Rise In Core Temperature Research Articles

Softwood heating in radio frequency fields

The aim of this study was to investigate the heating rate of lodgepole pine (Pinus contorta) and western red cedar (Thuja plicata) during radio frequency (RF) heating. Wood specimens (40 × 150 × 1000 mm3) with various moisture content and power density were heated using a laboratory size RF dryer at a frequency of 40.7 MHz, until shell temperature reached 56 °C that is approved as a lethal temperature for phytosanitation. Heating rate was positively correlated with power density and negatively correlated with moisture content. The ratio of heating rate to power density had a negative correlation with moisture content and density in both pine and cedar. The regression lines for moisture content had good coefficient of determination (R2) values of 0.63 and 0.61 °C m3/min kW (pine), 0.50 and 0.55 °C m3/min kW (red cedar) in both shell and core, respectively. The results demonstrate that the ratio of heating rate to power density is a useful parameter to estimate heating rate. The derived empirical equations made possible the calculation of the heating rate within test conditions applied to this study. The initial temperature rise in shell and core allowed a rather accurate determination of local power density. One dimensional mathematical model to describe the heating rate of wood during RF heating that was derived from the governing heat transfer equation combined with internal heat generation was developed and verified. The model using local power density had high R2 of 0.71 and 0.93 in both shell and core, respectively, indicating that the model was able to predict heating rate of wood with various moisture content under the known power density distribution.

Dual Roles for Perivascular Macrophages in Immune-to-Brain Signaling

Cytokines produced during infection/inflammation activate adaptive central nervous system (CNS) responses, including acute stress responses mediated by the hypothalamo-pituitary-adrenal (HPA) axis. The mechanisms by which cytokines engage HPA control circuitry remain unclear, though stimulated release of prostanoids from neighboring vascular cells has been implicated in this regard. How specific vascular cell types, endothelial cells (ECs) versus perivascular cells (PVCs; a subset of brain-resident macrophages), participate in this response remains unsettled. We exploited the phagocytic activity of PVCs to deplete them in rats by central injection of a liposome-encapsulated proapoptotic drug. This manipulation abrogated CNS and hormonal indices of HPA activation under immune challenge conditions (interleukin-1) that activated prostanoid synthesis only in PVCs, while enhancing these responses to stimuli (lipopolysaccharide) that engaged prostanoid production by ECs as well. Thus, PVCs provide both prostanoid-mediated drive to the HPA axis and an anti-inflammatory action that constrains endothelial and overall CNS responses to inflammatory insults.

The Heat Intolerant Phenotype. Physiological Responses And Lymphocyte Transcriptome

INTRODUCTION: During physical training in the heat, extreme metabolic heat storage manifests (pending on the individual features) as a rise in body core temperature (Tc). Individuals, previously exposed to heat exhaustion/stroke and demonstrating an earlier/faster Tc and heart rate rise within a cohort study, are defined as "heat intolerant" (HI). Whether HI is a transient phenotypic or genotypic response is yet unknown. PURPOSE: To investigate whether HI and heat tolerant (HT) subjects differ in their lymphocyte gene profile. METHODS: 68 healthy young male volunteers, 1-3 months post-exertion heatstroke, underwent a heat tolerance test (HTT), consisting of walking on a treadmill for 2h at a speed of 5 km·h-1 and 2% grade in a climatic chamber (40°C, 40% relative humidity). Tc, Tskin (3 sites), and heart rate were continuously monitored and recorded. Blood samples were drawn before, at the end of the HTT and after 1h of recovery in an air-conditioned room (23°C). Global gene profile of 6 HT and 6 HI lymphocytes RNA samples (2 pools per group) was detected and analyzed using two-color gene chips and bioinformatic tools. RESULTS: According to the HTT, 10 subjects were diagnosed as HI and 58 subjects as HT. Tc at the end of HTT was elevated by 1.4 and 0.77°C in the HI and the HT subjects, respectively. Tskin vs. Tc, indicative of skin blood flow, implied a HI sluggish response (vs. HT) (P<0.01). Two different gene chip experimental paradigms indicated differences in gene profiles of the HI vs. the HT group, prior to and following recovery from HTT. Basal differences in biological functional categories among the groups included genes associated with immune responses, stress (e.g., apoptotic pathways), transport, molecular processes (DNA and RNA regulation and organization) and metabolism. CONCLUSIONS:: This study (as well as our previous reports) characterizes a distinct HI physiological phenotype. This characterization of the HI phenotype demonstrates a differential genomic profile found even prior to heat stress tests, adding a novel category to the defined reasons for potential congenital HI.

