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The principal aim of the present study was to monitor the core temperature (Tc) of a population of saturation divers conducting routine deep dives at different locations in the United Kingdom sector of the North Sea and to assess whether current dive procedures are adequate in preventing deleterious decreases in Tc. A total of 30 divers, with an average (SD) of 19.3 (6.6) yr of experience as saturation divers, participated in the study. The survey included 59 dives conducted at six locations (Scott Field, Norfra Pipeline, Hudson Field, Pierce Field, Forties Field, and Bruce Field) from four Diver Support Vessels (Rockwater 1, Semi 2, Bar Protector, and Discovery). The depth of the dives monitored ranged from 54 to 160 meters of seawater (msw), and the duration of the dives from 31 min to 7 h 30 min. before each dive, divers were requested to ingest a radio pill and strap a data logger to their abdomen. Upon returning to the chamber within the Diver Support Vessel following a dive, they provided subjective ratings of thermal perception (7 point scale) and thermal comfort (4 point scale) for the period just before, during, and immediately after the dive. In 55 dives, Tc of saturation divers working at depths to 160 msw for up to 6 h with water temperatures ranging from 4 degrees to 6 degrees C increased above the pre-dive core temperature of 37.4 degrees (0.620+/-0.6 degrees C). In four dives there was a decrease in Tc: 2 divers had a 0.2 degrees C fall in Tc, and 2 bellmen had a decrease of 0.4 degrees and 1.0 degrees C. The subjective responses of divers indicated that they were thermally neutral (neither warm nor cold) and comfortable before and immediately after the dives. The current practice of providing thermal protection with hot water suits to saturation divers working in the North Sea is adequate for preventing the risk of hypothermia and maintaining thermal comfort.

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1. The initial respiratory and cardiac responses to cold water immersion are thought to be responsible for a significant number of open water deaths each year. Previous research has demonstrated that the magnitude of these responses can be reduced by repeated immersions in cold waterwhether the site of habituation is central or peripheral. 2. Two groups of subjects undertook two 3 min head-out immersions in stirred water at 10 C of the right-hand side of the body (R). Between these two immersions (3 whole days) the control group (n = 7) were not exposed to cold water, but the habituation group (n = 8) undertook a further six 3 min head-out immersions in stirred water at 10 C of the left-hand side of the body (L). 3. Repeated L immersions reduced (P < 0.01) the heart rate, respiratory frequency and volume responses. During the second R immersion a reduction (P < 0.05) in the magnitude of the responses evoked was seen in the habituation group but not in the control group, despite both groups having identical skin temperature profiles. 4. It is concluded that the mechanisms involved in producing habituation of the initial responses are located more centrally than the peripheral receptors.

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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.

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Many drowning victims have alcohol in their blood, but it is not clear whether there is a causal relationship. This study examined the effect of moderate alcohol consumption on the initial responses to cold water immersion. Sixteen subjects wearing swimming costumes undertook two, 3-min head-out seated immersions in water at 15 degrees C. One hour before immersion, subjects drank either 3.7 ml.kg body water-1 of 40% v:v alcohol as vodka, or an equivalent volume of water (control) mixed with squash. On immersion, the average blood alcohol concentration was 23 mmol.l-1 (105 mg.100 ml-1) after alcohol consumption and zero in the control condition. Respiratory frequency in the first 20 s of immersion was found to be reduced (P < 0.05) by 10% (a total of 2-3 breaths) after alcohol consumption compared to the control immersion. Tidal volume, heart rate, rectal temperature and skin temperatures did not differ significantly between immersions. It is concluded that moderate alcohol consumption does not attenuate the initial "cold shock" responses to a practically significant extent and is thus unlikely to reduce the risk of drowning on immersion in cold water.

