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The influence of sleep deprivation and knowledge of results on perceptual encoding
Acta Psychologica North-Holland
173
66 (1987) 173-187
THE INFLUENCE OF SLEEP DEPRIVATION AND KNOWLEDGE OF RESULTS ON PERCEPTUAL ENCODING * Frank J.J.M. STEYVERS Tilburg University, The Netherlands Accepted
June 1987
This study investigates the way sleep deprivation effects on perceptual processes are modulated by knowledge of results (KR). In a choice-reaction task, signal quality was manipulated, combined with and without KR and under increasing levels of lack of sleep. It was found that the decrease of performance due to sleep deprivation was larger when stimuli were degraded. KR counteracted the effect of sleep deprivation; however, KR improved performance irrespective of signal quality. Hence, sleep deprivation seems to have a twofold effect on performance; one effect on perceptual processing, which is insensitive to KR, and another effect on some different processing stage, which is sensitive to KR. The results were interpreted in terms of a model of human performance (Sanders 1983) in which a distinction is made between two energetical mechanisms, ‘arousal’ and ‘activation’, subserving perceptual and motor stages of information processing, respectively. Thus, KR appears to compensate for the deficiency of one type of energetical mechanism, caused by sleep deprivation. Yet, this compensation does not appear to be the result of increased arousal, because, irrespective of KR, the performance decrement caused by signal degradation was more pronounced with lack of sleep.
Traditionally, performance in reaction tasks has been investigated in two almost exclusive research areas, concerning either energetical or computational aspects of the processes underlying performance. Recently, Sanders (1983) proposed an integration of these approaches by relating the notion of multiple resources (Navon and Gopher 1979; Gopher and Navon 1980; Gopher et al. 1982) to a linear-stage model of information processing (Sternberg 1969; Sanders 1980; Gopher and Sanders 1984). In this model, two processing stages are subserved by * This paper was supported by grant 560-259-021 of The Netherlands’ Organisation for Pure Scientific Research (ZWO). The author gratefully acknowledges the advice and support of A.J.P. Hendrikx, A.F. Sanders, A.W.K. Gaillard, and C.H.M. Brunia during all phases of this study, the assistance of A. Mannaerts during the execution of the experiment, and the critical comments of M.G.H. Coles, A.J.W. Boelhouwer, P. Kop, and P.J. Venemans on earlier drafts of this paper. Authors’ address: F. Steyvers, Dept. of Psychology, Tilburg University, P.O. Box 90153, 5000 LE Tilburg, The Netherlands.
OOOl-6918/87/$3.50
0 1987, Elsevier Science Publishers
B.V. (North-Holland)
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of KR after sleep deprivation
two separate pools of resources, or ‘energetical mechanisms’. The model also proposes that an arousal mechanism supplies energy to a perceptual-encoding stage, and that an activation mechanism furnishes a motor-adjustment stage. Under normal circumstances arousal and activation provide sufficient resources to the respective processing stages. However, under influence of a stressor, such as sleep deprivation, drugs or loud noise, the energetical supply from arousal and/or activation becomes inadequate, resulting in a performance decrement. The model further proposes an effort mechanism, which serves to compensate for insufficient energetical supply from the arousal or activation mechanism. However, the compensating effect of effort requires that the subject is aware of his or her below-standard performance, and is also willing and able to mobilize the extra effort (Kahneman 1973). Thus, compensatory effect requires subjects to evaluate their performance. Knowledge of results (KR) may facilitate this evaluation. The effect of KR on performance has been studied by Wilkinson (1961) in a self-placed continuous reaction task. After sleep deprivation, performance deteriorated; presentation of KR restored performance to the level of performance after normal sleep. After normal sleep, KR had no effect on performance. In terms of Sanders’ (1983) model, these results can be explained by assuming that, as a result of KR, the level of energetical supply is restored, and the detrimental effects of sleep deprivation are counteracted. Wilkinson’s (1961) experiment did not involve task variables related to particular processing stages; therefore the question whether the effect of KR is on particular processing stages, by way of exciting one or more energetical mechanisms, cannot be answered. This study aims at taking a closer view to the locus of effect of KR after sleep deprivation. There is some evidence that perceptual as well as motoric processes are affected by lack of sleep. Sanders et al. (1982) found that sleep deprivation enhanced the detrimental effect of signal degradation. According to additive-factors logic this suggests that sleep deprivation affects perceptual encoding (Sanders 1980). In addition, Frowein et al. (1981b) reported that sleep deprivation enhanced the effect of time uncertainty. This suggests an effect of sleep deprivation on the motor-adjustment stage (Sanders 1980). Sanders (1983) integrates these findings in his model and proposes that these studies contain evidence for an influence of sleep deprivation on both the arousal and the activation mechanism.
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The aim of the present study is to investigate whether the compensatory activity of KR after sleep deprivation involves arousal. A manual six-choice reaction task was used, in which signal quality was manipulated. It is expected that sleep deprivation impairs performance, and more so when signals are degraded. KR is expected to compensate for this performance decrement. Thus, a second-order interaction is expected between sleep deprivation, signal degradation and KR; after sleep deprivation, KR will improve performance and reduce the combined effect of signal degradation and lack of sleep. In terms of Sanders’ (1983) model, sleep deprivation impairs performance by reducing the level of arousal, and arousal becomes critical to performance in case of degraded stimuli. KR restores performance by evoking compensatory effort. After normal sleep, KR will not improve performance, because the arousal level suffices to process degraded as well as intact signals adequately. Since effects of lack of sleep seem to appear only after some time (Wilkinson 1961; Sanders 1983), it is expected that these effects will occur more clearly in the second half of the working period. The demands on information processing are reflected in certain aspects of the evoked cardiac response (ECR) (e.g., Lacey 1967; Coles and Strayer 1985; Orlebeke et al. 1985). Heartrate deceleration preceding the action signal has been shown to depend on the expected difficulty of the forthcoming stimulus (Coles 1974; Duncan-Johnson and Coles 1974). Therefore, the present study tests the hypothesis that enhanced demands on stimulus encoding will enlarge the heartrate deceleration preceding the action signal in the ECR, but only when the system copes effectively with these demands. It is expected that the deceleration will be larger when signals are degraded. This effect should be independent of KR after normal sleep. After sleep deprivation and without KR, this effect should diminish. When the presentation of KR leads to improved performance, the deceleration will again become larger for degraded than for intact signals. Method Subjects Sixteen healthy, male persons, between 20 and 32 years of age, served as subjects. All subjects were right-handed and they had no prior experience with the experimental task. They received Dfl.300,- for participation.
