Simulated Jet Lag Research Articles

Simulated Chronic Jet Lag Affects the Structural and Functional Complexity of Hippocampal Neurons in Mice

There has been a long history that chronic circadian disruption such as jet lag or shift work negatively affects brain and body physiology. Studies have shown that circadian misalignment act as a risk factor for developing anxiety and mood-related depression-like behavior. Till date, most studies focused on simulating jet lag in model animals under laboratory conditions by repeated phase advances or phase delay only, while the real-life conditions may differ. In the present study, adult male mice were subjected to simulated chronic jet lag (CJL) by alternately advancing and delaying the ambient light–dark (LD) cycle by 9 h every 2 days, thereby covering a total of 24 days. The effect of CJL was then examined for a range of stress and depression-related behavioral and physiological responses. The results showed that mice exposed to CJL exhibited depression-like behavior, such as anhedonia. In the open field and elevated plus maze test, CJL-exposed mice showed increased anxiety behavior compared to LD control. In addition, CJL-exposed mice showed an increased level of serum corticosterone and proinflammatory cytokine, TNF-α in both serum and hippocampus. Moreover, CJL-exposed mice exhibited a reduction in structural complexity of hippocampal CA1 neurons along with decreased expression of neurotrophic growth factors, BDNF and NGF in the hippocampus compared to LD control. Taken together, our findings suggest that simulated chronic jet lag adversely affects structural and functional complexity in hippocampal neurons along with interrelated endocrine and inflammatory responses, ultimately leading to stress, anxiety, and depression-like behavior in mice.

P15-013-23 Changes in Human Metabolism and Post-Prandial Responses Following a 5-Hour Simulated Jet-Lag

P15-013-23 Changes in Human Metabolism and Post-Prandial Responses Following a 5-Hour Simulated Jet-Lag

Atypical behavioral and thermoregulatory circadian rhythms in mice lacking a microbiome

Trillions of microbial oscillators reside throughout the mammalian body, yet their contributions toward fundamental features of host circadian rhythms (CRs) have not been characterized. Here, we demonstrate that the microbiome contributes to host CRs in activity and thermoregulation. Mice devoid of microbes (germ-free, GF) exhibited higher-amplitude CRs in a light–dark cycle and longer circadian periods in constant darkness. Circadian entrainment to food was greater in GF mice, but resetting responses to simulated jet-lag were unaffected. Microbial transplantation with cecal contents of conventionally-raised mice normalized CRs of GF mice, indicating that the concurrent activity of gut microbes modulates host circadian networks. Obesogenic effects of high-fat diet were absent in GF mice, but some circadian-disruptive effects persisted. Transkingdom (host-microbe) interactions affect circadian period and entrainment of CRs in diverse traits, and microbes alter interactions among light- and food-entrainable circadian processes in the face of environmental (light, diet) perturbations.

Vasopressin regulates daily rhythms and circadian clock circuits in a manner influenced by sex

Arginine vasopressin (AVP) is a neurohormone that alters cellular physiology through both endocrine and synaptic signaling. Circadian rhythms in AVP release and other biological processes are driven by the suprachiasmatic nucleus (SCN) of the anterior hypothalamus. Loss of vasopressin signaling alters circadian behavior, but the basis of these effects remains unclear. Here we investigate the role of AVP signaling in circadian timekeeping by analyzing behavior and SCN function in a novel AVP-deficient mouse model. Consistent with previous work, loss of AVP signaling increases water consumption and accelerates recovery to simulated jetlag. We expand on these results to show that loss of AVP increases period, imprecision and plasticity of behavioral rhythms under constant darkness. Interestingly, the effect of AVP deficiency on circadian period was influenced by sex, with loss of AVP lengthening period in females but not males. Examining SCN function directly with ex vivo bioluminescence imaging of clock protein expression, we demonstrate that loss of AVP signaling modulates the period, precision, and phase relationships of SCN neurons in both sexes. This pattern of results suggests that there are likely sex differences in downstream targets of the SCN. Collectively, this work indicates that AVP signaling modulates circadian circuits in a manner influenced by sex, which provides new insight into sexual dimorphisms in the regulation of daily rhythms.

High-throughput discovery of genetic determinants of circadian misalignment.