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Twelve subjects undertook one submersion into water at 5 degrees C and two at 10 degrees C wearing either a wet or dry suit. During the submersions the subjects held their breath for as long as they could and then breathed through respiratory tubing for a further 10 s before being removed from the water. Bradycardia (heart rate < 60 beats/min) was observed during breath holding in 10 subjects in 28 of the 36 submersions. Ectopic arrhythmias were observed in 11 subjects in 29 of the 36 submersions, a much higher frequency than previously reported. These ectopic arrhythmias included premature atrial and junctional complexes, runs of supraventricular tachycardia, and premature ventricular complexes. They occurred predominantly in the 10-s period of submersion after the cessation of breath holding. The possible etiology of these arrhythmias and their significance are discussed and it is concluded that after breath-hold termination during cold-water submersion there is a short time during which the heart may be particularly susceptible to supraventricular ectopic arrhythmias.

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The surface toe temperature of 10 subjects was monitored in the field in Arctic Norway (minimum air temperature -27 degrees C). The lowest skin temperature recorded was 1.9 degrees C. The mean estimated time for the toe temperature to cool from 25 degrees C to 5 degrees C was 109 minutes (SD, 10.2) at an ambient temperature of -21 degrees C. One subject experienced a toe temperature below 5 degrees C for 2.9 hours during a 27-hour period. Surprisingly none of the subjects demonstrated clinical signs of cold injury, but this does not mean that this exposure was without risk. Cold sensitization could have occurred.

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1. The present investigation was designed to examine human adaptation to intermittent severe cold exposure and to assess the effect of exercise on any adaptation obtained. 2. Sixteen subjects were divided into two equal groups. Each subject performed ten head-out immersions; two into thermoneutral water which was then cooled until they shivered vigorously, and eight into water at 15 degrees C for 40 min. During the majority of the 15 degrees C immersions, one group (dynamic group) exercised whilst the other (static group) rested. 3. Results showed that both groups responded to repeated cold immersions with a reduction in their initial responses to cold. The time course of these reductions varied, however, between responses. 4. Only the static group developed a reduced metabolic response to prolonged resting immersion. 5. It is concluded that repeated resting exposure to cold was the more effective way of producing an adaptation. The performance of exercise during repeated exposure to cold prevented the development of an adaptive reduction in the metabolic response to cold during a subsequent resting immersion. In addition, many of the adaptations obtained during repeated resting exposure were overridden or masked during a subsequent exercising immersion.

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Twelve healthy male subjects performed three 10-min head-out immersions in water at 10 degrees C. The responses of the subjects to immersion were recorded under three conditions: a) Control condition (CC)--torso and limbs exposed; b) Torso protected/limbs exposed condition (TPC); and c) Limbs protected/torso exposed condition (LPC). Results showed that the LPC significantly reduced the heart rate (p less than 0.01), minute ventilation (p less than 0.05), and respiratory frequency (p less than 0.05) during the first minute of immersion compared to the CC. Subjects also found the LPC the most comfortable. The TPC significantly reduced minute ventilation (p less than 0.01) and respiratory frequency (p less than 0.01) on immersion compared to the CC, but did not significantly lower the heart rate response. A comparison of the LPC and TPC revealed no significant difference in minute ventilation and respiratory frequency recorded on immersion. The LPC however, produced significantly lower heart rates on immersion (p less than 0.05) than the TPC. It was concluded that the limbs may be more important than the torso for the initiation of cardiac response to cold water immersion.

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1. Exercise during immersion in cold water has been reported by several authors to accelerate the rate of fall of core temperature when compared with rates seen during static immersion. The nature of the exercise performed, however, has always been whole-body in nature. 2. In the present investigation fifteen subjects performed leg exercise throughout a 40 min head-out immersion in water at 15 degrees C. The responses obtained were compared with those seen when the subjects performed an identical static immersion. 3. Aural and rectal temperatures were found to fall by greater amounts during static immersion. 4. It is concluded that 'the type of exercise performed' should be included in the list of factors which affect core temperature during cold water immersion.

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1. All immersion casualties should be admitted to hospital for observation. If water has been inhaled and there are clinical signs in the chest they should be admitted to an ITU. 2. Attempts at resuscitation should always be made in apparently dead hypothermic immersion victims and only abandoned if unsuccessful after rewarming has occurred. 3. Always consider the possibility that an underlying pathological disturbance caused the incapacitation that led to the immersion incident. 4. If ventilatory support is required PEEP should be instituted as early as possible.

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