Injectorless quantum cascade laser with low voltage defect and improved thermal performance grown by metal-organic chemical-vapor deposition

We demonstrate a strain-compensated injectorless quantum cascade laser (I-QCL), grown by metal-organic chemical-vapor deposition, with a very low voltage defect operating up to room temperature. We experimentally study the effect of voltage defect on thermal performance by comparing the rise in core temperature over a 300 ns pulse width of I-QCL and conventional QCL, working in pulsed mode using time-resolved step scan. I-QCL shows approximately eight times lower rate of rise in core temperature compared to conventional QCL.

Roles of two preoptic cell groups in tonic and febrile control of rat tail sympathetic fibers

In response to cold and in fever, heat dissipation from the skin is reduced by sympathetic vasoconstriction. The preoptic region has been implicated in regulating basal, thermal, and febrile vasoconstriction of cutaneous vessels such as the rat's tail, but the neurons responsible for these functions have not been well localized. We recorded activity from single sympathetic nerve fibers supplying tail vessels in urethane-anesthetized rats, while microinjections of GABA (300 mM, 15-30 nl) were used to inhibit neurons in different parts of the preoptic region. Tail fiber activity increased promptly after GABA injections in two distinct regions: a rostromedial preoptic region (RMPO) centered around the organum vasculosum of the lamina terminalis, and a second region centered approximately 1 mm caudolaterally (CLPO). Responses to GABA within each region were similar. The febrile mediator, PGE(2) (0.2 or 1 ng in 15 nl) was then microinjected into GABA-sensitive preoptic sites. Injections of PGE(2) into the RMPO induced a rapid increase in tail fiber activity followed by a rise in core temperature; injections into the rostromedial part of CLPO gave delayed tail fiber responses; injections into the central and caudal parts of CLPO were without effect. These results indicate that neurons in two distinct preoptic regions provide tonic inhibitory drive to the tail vasoconstrictor supply, but febrile vasoconstriction is mediated by PGE(2) selectively inhibiting neurons in the rostromedial region.

Melatonin as an ergogenic aid

The possible ways in which a substance or technique can be regarded as “ergogenic” are first listed, and then a systematic account of the evidence that melatonin fulfils the requirements of such roles is undertaken. There is no evidence to indicate that the soporific and hypothermic effects of melatonin cause a decrease in physical performance, though its ability to decrease alertness and cognitive performance has been well established. The hypothermic effects of melatonin might, on the other hand, increase physical performance in two ways. First, they might allow more exercise to be performed before a “critical” temperature that causes the central nervous system to inhibit physical activity is reached. Second, the cutaneous vasodilatation produced by melatonin might promote heat loss during steady-state exercise and so guard against the rise of core temperature. Evidence for either of these roles is currently inadequate and insufficient for a confident judgement to be made. When the role of melatonin in promoting recovery from exercise is addressed, again, the data are too sparse and have often been obtained upon animals rather than humans. This is especially so with respect to the notion that melatonin might change favourably the metabolic responses to exercise. The general conclusion is that the case for/against melatonin as having a substantial ergogenic role has still to be made, and that far more evidence will be required before this can be done conclusively.