Circadian systems provide a fitness advantage to organisms by allowing them to adapt to daily changes of environmental cues, such as light/dark cycles. The molecular mechanism underlying the circadian clock has been well characterized. However, how internal circadian clocks are entrained with regular daily light/dark cycles remains unclear. By collecting and analyzing indirect calorimetry (IC) data from more than 2000 wild-type mice available from the International Mouse Phenotyping Consortium (IMPC), we show that the onset time and peak phase of activity and food intake rhythms are reliable parameters for screening defects of circadian misalignment. We developed a machine learning algorithm to quantify these two parameters in our misalignment screen (SyncScreener) with existing datasets and used it to screen 750 mutant mouse lines from five IMPC phenotyping centres. Mutants of five genes (Slc7a11, Rhbdl1, Spop, Ctc1 and Oxtr) were found to be associated with altered patterns of activity or food intake. By further studying the Slc7a11tm1a/tm1a mice, we confirmed its advanced activity phase phenotype in response to a simulated jetlag and skeleton photoperiod stimuli. Disruption of Slc7a11 affected the intercellular communication in the suprachiasmatic nucleus, suggesting a defect in synchronization of clock neurons. Our study has established a systematic phenotype analysis approach that can be used to uncover the mechanism of circadian entrainment in mice.

Responses of activity rhythms to temperature cues evolve in Drosophila populations selected for divergent timing of eclosion.

Even though the rhythms in adult emergence and locomotor activity are two different phenomena that occur at distinct life stages of the fly life cycle, previous studies have hinted at similarities in certain aspects of the organisation of the circadian clock driving these two rhythms. For instance, the period gene plays an important regulatory role in both rhythms. In an earlier study, we have shown that selection on timing of adult emergence behaviour in populations of Drosophila melanogaster leads to the co-evolution of temperature sensitivity of circadian clocks driving eclosion. In this study, we investigated whether temperature sensitivity of the locomotor activity rhythm evolved in our populations separately from the adult emergence rhythm, with the goal of understanding the extent of similarity (or lack thereof) in circadian organisation underlying the two rhythms. We found that in response to simulated jetlag with temperature cycles, late chronotypes (populations selected for predominant emergence during dusk) indeed re-entrained faster than early chronotypes (populations selected for predominant emergence during dawn) to 6 h phase delays, thereby indicating enhanced sensitivity of the activity/rest clock to temperature cues in these stocks (entrainment is the synchronisation of internal rhythms to cyclic environmental time cues). Additionally, we found that late chronotypes show higher plasticity of phases across regimes, day-to-day stability in phases and amplitude of entrainment, all indicative of enhanced temperature-sensitive activity/rest rhythms. Our results highlight remarkably similar organisation principles between circadian clocks regulating emergence and activity/rest rhythms.

Differences in post-chronic jet lag parameters in male and female mice

ABSTRACT Chronic jet lag has deleterious effects on many physiological parameters. Most simulations of chronic jet lag consist of repeated advances only, while real-life conditions may differ. We compared number of transients, activity (α) and rest (ρ), and robustness of rhythm by autocorrelation in male and female AKR mice; before, during, and after simulated chronic jet lag (CJL); and phase angle of entrainment and accuracy before and after CJL, using alternate 9-h advances and delays of the light-dark schedule. Females exhibited no scalloping. Compared to pre-CJL values, α was significantly more in females post-CJL, indicating α decompression. The levels of activity increased during and after CJL, particularly in females, indicating behavioural feedback on the circadian rhythm. Robustness of rhythm (autocorrelation coefficient, and amplitude) was significantly suppressed during CJL in both males and females. Females took more transients than males to re-entrain to the final LD shift at the end of CJL. More transients were needed to re-entrain at the end of CJL, compared to a single shift. The study suggests that animals undergoing CJL incorporating alternating advances and delays are able to avoid α compression associated with jet lag, and also that females are detrimentally affected more than males. Abbreviations: SCN: Suprachiasmatic Nuclei; CJL: Chronic Jet Lag; LD: Light-dark

Effects of a 20-Min Nap Post Normal and Jet Lag Conditions on P300 Components in Athletes.