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Task A subject was seated in a sound-attenuated, dimly illuminated cubicle at a slanted table, in front of a backprojection screen. An array of eight response buttons (1.09 cm2) was mounted on the table in a semi-circular configuration and labeled 1 to 8 in clockwise order. A home-key was mounted in the center of this semi-circle at a distance of 15 cm from the target-keys. Subjects were instructed to react as fast as possible to the signals with the right index finger, starting from the home-key towards one of the target-keys. A correct response consisted of pressing the key with the same label as the action signal (AS). Keys 1 and 8 were not used because of their anchor positions. AS duration was maximally 800 msec, but home-key release within 800 msec after AS onset terminated AS presentation immediately. A warning signal (WS) of 800 msec duration was presented 4 set before every AS. The response was followed by KR presentation, separately for response speed and accuracy. KR lasted until WS-onset of the next trial. Stimuli and apparatus The stimuli consisted of slides projected on the back of the screen, covering an area of 12 x 14.5 cm; a visual angle of 6.4 degrees. The screen had an overall luminance of 5 cd/m2, and the luminance of the stimuli was 30 cd/m2. The AS was composed of a dot pattern, shaped as any one of the digits 2 through 7 in a rectangular dotted frame (Frowein et al. 1981a). The WS consisted of an arrow-shaped dot pattern placed in a dotted frame, identical to the frame of the AS. The arrow pointed either to the left or to the right, indicating whether the next AS would belong either to the subset (2, 3, 4) or to the subset (5, 6, 7) respectively. In order to obtain an equal overall luminance, all
Fig. 1. Examples of the stimuli. Above: action signal # 2. Below: warning right. At the left intact signals, at the right degraded signals.
signal
arrow
to the
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stimuli were composed of a constant number of dots; 46 for WS and 50 for AS. Stimuli were degraded by placing dots from the surrounding frame of the intact stimuli to random positions within the frame on places not occupied by dots of the arrow (WS) or digit (AS). An example of each is shown in fig. 1. KR was presented through a 6 X 10 cm display, with two columns of lights mounted on the table surface. One column, at the upper left side of the display, consisted of four yellow lights (20 cd/m2 LEDs), labeled respectively with the Dutch equivalents of the ‘moderate’ and ‘bad’, from top to bottom. The label words ‘good’, ‘reasonable’, assigned a quality judgement of the response latency as compared to an individually preassigned criterion (see procedure section). The other column at the right lower side of the display consisted of one green light (15 cd/m* LED) labeled ‘correct’ and one red light (18 cd/m2 LED) labeled ‘wrong’, indicating the correctness of the response. In the KR condition illumination of one of the lights of the upper-left, and one of the lights of the lower-right column were used to express the judgement of response speed and response accuracy respectively. In the no-KR condition the judgement ‘reasonable’ for response speed, and the judgement ‘good for response accuracy were always given, independent of the actual response. In this condition subjects always knew that the KR-signals were fake. The timing of trials and acquisition of response data was controlled by a DEC PDP 11/02 computer. Ambient noise level in the cubicle was 28 dB(A). The subject chair was especially designed for this kind of reaction task (Ruzius and Steyvers 1980). Siemens Ag-AgCl surface electrodes were used for heartrate measurement. The signal was amplified by a Hellige amplifier, set to a time constant of 0.03 set and an upper cut-off frequency of 35 Hz. The amplifier heart signal was led into a Schmidt trigger, producing a pulse at the R-peaks that started and stopped a clock. In this way, the interbeat interval values were assessed to the nearest msec. Design The interval between onset of AS and of WS of the next trial, the intertrial interval (ITI), was either constant (8.5 set; fixed ITI) or variable (ranging from 7.5 to 10 set in 0.5 set steps of equal probability; variable ITI). The ITI variable was added in order to evaluate its influence on the measurement of heartrate, but this is beyond the scope of the present paper and results of ITI-effects will not be reported here. The 16 subjects were randomly assigned to two groups of 8 subjects. IT1 condition (fixed vs. variable) was varied between groups, while the remaining conditions (sleep deprivation, degradation of signals, KR and time on task) were varied within groups. Sleep deprivation was induced by keeping the subjects awake from 9.00 h until about 17.00 h of the next day, thus spending about 32 hours without sleep. Sleep deprivation effects were assessed in three sessions during these two successive days. In each session four blocks were presented of 144 trials each. Across trial blocks KR was given or withheld in an ABBA order. AS quality was in alternating order (degraded, intact, degraded, intact or vice versa) across blocks. In this way all four possible combinations of KR and AS quality were presented, once per session to every subject. Within each block WS quality was varied between four successive 36-trial parts in alternating order (intact, degraded, intact, degraded or vice versa). The first and the second half of each block established
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Effect of KR after
sleep deprrvation
two levels of time on task. The total duration of one block of 144 trials was about 30 minutes. All three sessions were preceded by 36 warm-up trials. A warm-up trial consisted of a warning tone (1000 Hz, 55 dB, 200 msec) that was followed after 5 set by AS, consisting of a 800-msec homogenous light flash on the screen. Subjects responded by releasing the home-key and pressing the key at position eight. Procedure Two subjects participated in alternation on three consecutive days. On the first day the subjects received instruction about task demands, followed by 36 warm-up trials, one practice block of 72 trials with intact AS and one practice block of 72 trials with degraded AS. KR was presented in all practice blocks. The practice blocks of the experimental conditions consisted of two parts of 36 trials; one with an intact WS and the other one with a degraded WS. Every block started with a l-mm adaptation interval in which no trials were given. Information about the kind of AS and KR of the block was always given before each block. The training session was concluded with instruction about their conduct that evening (no alcohol. no exessive exercises, normal sleep, etc.). The KR criterion was defined as the mean RT, calculated separately for intact and for degraded stimuli, of the last half of the practice sessions, rounded to the nearest multiple of 25 msec. The qualification ‘good’ was presented when the RT was less than this criterion minus 25 msec; ‘reasonable’ was given when the RT was less than the criterion plus 75 msec, and worse than the good criterion; ‘moderate’ was presented when an RT was less than the criterion plus 150 msec, and worse than the criterion for reasonable, and ‘bad’ was given when RT was slower than the moderate criterion. Additionally, when the MT was more than 300 msec, the score was lowered with one category: ‘good’ became ‘reasonable’, ‘ reasonable’ became ‘ moderate’. etc. On the second day, the subjects reported at the lab at 9.00 h, 12.00 h and 15.00 h, in order to prevent unscheduled sleeping. The actual experiment started at 19.00 h of the second day and lasted about 22 hours. At 19.00 h the electrodes for heartrate registration were connected to the subjects: one at the point of the left twelfth rib, the second about 5 cm below the middle of the right claviculum and the reference electrode about 5 cm to the right of the point of the sternum. The subjects alternated in running the 30-min trial blocks; when one subject was in the cubicle, the other subject was supervised by an assistant, in order to assure that the subject would stay awake. During the waiting time between the blocks, light food and non-alcoholic drinks or decaffeinated coffee were available, as well as books, board games, and video-tapes. The three sessions of a warm-up block and four experimental trial blocks per subject were executed from 19.30-1.00 h, again from 3.30-9.00 h and a third time from 11.30-17.00 h, thus establishing the three levels of sleep deprivation. Dependent variables and data analysis The dependent variables home-key release), movement
were reaction time (RT; time between AS-onset and time (MT; time between home-key release and target-key
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press), proportion of errors and proportion of omissions (trials in which no response was given within 3500 msec after AS-onset) and interbeat interval of the electro cardiogram (ECG). For the calculation of the mean RT and mean MT only trials with correct responses were used. When RT was above 2500 msec or below 50 msec or MT was above 1000 msec or below 25 msec, the concerning trial was excluded. Due to apparatus malfunction, less than 0.5% of the trials had to be excluded. Only the results of the intact-WS conditions are presented, because the signal quality of the WS is not part of the question in the present study. All ANOVAs were calculated by using the BMDP package, program 8V, adapted for use on a DEC VAX 11/785 computer.
Results Performance
data
Fig. 2 presents mean RTs and MTs, as well as proportions of errors and omissions as a function of sleep deprivation, KR and signal degradation. Separate ANOVAs (Session X signal quality x KR x time on task) were run on individual mean RTs, on individual mean MTs, and on individual proportion of errors and proportion of omissions. The individual proportions were arcsine transformed (Winer 1971). Based upon preliminary analyses, which showed no effects of ITI, the data were pooled over ITI-groups. The results of these ANOVAs are summarized in table 1.
