Reduced visual processing capacity in sleep deprived persons

Multiple experiments have found sleep deprivation to lower task-related parietal and extrastriate visual activation, suggesting a reduction of visual processing capacity in this state. The perceptual load theory of attention (Lavie, 1995) predicts that our capacity to process unattended distractors will be reduced by increasing perceptual difficulty of task-relevant stimuli. Here, we evaluated the effects of sleep deprivation and perceptual load on visual processing capacity by measuring neural repetition-suppression to unattended scenes while healthy volunteers attended to faces embedded in face-scene pictures. Perceptual load did not affect repetition suppression after a normal night of sleep. Sleep deprivation reduced repetition suppression in the parahippocampal place area (PPA) in the high but not low perceptual load condition. Additionally, the extent to which task-related fusiform face area (FFA) activation was reduced after sleep deprivation correlated with behavioral performance and lowered repetition suppression in the PPA. The findings concerning correct responses indicate that a portion of stimulus related activation following a normal night of sleep contributes to potentially useful visual processing capacity that is attenuated following sleep deprivation. Finally, when unattended stimuli are not highly intrusive, sleep deprivation does not appear to increase distractibility.     

Functional imaging correlates of impaired distractor suppression following sleep deprivation

Sleep deprivation (SD) has been shown to affect selective attention but it is not known how two of its component processes: target enhancement and distractor suppression, are affected. To investigate, young volunteers either attended to houses or were obliged to ignore them (when attending to faces) while viewing superimposed face-house pictures. MR signal enhancement and suppression in the parahippocampal place area (PPA) were determined relative to a passive viewing control condition. Sleep deprivation was associated with lower PPA activation across conditions. Critically SD specifically impaired distractor suppression in selective attention, leaving target enhancement relatively preserved. These findings parallel some observations in cognitive aging. Additionally, following SD, attended houses were not significantly better recognized than ignored houses in a post-experiment test of recognition memory contrasting with the finding of superior recognition of attended houses in the well-rested state. These results provide evidence for co-encoding of distracting information with targets into memory when one is sleep deprived.     

Sleep deprivation reduces default mode network connectivity and anti-correlation during rest and task performance

Sleep deprivation (SD) can alter extrinsic, task-related fMRI signal involved in attention, memory and executive function. However, its effects on intrinsic low-frequency connectivity within the Default Mode Network (DMN) and its related anti-correlated network (ACN) have not been well characterized. We investigated the effect of SD on functional connectivity within the DMN, and on DMN-ACN anti-correlation, both during the resting state and during performance of a visual attention task (VAT). 26 healthy participants underwent fMRI twice: once after a normal night of sleep in rested wakefulness (RW) and once following approximately 24 h of total SD. A seed-based approach was used to examine pairwise correlations of low-frequency fMRI signal across different nodes in each state. SD was associated with significant selective reductions in DMN functional connectivity and DMN-ACN anti-correlation. This was congruent across resting state and VAT analyses, suggesting that SD induces a robust alteration in the intrinsic connectivity within and between these networks.     

Effects of sleep deprivation on cortical activation during directed attention in the absence and presence of visual stimuli

Sleep deprivation (SD) can give rise to faltering attention but the mechanics underlying this remain uncertain. Using a covert attention task that required attention to a peripheral target location, we compared the effects of attention and SD on baseline activity prior to visual stimulation as well as on stimulus-evoked activity. Volunteers were studied after a night of normal sleep (RW) and a night of SD. Baseline signal elevations evoked by preparatory attention in the absence of visual stimulation were attenuated within rFEF, rIPS (sparing SEF) and all retinotopically mapped visual areas during SD, indicative of impaired endogenous attention. In response to visual stimuli, attention modulated activation in higher cortical areas and extrastriate cortex (hV4, ventral occipital areas) after RW. SD attenuated rFEF, rIPS, V3a and VO stimulus-evoked activation regardless of whether stimuli were attended. Notably, the modulation of stimulus-evoked activation by attention was not affected by SD unlike for the preparatory period, suggesting a reduced number, but still functional circuits during SD. Deficits in endogenous attention in SD dominate in the preparatory period, whereas changes in stimulus-related activation arise from an interaction between compromised fronto-parietal top-down control of attention and reduced sensitivity of extrastriate visual cortex to top-down or bottom-up inputs.     