Post-lunch sleepiness belongs to biological rhythms. Athletes take a nap to counteract afternoon circadian nadir, in prevision of disturbed sleep. This study examined the effects of brief post-lunch nap on vigilance in young and healthy athletes. The P300 components, physiological and cognitive performances were assessed either after nap or rest, following a night of normal sleep (NSC) or simulated jet lag condition (5-h advance-JLC). P300 wave is the positive deflection at about 300 ms in response to a rare stimulus, representing higher information processing. P300 amplitude reflects the amount of attention allocated whereas P300 latency reflects time spent on stimulus classification. P300 amplitude was significantly increased (Fz:11.14±3.0vs9.05±3.2 µV; p<0.05) and P300 latency was shorter (Pz:327.16±18.0vs344.90±17.0 ms; p<0.01) after nap in NSC. These changes were accompanied by lower subjective sleepiness (19.7±9.6vs27.5±16.5; p<0.05) and decrease in mean reaction times (MRT: divided attention, 645.1±74.2vs698±80.4 ms; p<0.05). In contrast, in JLC, only P300 amplitudes (Fz:10.30±3.1vs7.54±3.3 µV; p<0.01 and Cz: 11.48±3.1vs9.77±3.6 µV; p<0.05) increased but P300 latencies or MRT did not improve. These results indicated improvements in speed of stimulus evaluation time. Napping positively impacts on cognitive processing, especially when subjects are on normal sleep schedules. A nap should be planned for athletes whose performance requires speedy and accurate decisions.

Age-related circadian disorganization caused by sympathetic dysfunction in peripheral clock regulation

The ability of the circadian clock to adapt to environmental changes is critical for maintaining homeostasis, preventing disease, and limiting the detrimental effects of aging. To date, little is known about age-related changes in the entrainment of peripheral clocks to external cues. We therefore evaluated the ability of the peripheral clocks of the kidney, liver, and submandibular gland to be entrained by external stimuli including light, food, stress, and exercise in young versus aged mice using in vivo bioluminescence monitoring. Despite a decline in locomotor activity, peripheral clocks in aged mice exhibited normal oscillation amplitudes under light–dark, constant darkness, and simulated jet lag conditions, with some abnormal phase alterations. However, age-related impairments were observed in peripheral clock entrainment to stress and exercise stimuli. Conversely, age-related enhancements were observed in peripheral clock entrainment to food stimuli and in the display of food anticipatory behaviors. Finally, we evaluated the hypothesis that deficits in sympathetic input from the central clock located in the suprachiasmatic nucleus of the hypothalamus were in part responsible for age-related differences in the entrainment. Aged animals showed an attenuated entrainment response to noradrenergic stimulation as well as decreased adrenergic receptor mRNA expression in target peripheral organs. Taken together, the present findings indicate that age-related circadian disorganization in entrainment to light, stress, and exercise is due to sympathetic dysfunctions in peripheral organs, while meal timing produces effective entrainment of aged peripheral circadian clocks.

Circadian waveform bifurcation, but not phase-shifting, leaves cued fear memory intact

In mammals, memory acquisition and retrieval can be affected by time of day, as well as by manipulations of the light/dark cycle. Under bifurcation, a manipulation of circadian waveform, two subjective days and nights are experimentally induced in rodents. We examined the effect of bifurcation on Pavlovian fear conditioning, a prominent model of learning and memory. Here we demonstrate that bifurcation of the circadian waveform produces a small deficit in acquisition, but not on retrieval of fear memory. In contrast, repeated phase-shifting in a simulated jet-lag protocol impairs retrieval of memory for cued fear. The results have implications for those attempting to adjust to shift-work or other challenging schedules.

Neural correlates of individual differences in circadian behaviour.

Daily rhythms in mammals are controlled by the circadian system, which is a collection of biological clocks regulated by a central pacemaker within the suprachiasmatic nucleus (SCN) of the anterior hypothalamus. Changes in SCN function have pronounced consequences for behaviour and physiology; however, few studies have examined whether individual differences in circadian behaviour reflect changes in SCN function. Here, PERIOD2::LUCIFERASE mice were exposed to a behavioural assay to characterize individual differences in baseline entrainment, rate of re-entrainment and free-running rhythms. SCN slices were then collected for ex vivo bioluminescence imaging to gain insight into how the properties of the SCN clock influence individual differences in behavioural rhythms. First, individual differences in the timing of locomotor activity rhythms were positively correlated with the timing of SCN rhythms. Second, slower adjustment during simulated jetlag was associated with a larger degree of phase heterogeneity among SCN neurons. Collectively, these findings highlight the role of the SCN network in determining individual differences in circadian behaviour. Furthermore, these results reveal novel ways that the network organization of the SCN influences plasticity at the behavioural level, and lend insight into potential interventions designed to modulate the rate of resynchronization during transmeridian travel and shift work.

