In normal men, the majority of GH secretion occurs in a single large postsl
eep onset pulse that is suppressed during total sleep deprivation. We exami
ned the impact of semichronic partial sleep loss, a highly prevalent condit
ion, on the 24-h growth hormone profile. Eleven young men were studied afte
r six nights of restricted bedtimes (0100-0500) and after 7 nights of exten
ded bedtimes (2100-0900). Slow-wave sleep (SWS) was estimated as the durati
on of stages III and IV. Slow-wave activity (SWA) was calculated as electro
encephalogram power density in the 0.5- to 3-Hz frequency range. During the
state of sleep debt, the GH secretory pattern was biphasic, with both a pr
esleep onset "circadian" pulse and a postsleep onset pulse. Postsleep onset
GH secretion was negatively related to presleep onset secretion and tended
to be positively correlated with the amount of concomitant SWA. When sleep
was restricted, both SWS and SWA were increased during early sleep. Unexpe
ctedly, the increase in SWA affected the second, rather than the first, SWA
cycle, suggesting that presleep onset GH secretion may have limited SWA in
the first cycle, possibly via an inhibition of central GH-releasing hormon
e activity. Thus neither the GH profile nor the distribution of SWA conform
ed with predictions from acute sleep deprivation studies, indicating that a
daptation mechanisms are operative during chronic partial sleep loss.