Functional imaging of working memory following normal sleep and after 24 and 35 h of sleep deprivation: Correlations of fronto-parietal activation with performance

Working memory was evaluated after normal sleep, and at 24 and 35 h of sleep deprivation (SD) in 26 healthy young adults to examine the neural correlates of inter-individual differences in performance. The extent of performance decline was not significantly different between the two SD test periods although there was greater variability in performance at SD35. In both SD sessions, there was reduced task-related activation (relative to normal sleep) in both superior parietal regions and the left thalamus. Activation of the left parietal and left frontal regions after normal sleep was negatively correlated with performance accuracy decline from normal sleep to SD24 thus differentiating persons who maintained working memory performance following SD from those who were vulnerable to its effects.     

Sleep Deprivation Is an Additional Stress for Parents Staying in Hospital

PURPOSE.  This study aims to describe the sleep experience of parents staying overnight with their children in hospital.
DESIGN AND METHODS.  Parents ( n  = 102) completed the Verran and Snyder-Halpern Sleep Scale following a night spent with their children in an Australian tertiary pediatric hospital .
RESULTS.  Parents experienced sleep deprivation and poor quality of sleep, reporting a mean sleep period of 4.6 hr ( SD  = 2.1). Having only one child in the room was the only variable that significantly influenced the quality or amount of parental sleep .
PRACTICE IMPLICATIONS.  Parental sleep deprivation needs to be acknowledged and accommodated when nurses and parents negotiate the care of children in hospital .     

Acute sleep deprivation is associated with increased electrocardiographic P-wave dispersion in healthy young men and women

Background: Sleep deprivation (SD) is associated with worse cardiovascular outcome including mortality. Prolonged P-wave duration and P-wave dispersion (Pd) are known to represent inhomogeneous conduction of sinus impulses and are known to be electrophysiologic predictors of atrial fibrillation. Pd in normal subjects has been reported to be influenced by the autonomic tone. Because autonomic tone is affected by sleep and sleep duration, we evaluated the effect of acute SD on P-wave duration and Pd in healthy young adults and whether the effect was gender selective.
Methods : We obtained electrocardiograms of 37 healthy young volunteers (age: 28.45 ± 7.97; 11 women) after a night of regular sleep and repeated after a night with sleep debt. We measured minimum and maximum P-wave durations (Pmin, Pmax) and Pd in milliseconds.
Results : Average sleep time of the subjects were 7.7 ± 0.8 hours during regular sleep and 1.7 ± 1.6 hours during a night of sleep debt (P < 0.001). Subjects had significantly lower values of Pmin in milliseconds after a night of sleep debt when compared to regular sleep (65.13 ± 8.03 vs 74.86 ± 10.95; P < 0.001), whereas they had significantly higher values of Pmax and Pd (102.16 ± 9.46 vs 95.13 ± 11.21; P < 0.001 and 37.02 ± 8.11 vs 20.27 ± 11.42; P < 0.001, respectively). In Pearson's correlation analysis Pmin was positively and Pmax and Pd were negatively correlated with sleep time (P < 0.001, r = 0.465; P = 0.003, r =−0.336 and P < 0.001, r =–0.698 respectively). Effect of SD on P-wave duration and Pd was similar for both men and women.
Conclusions : In conclusion, prolongation of Pmax and Pd in acute SD suggests that acute SD might contribute to development and/or recurrence of atrial fibrillation.     