A 20-min nap in athletes changes subsequent sleep architecture but does not alter physical performances after normal sleep or 5-h phase-advance conditions

The aim of the study was to examine the effects of a post-prandial 20 min nap on a short-term physical exercise and subsequent sleep in athletes keeping their usual sleep schedules and in 5-h phase-advance condition. Sixteen healthy young male athletes (age 22.2 ± 1.7 years, non-habitual nappers) participated in the study. After a baseline 8-h time in bed in normal and 5-h advanced sleep schedules, a standardized morning and lunch in a laboratory environment, subjects underwent either a nap (20 min of sleep elapsed from 3 epochs of stage 1 or 1 epoch of stage 2), or a rest without sleep by lying in a bed, between 13:00 and 14:00 hours in non-shifted condition or 08:00 and 09:00 hours in shifted condition, after which anaerobic exercises were performed twice 2 h apart. Core body temperature was recorded throughout the study period. The nap extended sleep onset latency from 6.72 ± 3.83 to 11.84 ± 13.44 min, after shifted condition but did not modify sleep architecture of the post-trial night among athletes, whether shifted or not. Moreover, napping did not improve physical performance but it delayed acrophase and batyphase of core body temperature rhythm parameters. Napping showed no reliable benefit on short-term performances of athletes exercising at local time or after a simulated jet lag.

Variations in the rate and direction of re-entrainment to acute simulated jet lag in the diurnal North Indian palm squirrel

We report the presence of variations in the rate and direction of re-entrainment to acute simulated jet lag in wild-caught North Indian palm squirrels (Funambulus pennanti). Adult laboratory and wheel-acclimated (Lafayette, USA) males (N = 30) were entrained to a 12:12 h light/dark (LD) schedule, followed by a 9 h advance of the LD schedule to simulate acute jet lag. The direction and rate of re-entrainment, i.e. the number of orthodromic (advancing) and antidromic (delaying) transients, the acrophases of daily rhythms in each case, duration of activity (α) and phase angle relationship (ψ) were noted using Clocklab (Coulbourn, USA). The squirrels exhibited distinct variations in their response to simulated acute jet lag, re-entraining either slowly (14/30) or rapidly (10/30) by advancing transients, or undergoing antidromic re-entrainment slowly (5/30), and, in only one individual, rapidly. Acrophases re-entrained slower than onsets. α underwent compression during re-entrainment, particularly during fast orthodromic responses. ψ was not significantly different in any of the groups before or after re-entrainment. This phenomenon has scope for further investigation and highlights the need for individual assessment of re-entrainment patterns before taking preventive measures for jet lag.

Aging Differentially Affects the Re-entrainment Response of Central and Peripheral Circadian Oscillators

Aging produces a decline in the amplitude and precision of 24 h behavioral, endocrine, and metabolic rhythms, which are regulated in mammals by a central circadian pacemaker within the suprachiasmatic nucleus (SCN) and local oscillators in peripheral tissues. Disruption of the circadian system, as experienced during transmeridian travel, can lead to adverse health consequences, particularly in the elderly. To test the hypothesis that age-related changes in the response to simulated jet lag will reflect altered circadian function, we examined re-entrainment of central and peripheral oscillators from young and old PER2::luciferase mice. As in previous studies, locomotor activity rhythms in older mice required more days to re-entrain following a shift than younger mice. At the tissue level, effects of age on baseline entrainment were evident, with older mice displaying earlier phases for the majority of peripheral oscillators studied and later phases for cells within most SCN subregions. Following a 6 h advance of the light:dark cycle, old mice displayed slower rates of re-entrainment for peripheral tissues but a larger, more rapid SCN response compared to younger mice. Thus, aging alters the circadian timing system in a manner that differentially affects the re-entrainment responses of central and peripheral circadian clocks. This pattern of results suggests that a major consequence of aging is a decrease in pacemaker amplitude, which would slow re-entrainment of peripheral oscillators and reduce SCN resistance to external perturbation.

Effect of chronic jet lag after induction of Dalton's lymphoma in male and female mice

Biological rhythms are ubiquitous phenomena that enable an organism to temporally adapt to the environment. Jet lag occurs during rapid transmeridial transport and disrupts the normal biological rhythm. Disruption of the biological rhythm is known to reduce survival and hasten tumorigenesis in male mice. Dalton's lymphoma (DL) is a spontaneous and highly invasive T-cell lymphoma that develops as an ascitic tumor in murines. DL was induced by serial implantation of live ascite cells in laboratory-acclimated age-matched male and female AKR mice. The mice were then subjected to simulated chronic jet lag (CJL) by rapidly and alternately advancing and delaying the ambient light dark cycle by 8 h every 2 days. Females, but not males, with DL became arrhythmic after exposure to simulated CJL. Survival was significantly curtailed in both male and female mice with DL + CJL compared to survival in mice with DL alone or CJL alone (∼16 days after DL induction in mice and facing jet lag, and ∼28 days after DL induction in mice bearing but not undergoing jet lag simulation). These results suggest that female mice may be more at risk from jet lag associated effects if they have cancer prior to facing jet lag, and DL + CJL may detrimentally impact the female circadian clock more than that of the males.