Table I Summary of the ANOVA results on individual proportions of errors and omissions. Source
df
RT F
S A K T SxA SxK SxT KxA AxT
2.30 1,15 1,15 1,15 2,30 2,30 2.30 1.15 1,15
13.63 26.32 13.21 4.77 3.87 9.15 4.78 Cl.0 3.85
mean
RT, mean
MT F d d d a a c a
4.91 8.28 4.91 5.12 11.0 4.95 6.69 1.47 8.00
MT and arcsine
Errors F = a = a = a d
Abbreuiations: S = sleep deprivation; A = action signal quality; on task; RT = mean RT; MT = mean MT; errors = arcsine omissions = arcsine transformed proportion of omissions. a p
9.17 41.99 11.0 5.63 2.14 3.62 3.02 11.0 Cl.0
transformed
Omissions F d d a a
11.29 Cl.0 9.24 5.33 Cl.0 11.0 4.66 1.26 < 1.0
d ’ a
a
K = knowledge of results; T = time transformed proportion of errors;
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F.J.J.M.
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/ Ejfeect of KR after sleep deprivation
800
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Fig. 2. Mean RT (upper left panel), Mean MT (upper right panel), mean proportion of errors (lower left panel) and mean proportion of omissions (lower right panel) pooled for time on task. and averaged over subjects.
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Both signal degradation and time on task resulted in a rise of RT. Also, sleep deprivation increased RT, whereas presentation of KR caused RT to decrease. With sleep deprivation, stronger effects of KR, of signal degradation and of time on task were observed. However, the combined effect of signal degradation and sleep deprivation was independent of the effect of KR. The RT increase after lack of sleep was a conservative estimation of the sleep deprivation effect, because sleep deprivation was confounded with level of practice, which would result in an opposing tendency. For mean MTs there were significant main effects of stimulus quality, time on task, sleep deprivation and KR. The effect of KR increased with more lack of sleep. Also the time-on-task effect increased with lack of sleep. The effect of signal degradation became less pronounced in the second half of a trial block. The direction of the effects of KR on MT suggests no trade-off between RT and MT. The proportions of errors showed significant effects of signal degradation, of time on task and of sleep deprivation. The presentation of KR had no effect without lack of sleep; with sleep deprivation, however, the proportion of errors was somewhat larger with KR than without KR. The results on the proportions of omissions showed significant main effects of time on task, sleep deprivation and of KR. An interaction was found between the effect of time on task and sleep deprivation. Because of a significant signal-quality effect on mean MT, it was decided to reanalyze the performance data. Trials were excluded when the MT exceeded an individually assigned criterion value (see appendix). The only clear difference with the above-mentioned ANOVAs was that the main effect of signal quality on MT disappeared. Therefore, the original ANOVAs, as reported in table 1 will be used. The results on mean RT and on the proportion of errors suggest a speed-accuracy trade-off in the interaction of sleep deprivation and KR; with more lack of sleep RT decreases with the presentation of KR, whereas the proportion of errors increases. For each level of sleep deprivation, a correlation coefficient (r) was calculated between the individual KR-effects on mean RT and on proportion of errors. A speed-accuracy trade-off should have resulted in a significant negative correlation. The r-values for the increasing levels of lack of sleep were - 0.33, - 0.03, and - 0.14 respectively, none of which is significant (df= 15; one-sided test. Critical value for p = 0.05 in this case: - 0.412). Especially with more lack of sleep, when a speed-accuracy trade-off appeared from the ANOVAs and from fig. 2, the correlation coefficient is far from significant. Therefore, it is unlikely that the entire effect of KR presentation consists of a strategy shift towards faster and less accurate responses. Heartrate
data
The following heartrate measures were taken. From 4 seconds before WS to 3 seconds after AS (a total period of 11 set) heartrate (HR) was calculated per 0.5-set period according to Graham’s (1978) algorithm. Mean values were calculated per condition and per subject, omitting the trials without response. Thus, the ECR was obtained across a time interval of 22 periods with a duration of 0.5 sec. The ECR had a typical (e.g., Lang et al. 1978; Bohlin and Kjellberg 1979) triphasic wave pattern of a minimum (occurring next to WS), a subsequent maximum and a second minimum
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F.J.J.M.
Table 2 Summary of the ANOVAs in significant effects.
Steyvers
/ Effect of KR after sleep deprivation
on the heartrate
data. Only the analyses
are presented,
which resulted
Source
df
mHR F
bslHR F
dlHR F
aHR F
d2HR F
S T
2.30 1.15
12.05 ’ 23.56 a
12.44 B 17.05 il
12.62 a 20.53 a
10.72 a 19.94 ‘I
9.09 ‘l 22.85 *
Abbrevmtrons: mHR = mean overall heartrate; bslHR = heartrate of the baseline; dlHR = heartrate of the first minimum in the evoked cardiac response (ECR); aHR = heartrate of the maximum in the ECR; d2HR = heartrate of the second minimum in the ECR; S = sleep deprivation; T = time on task. a p < 0.001.
next to AS). By means of visual pattern scanning (per condition and per it was determined in which one of the 22 periods occurred the first minimum HR, the following maximum HR and the second minimum HR. Ten measures were defined and assessed: (a) the mean overall HR of all 22 periods; (b) a HR baseline (as such the mean of the first two measurement periods of the obtained ECR were taken); the HRs of respectively (c) the first minimum, (d) the maximum, and (e) the second minimum; (f) the HR of the first minimum minus the baseline HR; (g) the HR of the maximum minus the baseline HR; (h) the HR of the second minimum minus the baseline HR (thus obtaining baseline-corrected values); (i) an acceleration measure (the HR of the maximum minus the HR of the first minimum), and (j) a deceleration (occurring
subject)
80
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Fig. 3. Heartrate data, pooled for time on task and averaged over subjects. Left panel: overall heartrate. Middle panel: heartrate of the second minimum minus baseline. Right panel: heartrate of the maximum minus heartrate of the second minimum.
3
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measure (the HR of the maximum minus the HR of the second minimum). The data are pooled over ITI-group. Ten separate ANOVAs (session x signal quality x KR x time on task) were performed one for each heartrate measure. A summary of the significant effects, is presented in table 2. A significant main effect of sleep deprivation was found for the overall mean heartrate (67.7; 66.2 and 72.4 beats/mm for increasing levels of sleep deprivation respectively: see fig. 3, leftmost panel) as well as for the baseline HR, for the HR at the first minimum in the ECR, for the HR at the maximum in the ECR and for the HR at the second minimum in the ECR. There was also a main effect of time on task for these independent measures. There were no significant interactions. In the baseline-corrected measures of the HR at the first minimum, at the maximum, and at the second minimum in the ECR, and in the acceleration measure only one effect was found: the baseline-corrected HR at the second minimum increased with the three levels of sleep deprivation (F(2, 30) = 6.69; p < 0.005; see fig. 3, middle panel). In the deceleration measure, finally, it was found that without KR the deceleration was less than with KR (F(1.15) = 5.19; p < 0.05; see fig. 3, rightmost panel). Correlation
between performance
and heartrate
data
The ANOVAs suggest that, after sleep deprivation, there is a relation between phasic heartrate deceleration and KR, but not between phasic HR deceleration and signal quality. In order to evaluate whether the effects of KR and sleep deprivation on heartrate are related to performance, as stated in the introduction, correlation coefficients (r) were calculated in the following way: for each subject the KR-effect for mean RT and for the deceleration measure was calculated, separately for session 1, 2 and 3, thus obtaining three sets of sixteen pairs of values. The same was done for the signal-degradiation effect for these conditions. From these sets of value pairs, correlation coefficients were calculated. On the KR-effects, the r-values for session 1, 2 and 3 were respectively 0.15, -0.02 and -0.55. Only the last value was significant. On the signal-degradation effects, the results were -0.22, - 0.09 and -0.27 for session 1, 2, and 3, respectively, none of which is significant (df= 15; one-sided test). The critical value for p = 0.05 is -0.412 in all these cases.