The effects of total and REM sleep deprivation on laser-evoked potential threshold and pain perception

We investigated the effects of total and rapid eye movement (REM) sleep deprivation on the thermal nociceptive threshold and pain perception using the objective laser-evoked potential (LEP) and the subjective visual analogue scale (VAS). Twenty-eight male adult volunteers were assigned into Control (CTRL), Total (T-SD), and REM (REM-SD) Sleep Deprivation groups. The T-SD and REM-SD volunteers were totally or selectively deprived of sleep for 2 and 4 consecutive nights, respectively. Pain parameters were measured daily during the experimental period. Volunteers were stimulated on the back of the hand by blocks of 50 diode laser pulses. Intensities increased between successive blocks, ranging from nonnoxious to noxious levels, and the LEP threshold was identified based on the evoked-response onset. Both the LEP threshold and VAS ratings were significantly increased after the second night of T-SD. No significant variations were observed in the REM-SD group, suggesting a predominant role for slow wave sleep rather than selective REM-SD in pain perception. Also, for both sleep-deprived groups, the mean values of the LEP threshold and VAS ratings showed a gradual increase that was proportional to the SD deprivation time, followed by a decrease after 1 night of sleep restoration. These findings demonstrate a hyperalgesic modification to pain perception (as reflected by the augmented VAS) and a concomitant increase in the LEP threshold following T-SD, an apparently contradictory effect that can be explained by differences in the ways that attention affects these pain measurements.     

Hyperstimulation of striatal D2 receptors with sleep deprivation: Implications for cognitive impairment

Sleep deprivation interferes with cognitive performance but the mechanisms are poorly understood. We recently reported that one night of sleep deprivation increased dopamine in striatum (measured with [¹¹C]raclopride, a PET radiotracer that competes with endogenous dopamine for binding to D2 receptors) and that these increases were associated with impaired performance in a visual attention task. To better understand this association here we evaluate the relationship between changes in striatal dopamine (measured as changes in D2 receptor availability using PET and [¹¹C]raclopride) and changes in brain activation to a visual attention task (measured with BOLD and fMRI) when performed during sleep deprivation versus during rested wakefulness. We find that sleep induced changes in striatal dopamine were associated with changes in cortical brain regions modulated by dopamine (attenuated deactivation of anterior cingulate gyrus and insula) but also in regions that are not recognized targets of dopaminergic modulation (attenuated activation of inferior occipital cortex and cerebellum). Moreover, the increases in striatal dopamine as well as its associated regional activation and deactivation patterns correlated negatively with performance accuracy. These findings therefore suggest that hyperstimulation of D2 receptors in striatum may contribute to the impairment in visual attention during sleep deprivation. Thus, while dopamine increases in prefrontal regions (including stimulation of D1 receptors) may facilitate attention our findings suggest that hyperstimulation of D2 receptors in striatum may impair it. Alternatively, these associations may reflect a compensatory striatal dopamine response (to maintain arousal) that is superimposed on a larger response to sleep deprivation.     

Dissociation of cortical regions modulated by both working memory load and sleep deprivation and by sleep deprivation alone

Working memory is an important mental capacity that is compromised following sleep deprivation (SD). To understand how working memory load interacts with state to influence brain activation in load-sensitive regions, and the extent to which SD-related changes are common across different loads, we used fMRI to study twelve healthy subjects following 24 h of SD using a verbal n-back task with three load levels. Performance decline was observed by way of reduced accuracy and slower response times following SD. The left prefrontal region and thalamus showed load dependent activity modulation that interacted with state. The right parietal and anterior medial frontal regions showed load dependent changes in activity as well as an effect of state. The anterior cingulate and occipital regions showed activation that displayed state effects that were independent of working memory load. These findings represent a step toward identifying how different brain regions exhibit varying vulnerability to the deleterious effects of SD on working memory.     

