressive effects of sleep loss on eye movement density holds major biological implications for interrelations among sleep depth, NREM and REM sleep. Kurth et al's disregard of previous, highly relevant, well-substantiated data impedes research progress.

On 2016 Nov 15, IRWIN FEINBERG commented:

Kurth et al base their study on a faulty premise, stated in the first sentence: “Brain networks respond to sleep deprivation or restriction (emphasis added) with increased sleep depth which is quantified as slow-wave activity (SWA) in the sleep electroencephalogram (EEG)…” In fact, there is now abundant evidence that sleep restriction does not increase SWA in subsequent sleep, although it produces strong increases in behavioral sleepiness. We first observed this result in a 1991 study of the effects of acute termination of the last 3.5 h of sleep. This decrease in sleep duration did not produce the expected increase in either visually scored or computer measured SWA Feinberg I, 1991. This result so surprised us that we immediately repeated the experiment in a new group of subjects and obtained the same result Travis F, 1991. Since it was well established that a night of total sleep deprivation increases SWA, we sought to determine how much sleep restriction is needed to increase SWA. We limited sleep to 100 min and found that this restriction increased SWA. However, the increased SWA after 100 min of sleep differed from that after a night of total sleep deprivation (TSD). Whereas TSD reduced both the amplitude and incidence of slow waves, restriction to 100 min of sleep increased SW incidence but not amplitude Feinberg I, 1988. Subsequently, an extensive study by van Dongen et al showed that sleep restriction to 4 h/night for 14 consecutive nights does not increase SWA although it produces intense sleepiness and impaired vigilance Van Dongen HP, 2003. The previous studies were done with young adults so that it remained possible that the young subjects Kurth et al studied might have a different SWA response to sleep restriction. This is not the case. Sleep restriction in late childhood also failed to increase SWA Campbell IG, 2016. An incidental but reliable observation in our previous studies was that TSD Feinberg I, 1979 and partial sleep deprivation by restricted sleep (studies cited above) both reduce eye movement density in REM sleep. None of this previous work is cited or discussed by Kurth et al. The omissions are especially regrettable for two reasons. First, the failure of sleep restriction to increase SWA illustrates one of the major predictive failures of recovery models of SWA (both our own Feinberg I, 1974 and the similar two-process model Borbély AA, 2016). Second, the suppressive effects of sleep loss on eye movement density holds major biological implications for interrelations among sleep depth, NREM and REM sleep. Kurth et al's disregard of previous, highly relevant, well-substantiated data impedes research progress.