Core Temperature and Metabolic Responses After Carbohydrate Intake During Exercise at 30°C

Carbohydrate ingestion has recently been associated with elevated core temperature during exercise in the heat when testing for ergogenic effects. Whether the association holds when metabolic rate is controlled is unclear. Such an effect would have undesirable consequences for the safety of the athlete. To examine whether ingesting fluids containing carbohydrate contributed to an accelerated rise in core temperature and greater overall body heat production during 1 hour of exercise at 30 degrees C when the effort was maintained at steady state. Crossover design (repeated measures) in randomized order of treatments of drinking fluids with carbohydrate and electrolytes (CHO) or flavored-water placebo with electrolytes (PLA). The beverages were identical except for the carbohydrate content: CHO = 93.7 +/- 11.2 g, PLA = 0 g. Research laboratory. Nine physically fit, endurance-trained adult males. Using rectal temperature sensors, we measured core temperature during 30 minutes of rest and 60 minutes of exercise at 65% of maximal oxygen uptake (Vo(2) max) in the heat (30.6 degrees C, 51.8% relative humidity). Participants drank equal volumes (1.6 L) of 2 beverages in aliquots 30 minutes before and every 15 minutes during exercise. Volumes were fixed to approximate sweat rates and minimize dehydration. Rectal temperature and metabolic response (Vo(2), heart rate). Peak temperature, rate of temperature increase, and metabolic responses did not differ between beverage treatments. Initial hydration status, sweat rate, and fluid replacement were also not different between trials, as planned. Ingestion of carbohydrate in fluid volumes that minimized dehydration during 1 hour of steady-state exercise at 30 degrees C did not elicit an increase in metabolic rate or core temperature.

Change of fluctuation properties during non-local temperature rise in LHD from 2d phase contrast imaging

Fluctuation properties are analyzed in the Large Helical Device (LHD) for discharges exhibiting a non-local core temperature rise in response to edge cooling by injection of a Tracer Encapsulated Solid Pellet (TESPEL). Edge ion gyro-scale density fluctuation amplitudes, measured with a 2D CO2 phase contrast imaging system, are found to increase as the core temperature is rising and is therefore anti-correlated with a reduction of the total heat flux. This suggests that another mechanism, such as turbulence de-correlation has a stronger role on the heat flux than change of the density fluctuation level. The core fluctuation properties, in particular the phase velocity, change immediately in response to the edge temperature reduction, and possibly change of gradient, unresponsive to core gradients, suggesting a possible non-local transfer mechanism between the edge and core. Comparing different cases, it appears that the excitation of a fluctuation branch with higher core frequency and phase velocity (∼6km/s) is an essential ingredient for the core Te rise. After pellet injection, the amplitude of higher k components increases, implying a reduction of correlation length. One possible interpretation is that there may be increased E × B shear.

Physiological Effect of the RTX During Exercise in the Heat

PURPOSE: Core temperature regulation is critical to mission success during military operations in extreme thermal environments. Numerous cooling devices have been shown to significantly reduce heat strain during exercise in the heat. A device based on Rapid Thermal Exchange (RTX) technology is thought to reduce the rise in core temperature during exercise by dissipating heat through the hand via the application of negative pressure to the palm. This study was conducted to determine the physiological effects of the RTX on military personnel in a thermally challenging environment. METHODS: Eleven healthy, active-duty volunteers (age 29 ± 6 years; height 177 ± 8.5 cm; weight 80.2 ± 8.8 kg; BSA 1.97 ± 0.14 m2) participated in 2 heat trials (1 RTX [cooling] and 1 noncooling [NC]) that consisted of 180 min of exposure to a thermal environment of 100°F and 50%RH. All trials were randomized and consisted of 15 min of rest followed by a 30-min bout of exercise (treadmill walking at 3.5 mph at a 3% grade) every 45 min. Throughout the trial, all participants wore a battle dress uniform, a backpack weighing 25 lb, and a helmet. Heart rate, core temperature, and mean skin temperature (shoulder, chest, thigh, and calf temperatures) were measured each minute during the trials. Heat storage was calculated for the duration of the exposure. RESULTS: No difference was found between the RTX and NC trials for all analyses. Mean stay time values were RTX 124 ± 39 min and NC 132 ± 33 min. Mean end of test (EOT) core values were RTX 38.8 ± 0.4°C and NC 38.9 ± 0.4°C. Mean EOT heart rate values were RTX 136 ± 25 bpm and NC 143 ± 29 bpm. Mean heat storage values were RTX 48.9 ± 25.7 W/m2 and NC 47.5 ± 15.9 W/m2. Mean whole body sweat rate values were RTX 1.5 ± 0.4 L/hr and NC 1.3 ± 0.4 L/hr. Mean delta difference core values (increase in core temperature from baseline) were RTX 1.7 ± .4°C and NC 1.9 ± .5°C. CONCLUSIONS: The RTX technology used for this evaluation did not significantly reduce the level of heat strain. This RTX device did not significantly decrease heart rate, prevent a rise in core temperature, or change the heat storage values. These results suggest that this particular configuration of RTX technology provides no enhancement in military performance.