Antidepressive therapy by modifying sleep

Depressive symptoms are unspecific and occur in several psychiatric disorders. Sleep disturbances are also frequently present in depressed patients. As a consequence, it has been established that a number of modulations of the sleep-wake cycle can have an antidepressive effect. Total sleep deprivation or deprivation in the second half of the night have proven successful. The main limitation of the otherwise well tolerated treatment is the short duration of the antidepressive effect, which is mostly reversed in nearly all patients after the following night's sleep. New approaches are to shift the timing of sleep to earlier to ensure a possible longer-lasting effect. In clinical praxis the following manipulations should not be used: sleep deprivation in the first half of the night (not successful), REM-sleep deprivation (experimental setting), induced sleep prolongation (negative risk-benefit-ratio). In addition to patients with affective disorders sleep deprivation has proved relevant in patients with schizophrenia (depressed and/or with predominantly negative symptoms) and premenstrual dysphoric disorder. Very few side effects have been reported. Although many hypotheses have been tested, the mechanism of action underlying the antidepressive effect of sleep deprivation is still unknown.     

Acute sleep deprivation is associated with increased QT dispersion in healthy young adults

Background: Sleep deprivation (SD) is known to be associated with worse cardiovascular outcome including mortality. We investigated the association between acute SD and electrocardiographic maximum QT interval (QTmax), QT, and corrected QT dispersion (QTd/cQTd), which are known to be among predictors of ventricular arrhythmias and sudden death.
Methods: We obtained electrocardiograms of 37 healthy young volunteers (age: 28.45 ± 7.97 years; 11 women) after a night with regular sleep and repeated after a night with sleep debt. We measured minimum QT interval (QTmin), QTmax, QTd, and cQTd in milliseconds.
Results: Average sleep time of the subjects were 7.7 ± 0.8 hours during regular sleep and 1.7 ± 1.6 hours during a night with sleep debt (P < 0.001). Subjects had similar values of QTmin in milliseconds after a night of sleep debt when compared to after regular sleep (347.56 ± 29.75 vs 344.59 ± 20.89; P = 0.51), whereas they had significantly higher values of QTmax, QTd, and cQTd (396.48 ± 30.11 vs 378.10 ± 23.90; P = 0.001, 49.45 ± 9.11 vs 33.51 ± 10.05; P < 0.001 and 54.92 ± 10.42 vs 37.23 ± 10.81; P < 0.001, respectively). In Pearson's correlation analysis, QTmax, QTd, and cQTd were inversely correlated with sleep time (P = 0.012, r =–0.291; P < 0.001, r =–0.625 and P < 0.001, r =–0.616, respectively)
Conclusions: In conclusion, we clearly demonstrated that even one night of SD is associated with significant increase in QTmax, QTd, and cQTd in healthy young adults despite remaining within normal limits. These electrocardiographic changes in acute SD might contribute to development and/or recurrence of arrhythmias. This implication deserves further studies for clarifying the possible linkage between SD and arrhythmias.     

Sleep Fragmentation Hypersensitizes Healthy Young Women to Deep and Superficial Experimental Pain

The effect of sleep deprivation on pain sensitivity has typically been studied using total and partial sleep deprivation protocols. These protocols do not mimic the fragmented pattern of sleep disruption usually observed in individuals with clinical pain conditions. Therefore, we conducted a controlled experiment to investigate the effect of sleep fragmentation on pain perception (deep pain: forearm muscle ischemia, and superficial pain: graded pin pricks applied to the skin) in 11 healthy young women after 2 consecutive nights of sleep fragmentation, compared with a normal night of sleep. Compared with normal sleep, sleep fragmentation resulted in significantly poorer sleep quality, morning vigilance, and global mood. Pin prick threshold decreased significantly (increased sensitivity), as did habituation to ischemic muscle pain (increased sensitivity), over the course of the 2 nights of sleep fragmentation compared with the night of normal sleep. Sleep fragmentation did not increase the maximum pain intensity reported during muscle ischemia (no increase in gain), and nor did it increase the number of spontaneous pains reported by participants. Our data show that sleep fragmentation in healthy, young, pain-free women increases pain sensitivity in superficial and deep tissues, indicating a role for sleep disruption, through sleep fragmentation, in modulating pain perception.

