Cold water submersion can induce a high incidence of cardiac arrhythmias in healthy volunteers. Submersion and the release of breath holding can activate two powerful and antagonistic responses: the ...‘cold shock response’ and the ‘diving response’. The former involves the activation of a sympathetically driven tachycardia while the latter promotes a parasympathetically mediated bradycardia. We propose that the strong and simultaneous activation of the two limbs of the autonomic nervous system (‘autonomic conflict’) may account for these arrhythmias and may, in some vulnerable individuals, be responsible for deaths that have previously wrongly been ascribed to drowning or hypothermia. In this review, we consider the evidence supporting this claim and also hypothesise that other environmental triggers may induce autonomic conflict and this may be more widely responsible for sudden death in individuals with other predisposing conditions.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
Many stressors cause an increase in ventilation in humans. This is predominantly reported as an increase in minute ventilation (V̇E). But, the same V̇E can be achieved by a wide variety of changes in ...the depth (tidal volume, VT) and number of breaths (respiratory frequency, ƒR). This review investigates the impact of stressors including: cold, heat, hypoxia, pain and panic on the contributions of ƒR and VT to V̇E to see if they differ with different stressors. Where possible we also consider the potential mechanisms that underpin the responses identified, and propose mechanisms by which differences in ƒR and VT are mediated. Our aim being to consider if there is an overall differential control of ƒR and VT that applies in a wide range of conditions. We consider moderating factors, including exercise, sex, intensity and duration of stimuli. For the stressors reviewed, as the stress becomes extreme V̇E generally becomes increased more by ƒR than VT. We also present some tentative evidence that the pattern of ƒR and VT could provide some useful diagnostic information for a variety of clinical conditions. In The Physiological Society's year of ‘Making Sense of Stress’, this review has wide‐ranging implications that are not limited to one discipline, but are integrative and relevant for physiology, psychophysiology, neuroscience and pathophysiology.
Schematic of the tidal volume and breathing (respiratory) frequency responses to a range of stressors.
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FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
Despite previous reviews and commentaries, significant misconceptions remain concerning deep-body (core) and skin temperature measurement in humans. Therefore, the authors have assembled the ...pertinent Laws of Thermodynamics and other first principles that govern physical and physiological heat exchanges. The resulting review is aimed at providing theoretical and empirical justifications for collecting and interpreting these data. The primary emphasis is upon deep-body temperatures, with discussions of intramuscular, subcutaneous, transcutaneous and skin temperatures included. These are all turnover indices resulting from variations in local metabolism, tissue conduction and blood flow. Consequently, inter-site differences and similarities may have no mechanistic relationship unless those sites have similar metabolic rates, are in close proximity and are perfused by the same blood vessels. Therefore, it is proposed that a gold standard deep-body temperature does not exist. Instead, the validity of each measurement must be evaluated relative to one's research objectives, whilst satisfying equilibration and positioning requirements. When using thermometric computations of heat storage, the establishment of steady-state conditions is essential, but for clinically relevant states, targeted temperature monitoring becomes paramount. However, when investigating temperature regulation, the response characteristics of each temperature measurement must match the forcing function applied during experimentation. Thus, during dynamic phases, deep-body temperatures must be measured from sites that track temperature changes in the central blood volume.
•Thermodynamic principles govern physical and biological heat exchanges.•Inter-site tissue temperatures may be unrelated unless perfused by the same blood vessel.•Measurement validity must be evaluated relative to one's research objectives.•Measurement sensitivity must match the forcing function that disturbs homoeostasis.•During dynamic phases, measurements should track central blood temperature.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPUK
•Acute exercise in the heat increases IL-6 regardless of hydration status.•Acute exercise in the heat increases cortisol only when fluid-intake is restricted.•This cortisol response was strongly ...correlated with whole body sweat loss.•Cortisol, IL-6 and CRP were not augmented after heat acclimation.