Carcinogenicity of shift-work, painting, and fire-fighting

In October, 2007, 24 scientists from ten countries met at the International Agency for Research on Cancer (IARC), Lyon, France, to assess the carcinogenicity of shift-work, painting, and fi re-fi ghting. These assessments will be published as volume 98 of the IARC Monographs. About 15–20% of the working population in Europe and the USA is engaged in shift-work that involves nightwork, which is most prevalent (above 30%) in the health-care, industrial manufactur ing, mining, transport, communication, leisure, and hospitality sectors. Among the many diff erent patterns of shiftwork, those including nightwork are the most disruptive for the circadian clock. Six of eight epidemiological studies from various geographical regions, most notably two independent cohort studies of nurses engaged in shiftwork at night, have noted a modestly increased risk of breast cancer in long-term employees compared with those who are not engaged in shiftwork at night. These studies are limited by potential confounding and inconsistent defi nitions of shiftwork, with several focused on a single profession. The incidence of breast cancer was also modestly increased in most cohorts of female fl ight attendants, who also experience circadian disruption by frequently crossing time zones. Limitations of studies in these fl ight attendants include the potential for detection bias, proxy measures of exposure, and potential uncontrolled confounding by reproductive factors and cosmic radiation. Several diff erent rodent models have been used to test the eff ect of disruption of the circadian system on tumour development. More than 20 studies investigated the eff ect of constant light, dim light at night, simulated chronic jet lag, or circadian timing of carcinogens, and most showed a major increase in tumour incidence. No clear eff ect was seen for light pulses at night or constant darkness. A similar number of studies investigated the eff ect of reduced nocturnal melatonin concentrations or removal of the pineal gland (where melatonin is produced) in tumour development and most showed increases in the incidence or growth of tumours. Exposure to light at night disturbs the circadian system with alterations of sleep-activity patterns, suppression of melatonin production, and de regul ation of circadian genes involved in cancer-related pathways. Inactivation of the circadian Period gene, Per2, promotes tumour develop ment in mice, and in human breast and endo metrial tumours, the expression of PERIOD genes is inhibited. In animals, melatonin suppression can lead to changes in the gonadotrophin axis. In humans, sleep deprivation and the ensuing melatonin suppression lead to immunodefi ciency. For example, sleep deprivation suppresses natural killer-cell activity and changes the T-helper 1/T-helper 2 cytokine balance, reducing cellular immune defence and surveillance. On the basis of “limited evidence in humans for the carcinogenicity of shift-work that involves nightwork”, and “suffi cient evidence in experimental animals for the carcinogenicity of light during the daily dark period (biological night)”, the Working Group concluded that “shift-work that involves circadian disruption is probably carcinogenic to humans” (Group 2A). Painters are potentially exposed to many chemicals used as pigments, extenders, binders, solvents, and additives. Painters can also be exposed to other workplace hazards, such as asbestos or crystalline silica. Cohort and linkage studies of painters have shown consistent and signifi cant increases in lung cancer compared with the general population. No information on tobacco smoking was available in the cohort studies; however, the increases are comparable to results from many case–control studies that controlled for smoking. A meta-analysis by the Working Group of all independent studies, including two recent large studies, showed a signifi cant excess risk of about 20% overall, and of 50% when the analysis was restricted to smoking-adjusted estimates from population-based case–control studies. Increased mortality from mesothelioma was consistently noted. Similarly, cohort and linkage studies showed consistent 20–25% increases in the occurrence of urinary bladder cancer in painters, and similar increases were noted in case– control studies that controlled for smoking. Although fi ndings for lymphatic and haemopoietic cancers in painters were inconsistent, four of fi ve case– control studies reported signifi cant increases in childhood leukaemia associated with maternal exposure to paint. The risks tended to be greater when mothers were exposed before or during, rather than after, pregnancy, and two studies showed some evidence of an increasing risk with increasing exposure. Upcoming meetings February 5–12, 2008 Industrial and cosmetic dyes and related exposures

Temporal Variations of Coagulation Factor VII Activity in Mice Are Influenced by Lighting Regime

