New research by scientists in the U.S. has revealed that the disrupted sleep which results from jet lag and shift work occurs in two separate but linked groups of neurons below the hypothalamus at the base of the brain.
The fatigue caused by jet lag and shift work is a direct result of disruption to the body's normal rhythms and is a problem for both travellers and those who work in rotating shifts.
The symptoms of jet lag include fatigue, sleepiness, digestive upsets, impaired judgement and decision making, memory lapses, irritability and apathy.
The body is synchronised to night and day by the effect of sunlight through brain chemicals or neurotransmitters, especially melatonin and many bodily processes are set by this 24-hour physiological ‘clock’ - these include temperature, hormones, digestion, heart rate, blood pressure and brain states.
This changing rate of activity over each 24-hour period is called the circadian rhythm (‘circadian’ means approximately one day).
The new research from the University of Washington (UW) shows the disruption occurs in two separate but linked groups of neurons in a structure called the suprachiasmatic nucleus, below the hypothalamus at the base of the brain - one group is synchronized with deep sleep that results from physical fatigue and the other controls the dream state of rapid eye movement, or REM, sleep.
The ventral, or bottom, neurons receive light information directly from the eyes and govern rhythms in tune with periods of light and dark - while the dorsal, or top, neurons do not receive direct light information and so govern rhythms as a more independent internal, or circadian, biological clock.
Dr Horacio de la Iglesia, a UW associate professor of biology, and the lead author of the study, says it appears that some of the body's rhythms are "more loyal" to the ventral neurons and others are much more in tune with the dorsal neurons.
In normal circumstances the two neuron groups are synchronized with each other, but disruptions such as jet travel across time zones or shift work can throw the cycles out of kilter.
Deep sleep is most closely tied to light-dark cycles and typically adjusts to a new schedule in a couple of days, but REM sleep is more tied to the light-insensitive dorsal neurons and can be out of sync for a week or more.
Dr de la Iglesia says when a 22-hour light-dark cycle is imposed on animals, the ventral center can catch up but the dorsal doesn't adapt and defaults to its own inner cycle.
For his research he used laboratory rats with a normal cycle of 25 hours and when the artificial 22-hour light-dark schedule was imposed, he found that the rats' deep sleep, largely governed by light but also a response to fatigue, quickly adapted to the 22-hour cycle, while their REM sleep continued to follow a 25-hour cycle and as a result, REM sleep did not occur in a normal progression following deep sleep.
Dr de la Iglesia says they found that after exposing rats to a shift of the light-dark timing that simulates a trip from Paris to New York, REM sleep needed 6 to 8 days to catch up with non-REM, or deep, sleep - the sleep you usually experience in the first part of the night.
He says the two types of sleep overlap immediately after the simulated jet lag occurs and there is a greater likelihood of the animals entering REM sleep earlier than they should and this possibly explains why it can take several days for travellers and shift workers to adapt to their new schedules and could also explain why jet lag is associated with lower learning performance because the disruption of the normal circadian sequence of sleep states is very detrimental to learning.
Dr de la Iglesia says one of the problems is that you are doing things at times that your body isn't prepared to do them - one group of neurons is telling your body it is Paris time and another that it is New York time and as a result the body is internally desynchronized.
Previous research has indicated that treatments such as physical activity can help the body resynchronize its rhythms following jet lag and Dr de la Iglesia believes his research could be useful in fine-tuning pharmaceutical and other therapies.
The study was funded by the National Institutes of Health and the Mary Gates Endowment for Students at the UW and is published online in Current Biology.