This study examined the acute and chronic effects of euhydrated and hypohydrated heat exposure, on biomarkers of stress and inflammation. Eight trained males mean (SD) age: 21 (3) y; mass: 77.30 (4.88) kg; V̇O2max: 56.9 (7.2) mL kg−1 min−1 undertook two heat acclimation programmes (balanced cross-over design), once drinking to maintain euhydration and once with restricted fluid-intake (permissive dehydration). Days 1, 6, and 11 were 60 min euhydrated exercise-heat stress tests (40 °C; 50% RH, 35% peak power output), days 2–5 and 7–10 were 90 min, isothermal-strain (target rectal temperature: 38.5 °C) exercise-heat sessions. Plasma was obtained pre- and post- exercise on day 1, 2, and 11 and analysed for cortisol, interleukin-6 (IL-6), and C-reactive protein (CRP). Cortisol and CRP were also assessed on day 6. IL-6 was elevated following the initial (acute) 90 min isothermal heat strain exercise-heat exposure (day 2) with permissive dehydration ((pre exercise: 1.0 pg mL−1 0.9, post-exercise: 1.8 pg mL−1 1.0, P = .032) and when euhydrated (pre-exercise: 1.0 pg mL−1 1.4, post-exercise: 1.6 pg mL−1 2.1, P = .048). Plasma cortisol levels were also elevated but only during permissive dehydration (P = .032). Body mass loss was strongly correlated with Δcortisol (r = −0.688, P = .003). Although there was a trend for post-exercise cortisol to be decreased following both heat acclimation programmes (chronic effects), there were no within or between intervention differences in IL-6 or CRP. In conclusion, acute exercise in the heat increased IL-6 and cortisol only when fluid-intake is restricted. There were no chronic effects of either intervention on biomarkers of inflammation as evidenced by IL-6 and CRP returning to basal level at the end of heat acclimation.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPUK, ZRSKP
Abstract
Background
Death by drowning is a leading cause of accidental death in the United Kingdom (UK) and worldwide. The World Health Organization (WHO) states that effective documentation of ...drowning is required to describe drowning frequency and to underpin effective drowning prevention intervention, thus improving the quality of data describing drowning frequency represents a key initiative. The water incident database (WAID) has been used to document UK fatal and non-fatal water-based incidents since 2009. WAID has not undergone a systematic evaluation of its data or data collection procedures to establish if the database meets the WHO requirements. The present study investigated the characteristics of UK fatal drowning incidents and audited current WAID data capture procedures.
Methods
Data for the fatal drowning cases recorded between 2012 and 2019 were reviewed. Descriptive data were generated 1) to describe fatal drownings in the UK’s WAID in this period; 2) a sub-set of drownings were audited i) for completeness of data entry and, based on source documents, ii) for quality of data entry; 3) these processes were used to make recommendations for onward revisions to WAID.
Results
A total of 5051 fatalities were recorded between 2012 and 2019. Drowning was most frequent amongst males aged 35 to 60 years (
n
= 1346), whilst suspected accidents and suicides accounted for 44 and 35% of fatalities. Suicide by drowning was at a peak in the most recent year of data analysed (i.e., 2019; 279 cases) highlighting an urgent need for targeted intervention. Audit part 2i) indicated that 16% of all fields were incomplete, thus indicating potential redundancy, duplication, or the need for onward review. Audit part 2ii) indicated high levels of agreement (80 ± 12%) between audited cases and the ‘true’ WAID entries.
Conclusions
This study confirms WAID as a rigorous, transparent and effective means of documenting UK drownings thereby meeting WHO requirements for data quality; yet future improvements are recommended. Such findings allow researchers and policy makers to use WAID to further investigate UK drowning with a view to improving public safety measures and drowning prevention interventions
.