Heat Acclimation of an Individual with a Spinal Cord Injury: A Case Report

Individuals with spinal cord injury (SCI) have impaired temperature regulation because of disrupted autonomic neural pathways. Additionally, thermal afferent feedback from sensory nerves is decreased, thus reducing the stimulus for an appropriate thermoregulatory effector response from areas of sensate skin. These events lead to increased cardiovascular and thermoregulatory strain during physical activity. Heat acclimation reduces cardiovascular and thermal strain during heat exposure in healthy able-bodied individuals, but responses in individuals with SCI are unknown. PURPOSE: To test the hypothesis that a 7-day heat acclimation regimen attenuates cardiovascular and thermal strain during exercise-heat stress of an individual with an American Spinal Injury Association A "complete" spinal cord lesion at the eighth thoracic vertebra. METHODS: A 34-year-old man with an SCI lesion at T8 performed arm-crank ergometry exercise at 40% of mode-specific peak oxygen uptake in a climatic chamber set to 40 °C and 30% relative humidity for 60 min (two 30-min sessions separated by 5 min of rest) each day for 7 d (all days were successive except for 1 day between acclimation days 4 and 5). RESULTS: Between day 1 and day 7 of heat acclimation, final heart rate (164 vs. 147 beats·min-1) and the rise in core temperature (Tc) from baseline to the final minute of exercise (1.08 vs. 0.60 °C) decreased. Furthermore, for a given increase in T during exercise, the increase in sweat rate from the chest was enhanced from day 1 to day 7 (0.088 vs. 0.812 mg·cm−2·min−1/°C). Perceptual responses (rating of perceived exertion and thermal sensation) also were lower by the end of acclimation. CONCLUSION: Heat acclimation was effective in improving thermal tolerance in this individual with paraplegia, thereby increasing comfort and safety during exercise and situations involving elevated ambient temperature. Supported by NIH Grants HL61388 and HL84072.

Blood Flow Responses In Conduit Vessels Of The Inactive Limb During Passive Heating And Exercise

The response of skin blood flow in the forearm to a rise in core temperature (Tc) during passive heating is different from that during exercise. Although this difference in the forearm suggests that the changes in blood flow (BF) in the conduit artery and veins of the upper arm, which supplies blood to the forearm and returns blood from this site, would also differ between passive heating and exercise conditions, the BF response in the conduit vessels in the inactive limb during both conditions is not clear. PURPOSE: This study investigated the differences in the response of BF variables in the brachial artery, basilic vein (superficial vein), and brachial vein (deep vein) between passive heating and leg exercise. METHODS: Twenty young subjects rested in the supine position between a pair of tube-lined sheets. Hot water was circulated in the sheets to maintain a mean skin temperature of 37-38°C for 50 min as the passive heating trial (PH). Another fourteen young subjects performed supine cycling exercises at 60-69%VO2max for 30 min (Exercise trial: EX). The environmental conditions were an ambient temperature of 25-28°C and relative humidity of 50%. The blood velocity (V) and diameter (D) of each conduit vessel were measured using an ultrasound Doppler technique. BF was calculated from V and D. RESULTS: The BF in the artery and superficial vein increased linearly and significantly with a rise in ΔTc during PH and EX, although BF during PH was significantly higher than that during EX at ΔTc=0.1-0.8°C in the artery and at ΔTc=0.1-1.0°C in the superficial vein (P< 0.05). Examining the relation ΔTc-BF, the Tc thresholds for BF in the artery and superficial vein during EX were significantly higher than during PH (P< 0.05). Moreover, the V in the artery and superficial vein differed significantly between PH and EX at a given ΔTc (P< 0.05), while there was no remarkable difference in the D of the artery between conditions. By contrast, the BF variables in the deep vein did not change greatly with the rise in ΔTc during PH and EX, and there was no marked difference between the conditions. CONCLUSION: The BF responses in the conduit artery and superficial vein during passive heating are significantly higher than during exercise at a given ΔTc, while there was no significant difference in the BF response in the deep vein between conditions.

