| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
LETTERS TO THE EDITOR |
Laboratories of Neurochemistry, Sleep Research Laboratory, Section of Neuropharmacology
Laboratories of Neurochemistry, Section of Neuropharmacology, Department of Physiological Sciences, Instituto de Medicina Experimental, Universidad Central de Venezuela, Caracas, Venezuela
Sleep Disorders Center, Memorial Herman Hospital, Houston, TX
We read with interest the recently published article by Hall et al. (1) on the relationship between stress and heart rate variability during sleep. They used a standard speech task paradigm to elicit acute stress in the immediate presleep period. In addition, the high frequency of EKG component was used to index parasympathetic modulation, and the ratio of low to high frequency power of heart rate variability was used to index sympathetic balance. The authors concluded that acute stress was associated with decreased levels of parasympathetic modulation during nonrapid eye movement (non-REM) and rapid eye movement (REM) sleep and increased levels of sympatho-vagal balance during non-REM sleep. They also found that parasympathetic modulation increased across successive non-REM cycles in the control group. In addition, they reported that those increases were blunted in the stress group and remained essentially unchanged across successive non-REM periods. Finally, the authors stated that higher levels of sympatho-vagal balance during non-REM sleep were associated with poorer sleep maintenance and lower delta sleep activity. With respect to this, we would like to give some additional information dealing with the autonomic nervous system (ANS) changes registered in normal and stressed subjects throughout sleep periods.
The assessment of the ANS was performed not only through the heart rate plus blood pressure variability but also by measuring circulating neurotransmitters: noradrenaline, adrenaline, dopamine, platelet serotonin (p-5HT), plasma serotonin (f-5HT), and plasma tryptophane. These parameters were assessed at diurnal periods as well as nocturnal periods. The supine-resting + 1-minute orthostasis + 5-minute moderate exercise was performed in the morning (2–4), whereas the nocturnal assessment was performed at all sleep stages (SWS and REM; 5).
Summarizing, our results showed that the noradrenaline/adrenaline plasma ratio was greater than 3 during supine-resting and increased at one-minute orthostasis, in normal subjects. This noradrenaline/adrenaline ratio does not increase rather decrease in stressed subjects. On the other hand, the f-5HT values were found elevated in stressed but not in normal subjects. This f-5HT raised values were associated with an increase in platelet aggregability, always detected in the latter group (6–8).
These neurochemical findings were associated with increases of both heart rate and differential blood pressure (systolic less diastolic). The heart rate and blood pressure changes were found at both orthostasis and exercise periods. These findings are consistent with the postulation that stressed subjects present with predominance of adrenal over neural sympathetic activity (9,10).
The assessment of the ANS throughout the sleep cycle in normal subjects demonstrated that whereas adrenaline plasma levels fell at the first 10-minute period of supine-resting (wake), noradrenaline plasma level remained high, resulting in an increase of the noradrenaline:adrenaline ratio. Adrenaline plasma levels showed further and progressive decreases throughout the SWS and reached the minimal level at the REM sleep stage. On the other hand, noradrenaline plasma levels decreased slowly but reached minimal values at the REM sleep period, at which time both neural and adrenal sympathetic activities presented with almost zero values. This decrement of both neural plus adrenal sympathetic activities was opposed by an increase of plasma-5HT rise, which paralleled both blood pressure and heart rate falls. The well-known fact that circulating acetylcholine interferes with the uptake of plasma serotonin by platelets is consistent with the postulation that the f-5HT level is an index of parasympathetic activity in normal subjects (11).
Although both noradrenaline and adrenaline plasma levels showed parallel decreases throughout the supine-resting plus sleep periods, the noradrenaline:adrenaline ratio remained low (<1) in stressed subjects. In addition, the SWS periods were shorter than normal in these subjects, and a predominance of REM plus waking periods was registered throughout the nocturnal investigation. Although both systolic blood pressure (SBP) and diastolic blood pressure (DBP) did not fall before REM sleep periods, the differential pressure (SBP less DBP) was higher when compared with that observed in normal subjects. This finding is consistent with predominance of adrenal over neural sympathetic activity. However, both blood pressure and heart rate reached minimal levels at REM sleep (5,10). This finding is consistent with the absence of both neural and adrenal sympathetic activities (12).
The normal f5HT:p5HT ratio increase registered throughout SWS in normal subjects was not observed in stressed subjects (13). The fact that these subjects showed permanent elevated plasma-5HT plus adrenaline plasma levels plus increased platelet aggregability is consistent with this. Finally, the poor parasympathetic plus high adrenal sympathetic activities registered in stressed subjects are consistent with the frequent waking periods they show during nocturnal sleep cycles.
REFERENCES
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
