Clare Eglin

Immersion deaths and deterioration in swimming performance in cold water

BACKGROUND General hypothermia (deep body temperature <35 degrees C) has been implicated in immersion-related deaths, but many deaths occur too quickly for it to be involved. We investigated changes in swimming capability in cold water to find out whether such changes could lead to swim failure and drowning. METHODS Ten volunteers undertook three self-paced breaststroke swims in a variable-speed swimming flume, in water at 25 degrees C, 18 degrees C, and 10 degrees C, for a maximum of 90 min. During each swim, we measured oxygen consumption, rectal temperature, swim speed and angle, and stroke rate and length. Swim failure was defined as being unable to keep feet off the bottom of the flume. FINDINGS All ten swimmers completed 90 min swims at 25 degrees C, eight completed swims at 18 degrees C, and five at 10 degrees C. In 10 degrees C water, one swimmer reached swim failure after 61 min and four were withdrawn before 90 min with rectal temperatures of 35 degrees C when they were close to swim failure. Swimming efficiency and length of stroke decreased more and rate of stroke and swim angle increased more in 10 degrees C water than in warmer water. These variables seemed to characterise impending swim failure. INTERPRETATION Impaired performance and initial cardiorespiratory responses to immersion probably represent the major dangers to immersion victims. Consequently, treatment should be aimed at symptoms resulting from near-drowning rather than severe hypothermia.

The effect of repeated endurance exercise on IL-6 and sIL-6R and their relationship with sensations of fatigue at rest

Strenuous, prolonged exercise increases interleukin-6 (IL-6) release. The effect of IL-6 is dependent on the availability of IL-6 receptors. Few studies have addressed the impact of exercise on IL-6 receptor levels or procalcitonin (PCT), an indicator of systemic inflammation. Changes in these molecules may give insight into cytokine-related mechanisms underlying exercise-related fatigue. Thirteen trained male subjects partook in the study. They cycled a total distance of 468 km over 6 days. Blood samples were obtained prior to and immediately following Day 1 of the study and then each morning prior to exercise. Blood samples were analysed for plasma IL-6, soluble IL-6 receptor (sIL-6R), C-reactive protein (CRP), PCT, creatine kinase (CK) and cortisol concentrations. Subjects also completed mood state questionnaires each day prior to exercise. IL-6 was elevated immediately post-exercise on Day 1 but was unchanged at rest for the duration of the event. In contrast, sIL-6R, CRP, PCT and CK concentrations were unchanged immediately post-exercise on Day 1 but were significantly elevated at rest over the duration of the event compared with pre-event baseline. sIL-6R was highly correlated to CRP. Cortisol concentrations remained unchanged at all time points. In conclusion, strenuous, prolonged exercise stimulated an acute phase response which was maintained throughout the 6-day event. sIL-6R increase is associated with CRP and may affect subjective sensations of post-exercise fatigue at rest.

Habituation of the initial responses to cold water immersion in humans: a central or peripheral mechanism?

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.

Permanence of the habituation of the initial responses to cold-water immersion in humans

Abstract 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 °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 °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 °C. The H group showed a reduction in respiratory frequency (47 to 24 breaths · min−1), inspiratory minute volume (72.2 to 31.3 l · min−1) and heart rate (128 to 109 beats · 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 long-lasting (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.

Temperature dependence of habituation of the initial responses to cold-water immersion

Abstract 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°C, with smaller responses being observed following immersion in water at 15°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°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°C. Respiratory rate (fR), inspiratory minute volume (V˙I) and heart rate (fH) were measured continuously throughout each immersion. Following repeated immersions in water at 15°C, the fR, V˙I and fH responses of the H group over the first 30 s of immersion were reduced (P < 0.01) from 33.3 breaths · min−1, 50.5 l · min−1 and 114 beats · min−1 respectively, to 19.8 breaths · min−1, 26.4 l · min−1 and 98 beats · min−1, respectively. In water at 10°C these responses were reduced (P < 0.01) from 47.3 breaths · min−1, 67.6 l · min−1 and 128 beats · min−1 to 24.0 breaths · min−1, 29.5 l · min−1 and 109 beats · 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.

Habituation of the metabolic and ventilatory responses to cold-water immersion in humans.

An experiment was undertaken to answer long-standing questions concerning the nature of metabolic habituation in repeatedly cooled humans. It was hypothesised that repeated skin and deep-body cooling would produce such a habituation that would be specific to the magnitude of the cooling experienced, and that skin cooling alone would dampen the cold-shock but not the metabolic response to cold-water immersion. Twenty-one male participants were divided into three groups, each of which completed two experimental immersions in 12°C water, lasting until either rectal temperature fell to 35°C or 90min had elapsed. Between these two immersions, the control group avoided cold exposures, whilst two experimental groups completed five additional immersions (12°C). One experimental group repeatedly immersed for 45min in average, resulting in deep-body (1.18°C) and skin temperature reductions. The immersions in the second experimental group were designed to result only in skin temperature reductions, and lasted only 5min. Only the deep-body cooling group displayed a significantly blunted metabolic response during the second experimental immersion until rectal temperature decreased by 1.18°C, but no habituation was observed when they were cooled further. The skin cooling group showed a significant habituation in the ventilatory response during the initial 5min of the second experimental immersion, but no alteration in the metabolic response. It is concluded that repeated falls of skin and deep-body temperature can habituate the metabolic response, which shows tissue temperature specificity. However, skin temperature cooling only will lower the cold-shock response, but appears not to elicit an alteration in the metabolic response.