Discussion Performance is sensitive to lack of sleep and this effect is more pronounced with degraded signals. With this first-order interaction, the results of Sanders et al. (1982) are clearly confirmed. This suggests that, in terms of Sanders’ (1983) model, sleep deprivation impairs the arousal mechanism, thereby reducing the energetical supply to perceptual processes. KR resulted in better performance, but only after sleep deprivation. This suggests that KR does improve some energetical mechanism, that
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is impaired by lack of sleep. This explanation is well in accord with the model. The absence, however, of the predicted second-order interaction between the effects of KR, sleep deprivation and signal quality suggests that sleep deprivation has at least a twofold effect: (a) it impairs perceptual processing, irrespective of KR, and, (b) it impairs some other type of process: an impairment which is smaller when KR is presented. Thus, KR and signal quality appear to affect different processing stages. A similar picture emerges from the heartrate deceleration in the ECR; KR increases this deceleration, whereas manipulation of signal quality has no effect. The absence of a signal-degradation effect on heartrate was also reported by Gaillard et al. (1985). Additional support was found in the correlations between the HR deceleration of the ECR and RT. Individual differences were calculated between the conditions with and without KR, separately for the three levels of sleep deprivation. Only with lack of sleep there was a significant correlation between differential HR and RT. In contrast, no such significant correlation was found when individual differences were computed between high and low signal quality conditions (pooled over KR). Thus, beneficial effects of KR are concurrently reflected in RT and in HR, while this is not so for effects of signal quality. The evidence discussed so far suggests that the locus of the combined effect of KR and sleep deprivation is at some other stage than perceptual processing. Therefore, it is a plausible hypothesis, that, instead of compensating for a lack of arousal, KR affects some motoric process that depends on the level of activation. Some support for this hypothesis is provided by the effects of KR on MT. As an index of response execution, MT is dependent of the output of the motor adjustment stage (Frowein 1981), which is presumably subserved by the activation mechanism (Sanders 1983). In this way, KR effects may resemble the effects of amphetamine: Frowein et al. (1981b) found that amphetamine may decrease MT, which was longer after sleep deprivation. Only a future experiment can test this hypothesis, by investigating the combined effects of sleep deprivation, KR, and, for instance, time uncertainty. An alternative possibility suggested by Sanders’ (1983) model is the direct influence of KR-induced effort on information processing stages. Effort is assumed to affect the response selection stage. In order to test the hypothesis that the locus of effect of KR-induced compensation for
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sleep deprivation involves response selection, a task variable has to be introduced that is known to selectively affect this stage, such as stimulus-response compatibility (Sanders 1980). However, sleep deprivation and stimulus-response compatibility have shown additive effects (Sanders et al. 1982), which suggests that sleep deprivation does not impair the response selection stage. Hence, it is implausible that the locus of effect of KR-induced effort in compensating the detrimental effects of sleep deprivation on performance involves response selection. Wilkinson’s (1961) findings on KR are partly replicated: KR improves performance, in particular after sleep deprivation. In contrast with Wilkinson’s results, KR does not fully restore performance under sleep deprivation to the level of performance after normal sleep. One possible explanation is that Wilkinson’s performance measure in terms of ‘gaps’ (RTs longer than 1500 msec) is different from the measure of mean RT used here. Yet, fig. 3 shows that proportion of omissions, a measure that resembles gaps more than RT, did not show complete KR-induced improvement after lack of sleep. Furthermore, the KR of the present study was visual, whereas Wilkinson presented auditory KR. Also, in this study KR was given after every trial, whereas Wilkinson presented KR only after an error or a gap, and after every 5-min period. Finally, Wilkinson used a self-paced continuous RT-task, whereas in this study a discrete paced task was used. These differences may account for the incomplete compensation of performance by KR in the present study. Summarizing this study, there is evidence for at least two distinct effects of sleep deprivation; one effect interacts with signal quality and another effect interacts with KR. Sleep deprivation amplifies the effect of signal degradation, which reflects a depletion of arousal. KR compensates for lack of sleep, irrespective of signal quality. Hence, it appears that the compensation for lack of sleep by KR does not involve arousal.
Appendix Because a significant effect of signal quality on mean MT, the data were reanalyzed, using an individually assigned cut-off value for MTs. Trials with an MT exceeding this cut-off value were excluded. The aim of this correction was to obtain a trial set with more similar MT-distri-
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of KR aftersleep deprwation
butions across signal quality conditions. This is more or less a stipulation for additive-factors logic (Sanders 1980). For each block of 144 trials in the high signal quality condition, mean and sd of the MT was calculated. The cut-off value was defined as one sd above the mean. This value served as criterion to exclude trials from both high and low signal quality conditions. The mean cut-off value determined this way was 331 msec. The mean RTs were practically identical to the mean RTs of the uncorrected data. The individual mean RTs and mean MTs from the selected data were subjected to ANOVAs. The results of these ANOVAs were the same as the results of the ANOVAs on the uncorrected data: all effects of the independent variables were present, except for the main effect of time on task, which became marginally significant (0.05
References Bohlin, G. and A. KJellberg, 1979. ‘Orienting activity in two-stimulus paradigms as reflected in heart rate’. In: H.D. Kimmel. E.H. v. Olst and J.F. Orlebeke (eds.), The orienting reflex in humans. Hillsdale. NJ: Earlbaum. pp. 169-197. Coles, M.G.H., 1974. Physiological activity and detection: the effects of attention requirements and the predictions of performance. Biological Psychology 2, 113-I 25. Coles, M.G.H. and D.L. Strayer, 1985. ‘The psychophysiology of the cardiac cycle time effect’. In: J.F. Orlebeke, G. Mulder and L.J.P. van Doomen (eds.), Psychophysiology of cardiovascular control. New York/London: Plenum Press. pp. 517-534. Duncan-Johnson, CC. and M.G.H. Coles, 1974. Heart-rate and disjunctive reaction-time: the effects of discrimination requirements. Journal of Experimental Psychology 103. 1160-l 168. Frowein, H.W., 1981. Selective drug effects on information processing. Enschede: Sneldruk Boulevard. Frowem, H.W.. A.W.K. Gaillard and CA. Varey, 19Xla. EP components. visual processing stages. and the effect of a barbiturate. Biological Psychology 13. 239-249. Frowein. H.W.. D. Reitsma and C. Aquarius. 1981b. ‘Effects of two counteracting stresses on the reaction process’. In: J. Long and A. Baddeley (eds.), Attention and performance IX. Hillsdale, NJ: Erlbaum, pp. 575-590. Gaillard, A.W.K., CA. Varey and C.J. Verduin. 1985. ‘Heart-rate during a reaction-time and a reference task’. In: J.F. Orlebeke, G. Mulder and L.J.P. Van Doornen (eds.). Psychophysiology of cardiovascular control. New York/London: Plenum Press. pp. 465-477.