Activation of the prostaglandin system in response to sleep loss in healthy humans: Potential mediator of increased spontaneous pain

Insufficient duration of sleep is a highly prevalent behavioral pattern in society that has been shown to cause an increase in spontaneous pain and sensitivity to noxious stimuli. Prostaglandins (PGs), in particular PGE2, are key mediators of inflammation and pain, and we investigated whether PGE2 is a potential mediator in sleep-loss-induced changes in nociceptive processing. Twenty-four participants (7 females, age 35.1 ± 7.1 years) stayed for 7 days in the Clinical Research Center. After two baseline days, participants were randomly assigned to either 3 days of 88 h of sleep deprivation (TSD, N = 15) or 8 h of sleep per night (N = 9), followed by a night of recovery sleep. Participants rated the intensity of various pain-related symptoms every 2 h across waking periods on computerized visual analog scales. PGE2 was measured in 24-h-urine collections during baseline and third sleep deprivation day. Spontaneous pain, including headache, muscle pain, stomach pain, generalized body pain, and physical discomfort significantly increased by 5–14 units on a 100-unit scale during TSD, compared to the sleep condition. Urinary PGE2 metabolite significantly increased by about 30% in TSD over sleep condition. TSD-induced increase in spontaneous pain, in particular headache and muscle pain, was significantly correlated with increase in PGE2 metabolite. Activation of the PGE2 system appears to be a potential mediator of increased spontaneous pain in response to insufficient sleep.     

Sleep patterns in nonambulatory boys with Duchenne muscular dystrophy

Sleep patterns and respiratory function during sleep were studied in five nonambulatory boys with Duchenne muscular dystrophy to clarify why patients with this disease awaken frequently at night. It was hypothesized that hypoxemia during sleep due to severe restrictive lung disease might cause nighttime arousals. Each boy underwent electroencephalography, electro-oculography and electromyography. Also determined were arterial oxyhemoglobin saturation, airflow from the nose and mouth, chest and abdominal excursions, and carbon dioxide tension of exhaled breaths. All five subjects had pulmonary function abnormalities consistent with severe restrictive lung disease and respiratory muscle weakness but none had evidence of respiratory failure or cor pulmonale. The boys awakened three times more frequently than age-matched published norms and experienced sleep stage shifts twice as often as normal children. Rapid-eye movement (REM) sleep as a proportion of total sleep was significantly reduced; sleep stage I was increased compared to normal values. No subject developed oxyhemoglobin desaturation during sleep. End-tidal CO2 tensions rose during sleep stages I, II and V (REM) in association with reduced chest wall excursion, suggesting transient episodes of mild hypoventilation which were not associated with arousals. Sleep fragmentation, frequent arousals and REM sleep deprivation occur in some boys with Duchenne muscular dystrophy but are not associated with significant disorders in breathing during sleep.     

The Effects of Recovery Sleep on Experimental Pain

Recent research suggests that recovery sleep (RS) has the potential to restore pain sensitivity and modulation after hyperalgesia due to preceding sleep deprivation. However, it has not yet been systematically examined whether the restoration of these pain parameters is driven by sleep characteristics of RS. Thus, the present study assessed changes in experimental pain during RS after total sleep deprivation (TSD) to test whether RS parameters predicted the restoration of the pain system. Thirty healthy participants completed one night of habitual sleep, one night of TSD and a subsequent recovery night. At-home sleep during baseline and recovery was assessed using portable polysomnography and a questionnaire. Before and after each night pressure pain thresholds (PPTs), temporal pain summation (TSP) and conditioned pain modulation (CPM) were assessed. PPTs decreased after TSD and increased following RS, indicating a restoration of pain sensitivity after hyperalgesia. RS characteristics did not predict this restoration, suggesting other mechanisms (eg, changes in serotonergic activity) underlying the observed pain changes. TSP indicated a lack of effect of experimental sleep manipulations on excitatory processes whereas CPM lacked sufficient reliability to investigate inhibitory processes. Thus, results indicate moderate effects of sleep manipulations on pain sensitivity, but not on pain modulation.PerspectiveThis article highlights the potential of recovery sleep to let pain thresholds return to normal following their decrease after a night of total sleep deprivation. In contrast, endogenous pain modulation (temporal pain summation, conditioned pain modulation) was not affected by sleep deprivation and recovery sleep.     

