Why the study?
How does sympathetic skin nerve activity and effector function change during different sleep stages in healthy humans?
How does sympathetic skin nerve activity and effector function change during different sleep stages in healthy humans?
The study suggests the existence of specific sympathetic vasodilator fibers in the skin, as evidenced by unchanged multiunit SSA during non-REM sleep despite increases in skin resistance and blood flow.
Answers are grounded in this paper and cite their sources.
Sleep-stage sympathetic patterns should not alter practice; leaves open existence of specific skin vasodilator fibers in non-REM.
Multi-unit sympathetic skin nerve activity (SSA) in the peroneal nerve was recorded together with electrical skin resistance, skin blood flow and (in some subjects) finger blood pressure during sleep in 22 sleep-deprived healthy subjects. The average strength of sympathetic activity in different sleep stages was measured during 5-min periods as the area-under-curve of the integrated neurogram. Stage 2 sleep was reached by 15 subjects, stages 3-4 by nine and rapid eye movement (REM) sleep by six subjects. Non-REM sleep was always associated with an increased skin resistance, which was larger in glabrous than in hairy skin (293 +/- 48 vs. 175 +/- 4% of awake control level, n = 10, P < 0.05). Skin blood flow also increased during sleep, with a mean maximal increase of 397 +/- 79% of the awake control level (n = 11, P < 0.05). In spite of these changes of effector function no significant difference in mean SSA was found between the awake control period and periods of non-REM sleep, but during REM sleep SSA increased with 34% (P < 0.05) compared with the immediately preceding stage 2 period. In stage 2 sleep, K-complexes were associated with bursts of SSA followed by transient changes of skin resistance, blood flow and arterial blood pressure. When both skin resistance and blood flow were recorded within the innervation area of the impaled fascicle, single bursts or short periods of increased SSA could be succeeded by increased skin blood flow without concomitant skin resistance change. This indicates the existence of specific sympathetic vasodilator fibres in the skin. Therefore the unchanged strength of multiunit SSA during non-REM sleep in the face of increases of skin resistance and blood flow may be a consequence of an increased sympathetic vasodilator nerve activity combined with decreases of vasoconstrictor and sudomotor traffic.
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Noll et al. (1994) studied this question.
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