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Graham, F.K., 1978. Constraints on measuring heart-rate and period sequentially through real and cardiac time. Psychophysiology 15, 492-495. Gopher, D. and D. Navon, 1980. How is performance limited: testing the notion of central capacity. Acta Psychologica 46, 161-180. Gopher, D. and A.F. Sanders, 1984. ‘S-Oh-R: Oh Stages ! Oh Resources!’ In: W. Prim and A.F. Sanders (eds.), Cognition and motor processes. Berlin: Springer. pp. 231-253. difficulty manipulations interacted Gopher, D., M. Bricker and D. Navon, 1982. Different differently with task emphasis: evidence for multiple resources. Journal of Experimental Psychology: Human Perception and Performance 8, 146-157. Kahneman, D., 1973. Attention and effort. Englewood Cliffs, NJ: Prentice-Hall. Lacey, J.I., 1967. ‘Somatic response patterning and stress: some revisions of activation theory’. In: M.H. Appley and R. Trumball (eds.), Psychological stress: issues in research. New York: Appleton-Century Crofts. of anticipation’. In: J. Lang, P.J., A. Ohman and R.F. Simons, 1978. ‘The psychophysiology Requin (ed.), Attention and performance VII. Hillsdale, NJ: Erlbaum. pp. 469-485. Navon, D. and D. Gopher, 1979. On the economy of the human information processing system. Psychological Review 33, 177-184. Orlebeke. J.F., R.J.M. Somsen and M.W. van der Molen, 1985. ‘Anxiety and attentional processes as assessed with the additive factor method. In: J.F. Orlebeke, G. Mulder and L.J.P. van Doomen (eds.), Psychophysiology of cardiovascular control. New York/London: Plenum Press. pp. 549-563. Ruzius, M. and F. Steyvers, 1980. The design and the test of an individual adjustment criterion for the adjustment of a seat to be used in reaction-time tasks. Tilburg: Tilburg University, SPW-rapport SC 257 (in Dutch). Sanders, A.F.. 1980. ‘Stage analysis of reaction processes’. In: G.E. Stelmach and J. Requin (eds.), Tutorials in motor behavior. Amsterdam: North-Holland. pp. 331-354. Sanders, A.F., 1983. Towards a model of stress and human performance. Acta Psychologica 53, 61-97. Sanders, A.F., J.C.C. Wijnen and A.E. van Arkel. 1982. An additive factor analysis on the effects of sleep loss and reaction processes. Acta Psychologica 51, 41-59. Stemberg. S., 1969. ‘The discovery of processing stages: extension of Donders’ method’. In: W.G. Koster (ed.), Attention and performance II. Amsterdam: North-Holland. pp. 276-315. Wilkinson, R.T.. 1961. Interaction of lack of sleep with knowledge of results, repeated testing and individual differences. Journal of Experimental Psychology 62, 263-271. Winer, B.J., 1971. Statistical principles in experimental design (2nd ed.). New York: McGraw-Hill.
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66 (1987) 173-187
THE INFLUENCE OF SLEEP DEPRIVATION AND KNOWLEDGE OF RESULTS ON PERCEPTUAL ENCODING * Frank J.J.M. STEYVERS Tilburg University, The Netherlands Accepted
June 1987
This study investigates the way sleep deprivation effects on perceptual processes are modulated by knowledge of results (KR). In a choice-reaction task, signal quality was manipulated, combined with and without KR and under increasing levels of lack of sleep. It was found that the decrease of performance due to sleep deprivation was larger when stimuli were degraded. KR counteracted the effect of sleep deprivation; however, KR improved performance irrespective of signal quality. Hence, sleep deprivation seems to have a twofold effect on performance; one effect on perceptual processing, which is insensitive to KR, and another effect on some different processing stage, which is sensitive to KR. The results were interpreted in terms of a model of human performance (Sanders 1983) in which a distinction is made between two energetical mechanisms, ‘arousal’ and ‘activation’, subserving perceptual and motor stages of information processing, respectively. Thus, KR appears to compensate for the deficiency of one type of energetical mechanism, caused by sleep deprivation. Yet, this compensation does not appear to be the result of increased arousal, because, irrespective of KR, the performance decrement caused by signal degradation was more pronounced with lack of sleep.
Traditionally, performance in reaction tasks has been investigated in two almost exclusive research areas, concerning either energetical or computational aspects of the processes underlying performance. Recently, Sanders (1983) proposed an integration of these approaches by relating the notion of multiple resources (Navon and Gopher 1979; Gopher and Navon 1980; Gopher et al. 1982) to a linear-stage model of information processing (Sternberg 1969; Sanders 1980; Gopher and Sanders 1984). In this model, two processing stages are subserved by * This paper was supported by grant 560-259-021 of The Netherlands’ Organisation for Pure Scientific Research (ZWO). The author gratefully acknowledges the advice and support of A.J.P. Hendrikx, A.F. Sanders, A.W.K. Gaillard, and C.H.M. Brunia during all phases of this study, the assistance of A. Mannaerts during the execution of the experiment, and the critical comments of M.G.H. Coles, A.J.W. Boelhouwer, P. Kop, and P.J. Venemans on earlier drafts of this paper. Authors’ address: F. Steyvers, Dept. of Psychology, Tilburg University, P.O. Box 90153, 5000 LE Tilburg, The Netherlands.
OOOl-6918/87/$3.50
0 1987, Elsevier Science Publishers
B.V. (North-Holland)
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two separate pools of resources, or ‘energetical mechanisms’. The model also proposes that an arousal mechanism supplies energy to a perceptual-encoding stage, and that an activation mechanism furnishes a motor-adjustment stage. Under normal circumstances arousal and activation provide sufficient resources to the respective processing stages. However, under influence of a stressor, such as sleep deprivation, drugs or loud noise, the energetical supply from arousal and/or activation becomes inadequate, resulting in a performance decrement. The model further proposes an effort mechanism, which serves to compensate for insufficient energetical supply from the arousal or activation mechanism. However, the compensating effect of effort requires that the subject is aware of his or her below-standard performance, and is also willing and able to mobilize the extra effort (Kahneman 1973). Thus, compensatory effect requires subjects to evaluate their performance. Knowledge of results (KR) may facilitate this evaluation. The effect of KR on performance has been studied by Wilkinson (1961) in a self-placed continuous reaction task. After sleep deprivation, performance deteriorated; presentation of KR restored performance to the level of performance after normal sleep. After normal sleep, KR had no effect on performance. In terms of Sanders’ (1983) model, these results can be explained by assuming that, as a result of KR, the level of energetical supply is restored, and the detrimental effects of sleep deprivation are counteracted. Wilkinson’s (1961) experiment did not involve task variables related to particular processing stages; therefore the question whether the effect of KR is on particular processing stages, by way of exciting one or more energetical mechanisms, cannot be answered. This study aims at taking a closer view to the locus of effect of KR after sleep deprivation. There is some evidence that perceptual as well as motoric processes are affected by lack of sleep. Sanders et al. (1982) found that sleep deprivation enhanced the detrimental effect of signal degradation. According to additive-factors logic this suggests that sleep deprivation affects perceptual encoding (Sanders 1980). In addition, Frowein et al. (1981b) reported that sleep deprivation enhanced the effect of time uncertainty. This suggests an effect of sleep deprivation on the motor-adjustment stage (Sanders 1980). Sanders (1983) integrates these findings in his model and proposes that these studies contain evidence for an influence of sleep deprivation on both the arousal and the activation mechanism.