睡眠剥夺引起大鼠海马神经元凋亡与丝裂素活化蛋白激酶表达的变化

背景:丝裂素活化蛋白激酶是一组与神经元的存活凋亡有关的蛋白激酶,睡眠剥夺可以引起神经元凋亡。目的:观察睡眠剥夺大鼠丝裂素活化蛋白激酶表达的变化并分析其可能的意义。设计:完全随机分组的前瞻性研究。单位:郑州大学生理学教研室神经研究室。材料:实验于2000-06/2002-10在郑州大学完成。选取成年健康SD大鼠24只。方法:24只大鼠随机分为快眼动睡眠剥夺组、快眼动睡眠剥夺对照组和正常对照组3组,每组8只。睡眠剥夺组从早晨8点始,连续剥夺睡眠72h。正常对照组则置饲养笼中饲养,维持正常的睡眠-觉醒周期。观察其形态学变化。另取24只大鼠分组同上用于丝裂素活化蛋白激酶的检测。采用TUNEL染色法观察睡眠剥夺大鼠的海马神经元形态学变化,观察细胞外信号调节激酶活性的变化和c-Jun氨基末端激酶蛋白表达量的变化。主要观察指标:①观察睡眠剥夺大鼠海马神经元的形态学变化。②观察海马神经元细胞外信号调节激酶和c-Jun氨基末端激酶表达的变化。结果:①海马神经元形态学变化:快眼动睡眠剥夺组大鼠CA1和CA3区可见较多的凋亡阳性细胞,主要分布在海马的锥体细胞层。CA2区仅见极少量凋亡细胞,CA4区偶见凋亡细胞。正常对照组和快眼动睡眠剥夺对照组海马组织切片中未见明显阳性细胞。②细胞外信号调节激酶活性的变化:快眼动睡眠剥夺组明显低于快眼动睡眠剥夺对照组和对照组(1764.00±941.56,6139.67±2863.62,566.700±2763.41,t=3.2111,0.9863,P<0.05)。③c-Jun氨基末端激酶的阳性表达:快眼动睡眠剥夺组明显高于快眼动睡眠剥夺对照组和对照组(87.5%,25%,75%,t=3.4121,P<0.05)。结论:睡眠剥夺可引起大鼠海马神经元丝裂素活化蛋白激酶活性的变化,可能与神经元的凋亡有关。     

Partial Sleep Restriction Decreases Insulin Sensitivity in Type 1 Diabetes

OBJECTIVE

Sleep restriction results in decreased insulin sensitivity and glucose tolerance in healthy subjects. We hypothesized that sleep duration is also a determinant of insulin sensitivity in patients with type 1 diabetes.

RESEARCH DESIGN AND METHODS

We studied seven patients (three men, four women) with type 1 diabetes: mean age 44 ± 7 years, BMI 23.5 ± 0.9 kg/m², and A1C 7.6 ± 0.3%. They were studied once after a night of normal sleep duration and once after a night of only 4 h of sleep. Sleep characteristics were assessed by polysomnography. Insulin sensitivity was measured by hyperinsulinemic euglycemic clamp studies with an infusion of [6,6-²H₂]glucose.

