Previously, we found that regular sleep fragmentation, similar to that foun
d in patients with sleep apnoea/hypopnoea syndrome (SAHS), impairs daytime
function. Apnoeas and hypopnoeas occur in groups in patients with REM or po
sture related SAHS. Thus, we hypothesised that clustered sleep fragmentatio
n would have a similar impact on daytime function as regular sleep fragment
ation. We studied 16 subjects over two pairs of 2 nights and 2 days. The fi
rst night of each pair was for acclimatisation. On the second night, subjec
ts either had their sleep fragmented regularly every 90 s, or fragmented ev
ery 30 s for 30 min every 90 min, the remaining 60 min being undisturbed. W
e fragmented sleep with tones to produce a minimum 3 s increase in EEG freq
uency. During the days following each pair of nights we tested subjects day
time function. Total sleep time (TST) and microarousal frequency were simil
ar on both study nights. We found significantly less stage 2 (55 SD 4, 62 /- 7%; P = 0.001) and more slow wave sleep (21 SD 3, 12 +/- 6%; P < 0.001)
on the clustered night. Mean sleep onset latency was similar on MSLT (clust
ered 10 SD 5, regular 9 +/- 4 min; P = 0.7) and MWT (clustered 32 SD 7, reg
ular 30 +/- 7 min; P = 0.2). There was no difference in subjects mood or co
gnitive function after either study night. These results suggest that altho
ugh there is more slow wave sleep (SWS) on the clustered night, similar num
bers of sleep fragmenting events produced similar daytime function whether
the events were evenly spaced or clustered.