Selective slow-wave sleep (SWS) deprivation through acoustic stimulation and SWS rebound

Visuall) scorcd dclta acti\it! (SWS) increases alter total and partiid \Iccp dcpri\ation. Ho\\e\cr, i t is not clear \\ hcthcr SWS amount is onl) a lunction 0 1 pnor waking duration, as prcdictcd b) thc r i v i ~ - ~ ~ r i ~ ~ ' r ~o r. s\\ ~hc~th~c~r ii~t iis/ arl/s.o rclatcd l o tlic structurc 01 thc prc\ ious sleep period (it.t o the timc spent in SWS). In lael, sc\craI sludics ha\c rho\\ n that SWS l o v t during partial o r wIccti\c 4ccp dcpri\ation I\ rcco\crcd through a compensatnc rcbound in thc succcssi\ e period of slecp (c.g. 1-2). Oihcr idcnccs sccnl to qucstion thc dcpcndcncc ol SWS o n prior \\ aking duration: lor e\aniplc. i t has bccn Iiund that 3.5-4 h ol sleep curtailmcnt do not cause an! SWS rch)und in thc rcco\cr) night (3-5)T he aim 01 thi\ \tud) is lo \clccti\cl! depri\c SWS during tuoconsecutivc nights \rithout both disrupting slccp structure and changing thc total slccp duiation. and to ohcch eithci thc prcscncc or thc ab\cncc of a cornpenhati\ e SWS rchwnd in thc folio\\ ing rcco\erq night. METHODS. Ten normal male Ss. partccipatcd to 6 c(insccuti\c Iah)r~kir) nights: I ) Adaptation; 3) Basclinc (BSL); 3) Baseline nith awakenings (BSL-A): 4) SWS Depmauon-l (DEP-I): -5) SWS Dcpri\ation-2 (DEP-2),6) Rcco\cr) (REC). Dui-in@ thc nights #4 and #5. SWS depn\atton was accomplished b) sounding a tonc (frcqucnc): INX) HI; intensit): 4 0 1 10 dB) \\hcnc\cr at least 2 dclta \\a\cs ((1.5-3.S HI: >75 1iV) appeared in a IS-scc recording inter\al Bcginning Irom the loncst intensit). 11 \\as increascd i n \reps olS dB il no rcsponsc occurrcd (\lccp stagc \hilt, K complc\. EEG dcsinchronization. alpha burst. musclc tone increase. sIo\! e ) c mi\ emcnh). RESULTS. A one-ma! ANOVA vith Niqlrr as S-le\el\ lactoi (BSL. BSL-A. DEP-I, DEP-2, REC) \\as carricd out on pcrccntagc and latcnc) 01 each slecp stagc, Wakcfulncss (W). Total Slccp Timc (TST), Total Bcd Timc (TBT), numbcr 01 a\\ akcninp (NA), and Sleep Elficicnc) Indcx (SEI). Being stages 3. 4 and SWS (3+4) \irtuall) absent during DEP-I and DEP-2 (mcan pcrccntagc 01 SWS \\as 0.2Y'Z and (1.6S'Z in DEP- I and DEP-2 rcspccti\cl)). \\c compared only BSL, BSL-A and REC nights lor these siagcs. ANOVAs sho\\cd a signil~icanti ncrcasc 01 QS4(F=16.59:p = 003). VSWS (Fz21.34: p=.O()I) and of SEI (F=S.42: p=.o03) in the REC. a\ compared to thc BSL-A: thcsc cllccts ncre parallclcd b) a signilicant khortcning 01 S3 (F=7.70: p=.O2) and S4 (F=l1.37, p=.Ol) Iaicncics. As a consequence 0 1 SWS dcpri\alion. 'ZS2 signilicantl) increased in the DEP nights uith rc\pcct to BSL. BSL-A and REC night\ (F=17.Yl; p=.ON)I), nhilc Q W incrcascd (F=3.5: p=.O2) in the DEP-I night as compared to the othcr nights (duc to one outla)cr Suhjcct). No othcr signilicant dillcrences bctnccn nights were lound. CONCLUSIONS. The \cr) cllccti\c scIccti\c SWS dcpri\ation obtaincd lor 2 conscculi\c nights \\a\ accompanicd b) an increase o l n.akefulncss onl) during the DEP-I night. This result \!as duc to onc subjccr that during DEP-I night sho\\cd to bc \cr! sensiti\c to thc acoustic stimulation. being aaakcned several limcs by the tones. Discarding his data, the dillcrcncc in perccnvage o l \\akclulncss bctnccn DEP-I and thc other nights is ire/ .\i,qrrifii.~r~O/. n the other hand, thc lack of signilicant dillercnccs among nights nith regard to perccntagc 01' REM slccp. stagc I , MT and NA indicates that the acoustic stimulation technique did not disrupt normal slecparchitecturc. In addition, sclccti\c SWS dcpri\ation did not allcct TST. as SWS \\as replaced h) an increase ol slagc 2 . In conclusion, the SWS rebound n e lound during reco\cr! night lollon ing 2 night\ 01 SWS dcprn aiion. lurthcr support thc h) pothesis that dclta slccp amount IS more linked to SWS in the pre\ ious slecp perids than to the total slecp duration. SELECTIVE SWS DEPRIVATION DETERMINES A SWS REBOUND.