RESULTS

Sleep duration was shorter in the night with sleep restriction than in the unrestricted night (469 ± 8.5 vs. 222 ± 7.1 min, P = 0.02). Sleep restriction did not affect basal levels of glucose, nonesterified fatty acids (NEFAs), or endogenous glucose production. Endogenous glucose production during the hyperinsulinemic clamp was not altered during the night of sleep restriction compared with the night of unrestricted sleep (6.2 ± 0.8 vs. 6.9 ± 0.6 μmol · kg lean body mass⁻¹ · min⁻¹, NS). In contrast, sleep restriction decreased the glucose disposal rate during the clamp (25.5 ± 2.6 vs. 22.0 ± 2.1 μmol · kg lean body mass⁻¹ · min⁻¹, P = 0.04), reflecting decreased peripheral insulin sensitivity. Accordingly, sleep restriction decreased the rate of glucose infusion by ∼21% (P = 0.04). Sleep restriction did not alter plasma NEFA levels during the clamp (143 ± 29 vs. 133 ± 29 μmol/l, NS).

CONCLUSIONS

Partial sleep deprivation during a single night induces peripheral insulin resistance in these seven patients with type 1 diabetes. Therefore, sleep duration is a determinant of insulin sensitivity in patients with type 1 diabetes.Intensive insulin therapy is essential for optimal glucoregulation in type 1 diabetes because the degree and duration of hyperglycemia determine the incidence of complications (1). However, glucoregulation cannot be normalized in patients with type 1 diabetes, as reflected by relatively large intra-individual variations of blood glucose levels. Subtle intra-individual variations in glucoregulation and insulin sensitivity in these patients depend on variations in physiological determinants such as dietary factors and exercise (2,3). In contrast to healthy subjects, however, patients with type 1 diabetes are unable to compensate for these physiological variations, other than by adaptations of the dose of exogenous insulin.Normal glucose homeostasis shows a diurnal pattern with variations in glucose tolerance, in which sleep characteristics play a key role (4). In this respect, sleep duration may be particularly relevant because sleep curtailment is a common aspect of our modern 24-h society (5,6). A reduction in sleep duration impairs glucose tolerance in healthy subjects (7). The effects of reduction of sleep duration on insulin sensitivity have not been studied in patients with type 1 diabetes.We hypothesized that partial sleep restriction decreases insulin sensitivity in patients with type 1 diabetes, which may contribute to intra-individual variations in glucoregulation. Therefore, we compared the effects of a single night of reduced sleep duration with those of a night of normal sleep duration on hepatic and peripheral insulin sensitivity, as assessed by hyperinsulinemic euglycemic clamp studies combined with tracer dilution of [6,6-²H₂]glucose in patients with type 1 diabetes.     

Effects of sleep deprivation on anaerobic exercise-induced changes in auditory brainstem evoked potentials

BACKGROUND: The present study was designed to assess how anaerobic exercise affects auditory brainstem response (ABR) parameters, and whether one night of sleep deprivation could alter these possible exercise-induced changes in ABRs. METHODS: Seven healthy, audiologically normal male students (mean age 22.4 +/- 1.0 years) participated in the study. All subjects underwent anaerobic Wingate test for three times: (i) baseline, (ii) following a full-night of habitual sleep and (iii) following one night of sleep deprivation. ABR measurements were performed before and after the second and the third Wingate tests. Oral body temperatures were recorded at the beginning of all ABR measurements. RESULTS: The latencies of wave III and V significantly shortened by anaerobic loading performed in the day after habitual sleep (4.13 +/- 0.10 versus 4.01 +/- 0.17 ms, P<0.02; and 5.84 +/- 0.26 versus 5.65 +/- 0.23 ms, P<0.03, respectively). One night of total sleep deprivation shortened pre-exercise latencies and altered exercise-induced changes in ABRs. CONCLUSION: The findings obtained in the present study show that acute anaerobic exercise is effective on ABR wave latencies independent from body temperature changes, and sleep deprivation has some modulatory effects on exercise-induced changes in ABR.     