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The aim of the present study is to investigate whether the compensatory activity of KR after sleep deprivation involves arousal. A manual six-choice reaction task was used, in which signal quality was manipulated. It is expected that sleep deprivation impairs performance, and more so when signals are degraded. KR is expected to compensate for this performance decrement. Thus, a second-order interaction is expected between sleep deprivation, signal degradation and KR; after sleep deprivation, KR will improve performance and reduce the combined effect of signal degradation and lack of sleep. In terms of Sanders’ (1983) model, sleep deprivation impairs performance by reducing the level of arousal, and arousal becomes critical to performance in case of degraded stimuli. KR restores performance by evoking compensatory effort. After normal sleep, KR will not improve performance, because the arousal level suffices to process degraded as well as intact signals adequately. Since effects of lack of sleep seem to appear only after some time (Wilkinson 1961; Sanders 1983), it is expected that these effects will occur more clearly in the second half of the working period. The demands on information processing are reflected in certain aspects of the evoked cardiac response (ECR) (e.g., Lacey 1967; Coles and Strayer 1985; Orlebeke et al. 1985). Heartrate deceleration preceding the action signal has been shown to depend on the expected difficulty of the forthcoming stimulus (Coles 1974; Duncan-Johnson and Coles 1974). Therefore, the present study tests the hypothesis that enhanced demands on stimulus encoding will enlarge the heartrate deceleration preceding the action signal in the ECR, but only when the system copes effectively with these demands. It is expected that the deceleration will be larger when signals are degraded. This effect should be independent of KR after normal sleep. After sleep deprivation and without KR, this effect should diminish. When the presentation of KR leads to improved performance, the deceleration will again become larger for degraded than for intact signals. Method Subjects Sixteen healthy, male persons, between 20 and 32 years of age, served as subjects. All subjects were right-handed and they had no prior experience with the experimental task. They received Dfl.300,- for participation.
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Task A subject was seated in a sound-attenuated, dimly illuminated cubicle at a slanted table, in front of a backprojection screen. An array of eight response buttons (1.09 cm2) was mounted on the table in a semi-circular configuration and labeled 1 to 8 in clockwise order. A home-key was mounted in the center of this semi-circle at a distance of 15 cm from the target-keys. Subjects were instructed to react as fast as possible to the signals with the right index finger, starting from the home-key towards one of the target-keys. A correct response consisted of pressing the key with the same label as the action signal (AS). Keys 1 and 8 were not used because of their anchor positions. AS duration was maximally 800 msec, but home-key release within 800 msec after AS onset terminated AS presentation immediately. A warning signal (WS) of 800 msec duration was presented 4 set before every AS. The response was followed by KR presentation, separately for response speed and accuracy. KR lasted until WS-onset of the next trial. Stimuli and apparatus The stimuli consisted of slides projected on the back of the screen, covering an area of 12 x 14.5 cm; a visual angle of 6.4 degrees. The screen had an overall luminance of 5 cd/m2, and the luminance of the stimuli was 30 cd/m2. The AS was composed of a dot pattern, shaped as any one of the digits 2 through 7 in a rectangular dotted frame (Frowein et al. 1981a). The WS consisted of an arrow-shaped dot pattern placed in a dotted frame, identical to the frame of the AS. The arrow pointed either to the left or to the right, indicating whether the next AS would belong either to the subset (2, 3, 4) or to the subset (5, 6, 7) respectively. In order to obtain an equal overall luminance, all
Fig. 1. Examples of the stimuli. Above: action signal # 2. Below: warning right. At the left intact signals, at the right degraded signals.
signal
arrow
to the
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of KR ufier sleep deprivation
171
stimuli were composed of a constant number of dots; 46 for WS and 50 for AS. Stimuli were degraded by placing dots from the surrounding frame of the intact stimuli to random positions within the frame on places not occupied by dots of the arrow (WS) or digit (AS). An example of each is shown in fig. 1. KR was presented through a 6 X 10 cm display, with two columns of lights mounted on the table surface. One column, at the upper left side of the display, consisted of four yellow lights (20 cd/m2 LEDs), labeled respectively with the Dutch equivalents of the ‘moderate’ and ‘bad’, from top to bottom. The label words ‘good’, ‘reasonable’, assigned a quality judgement of the response latency as compared to an individually preassigned criterion (see procedure section). The other column at the right lower side of the display consisted of one green light (15 cd/m* LED) labeled ‘correct’ and one red light (18 cd/m2 LED) labeled ‘wrong’, indicating the correctness of the response. In the KR condition illumination of one of the lights of the upper-left, and one of the lights of the lower-right column were used to express the judgement of response speed and response accuracy respectively. In the no-KR condition the judgement ‘reasonable’ for response speed, and the judgement ‘good for response accuracy were always given, independent of the actual response. In this condition subjects always knew that the KR-signals were fake. The timing of trials and acquisition of response data was controlled by a DEC PDP 11/02 computer. Ambient noise level in the cubicle was 28 dB(A). The subject chair was especially designed for this kind of reaction task (Ruzius and Steyvers 1980). Siemens Ag-AgCl surface electrodes were used for heartrate measurement. The signal was amplified by a Hellige amplifier, set to a time constant of 0.03 set and an upper cut-off frequency of 35 Hz. The amplifier heart signal was led into a Schmidt trigger, producing a pulse at the R-peaks that started and stopped a clock. In this way, the interbeat interval values were assessed to the nearest msec. Design The interval between onset of AS and of WS of the next trial, the intertrial interval (ITI), was either constant (8.5 set; fixed ITI) or variable (ranging from 7.5 to 10 set in 0.5 set steps of equal probability; variable ITI). The ITI variable was added in order to evaluate its influence on the measurement of heartrate, but this is beyond the scope of the present paper and results of ITI-effects will not be reported here. The 16 subjects were randomly assigned to two groups of 8 subjects. IT1 condition (fixed vs. variable) was varied between groups, while the remaining conditions (sleep deprivation, degradation of signals, KR and time on task) were varied within groups. Sleep deprivation was induced by keeping the subjects awake from 9.00 h until about 17.00 h of the next day, thus spending about 32 hours without sleep. Sleep deprivation effects were assessed in three sessions during these two successive days. In each session four blocks were presented of 144 trials each. Across trial blocks KR was given or withheld in an ABBA order. AS quality was in alternating order (degraded, intact, degraded, intact or vice versa) across blocks. In this way all four possible combinations of KR and AS quality were presented, once per session to every subject. Within each block WS quality was varied between four successive 36-trial parts in alternating order (intact, degraded, intact, degraded or vice versa). The first and the second half of each block established
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Effect of KR after
sleep deprrvation
two levels of time on task. The total duration of one block of 144 trials was about 30 minutes. All three sessions were preceded by 36 warm-up trials. A warm-up trial consisted of a warning tone (1000 Hz, 55 dB, 200 msec) that was followed after 5 set by AS, consisting of a 800-msec homogenous light flash on the screen. Subjects responded by releasing the home-key and pressing the key at position eight. Procedure Two subjects participated in alternation on three consecutive days. On the first day the subjects received instruction about task demands, followed by 36 warm-up trials, one practice block of 72 trials with intact AS and one practice block of 72 trials with degraded AS. KR was presented in all practice blocks. The practice blocks of the experimental conditions consisted of two parts of 36 trials; one with an intact WS and the other one with a degraded WS. Every block started with a l-mm adaptation interval in which no trials were given. Information about the kind of AS and KR of the block was always given before each block. The training session was concluded with instruction about their conduct that evening (no alcohol. no exessive exercises, normal sleep, etc.). The KR criterion was defined as the mean RT, calculated separately for intact and for degraded stimuli, of the last half of the practice sessions, rounded to the nearest multiple of 25 msec. The qualification ‘good’ was presented when the RT was less than this criterion minus 25 msec; ‘reasonable’ was given when the RT was less than the criterion plus 75 msec, and worse than the good criterion; ‘moderate’ was presented when an RT was less than the criterion plus 150 msec, and worse than the criterion for reasonable, and ‘bad’ was given when RT was slower than the moderate criterion. Additionally, when the MT was more than 300 msec, the score was lowered with one category: ‘good’ became ‘reasonable’, ‘ reasonable’ became ‘ moderate’. etc. On the second day, the subjects reported at the lab at 9.00 h, 12.00 h and 15.00 h, in order to prevent unscheduled sleeping. The actual experiment started at 19.00 h of the second day and lasted about 22 hours. At 19.00 h the electrodes for heartrate registration were connected to the subjects: one at the point of the left twelfth rib, the second about 5 cm below the middle of the right claviculum and the reference electrode about 5 cm to the right of the point of the sternum. The subjects alternated in running the 30-min trial blocks; when one subject was in the cubicle, the other subject was supervised by an assistant, in order to assure that the subject would stay awake. During the waiting time between the blocks, light food and non-alcoholic drinks or decaffeinated coffee were available, as well as books, board games, and video-tapes. The three sessions of a warm-up block and four experimental trial blocks per subject were executed from 19.30-1.00 h, again from 3.30-9.00 h and a third time from 11.30-17.00 h, thus establishing the three levels of sleep deprivation. Dependent variables and data analysis The dependent variables home-key release), movement
were reaction time (RT; time between AS-onset and time (MT; time between home-key release and target-key
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press), proportion of errors and proportion of omissions (trials in which no response was given within 3500 msec after AS-onset) and interbeat interval of the electro cardiogram (ECG). For the calculation of the mean RT and mean MT only trials with correct responses were used. When RT was above 2500 msec or below 50 msec or MT was above 1000 msec or below 25 msec, the concerning trial was excluded. Due to apparatus malfunction, less than 0.5% of the trials had to be excluded. Only the results of the intact-WS conditions are presented, because the signal quality of the WS is not part of the question in the present study. All ANOVAs were calculated by using the BMDP package, program 8V, adapted for use on a DEC VAX 11/785 computer.
