Temperature最新文献

Purpose: Recent field studies of physical exertion in challenging environmental conditions have reported dissociation between elevation in body core temperature (T_c) and successful task completion. This prompted us to further examine physiological mechanisms that might underlie variability in the response to exertional heat exposure. We hypothesized that, in response to exercise in the heat, systematic differences in central and peripheral physiological variables would be apparent between participants who successfully completed the task, versus those who became hyperthermic or symptomatic.

Methods: Thirty-eight healthy participants attempted a 120-min walk (5 km/h, 2% grade) in a climate-controlled chamber (40°C, 50%RH). At rest and at regular intervals during the walk, measures of physiological heat strain were assessed. Twenty-seven participants were Completers, seven were stopped because their T_c exceeded 39°C (Hyperthermics), and four became Symptomatic (e.g. lightheaded, headache, dizzy) and did not complete the walk.

Results: Visceral adipose tissue was higher in those who became Hyperthermic, compared to the Completers (437 ± 183 vs 245 ± 268 g; p = 0.034), despite similar height and body mass. Hyperthermics also had higher heart rate (p = 0.009), and lower end-diastolic volume (p = 0.031), and stroke volume (p = 0.031) during the early stages of walking, compared to the Completers. None of the Symptomatics reached a T_c >39°C (symptoms occurred at 38.1 ± 0.4°C), and none of the Hyperthermics reported symptoms.

Conclusions: During exertional heat exposure, adiposity and exaggerated early-stage hemodynamic responses were related to T_c elevation, but hyperthermia was not related to the development of symptoms, and baseline parameters relating to body composition and fitness were not related to symptom development.

Military cold weather operations (CWOs) introduce a range of challenges, including extreme temperatures, strong winds, difficult terrain, and exposure to snow, ice, and water. Personnel undertaking these missions face a heightened risk of cold weather injury (CWI), such as hypothermia, freezing cold injuries, and non-freezing cold injuries. The risk of these injuries is influenced by various factors, including age, sex, and body composition. To ensure optimal and safe performance in CWOs, it is crucial to implement effective preventive measures against CWI. This article emphasizes the most pertinent strategies for CWI prevention in CWOs. Initially, it is important to assess individual vulnerability to CWI. Education and training on CWI prevention should be provided before deployment in CWOs. During CWOs, attention should be given to crucial behaviors such as using a proper layered clothing system, recognizing the risks associated with prolonged stationary periods in cold conditions, consuming adequate calories, and staying hydrated. Additionally, environmental monitoring using tools like the windchill index and regular checks on physical status are essential. Although monitoring by itself does not prevent CWI, it can prompt necessary behavioral adjustments. Education and behavioral modifications are central to preventing CWI. Given the limited research on CWI prevention in military settings, despite the frequent occurrence of these injuries, there is a pressing need for further studies to evaluate effective preventive strategies within this specific operational framework.

Core temperature (T_C) changes, alongside exercise, affect hemodynamic responses across different conduit and microvascular beds. This study investigated impacts of ecologically valid environmental heat and exercise exposures on cerebral, skin and retinal vascular responses by combining physiological assessments alongside computational fluid dynamics (CFD) modeling. Young, healthy participants (n = 12) were exposed to environmental passive heating (PH), and heated exercise (HE) (ergometer cycling), in climate-controlled conditions (50 mins, 40°C, 50% relative humidity) while maintaining upright posture. Blood flow responses in the common carotid (CCA), internal carotid (ICA) and central retinal (CRA) arteries were assessed using Duplex ultrasound, while forearm skin microvascular blood flow responses were measured using optical coherence tomography angiography. Three-dimensional retinal hemodynamics (flow and pressure) were calculated via CFD simulation, enabling assessment of wall shear stress (WSS). T_C rose following PH (+0.2°C, p = 0.004) and HE (+1.4°C, p < 0.001). PH increased skin microvascular blood flow (p < 0.001), whereas microvascular CRA flow decreased (p = 0.038), despite unchanged ICA flow. HE exacerbated these differences, with increased CCA flow (p = 0.007), unchanging ICA flow and decreased CRA flow (p < 0.001), and interactions between vascular (CCA vs. ICA p = 0.018; CCA vs. CRA p = 0.004) and microvascular (skin vs. retinal arteriolar p < 0.001) territories. Simulations revealed patterns of WSS and lumen pressure that uniformly decreased following HE. Under ecologically valid thermal challenge, different responses occur in distinct conduit and microvascular territories, with blood flow distribution favoring systemic thermoregulation, while flow may redistribute within the brain.

Passively elevating body temperature can trigger a potentially beneficial acute inflammatory response. However, heat therapy often causes discomfort and negative thermal perceptions, particularly in females who generally have lower heat tolerance than males. This study aimed to evaluate the impact of facial cooling on thermal comfort and interleukin-6 concentration in response to 60 minutes of dry heat exposure, and to investigate sex differences in physiological responses and perceptions. 22 healthy young adults (10 females, 12 males; age: 24.4 ± 3.3 years) completed three trials in randomized order using a dry sauna device: 1) Hyperthermia (71.1 ± 1.9°C; HEAT), 2) Hyperthermia with facial cooling via fans (71.1 ± 3.0°C; FAN), and 3) Normothermia (27.0 ± 0.9°C; CON). Blood samples to determine interleukin-6 (IL-6) plasma concentration were collected before and after exposure; basic affect and thermal comfort, rectal and skin temperature were assessed throughout the intervention. Rectal temperature following HEAT (38.0 ± 0.3°C) and FAN (37.8 ± 0.3°C) did not differ between males and females (p = 0.57). Females had higher forehead skin temperatures than males (p ≤ 0.019). Thermal comfort remained more positive in FAN compared to HEAT (p ≤ 0.002). Females felt more thermal discomfort than males in HEAT (p ≤ 0.03), but not in FAN (p = 0.28). The increase in IL-6 plasma concentration was similar between HEAT and FAN (p = 1.00), and higher than CON (p ≤ 0.02); there was no difference between males and females (p = 0.69). This study showed that facial cooling alleviated the thermal discomfort during heat exposure, particularly benefitted females, and did not impede the acute IL-6 response.

Our body temperature is normally kept within a narrow range of 1°C. For example, if our body temperature rises, such as in a hot environment or due to strenuous exercise, our thermoregulatory system will trigger a powerful heat defense response with vasodilation, sweating, and lowered metabolism. During fever, which often involves body temperatures of up to 41°C, this heat defense mechanism is apparently inhibited; otherwise, the rising body temperature would be immediately combated, and fever would not be allowed to develop. New evidence suggests how and where this inhibition takes place. In two consecutive studies from Cheng et al. and Xu et al., it has been shown that prostaglandin E₂, which generates fever by acting on thermosensory neurons in the preoptic hypothalamus, also acts on neurons in the brainstem parabrachial nucleus, which receive temperature information from temperature-activated spinal cord neurons and relay this information to the thermoregulatory center in the hypothalamus to either induce cold or heat defenses. By acting on the same type of prostaglandin E₂ receptor that is critical for fever generation in the preoptic hypothalamus, the EP₃ receptor, prostaglandin E₂ inhibits the signaling of the heat-responsive parabrachial neurons, while stimulating the cold-responsive neurons. These novel findings thus show that prostaglandin E₂, by binding to the same receptor subtype in the parabrachial nucleus as in the preoptic hypothalamus, adjusts the sensitivity of the thermosensory system in a coordinated manner to allow the development of febrile body temperatures.