Microvascular Injury, Thrombosis, Inflammation, and Apoptosis in the Pathogenesis of Heatstroke

Severe heatstroke is a leading cause of morbidity and mortality during heat waves. The pathogenesis of tissue injury, organ failure, and death in heatstroke is not well understood. We investigated the pathways of heatstroke-induced tissue injury and cell death in anesthetized baboons (Papio hamadyras) subjected to environmental heat stress until core temperature attained 42.5 degrees C (moderate heatstroke; n = 3) or onset of severe heatstroke (n = 4) signaled by a fall in systolic blood pressure to < 90 mm Hg and rise in core temperature to 43.1+/-0.1 degrees C. Three sham-heated animals served as controls. Light and electron microscopy revealed widespread hemorrhage and thrombosis, transmural migration of leukocytes, and microvascular endothelium injury in severe heatstroke. Immunohistology and ultrastructural analysis demonstrated increased staining of endothelial von Willebrand factor (vWF), tissue factor (TF), and endothelial leukocyte-platelet interaction. Extensive apoptosis was noted in spleen, gut, and lung, and in hematopoeitic cells populating these organs. Double-labeling studies colocalized active caspase-3 and TF with apoptotic cells. Findings in sham-heated animals were unremarkable. These data suggested that microvascular injury, thrombosis, inflammation, and apoptosis may play an important role in the pathogenesis of heatstroke injury.

Effects of biting on elevation of blood pressure and other physiological responses to stress in rats: Biting may reduce allostatic load

We have investigated how biting modulates some of the physiological changes (blood pressure, core temperature, and chemical mediators in the serum) that are induced by restraint stress. We exposed rats to restraint stress for 60 min. Biting on a wooden stick during restraint significantly suppressed the increase of blood pressure at 30, 45, 60, and 75 min and significantly inhibited the rise in core temperature at 30, 60, 120, and 180 min compared with rats that were restrained but did not bite anything. These differences were visible in infrared thermal images of the restraint-only and restraint-with-biting rats after 60 min. Biochemical analysis revealed that biting significantly suppressed increases of plasma interleukin-1β, interleukin-6, and leptin and that it significantly suppressed a decrease of thyroid-stimulating hormone. These observations suggest that biting produces an anti-stress effect and that para-functional masticatory activity plays an important role in coping with stressful events.

If It Quacks Like a Duck Then …!

