Endotoxin, a lipopolysaccharide (0.4 or 0.8 ng/kg body weight), was in
jected at 1900 hours in 17 healthy men in a single-blind, placebo-cont
rolled experiment. The administration was followed by a 4-hour period
of quiet wakefulness in bed (light intensity <200 lux). Unlimited slee
p was allowed after 2300 hours (lights off) until the next morning. Th
e electroencephalogram (EEG), electromyogram, electrooculogram, electr
ocardiogram and rectal temperature were recorded throughout the experi
mental session. Standard sleep stages were assessed, and the EEG was s
ubmitted to a state-specific, serial spectral analysis. Endotoxin admi
nistration induced a rise of body temperature and heart rate, which st
arted approximately 2 hours after the injection and persisted through
most of the sleep period. Sleep latency remained unchanged, whereas ra
pid eye movement (REM) sleep latency increased from 60.3 to 89.0 minut
es (paired t test; p = 0.06) compared to control values. Stage 2 sleep
was elevated from 45.5 to 49.0% of time in bed (p < 0.05), and total
nonrapid eye movement (NREM) sleep from 64.2 to 69.1% (p < 0.05). No s
ignificant change could be observed in slow-wave sleep (SWS, stages 3
and 4). During the first 4 hours of the sleep period, NREM sleep EEG s
pectral power was distinctly and markedly increased between 8 and 12 H
z (alpha) and 15 and 20 Hz (beta) (p < 0.05), whereas at the same time
EEG power between 1 and 8 Hz (delta, theta) was not significantly cha
nged. We conclude that in humans the primary host response induced by
endotoxin initially suppresses REM sleep and increases stage 2 NREM sl
eep, but does not affect SWS. No clear modification of sleep EEG delta
activity could be observed after endotoxin injection, despite marked
endocrinological and physiological changes such as the elevation of bo
dy temperature. Numerous factors related to the human primary host res
ponse may be responsible for the EEG intensification of the alpha and
beta range.