Cold sensitivity test for individuals with non-freezing cold injury: the effect of prior exercise

BackgroundOne of the chronic symptoms of non-freezing cold injury (NFCI) is cold sensitivity. This study examined the effects of prior exercise on the response to a cold sensitivity test (CST) in NFCI patients with the aim of improving diagnostic accuracy.MethodsTwenty three participants, previously diagnosed with NFCI by a Cold Injuries Clinic, undertook two CSTs. Participants either rested (air temperature 31°C) for approximately 80 min (prior rest condition (REST)) or rested for 30 min before exercising gently for 12 min (prior exercise condition (EX)). Following REST and EX, the participants placed their injured foot, covered in a plastic bag, into 15°C water for 2 min; this was followed by spontaneous rewarming in 31°C air for 10 min.ResultsThe great toe skin temperature (Tsk) before immersion averaged 32.5 (3.4)°C in both conditions. Following immersion, the rate of rewarming of the great toe Tsk was faster in EX compared to REST and was higher 5 min (31.7 (3.4)°C vs. 29.8 (3.4)°C) and 10 min (33.8 (4.0)°C vs. 32.0 (4.0)°C) post-immersion. Over the first 5 min of rewarming, changes in the great toe Tsk correlated with the changes in skin blood flow (SkBF) in EX but not the REST condition. No relationship was observed between Tsk in either CST and the severity of NFCI as independently clinically assessed.ConclusionsExercise prior to the CST increased the rate of the toe Tsk rewarming, and this correlated with the changes in SkBF. However, the CST cannot be used in isolation in the diagnosis of NFCI, although the EX CST may prove useful in assessing the severity of post-injury cold sensitivity for prognostic and medico-legal purposes.

Sublingual glyceryl trinitrate and the peripheral thermal responses in normal and cold-sensitive individuals

Non-freezing cold injury (NFCI) is a prevalent, but largely undiagnosed and poorly understood syndrome afflicting many who, as part of their work or leisure, expose their extremities to cold temperatures. The long term sequelae of NFCI are hyperhidrosis, cold-sensitivity and pain; these can last a lifetime. We tested the hypothesis that, in comparison with a placebo, sublingual glyceryl trinitrate (GTN) would increase the peripheral microcirculation during and after a mild cold challenge of individuals who had not been diagnosed with NFCI, but were cold-sensitive. Naive participants were categorised into two cohort groups: control (n=7) or cold-sensitive (n=6). All participants undertook a standardised two minute cold exposure of their right foot while toe skin temperature (Tsk; infra-red thermograms) and blood flow (toe pad laser Doppler) were measured. GTN increased the rate of rewarming and absolute Tsk of the coldest toe after the cold challenge in cold-sensitive individuals. GTN also increased the blood flow in the great toe during rewarming in some cold-sensitive individuals. We accept our hypothesis and suggest that the impairment in the vasodilatory response seen in individuals with cold-sensitivity can be overcome by the use of GTN, an endothelial-independent NO donor, and thereby improve the rewarming of cooled peripheral tissues.

Role of cyclooxygenase in the vascular response to locally delivered acetylcholine in Caucasian and African descent individuals

INTRODUCTION Individuals of African descent (AFD) are more susceptible to non-freezing cold injury (NFCI) compared with Caucasian individuals (CAU). Vasodilatation to acetylcholine (ACh) is lower in AFD compared with CAU in the non-glabrous foot and finger skin sites; the reason for this is unknown. Prostanoids are responsible, in part, for the vasodilator response to ACh, however it is not known whether the contribution differs between ethnicities. METHODS 12 CAU and 12 AFD males received iontophoresis of ACh (1 w/v%) on non-glabrous foot and finger skin sites following placebo and then aspirin (600mg, single blinded). Aspirin was utilised to inhibit prostanoid production by inhibiting the cyclooxygenase (COX) enzyme. Laser Doppler flowmetry was utilised to measure changes in skin blood flow. RESULTS Not all participants could receive iontophoresis charge due to high skin resistance; these participants were therefore excluded from the analyses. Foot: ACh elicited greater maximal vasodilatation in CAU than AFD following placebo (P=0.003) and COX inhibition (COXib) (P<0.001). COXib did not affect blood flow responses in AFD, but caused a reduction in the area under the curve for CAU (P=0.031). Finger: ACh elicited a greater maximal vasodilatation in CAU than AFD following placebo (P=0.013) and COXib (P=0.001). COXib tended to reduce the area under the curve in AFD (P=0.053), but did not affect CAU. CONCLUSIONS CAU have a greater endothelial reactivity than AFD in both foot and finger skin sites irrespective of COXib. It is concluded that the lower ACh-induced vasodilatation in AFD is not due to a compromised COX pathway.

Role of cyclooxygenase in the vascular responses to extremity cooling in Caucasian and African males

What is the central question of this study? Compared with Caucasians, African individuals are more susceptible to non‐freezing cold injury and experience greater cutaneous vasoconstriction and cooler finger skin temperatures upon hand cooling. We investigated whether the enzyme cyclooxygenase is, in part, responsible for the exaggerated response to local cooling. What is the main finding and its importance? During local hand cooling, individuals of African descent experienced significantly lower finger skin blood flow and skin temperature compared with Caucasians irrespective of cyclooxygenase inhibition. These data suggest that in young African males the cyclooxygenase pathway appears not to be the primary reason for the increased susceptibility to non‐freezing cold injury.