In Response: Drs. Girard and Urwyler (1) take issue with our recent diagnosis and treatment of a hypermetabolic state (2). We agree that not all hypermetabolic states are due malignant hyperthermia (MH). Our differential diagnosis included sepsis and hypoperfusion. Neuroleptic malignant syndrome was ruled out as no agents implicated in the neuroleptic syndrome were used. Hypoperfusion was a possibility. However, the patient had a stable hemodynamic profile (cardiac index of greater than 2.5 L/min) upon arrival to the intensive care unit and the hypotension and decrease in MVO2 was precipitous. We were unable to acutely rule out sepsis. This patient’s clinical presentation was entirely consistent with MH, including a combined respiratory and metabolic acidosis, skin mottling, skeletal muscle rigidity, a rapid rise in core temperature, and a drop in mixed venous oxygen saturation. The diagnosis was supported by the family history of unexplained intraoperative hyperpyrexia and acidosis in two different blood relatives under anesthesia. The most conservative course of action was to assume the worst and treated accordingly. Following the administration of dantrolene there was complete resolution of his metabolic derangement. Impending septic or cardiogenic shock would not have resolved following dantrolene. There are several problems with attributing this patient’s hypermetabolic state to propofol infusion syndrome. The patent developed a combined respiratory and lactic acidosis despite adequate minute ventilation. The propofol infusion lasted only 3 h at a rate of 100 mcg/kg/min, and was discontinued well before the event in question. Drs. Girard and Urwyler’s assertion that MH is strictly a pharmacogenetic disease requiring a pharmacological trigger has been disproven in the literature as evidenced by MH occurring without a classic trigger (3). We elected to administer oral dantrolene to this patient due to his size (100 kg) and muscular build. The use of oral dantrolene for several days following an acute event of MH is described on page 538 in the most recent edition of the textbook Clinical Anesthesia (4). We proposed off-pump CABG as a means to avoid systemic rewarming from cardiopulmonary bypass based on our theory that warming was the inciting cause of this case report. This theory is not without both clinical human and experimental animal support. Obviously we cannot force a patient to undergo diagnostic testing, but this patient did ultimately consent for molecular diagnostic studies. His RYR1 gene sequencing was negative for known pathological variants associated with MH. However, the clinical sensitivity of this test is roughly 40%, leaving the other 60% of the MH susceptible individuals unaccounted for. As such, we look forward to new and better diagnostic studies in the future (5). This patient’s daughter will require a tonsillectomy in the near future. Any takers? Adam D. Lichtman, MD Department of Anesthesiology Weill-Cornell Medical Center New York New York [email protected] Charles Oribabor, MD Cardiothoracic Intensive Care Unit New York Methodist Hospital Brooklyn New York

Effect of Palm Cooling on Heat Extraction During Exercise in a Hot Dry Environment

Athletes, military personnel, astronauts, and firefighters are often required to perform in hot environments, increasing the risk of hyperthermia. Several methods of body cooling have been studied but most are dependent upon heavy equipment or an external power source, and may be impractical for use in the field. A portable palm cooling with negative pressure device (RTX) has been used to extract heat through the palm of the hand and attenuate hyperthermia. PURPOSE: To evaluate the effectiveness of the RTX in slowing the development of hyperthermia and associated symptoms to three other conditions [hand immersed in water bath (WB), water-perfused vest (VEST), no-cooling condition (NC)] in subjects exercising in a hot environment wearing summer fatigues, a backpack and body armor. METHODS: 10 subjects (age 25 ± 3 yrs; weight 74 ± 6 kg; height 177 ± 6 cm; VO2max 54 ± 9 mL kg-1.min-1) performed four heat stress tests in a counter-balanced order (NC / RTX/WB/VEST). The protocol consisted of two bouts [1st and 2nd bouts were terminated at a core temperature (TC) of 38.5°C and 39°C, respectively] of treadmill walking (at 50% VO2max), separated by a 41 -min cooling and rehydration period in a hot, dry environment (42°C, 30% rh). Time duration, rate of rise in core temperature (Tcslope) and heart rate (HR) were evaluated using a 2-way repeated-measures ANO VA. RESULTS: The time to reach the pre-determined TC in the 1st and 2nd bouts were not different among RTX (mean ± SD; 52 ± 14 and 42 ± 12 min respectively), NC (49 ± 13 and 41 ± 14 min respectively), and WB (54 ± 14 and 55 ± 20 min respectively), but was longer for the VEST (85 ± 30, and 65 ± 12 min respectively) in both bouts (p<0.05). The Tcslope (°C/min) was significantly lower for VEST in the 1st and 2nd bouts versus the other conditions (p<0.05), and no differences were observed during recovery. HR was not different at 10, 20 and 30 minutes of exercise in the 1st bout among RTX, NC, and WB, but was lower for VEST in the 1st bout (p<0.05). HR was not different among conditions in the 2nd bout. CONCLUSION: The RTX was not effective in slowing the development of hyperthermia in the present protocol. Aspects related to hand vasoconstriction and the severe work/heat stress conditions used in the present study possibly prevented the expected heat extraction. Supported by DARPA grant # W911NF-06-1 -0025

