Sleep during the Antarctic winter: preliminary observations on changing the spectral composition of artificial light.

Antarctic Base personnel live for 3 months in winter with no natural sunlight. This project compared sleep, by actigraphy, during periods of increased exposure to white light or blue enriched light in 2003. The primary aim was to help define the optimum spectral composition and intensity of artificial environmental light. Nine men and one woman (33 +/- 7 years, mean +/- SD), wore activity and light monitors continuously from 28.2 to 9.10, and kept sleep diaries. Extra light was provided by light boxes (standard white, 5300 K, or prototype blue enriched, 10,000 K, Philips Lighting), which were turned on in bedrooms and in communal/work areas approximately 08.00-18.00 hours. After a no-treatment control period, 28.2-20.3, sequential 4-5 week periods of first white, then blue light, were imposed with a further control period 19.9-9.10. A limited baseline study in 2002 (no interventions) similarly measured light and activity in seven men and one woman (30 +/- 7 years). Daily light exposure in winter (lux, mean +/- SD) was doubled in 2003 (maximum 1039 +/- 281, average 64 +/- 21), compared to 2002 (572 +/- 276 and 30 +/- 11), P < 0.05 and P < 0.01, with no differences between white and blue light. There were no major differences in sleep between light conditions in 2003. A delay in sleep timing was found in midwinter compared to control (2003, bedtime, P < 0.05, sleep start, P < 0.05, sleep end, P < 0.01) and sleep fragmentation increased (P < 0.05). Sleep efficiency was slightly higher during all blue light periods compared to all white periods (P < 0.05). The use of higher intensity light of suitable spectral composition is proposed.

Expression of hexokinase isoforms in the dorsal root ganglion of the adult rat and effect of experimental diabetes.

The effect of streptozotocin (STZ)-induced diabetes on expression and activity of hexokinase, the first enzyme and rate-limiting step in glycolysis, was studied in sensory neurons of lumbar dorsal root ganglia (DRG). The DRG and sciatic nerve of adult rats expressed the hexokinase I isoform only. Immunofluorescent staining of lumbar DRG demonstrated that small-medium neurons and satellite cells exhibited high levels of expression of hexokinase I. Large, mainly proprioceptive neurons, had very low or negative staining for hexokinase I. Intracellular localization and biochemical studies on intact DRG from adult rats and cultured adult rat sensory neurons revealed that hexokinase I was almost exclusively found in the mitochondrial compartment. Duration of STZ-diabetes of 6 or 12 weeks diminished hexokinase activity by 28% and 30%, respectively, in lumbar DRG compared with age matched controls (P<0.05). Quantitative Western blotting showed no effect of diabetes on hexokinase I protein expression in homogenates or mitochondrial preparations from DRG. Immunofluorescent staining for hexokinase I showed no diabetes-dependent change in small-medium neuron expression in DRG, however, large neurons became positive for hexokinase I (P<0.05). Such complex effects of diabetes on hexokinase I expression in the DRG may be due to glucose-driven up-regulation of expression or the result of impaired axonal transport and perikaryal accumulation in the large neuron sub-population. Because hexokinase is the rate-limiting enzyme of glycolysis these results imply that metabolic flux through the glycolytic pathway is reduced in diabetes. This finding, therefore, questions the role of high glucose-induced metabolic flux as a key driving force in reactive oxygen species generation by mitochondria.

Sleep and circadian phase in a ship's crew.

Numerous factors influence the increased health risks of seamen. This study investigated sleep (by actigraphy) and the adaptation of the internal clock in watch-keeping crew compared to day workers, as possible contributory factors. Fourteen watch keepers, 4 h on, 8 h off (0800-1200/2000-2400 h, 1200-1600/2400-0400 h, 1600-2000/0400-0800 h) (fixed schedule, n = 6; rotating by delay weekly, n = 8), and 12 day workers participated during a voyage from the United Kingdom to Antarctica. They kept daily sleep diaries and wore wrist monitors for continuous recording of activity. Sleep parameters were derived from activity using the manufacturer's software and analyzed by repeated-measures ANOVA using SAS 8.2. Sequential urine samples were collected for 48 h weekly for 6-sulphatoxymelatonin measurement as an index of circadian rhythm timing. Individuals working watches of 1200-1600/2400-0400 h and 1600-2000/0400-0800 h had 2 sleeps daily, analyzed separately as main sleep (longest) and 2nd sleep. Main sleep duration was shorter in watch keepers than in day workers (p < 0.0001). Objective sleep quality was significantly compromised in rotaters compared to both day workers and fixed watch keepers, the most striking comparisons being sleep efficiency (percentage desired sleep time spent sleeping) main sleep (p < 0.0001) and sleep fragmentation (an index of restlessness) main sleep (p < 0.0001). The 2nd sleep was substantially less efficient than was the main sleep (p < 0.0001) for all watch keepers. There were few significant differences in sleep between the different watches in rotating watch keepers. Circadian timing remained constant in day workers. Timing of the 6-sulphatoxymelatonin rhythm was later for the watch of 1200-1600/2400-0400 h than for all others (1200-1600/2400-0400 h, 5.90 +/- 0.85 h; 1600-2000/0400-0800 h, 1.5 +/- 0.64 h; 0800-1200/ 2000-2400 h, 2.72 +/- 0.76 h; days, 2.09 +/- 0.68 h [decimal hours, mean +/- SEM]: ANOVA, p < 0.01). This study identifies weekly changes in watch time as a cause of poor sleep in watch keepers. The most likely mechanism is the inability of the internal clock to adapt rapidly to abrupt changes in schedule.