Observations alongside several expert recommendations have informed a revised version of WAID.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
It has been suggested that dehydration is an independent stimulus for heat acclimation (HA), possibly through influencing fluid-regulation mechanisms and increasing plasma volume (PV) expansion. ...There is also some evidence that HA may be ergogenic in temperate conditions and that this may be linked to PV expansion. We investigated: (i) the influence of dehydration on the time-course of acquisition and decay of HA; (ii) whether dehydration augmented any ergogenic benefits in temperate conditions, particularly those related to PV expansion.
: Eight males VO
: 56.9(7.2) mL·kg
·min
undertook two HA programmes (balanced cross-over design), once drinking to maintain euhydration (HA
) and once with restricted fluid-intake (HA
). Days 1, 6, 11, and 18 were 60 min exercise-heat stress tests HST (40°C; 50% RH), days 2-5 and 7-10 were 90 min, isothermal-strain (
~ 38.5°C), exercise-heat sessions. Performance parameters VO
, lactate threshold, efficiency, peak power output (PPO) were determined pre and post HA by graded exercise test (22°C; 55%RH).
: During isothermal-strain sessions hypohydration was achieved in HA
and euhydration maintained in HA
average body mass loss -2.71(0.82)% vs. -0.56(0.73)%,
< 0.001, but aldosterone concentration, power output, and cardiovascular strain were unaffected by dehydration. HA was evident on day 6 {reduced end-exercise
-0.30(0.27)°C and exercise heart rate -12(15) beats.min
, increased PV +7.2(6.4)% and sweat-loss +0.25(0.22) L.h
,
< 0.05} with some further adaptations on day 11 {further reduced end-exercise
-0.25(0.19)°C and exercise heart rate -3(9) beats.min
,
< 0.05}. These adaptations were not notably affected by dehydration and were generally maintained 7-days post HA. Performance parameters were unchanged, apart from increased PPO (+16(20) W, irrespective of condition).
: When thermal-strain is matched, permissive dehydration which induces a mild, transient, hypohydration does not affect the acquisition and decay of HA, or endurance performance parameters. Irrespective of hydration, trained individuals require >5 days to optimize HA.
There is a need to rapidly screen individuals for heat strain and fever using skin temperature (Tsk) as an index of deep body temperature (Tb). This study’s aim was to assess whether Tsk could serve ...as an accurate and valid index of Tb during a simulated heatwave. Seven participants maintained a continuous schedule over 9-days, in 3-day parts; pre-/post-HW (25.4 °C), simulated-HW (35.4 °C). Contact thermistors measured Tsk (Tforehead, Tfinger); radio pills measured gastrointestinal temperature (Tgi). Proximal-distal temperature gradients (ΔTforehead–finger) were also measured. Measurements were grouped into ambient conditions: 22, 25, and 35 °C. Tgi and Tforehead only displayed a significant relationship in 22 °C (r: 0.591; p < 0.001) and 25 °C (r: 0.408; p < 0.001) conditions. A linear regression of all conditions identified Tforehead and ΔTforehead–finger as significant predictors of Tgi (r2: 0.588; F: 125.771; p < 0.001), producing a root mean square error of 0.26 °C. Additional residual analysis identified Tforehead to be responsible for a plateau in Tgi prediction above 37 °C. Contact Tforehead was shown to be a statistically suitable indicator of Tgi in non-HW conditions; however, an error of ~1 °C makes this physiologically redundant. The measurement of multiple sites may improve Tb prediction, though it is still physiologically unsuitable, especially at higher ambient temperatures.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
To investigate inter-individual variance in adaptive responses to heat acclimation (HA).
17 males (VO2max=58.8(8.4) mL·kg−1·min−1) undertook 10-days (exercise + heat-stress 40 °C, 50%RH) HA. ...Adaptation was assessed by heat stress tests (HST; 60–minutes cycling, 35% peak power output) pre- and post-HA.
