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The study examined the effects of a 10-day normobaric hypoxic confinement (FiO2: 0.14), with [hypoxic exercise training (HT); n = 8)] or without [hypoxic ambulatory (HA; n = 6)] exercise, on the hand temperature responses during and after local cold stress. Before and after the confinement, subjects immersed their right hand for 30 min in 8 °C water [cold water immersion (CWI)], followed by a 15-min spontaneous rewarming (RW), while breathing either room air (AIR), or a hypoxic gas mixture (HYPO). The hand temperature responses were monitored with thermocouples and infrared thermography. The confinement did not influence the hand temperature responses of the HA group during the AIR and HYPO CWI and the HYPO RW phases; but it impaired the AIR RW response (-1.3 °C; P = 0.05). After the confinement, the hand temperature responses were unaltered in the HT group throughout the AIR trial. However, the average hand temperature was increased during the HYPO CWI (+0.5 °C; P ≤ 0.05) and RW (+2.4 °C; P ≤ 0.001) phases. Accordingly, present findings suggest that prolonged exposure to normobaric hypoxia per se does not alter the hand temperature responses to local cooling; yet, it impairs the normoxic RW response. Conversely, the combined stimuli of continuous hypoxia and exercise enhance the finger cold-induced vasodilatation and hand RW responses, specifically, under hypoxic conditions., (© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

The roles of histaminergic and cholinergic neuron systems in the regulation of body temperature have been studied almost exclusively in animals. Recently, we have found that motion sickness, i.e. a condition where hippocampal cholinergic mismatch signals induce a release of histamine in the vomiting centre, accelerates the decline in body temperature in men during exposure to cold. In the present study we measured the thermoregulatory effects of two substances commonly used against motion sickness, i.e. the histamine (H1) receptor blocker dimenhydrinate (DMH) and the muscarine receptor blocker scopolamine (SCOP). In three trials, control (CN), DMH and SCOP, 10 male subjects were immersed in 15 degrees C water for a maximum of 90 min. The trials were separated by a minimum of three days and their order was alternated between subjects. In all trials the subject received, in a double blind fashion, a transdermal patch (SCOP or placebo) 12-14 h before immersion and a tablet (DMH or placebo) 1h before immersion. Mean skin temperature, rectal temperature (T(rec)), the difference in temperature between the non-immersed right forearm and 3rd finger of the right hand (T(ff)), and oxygen uptake (VO(2)) were recorded. The fall in T(rec) was smaller in the DMH than in the CN and SCOP conditions. The recordings of T(ff) and VO(2) suggest that SCOP attenuates peripheral vasoconstriction while DMH increases shivering thermogenesis. Notably, thermal discomfort was reduced in the SCOP condition. Findings are thoroughly discussed in the context of animal studies on the neuropharmacology and neurophysiology of thermoregulation and motion sickness.

Sudden immersion in cold water initiates an inspiratory gasp response followed by uncontrollable hyperventilation and tachycardia. It is known that this response, termed the "cold shock" response, can be attenuated following repeated immersion. In the present investigation we examined how long this habituation lasts. Twelve healthy male volunteers participated in the experiment, they were divided into a control (C) group (n = 4), and a habituation (H) group (n = 8). In October, each subject undertook two 3-min head-out seated immersions into stirred water at 10 degrees C wearing swimming trunks. These immersions took place at the same time of day, with 4 days separating the two immersions. In the intervening period, the C group were not exposed to cold water, while the H group undertook six, 3-min head-out immersions in water at 15 degrees C. Two months (December), 4 months (February), 7 months (May) and 14 months (January) after their first immersion, all subjects undertook another 3-min head-out immersion in water at 10 degrees C. The H group showed a reduction in respiratory frequency (47 to 24 breaths x min(-1)), inspiratory minute volume (72.2 to 31.3 1 x min(-1)) and heart rate (128 to 109 beats x min(-1)) during the first 30 s of immersion on day 5 compared to day 1. Seven months later these responses were still significantly reduced compared to day 1. After 14 months, heart rate remained attenuated but respiratory frequency and inspiratory minute volume had returned towards pre-habituation levels. The responses of the C group during the first 30 s of immersion were not altered. Both groups showed an attenuation in the responses during the remaining 150 s of immersion following repeated immersions. It is concluded that repeated immersions in cold water result in a longlasting (7-14 months) reduction in the magnitude of the cold shock response. Less frequent immersions produced a decrease in the duration, but not the magnitude of the response.

The initial responses to cold-water immersion, evoked by stimulation of peripheral cold receptors, include tachycardia, a reflex inspiratory gasp and uncontrollable hyperventilation. When immersed naked, the maximum responses are initiated in water at 10 degrees C, with smaller responses being observed following immersion in water at 15 degrees C. Habituation of the initial responses can be achieved following repeated immersions, but the specificity of this response with regard to water temperature is not known. Thirteen healthy male volunteers were divided into a control (C) group (n = 5) and a habituation (H) group (n = 8). Each subject undertook two 3-min head-out immersions in water at 10 degrees C wearing swimming trunks. These immersions took place at a corresponding time of day with 4 days separating the two immersions. In the intervening period the C group were not exposed to cold water, while the H group undertook another six, 3-min, head-out immersions in water at 15 degrees C. Respiratory rate (fR), inspiratory minute volume (VI) and heart rate (fH) were measured continuously throughout each immersion. Following repeated immersions in water at 15 degrees C, the fR, VI and fH responses of the H group over the first 30 s of immersion were reduced (P < 0.01) from 33.3 breaths x min(-1), 50.5 l x min(-1) and 114 beats x min(-1) respectively, to 19.8 breaths x min(-1) 26.41 x min(-1) and 98 beats x min(-1), respectively. In water at 10 degrees C these responses were reduced (P < 0.01) from 47.3 breaths x min(-1), 67.61 x min(-1) and 128 beats x min(-1) to 24.0 breaths x min(-1), 29.5 l x min(-1) and 109 beats x min(-1), respectively over a corresponding period of immersion. Similar reductions were observed during the last 2.5 min of immersions. The initial responses of the C group were unchanged. It is concluded that habituation of the cold shock response can be achieved by immersion in warmer water than that for which protection is required. This suggests that repeated submaximal stimulation of the cutaneous cold receptors is sufficient to attenuate the responses to more maximal stimulation.

Five models predicting shivering thermogenesis on the basis of steady state skin and core temperature were evaluated: Hayward et al., Stolwijk and Hardy,; Nadel et al.,; Timbal et al., and Brown and Brengelmann, using the empirical data derived from a cold water immersion study by Morrison et al. A residual analysis indicated that all models generated substantial errors of prediction. The best overall predictors were expressions suggested by Hayward et al., while the predictive equation of Nadel et al. ranked second. Derivation of personal coefficients significantly improved the prediction of all models and a subsequent modification of the standard models, adding temperature derivative terms, further reduced the magnitude of the error. An analysis of the residuals indicated that peripheral and core temperatures should be weighted according to the characteristics of thermosensitive neural structures in these regions.