JOURNAL ARTICLE
RANDOMIZED CONTROLLED TRIAL

Cognitive workload and sleep restriction interact to influence sleep homeostatic responses

Namni Goel, Takashi Abe, Marcia E Braun, David F Dinges
Sleep 2014 November 1, 37 (11): 1745-56
25364070

STUDY OBJECTIVES: Determine the effects of high versus moderate workload on sleep physiology and neurobehavioral measures, during sleep restriction (SR) and no sleep restriction (NSR) conditions.

DESIGN: Ten-night experiment involving cognitive workload and SR manipulations.

SETTING: Controlled laboratory environment.

PARTICIPANTS: Sixty-three healthy adults (mean ± standard deviation: 33.2 ± 8.7 y; 29 females), age 22-50 y.

INTERVENTIONS: Following three baseline 8 h time in bed (TIB) nights, subjects were randomized to one of four conditions: high cognitive workload (HW) + SR; moderate cognitive workload (MW) + SR; HW + NSR; or MW + NSR. SR entailed 5 consecutive nights at 4 h TIB; NSR entailed 5 consecutive nights at 8 h TIB. Subjects received three workload test sessions/day consisting of 15-min preworkload assessments, followed by a 60-min (MW) or 120-min (HW) workload manipulation comprised of visually based cognitive tasks, and concluding with 15-min of postworkload assessments. Experimental nights were followed by two 8-h TIB recovery sleep nights. Polysomnography was collected on baseline night 3, experimental nights 1, 4, and 5, and recovery night 1 using three channels (central, frontal, occipital [C3, Fz, O2]).

MEASUREMENTS AND RESULTS: High workload, regardless of sleep duration, increased subjective fatigue and sleepiness (all P < 0.05). In contrast, sleep restriction produced cumulative increases in Psychomotor Vigilance Test (PVT) lapses, fatigue, and sleepiness and decreases in PVT response speed and Maintenance of Wakefulness Test (MWT) sleep onset latencies (all P < 0.05). High workload produced longer sleep onset latencies (P < 0.05, d = 0.63) and less wake after sleep onset (P < 0.05, d = 0.64) than moderate workload. Slow-wave energy-the putative marker of sleep homeostasis-was higher at O2 than C3 only in the HW + SR condition (P < 0.05).

CONCLUSIONS: High cognitive workload delayed sleep onset, but it also promoted sleep homeostatic responses by increasing subjective fatigue and sleepiness, and producing a global sleep homeostatic response by reducing wake after sleep onset. When combined with sleep restriction, high workload increased local (occipital) sleep homeostasis, suggesting a use-dependent sleep response to visual work. We conclude that sleep restriction and cognitive workload interact to influence sleep homeostasis.

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