Inter-individual variability was evident in adaptive responses e.g. mean(range) reduction in end-exercise Tre= −0.70(−0.20 to −1.32)°C, but, in the main, the variance in adaptation was unrelated across indices (thermal, sudomotor, cardiovascular, haematological), indicating independence between adaptation indices. Variance in adaptive responses was not correlated with aerobic capacity, history of previous HA, or the accrued thermal-dose. Some responses to the initial HST were related to the subsequent adaptations e.g. ∆T̅sk during the initial HST and the reduction in the within HST ΔTre after HA (r = −0.676), but responses to the initial HST may also have been influenced by HST design e.g. ΔTre correlated with metabolic heat production (r = 0.609). Metabolic heat production also correlated with the reduction in the within HST ΔTre after HA (r = −0.514).
HA indices are mainly independent; ‘low’, or ‘high’, responders on one index do not necessarily demonstrate similar response across other indices. Variance in HA responses was not related to aerobic capacity, previous HA, or thermal-dose. Thermo-physiological responses to a HST might identify individuals who will benefit from HA. However, some initial responses are influenced by HST design, which may also affect the scope for demonstrating adaption.
Variance in the HA response remains largely unaccounted for and future studies should identify factors contributing to this variance.
•Variance in the adaptive response to heat was not explained by aerobic capacity, previous heat acclimation, or thermal dose.•Acclimation indices (thermal, sudomotor, cardiovascular, haematological) appear to be largely independent of each other.•Classification of individuals as either ‘low’ or ‘high’ responders to heat may not be appropriate.•An initial heat stress test may identify initial ‘heat-readiness’ and also those who will benefit from heat acclimation.•Heat stress test design may affect the scope for evidencing adaption, but most of the variance in adaptation is unexplained.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPUK
Abstract There is some confusion, and consequent variation in policy, between the agencies responsible for the search, rescue and resuscitation of submersion victims regarding the likelihood of ...survival following a period of submersion. The aim of this work was to recommend a decision-making guide for such victims. This guidance was arrived at by a review of the relevant literature and specific case studies, and a “consensus” meeting on the topic. The factors found to be important for determining the possibility of prolonged survival underwater were: water temperature; salinity of water; duration of submersion; and age of the victim. Of these, only water temperature and duration are sufficiently clear to form the basis of guidance in this area. It is concluded that if water temperature is warmer than 6 °C, survival/resuscitation is extremely unlikely if submerged longer than 30 min. If water temperature is 6 °C or below, survival/resuscitation is extremely unlikely if submerged longer than 90 min.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPUK
Abstract A single exposure to menthol can, depending on concentration, enhance both cool sensations and encourage body heat storage. This study tested whether there is an habituation in either ...response after repeated-daily exposures. Twenty-two participants were assigned to one of three spray groups: Control (CON; n = 6), 0.05% l -menthol (M0.05% ; n = 8), and 0.2% l -menthol (M0.2% ; n = 8). On Monday (20 °C, 50% rh) participants were sprayed with 100 mL of solution and undertook 40 min of cycling at 45% of their peak power (Ex1 ), from Tuesday to Thursday (30 °C, 50% rh) they were sprayed twice daily whilst resting (R1 to R6 ), Friday was a repeat of Monday (Ex2 ). Thermal sensation (TS), thermal comfort, perceived exertion, irritation, rectal and skin temperature (Tsk ), skin blood flow (SkBF) and sweat rate were monitored. A two-way ANOVA (alpha = 0.05) compared responses from the beginning (Ex1 , R1 ) and end (Ex2 , R5 ) of the testing week. M0.2% induced significantly ( P < 0.05) cooler TS at the beginning of the week (Ex1 , R1 ) compared to the end (Ex2 , R5 ), indicating habituation of TS; this was not observed in M0.05% . No other perceptual or physiological responses habituated. 0.2% Menthol caused a heat storage response, mediated by vasoconstriction, at the beginning and end of the week, suggesting the habituation of TS occurred in a pathway specific to sensation. In summary, the cooling influence of 0.2% menthol habituates after repeated-daily exposures, but with no habituation in heat storage.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPUK
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