The Effect Of Exercise Induced Pre-Warming On Core Temperature During A Live Fire 'Search-and-Rescue' Task

Professional fire-fighters usually work 24-hour shifts. Although fighting fires is one of their most important tasks, other, non-fire fighting related physically demanding activities such as practicing, workouts and maintenance, form the main part of a shift. These activities may have a warm-up effect on the fire-fighter's body temperature. This rise in core temperature may lead to a faster onset of heat stress symptoms during fire fighting. It may also shorten the maximal acceptable working time of a fire fighting task. PURPOSE: To explore the effect of exercise-induced pre-warming on the body core temperature during a fire fighting task under realistic conditions. METHODS: 8 professional fire-fighters of the Amsterdam Fire Brigade performed a standardized live fire ‘search-and-rescue’ task twice over two days. Standard turn-out gear and SCBA (Self Contained Breathing Apparatus) were used. Prior to one of both ‘search-and-rescue’ tasks the fire-fighters carried out a 20-min. weight-dependent (1.5 W.kg-1) bicycle ergometer test to provoke an exercise-induced pre-warming effect. During both testing days, core temperature was recorded using an ingestible core body temperature pill (CorTempTM, HQ Inc., USA). Performance time on the ‘search-and-rescue’ task was also recorded. RESULTS: Preliminary results show a higher mean core temperature during the combined bicycle ergometer test / ‘search-and-rescue’ task when compared to the single ‘search-and-rescue’ task (37.84 (SD=0.30) vs 37.59°C (SD=0.21)). The absolute highest core temperature was also higher during the combined test (38.38 vs 38.02°C). Preliminary results also show that the mean performance time of the ‘search-and-rescue’ task during the combined bicycle ergometer test/ ‘search-and-rescue’ task was 6.2% higher when compared to the single ‘search-and-rescue’ task. CONCLUSIONS: Moderate, non-fire fighting related exercise prior to a fire fighting task may lead to a higher core temperature during fire fighting. Consequently, earlier onset of symptoms of heat stress during a common fire fighting task may occur.

Reduction in Platelet Activation by Citrate Anticoagulation Does Not Prevent Intradialytic Hemodynamic Instability

Background: The etiology of intradialytic hemodynamic instability is multifactorial. Of the various factors involved, a rise in core temperature seems to be crucial. In this respect, the bioincompatibility of hemodialysis (HD) treatment might play an important role. The application of cool dialysate reduces the number of periods of intradialytic hypotension (IDH) considerably. In rats, roller pump perfusion caused hypotension by shear stress induced platelet aggregation and subsequent serotonin release. During clinical HD, citrate anticoagulation abolished platelet activation almost completely. Hence, citrate anticoagulation might reduce IDH, whereas the beneficial effect of cool dialysate might be partly explained by reduced platelet activation. Methods: In the present study, blood pressure, IDH episodes, platelet activation, platelet aggregation, and serotonin release were studied crossover in 10 patients during HD with dalteparin anticoagulation at normal and low dialysate temperatures and during HD with citrate. Results: Citrate strongly reduced platelet activation, but did not improve IDH. The blood pressure was best preserved during cool-temperature HD, despite manifest platelet activation. Platelet activation was not accompanied by a rise in the plasma serotonin concentration. Conclusions: Three major conclusions can be drawn: (1) it is unlikely that platelet activation and subsequent serotonin release underlie IDH in the clinical situation; (2) the protective effects of cool dialysate on IDH appear to be independent of HD-induced platelet activation, and (3) extrapolating results from rat experiments to the human situation requires uppermost prudence.

