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Updated: Jan 24, 2026

Assessing Collagen and Elastin Pressure-dependent Microarchitectures in Live, Human Resistance Arteries by Label-free Fluorescence Microscopy
Published on: April 9, 2018
Revisiting the dermatomal recruitment of, and pressure-dependent influences on, human eccrine sweating
Remo Frei1, Sean R Notley1, Elizabeth A Taylor1
1Centre for Human and Applied Physiology, School of Medicine, University of Wollongong, Wollongong, NSW, 2522, Australia.
Abstract:
Herein we describe two experiments in which the recruitment and pressure-induced modifications of human eccrine sweating were investigated. In one experiment, the longstanding belief that glandular recruitment follows a gradual, caudal-to-rostral (dermatomal) recruitment pattern was re-evaluated. The onset of sweating was simultaneously determined (ventilated capsules) from four spinal (dermatomal) segments (forehead, dorsal hand, lower chest and dorsal foot) during the passive heating of supine participants (N = 8). No evidence was found to support either dermatomal or simultaneous glandular recruitment patterns. Instead, the results were more consistent with individualised (random) patterns of regional activation (P > 0.05), with significant time delays among sites. Such delays in the appearance of discharged sweat may reflect differences in neurotransmitter sensitivity, precursor sweat production or ductal reabsorption. In the second experiment, the pressure-induced hemihidrotic reflex (contralateral sudomotor enhancement) was revisited, using pressures applied over 10 cm2 areas of the chest (left side: 6 N cm-2) and left heel (3 N cm-2) during both supine and seated postures (N = 12). Participants were passively heated and thermally clamped before pressure application. Hemihidrosis was not observed from the contralateral surfaces within the same (chest) or lower spinal segments (abdomen; both P > 0.05) during chest pressure, but a generalised enhancement followed heel pressure when supine. We suggest that previous observations of hemihidrosis possibly resulted from elevated heat storage, rather than a neural reflex. Chest pressure significantly inhibited ipsilateral sweating (forehead, hand, chest; all P < 0.05), and that influence is hypothesised to result from interactions between ascending mechanoreceptor afferents and the descending sudomotor pathways.
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