Results Performance
data
Fig. 2 presents mean RTs and MTs, as well as proportions of errors and omissions as a function of sleep deprivation, KR and signal degradation. Separate ANOVAs (Session X signal quality x KR x time on task) were run on individual mean RTs, on individual mean MTs, and on individual proportion of errors and proportion of omissions. The individual proportions were arcsine transformed (Winer 1971). Based upon preliminary analyses, which showed no effects of ITI, the data were pooled over ITI-groups. The results of these ANOVAs are summarized in table 1.
Table I Summary of the ANOVA results on individual proportions of errors and omissions. Source
df
RT F
S A K T SxA SxK SxT KxA AxT
2.30 1,15 1,15 1,15 2,30 2,30 2.30 1.15 1,15
13.63 26.32 13.21 4.77 3.87 9.15 4.78 Cl.0 3.85
mean
RT, mean
MT F d d d a a c a
4.91 8.28 4.91 5.12 11.0 4.95 6.69 1.47 8.00
MT and arcsine
Errors F = a = a = a d
Abbreuiations: S = sleep deprivation; A = action signal quality; on task; RT = mean RT; MT = mean MT; errors = arcsine omissions = arcsine transformed proportion of omissions. a p
9.17 41.99 11.0 5.63 2.14 3.62 3.02 11.0 Cl.0
transformed
Omissions F d d a a
11.29 Cl.0 9.24 5.33 Cl.0 11.0 4.66 1.26 < 1.0
d ’ a
a
K = knowledge of results; T = time transformed proportion of errors;
180
F.J.J.M.
Steyvers
/ Ejfeect of KR after sleep deprivation
800
l
KR
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600
500 r;; E 2 400
300
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Fig. 2. Mean RT (upper left panel), Mean MT (upper right panel), mean proportion of errors (lower left panel) and mean proportion of omissions (lower right panel) pooled for time on task. and averaged over subjects.
F.J.J.M.
Steyuers / Effeci of KR after sleep depriuation
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Both signal degradation and time on task resulted in a rise of RT. Also, sleep deprivation increased RT, whereas presentation of KR caused RT to decrease. With sleep deprivation, stronger effects of KR, of signal degradation and of time on task were observed. However, the combined effect of signal degradation and sleep deprivation was independent of the effect of KR. The RT increase after lack of sleep was a conservative estimation of the sleep deprivation effect, because sleep deprivation was confounded with level of practice, which would result in an opposing tendency. For mean MTs there were significant main effects of stimulus quality, time on task, sleep deprivation and KR. The effect of KR increased with more lack of sleep. Also the time-on-task effect increased with lack of sleep. The effect of signal degradation became less pronounced in the second half of a trial block. The direction of the effects of KR on MT suggests no trade-off between RT and MT. The proportions of errors showed significant effects of signal degradation, of time on task and of sleep deprivation. The presentation of KR had no effect without lack of sleep; with sleep deprivation, however, the proportion of errors was somewhat larger with KR than without KR. The results on the proportions of omissions showed significant main effects of time on task, sleep deprivation and of KR. An interaction was found between the effect of time on task and sleep deprivation. Because of a significant signal-quality effect on mean MT, it was decided to reanalyze the performance data. Trials were excluded when the MT exceeded an individually assigned criterion value (see appendix). The only clear difference with the above-mentioned ANOVAs was that the main effect of signal quality on MT disappeared. Therefore, the original ANOVAs, as reported in table 1 will be used. The results on mean RT and on the proportion of errors suggest a speed-accuracy trade-off in the interaction of sleep deprivation and KR; with more lack of sleep RT decreases with the presentation of KR, whereas the proportion of errors increases. For each level of sleep deprivation, a correlation coefficient (r) was calculated between the individual KR-effects on mean RT and on proportion of errors. A speed-accuracy trade-off should have resulted in a significant negative correlation. The r-values for the increasing levels of lack of sleep were - 0.33, - 0.03, and - 0.14 respectively, none of which is significant (df= 15; one-sided test. Critical value for p = 0.05 in this case: - 0.412). Especially with more lack of sleep, when a speed-accuracy trade-off appeared from the ANOVAs and from fig. 2, the correlation coefficient is far from significant. Therefore, it is unlikely that the entire effect of KR presentation consists of a strategy shift towards faster and less accurate responses. Heartrate
data
The following heartrate measures were taken. From 4 seconds before WS to 3 seconds after AS (a total period of 11 set) heartrate (HR) was calculated per 0.5-set period according to Graham’s (1978) algorithm. Mean values were calculated per condition and per subject, omitting the trials without response. Thus, the ECR was obtained across a time interval of 22 periods with a duration of 0.5 sec. The ECR had a typical (e.g., Lang et al. 1978; Bohlin and Kjellberg 1979) triphasic wave pattern of a minimum (occurring next to WS), a subsequent maximum and a second minimum
182
F.J.J.M.
Table 2 Summary of the ANOVAs in significant effects.
Steyvers
/ Effect of KR after sleep deprivation
on the heartrate
data. Only the analyses
are presented,
which resulted
Source
df
mHR F
bslHR F
dlHR F
aHR F
d2HR F
S T
2.30 1.15
12.05 ’ 23.56 a
12.44 B 17.05 il
12.62 a 20.53 a
10.72 a 19.94 ‘I
9.09 ‘l 22.85 *
Abbrevmtrons: mHR = mean overall heartrate; bslHR = heartrate of the baseline; dlHR = heartrate of the first minimum in the evoked cardiac response (ECR); aHR = heartrate of the maximum in the ECR; d2HR = heartrate of the second minimum in the ECR; S = sleep deprivation; T = time on task. a p < 0.001.
next to AS). By means of visual pattern scanning (per condition and per it was determined in which one of the 22 periods occurred the first minimum HR, the following maximum HR and the second minimum HR. Ten measures were defined and assessed: (a) the mean overall HR of all 22 periods; (b) a HR baseline (as such the mean of the first two measurement periods of the obtained ECR were taken); the HRs of respectively (c) the first minimum, (d) the maximum, and (e) the second minimum; (f) the HR of the first minimum minus the baseline HR; (g) the HR of the maximum minus the baseline HR; (h) the HR of the second minimum minus the baseline HR (thus obtaining baseline-corrected values); (i) an acceleration measure (the HR of the maximum minus the HR of the first minimum), and (j) a deceleration (occurring
subject)
80
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Fig. 3. Heartrate data, pooled for time on task and averaged over subjects. Left panel: overall heartrate. Middle panel: heartrate of the second minimum minus baseline. Right panel: heartrate of the maximum minus heartrate of the second minimum.