The effect of the rate of rise in core temperature on serum Hsp70 during exercise in the heat

Exercise induces an increase in serum Hsp70 (sHsp70), which may modulate the innate immune response. When exercise is performed in a hot environment, heat exerts an additional stimulus to the immune system. However, we do not know if the sHSP70 is dependent on the rate of rise in core temperature (Tc). We hypothesized that sHsp70 post exercise in the heat will be smaller when the rate of rise in Tc is attenuated by applying cooling. Seven healthy male (age: 26±3years; height: 179±6cm; weight: 75.4±6.0kg; maximum oxygen uptake (VO2max): 58±8mL/kg/min) performed two identical tests in the heat (42°C, 30% rh). Subjects exercised with no cooling (no cool) and a water-perfused vest (cool) in two different trials. Subjects walked on a treadmill (~50% VO2max) in military summer fatigues, body armor, and a backpack (total gear equaled 15% of their body weight) until Tc reached 38.5°C or heart rate (HR) exceeded 95% HRmax. sHSP70 was measured pre and post exercise by ELISA. The exercise duration was longer for cool condition (88±33min) than for no cool (46±13min) (p<0.05). sHSP70 increased pre to post exercise from 0.57±0.61 to 1.69±0.66 ng/mL, in no cool (p<0.05). In the cool condition, sHSP70 changed from 0.81±1.30 to 1.70±0.67 ng/mL (p=0.08). Thus, there was no difference in post exercise sHSP70 between the two conditions (p>0.05). This suggests that sHsp70 during exercise in the heat is primarily determined by the core temperature attained rather than the rate of rise in core temperature.

Thermoregulation during Exercise in the Heat

As a result of the inefficiency of metabolic transfer, >75% of the energy that is generated by skeletal muscle substrate oxidation is liberated as heat. During exercise, several powerful physiological mechanisms of heat loss are activated to prevent an excessive rise in body core temperature. However, a hot and humid environment can significantly add to the challenge that physical exercise imposes on the human thermoregulatory system, as heat exchange between body and environment is substantially impaired under these conditions. This can lead to serious performance decrements and an increased risk of developing heat illness. Fortunately, there are a number of strategies that athletes can use to prevent and/or reduce the dangers that are associated with exercise in the heat. In this regard, heat acclimatisation and nutritional intervention seem to be most effective. During heat acclimatisation, the temperature thresholds for both cutaneous vasodilation and the onset of sweating are lowered, which, in combination with plasma volume expansion, improve cardiovascular stability. Effective nutritional interventions include the optimisation of hydration status by the use of fluid replacement beverages. The latter should contain moderate amounts of glucose and sodium, which improve both water absorption and retention.

Exercise in the Heat

This study examined changes in serum S100beta concentration, a peripheral marker of BBB permeability, in response to exercise in the heat with and without fluid ingestion. Eight physically active males completed up to 90 min of intermittent exercise at a power output corresponding to 55% VO2peak in a warm environment (35 degrees C, 56% rh). Trials were completed with (F trial) and without (NF trial) the replacement of sweat losses. During the fluid trial, an aliquot of plain water was ingested at 15-min intervals to match the volume of sweat lost during the previous period of exercise. Exercise time was 80.7 +/- 13.0 min in the NF trial and 85.1 +/- 9.5 min in the F trial (P = 0.107). Fluid ingestion resulted in a smaller rise in core temperature (P = 0.050) and heart rate (P = 0.027) during the latter stages of exercise. Serum S100beta concentrations were 0.08 +/- 0.02 microg.L at rest, increasing to 0.20 +/- 0.06 microg.L at the end of exercise in the NF trial, with this response attenuated by the ingestion of fluid (0.13 +/- 0.03 microg.L; P = 0.046). Both serum sodium concentration (P < 0.001) and serum osmolality (P = 0.003) were significantly lower at the end of exercise in the F trial than in the NF trial. The results of this study demonstrate that water ingestion can limit exercise-induced increases in serum S100beta, consistent with the preservation of BBB integrity. It is possible that this response was mediated through the maintenance of lower extracellular osmolality late in exercise, thus potentially limiting the osmotically driven movement of fluid across the BBB.