Physical exercise accelerates re-entrainment of human sleep-wake cycle but not of plasma melatonin rhythm to 8 h phase-advanced sleep schedule.
Effects of timed physical exercise were examined on the re-entrainment of sleep-wake cycle and circadian rhythms to an 8 hour phase-advanced sleep schedule. Seventeen male adults spent 12 days in a temporal isolation facility with dim light conditions. The sleep schedule was phase-advanced by 8 hours from their habitual sleep times for 4 days, which was followed by a free-run session for 6 days where the subjects were deprived of time cues. During the shift schedule, the exercise group (n=9) performed physical exercise with a bicycle ergometer in the early and middle waking period for 2 hours each. The control group (n=8) sat on a chair at those times. Their sleep-wake cycles were monitored everyday by polysomnography and/or weight sensor equipped with a bed. The circadian rhythm in plasma melatonin was measured on the baseline day before phase-shift, on the 4th day of shift schedule and the 5th day of free-run. As a result, the sleep-onset on the first day of free-run in the exercise group was significantly phase-advanced from that in the control and from the baseline. On the other hand, the circadian melatonin rhythm was significantly phase-delayed in the both groups, showing internal desynchronization of the circadian rhythms. The sleep-wake cycle resynchronized to the melatonin rhythm by either phase-advance or -delay shifts in the free-run session. These findings indicate that the re-entrainment of the sleep-wake cycle to a phase-advanced schedule occurs independent of the circadian pacemaker and is accelerated by timed physical exercise.
1 comment:
Somebody posted this study here;
http://www.jneurosci.org/cgi/content/abstract/28/12/3071
in the comments to Michael Eades recanting of intermittent fasting over at four hour work week. Calorie restriction and fasting increases hypothalamic levels of orexin.
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During periods of reduced food availability, animals must respond with behavioral adaptations that promote survival. Despite the fact that many psychiatric syndromes include disordered eating patterns as a component of the illness, little is known about the neurobiology underlying behavioral changes induced by short-term calorie restriction. Presently, we demonstrate that 10 d of calorie restriction, corresponding to a 20–25% weight loss, causes a marked antidepressant-like response in two rodent models of depression and that this response is dependent on the hypothalamic neuropeptide orexin (hypocretin). Wild-type mice, but not mice lacking orexin, show longer latency to immobility and less total immobility in the forced swim test after calorie restriction. In the social defeat model of chronic stress, calorie restriction reverses the behavioral deficits seen in wild-type mice but not in orexin knock-out mice. Additionally, chronic social defeat stress induces a prolonged reduction in the expression of prepro-orexin mRNA via epigenetic modification of the orexin gene promoter, whereas calorie restriction enhances the activation of orexin cells after social defeat. Together, these data indicate that orexin plays an essential role in mediating reduced depression-like symptoms induced by calorie restriction.
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Orexin stimulates hunger, and also olfactory sensitivity. It makes sense that calorie restriction and an increase in hunger should be accompanied by decreased social stress; the greater threat becomes starvation. Better to risk the owl's claws or being knocked around by a bigger mouse than to starve to death.
Social anxiety is a pretty big problem for me, so I've been reading up on orexin, hoping to find something practical to my own situation.
This article here is pretty interesting;
http://www.news-medical.net/news/2009/01/29/45355.aspx
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"Obese people are not deficient in leptin," Dr. Yanagisawa said. "They have tons of leptin floating around. The problem is that their brain isn't very sensitive to it." Orexin, which Dr. Yanagisawa discovered about a decade ago, is involved in controlling appetite and sleep. He found that reduced levels of orexin lead to the sleep disorder narcolepsy in both rodents and humans.
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The high-orexin mice had lower blood levels of leptin, implying that the leptin was more effective in controlling weight in these mice. In addition, when the researchers administered leptin to the high-orexin mice, the animals responded with a much greater loss of appetite and weight compared to normal mice given leptin.
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Anyways, your post made me wonder what timed exercise would do to sleep patterns if no time-shift is involved, and whether this might affect orexin levels, and through them, social anxiety. It might be time for a little self-experimentation.
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