It was recently reported that the circadian clock machinery controls plasma levels of factor (F) VII, the serine protease triggering blood coagulation. Here, by exploiting the mouse model, this study showed that variations of photoperiod (i.e., winter or summer conditions or simulated chronic jetlag conditions) have a strong impact on plasma FVII activity levels. Under conditions mimicking summer or winter photoperiods, FVII activity showed a clear 24 h rhythmicity. Interestingly, mean daily FVII activity levels were significantly reduced in mice exposed to summer photoperiods. Behavioral activity rhythms under both photoperiods were synchronized to LD cycles, and the amount of activity per 24 h was comparable. The authors also investigated the influence of chronic jetlag (CJL) on the FVII activity rhythms, which can be easily mimicked in mice through continuous abrupt shifts in the lighting schedule. The exposure of mice to simulated CJL of either consecutive westward or consecutive westward and eastward flights for 15 days did not abolish the behavioral activity rhythms but was associated with a period significantly different from 24 h. Intriguingly, both types of CJL exerted a strong influence on FVII activity rhythms, which were virtually suppressed. Moreover, the mean daily FVII activity was significantly lower in the CJL than in the winter photoperiod condition. Taken together, these findings in mice provide novel insights into the modulation of FVII activity levels, which might have implications for human pathophysiology.

Progressive elevation of plasma thyrotropin during adaptation to simulated jet lag: effects of treatment with bright light or zolpidem.

It is well known that TSH secretion is modulated by sleep and circadian rhythmicity, but effects of abrupt shifts of the sleep-wake and dark-light cycles such as occur in jet lag and shift work have not been investigated. The present study examines alterations in the 24-h profiles of plasma TSH and thyroid hormones following an 8-h advance shift achieved without enforcing prolonged sleep deprivation. The effects of bright light exposure or sleep facilitation with zolpidem were investigated in separate studies performed in the same subjects. Each study involved blood sampling at 20-min intervals for 68 h and included a baseline period with dim light during waking hours and 2300-0700 h bedtimes in total darkness. The 8-h shift was achieved by advancing bedtimes to 1500-2300 h. In the course of adaptation to the shift, TSH levels increased progressively in all three studies because daytime sleep failed to inhibit TSH and nighttime wakefulness was associated with large TSH elevations. The overall elevation of TSH tended to be paralleled by a small increase in T3, but not free T4, levels. In the absence of treatment, mean TSH levels following awakening from the second shifted sleep were more than 2-fold higher than during the same time interval following normal nocturnal sleep (2.10 +/- 0.22 mU/L vs. 1.04 +/- 0.14 mU/L; n = 8, P < 0.001). Bright light exposure limited the overall increase of TSH, and mean TSH levels at the end of the study were lower than in the absence of treatment (P < 0.03). Treatment with zolpidem during the first shifted night limited the overall increase in TSH levels during the following waking period (P < 0.05), but the beneficial effect was no longer significant following the second shifted night. Thus, the jet lag syndrome may be associated with a prolonged elevation of peripheral TSH levels that may be limited by treatment with bright light exposure or hypnotic facilitation of sleep.

Progressive elevation of plasma thyrotropin during adaptation to simulated jet lag: effects of treatment with bright light or zolpidem

Progressive elevation of plasma thyrotropin during adaptation to simulated jet lag: effects of treatment with bright light or zolpidem

Inducing jet lag in older people: Adjusting to a 6-hour phase advance in routine

A 15-day simulated jet lag experiment was performed in a time isolation laboratory using 15 old women (79–91 years, mean 82.9 years) and 10 old men (71–86 years, mean 80.5 years). After five full days and nights on the subject's habitual routine, the waketime of night 6 was advanced by 6 h, truncating the sleep episode. All subsequent events occurred 6 h earlier than normal. Adjustment to the phase shift was evaluated by the circadian rhythm in rectal temperature (measured every minute), polysomnography of each sleep episode, and daily averages of mood, activation, and performance speed. While the circadian rhythm amplitude reduction consequent upon the phase shift showed a tendency to be longer lived in the old men, both old groups showed fairly rapid adjustment of the timing of their circadian temperature rhythm, comparable (if not better) to that observed earlier in a study of middle aged men. However, sleep disruption (and daytime sleepiness) appeared to be longer lived in the elderly, showing little of the recovery over time observed in younger subjects. Thus, there appeared to be some separation in the elderly of the sheep disruption and circadian rhythm disruption effects of jet lag.