睡眠剥夺后急性力竭运动大鼠血清的氧化应激状态

背景:有研究表明,大负荷的运动训练可造成自由基的生成急剧增加这些内源性自由基生成增多以及由此导致的组织细胞及亚细胞的脂质过氧化加强,使组织细胞的结构和功能受损,从而导致运动能力下降。睡眠剥夺也可造成机体氧自由基增加。目的:观察不同睡眠剥夺时间后急性力竭运动大鼠血清丙二醛、谷胱甘肽含量和超氧化物歧化酶活力的变化。设计:随机对照动物实验。单位:湖南师范大学体育学院运动人体科学实验室。材料:选用30只健康雄性10周龄SD大鼠,体质量(220±13)g,清洁级,由湖南农业大学实验动物服务部提供。方法:实验于2006-04/05在湖南师范大学体育学院运动生物化学实验室完成,随机摸球法将大鼠分为5组,空白对照组,单纯运动组,剥夺睡眠24h组,剥夺睡眠24h组,剥夺睡眠72h组,每组6只;空白对照组大鼠正常睡眠、不运动;单纯运动组大鼠正常睡眠、急性力竭运动后处死;剥夺睡眠24,48,72h组大鼠分别在剥夺睡眠24,48,72h,进行急性力竭运动后处死。大鼠睡眠剥夺模型采用的是轻柔刺激法;单纯运动组和睡眠剥夺后力竭运动组大鼠依据Bedford建立的大鼠运动模型方案进行运动:跑台坡度为10°,速度为19.3m/min,所有运动大鼠至力竭(力竭标准:运动末期,大鼠先后滞留跑道后1/3处达3次以上,各种刺激驱赶均无效,停跑后体征表现为呼吸急促,神情倦怠,腹卧位,对刺激反应迟钝,捕捉时,逃避反应较运动前减弱)。各组大鼠于实验后麻醉处死,将血液取出,自然凝固后离心,取上清检测丙二醛、谷胱甘肽的含量及超氧化物歧化酶活性。主要观察指标:大鼠血清的丙二醛、谷胱甘肽含量和超氧化物歧化酶活力的变化。结果:纳入大鼠30只均进入结果分析。①单纯运动组丙二醛含量高于空白对照组[(4.37±0.26),(3.35±0.14)μmol/L,P<0.01]。剥夺睡眠24,48,72h组丙二醛含量分别为(4.89±0.20),(5.15±0.12),(7.29±0.42)μmol/L,均高于单纯运动组,其中睡眠剥夺72h组高于其他睡眠剥夺组,差异有统计学意义(P<0.01)。②单纯运动组的谷胱甘肽含量低于空白对照组[(83.33±1.73),(93.16±2.44)mg/g,P<0.01],剥夺睡眠24h组谷胱甘肽含量为(94.98±1.69),高于单纯运动组(P<0.01),剥夺睡眠48,72h组谷胱甘肽含量分别为(79.89±2.16),(72.38±3.19)mg/g,低于单纯运动组(P<0.05,0.01),睡眠剥夺各时间组差异均有统计学意义(P<0.01)。③单纯运动组超氧化物歧化酶活力低于空白对照组[(4.59±0.21),(5.21±0.11)mkat/g,P<0.01],剥夺睡眠24,48,72h组超氧化物歧化酶活力分别为(5.03±0.15),(3.95±0.19),(3.27±0.31)mkat/g,均低于单纯运动组(P<0.01),但睡眠剥夺48h和72h的超氧化物歧化酶明显低于空白对照组(P<0.01);睡眠剥夺各时间组差异均有统计学意义(P<0.01)。结论:睡眠剥夺能够引起大鼠血清氧化应激损伤;随着睡眠剥夺时间的加长并做力竭运动使大鼠血清的氧自由基产物堆积越多,清除氧自由基能力越差,对机体的损伤明显。