3
F.J.J.M.
Steyuers / Effect of KR after sleep deprmmon
183
measure (the HR of the maximum minus the HR of the second minimum). The data are pooled over ITI-group. Ten separate ANOVAs (session x signal quality x KR x time on task) were performed one for each heartrate measure. A summary of the significant effects, is presented in table 2. A significant main effect of sleep deprivation was found for the overall mean heartrate (67.7; 66.2 and 72.4 beats/mm for increasing levels of sleep deprivation respectively: see fig. 3, leftmost panel) as well as for the baseline HR, for the HR at the first minimum in the ECR, for the HR at the maximum in the ECR and for the HR at the second minimum in the ECR. There was also a main effect of time on task for these independent measures. There were no significant interactions. In the baseline-corrected measures of the HR at the first minimum, at the maximum, and at the second minimum in the ECR, and in the acceleration measure only one effect was found: the baseline-corrected HR at the second minimum increased with the three levels of sleep deprivation (F(2, 30) = 6.69; p < 0.005; see fig. 3, middle panel). In the deceleration measure, finally, it was found that without KR the deceleration was less than with KR (F(1.15) = 5.19; p < 0.05; see fig. 3, rightmost panel). Correlation
between performance
and heartrate
data
The ANOVAs suggest that, after sleep deprivation, there is a relation between phasic heartrate deceleration and KR, but not between phasic HR deceleration and signal quality. In order to evaluate whether the effects of KR and sleep deprivation on heartrate are related to performance, as stated in the introduction, correlation coefficients (r) were calculated in the following way: for each subject the KR-effect for mean RT and for the deceleration measure was calculated, separately for session 1, 2 and 3, thus obtaining three sets of sixteen pairs of values. The same was done for the signal-degradiation effect for these conditions. From these sets of value pairs, correlation coefficients were calculated. On the KR-effects, the r-values for session 1, 2 and 3 were respectively 0.15, -0.02 and -0.55. Only the last value was significant. On the signal-degradation effects, the results were -0.22, - 0.09 and -0.27 for session 1, 2, and 3, respectively, none of which is significant (df= 15; one-sided test). The critical value for p = 0.05 is -0.412 in all these cases.
Discussion Performance is sensitive to lack of sleep and this effect is more pronounced with degraded signals. With this first-order interaction, the results of Sanders et al. (1982) are clearly confirmed. This suggests that, in terms of Sanders’ (1983) model, sleep deprivation impairs the arousal mechanism, thereby reducing the energetical supply to perceptual processes. KR resulted in better performance, but only after sleep deprivation. This suggests that KR does improve some energetical mechanism, that
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is impaired by lack of sleep. This explanation is well in accord with the model. The absence, however, of the predicted second-order interaction between the effects of KR, sleep deprivation and signal quality suggests that sleep deprivation has at least a twofold effect: (a) it impairs perceptual processing, irrespective of KR, and, (b) it impairs some other type of process: an impairment which is smaller when KR is presented. Thus, KR and signal quality appear to affect different processing stages. A similar picture emerges from the heartrate deceleration in the ECR; KR increases this deceleration, whereas manipulation of signal quality has no effect. The absence of a signal-degradation effect on heartrate was also reported by Gaillard et al. (1985). Additional support was found in the correlations between the HR deceleration of the ECR and RT. Individual differences were calculated between the conditions with and without KR, separately for the three levels of sleep deprivation. Only with lack of sleep there was a significant correlation between differential HR and RT. In contrast, no such significant correlation was found when individual differences were computed between high and low signal quality conditions (pooled over KR). Thus, beneficial effects of KR are concurrently reflected in RT and in HR, while this is not so for effects of signal quality. The evidence discussed so far suggests that the locus of the combined effect of KR and sleep deprivation is at some other stage than perceptual processing. Therefore, it is a plausible hypothesis, that, instead of compensating for a lack of arousal, KR affects some motoric process that depends on the level of activation. Some support for this hypothesis is provided by the effects of KR on MT. As an index of response execution, MT is dependent of the output of the motor adjustment stage (Frowein 1981), which is presumably subserved by the activation mechanism (Sanders 1983). In this way, KR effects may resemble the effects of amphetamine: Frowein et al. (1981b) found that amphetamine may decrease MT, which was longer after sleep deprivation. Only a future experiment can test this hypothesis, by investigating the combined effects of sleep deprivation, KR, and, for instance, time uncertainty. An alternative possibility suggested by Sanders’ (1983) model is the direct influence of KR-induced effort on information processing stages. Effort is assumed to affect the response selection stage. In order to test the hypothesis that the locus of effect of KR-induced compensation for
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sleep deprivation involves response selection, a task variable has to be introduced that is known to selectively affect this stage, such as stimulus-response compatibility (Sanders 1980). However, sleep deprivation and stimulus-response compatibility have shown additive effects (Sanders et al. 1982), which suggests that sleep deprivation does not impair the response selection stage. Hence, it is implausible that the locus of effect of KR-induced effort in compensating the detrimental effects of sleep deprivation on performance involves response selection. Wilkinson’s (1961) findings on KR are partly replicated: KR improves performance, in particular after sleep deprivation. In contrast with Wilkinson’s results, KR does not fully restore performance under sleep deprivation to the level of performance after normal sleep. One possible explanation is that Wilkinson’s performance measure in terms of ‘gaps’ (RTs longer than 1500 msec) is different from the measure of mean RT used here. Yet, fig. 3 shows that proportion of omissions, a measure that resembles gaps more than RT, did not show complete KR-induced improvement after lack of sleep. Furthermore, the KR of the present study was visual, whereas Wilkinson presented auditory KR. Also, in this study KR was given after every trial, whereas Wilkinson presented KR only after an error or a gap, and after every 5-min period. Finally, Wilkinson used a self-paced continuous RT-task, whereas in this study a discrete paced task was used. These differences may account for the incomplete compensation of performance by KR in the present study. Summarizing this study, there is evidence for at least two distinct effects of sleep deprivation; one effect interacts with signal quality and another effect interacts with KR. Sleep deprivation amplifies the effect of signal degradation, which reflects a depletion of arousal. KR compensates for lack of sleep, irrespective of signal quality. Hence, it appears that the compensation for lack of sleep by KR does not involve arousal.
Appendix Because a significant effect of signal quality on mean MT, the data were reanalyzed, using an individually assigned cut-off value for MTs. Trials with an MT exceeding this cut-off value were excluded. The aim of this correction was to obtain a trial set with more similar MT-distri-
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butions across signal quality conditions. This is more or less a stipulation for additive-factors logic (Sanders 1980). For each block of 144 trials in the high signal quality condition, mean and sd of the MT was calculated. The cut-off value was defined as one sd above the mean. This value served as criterion to exclude trials from both high and low signal quality conditions. The mean cut-off value determined this way was 331 msec. The mean RTs were practically identical to the mean RTs of the uncorrected data. The individual mean RTs and mean MTs from the selected data were subjected to ANOVAs. The results of these ANOVAs were the same as the results of the ANOVAs on the uncorrected data: all effects of the independent variables were present, except for the main effect of time on task, which became marginally significant (0.05
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