Sympathetic Muscle Nerve Activity During Sleep in Man

Abstract

Muscle sympathetic activity (MSA) was recorded in the peroneal nerve during sleep in 14 sleep-deprived healthy subjects. Continuous noninvasive recordings of finger blood pressure were obtained in 7 subjects. In light sleep (stage 2 sleep) the number of sympathetic bursts/min decreased to 90 +/- 8% (mean +/- SEM) and total MSA (= burst/min x mean burst area) to 89 +/- 5% of the awake value (P less than 0.05, n = 14). In deep sleep (stage 3-4) total MSA decreased further, to 71 +/- 8% of the awake value (n = 5). There was no close correlation between variations of depth of sleep and variations of sympathetic activity but during continuously deepening sleep MSA decreased progressively with time. In stage 2 sleep, high amplitude K complexes were accompanied by short-lasting increases of sympathetic activity. Since these increases of MSA were not preceded by decreases of diastolic blood pressure, which is known to evoke increased sympathetic nerve traffic in muscle nerves, we suggest that K complex related increases of MSA are signs of arousal which elicit both cortical EEG phenomena and activation of cerebral sympathetic centres. During desynchronized (REM) sleep, total MSA increased to 124 +/- 12% of the value in awake state (n = 5). The increases occurred mainly in short irregular periods, often related to rapid eye movements and there was an inverse relationship between the duration of the desynchronized sleep and the increase of total MSA. Our findings are similar to the data obtained in animal experiments and may partly explain changes of blood pressure during synchronized and desynchronized sleep reported previously in man.

Baroreflex Buffering of Sympathetic Activation During Sleep

“…This overall picture points to a cardiac parasympathetic predominance during non-REM and to a peripheral sympathetic activation during REM, in agreement with studies that directly recorded peripheral sympathetic nerve traffic. [5][6][7] The lack of a tachycardic effect, despite the simultaneous increase sympathetic activation, frequently reported during REM 5,6,24,25 could be explained through a vagally mediated baroreflex mechanism offsetting cardiac sympathetic activation, as suggested by the increase in BRS in response to hypertensive stimuli. 25 As to the lack of significant changes in BRS downsequences, a different buffering effect of arterial baroreflex in response to increases and decreases in BP during sleep has Symbols indicate between-condition differences as follows: *Awake vs non-CAP; †Awake vs CAP; ‡Awake vs REM; §CAP vs non-CAP; ¶CAP vs REM; ʈNon-CAP vs REM; **Not significant vs non-CAP S2; † †Not significant vs non-CAP S2.…”

“…Previous studies dealing with sleep-related neural cardiovascular regulation [5][6][7][23][24][25] have focused on the conventional scoring defining the sleep macrostructure. 13 As in these studies, we observed a decrease in BP during S2 and SWS, with a recovery to the awake level during REM associated with parallel changes in LF SBP .…”

“…[5][6][7] Studies investigating sleep structure have led to the identification of a natural electroencephalographic arousal rhythm within the non-REM sleep stages, related to transient lightenings of sleep depth, known as the cyclic alternating pattern (CAP). 8,9 CAP corresponds to a prolonged oscillation of the arousal level, whereas the complementary condition, non-CAP (NCAP), is closely related to a degree of stability in sleep depth.…”

Sleep-Disordered Breathing in Heart Failure ― A Therapeutic Dilemma ―

“…17, 18 Cardiac metabolic gene expression anticipates and aligns with this circadian variation in myocardial workload. 19 Synchrony of these metabolic, temporal and autonomic rhythms, fundamental to normal cardiovascular homeostasis, 20 is disrupted profoundly by SDB.…”

Proceedings of the Physiological Society, 14‐15 February 1992, Bristol Meeting: Communications

“…The difference in thresholds and the response to analgesics in both legs before and after injury to the left suggests that there are both central and peripheral aspects to the increase in pain sensitivity. (Parmeggiani & Morrison, 1990) and in humans (Hornyak et al 1991), and it has been speculated that cardiac parasympathetic activity would increase during non-REM sleep. Using the absolute differences in consecutive R-R intervals in a continuous ECG (beat variability, BV) (Julu & Hondo, 1992), we have measured the BV during progressive stages (1-3) of non-REM sleep in 5 sleepdeprived subjects (10-53 years old).…”