An ingestible telemetric temperature sensor for measuring body core temperature (T_c) was first described 45 years ago, although the method has only recently gained widespread use for exercise applications. This review aims to (1) use Bland and Altman’s limits of agreement (LoA) method as a basis for quantitatively reviewing the agreement between intestinal sensor temperature (T_intestinal), oesophageal temperature (T_oesophageal) and rectal temperature (T_rectal) across numerous previously published validation studies; (2) review factors that may affect agreement; and (3) review the application of this technology in field-based exercise studies. The agreement between T_intestinaland T_oesophagealis suggested to meet our delimitation for an acceptable level of agreement (ie, systematic bias 0.1°C, although the 95% LoA is acceptable. T_intestinalresponds less rapidly than T_oesophagealat the start or cessation of exercise or to a change in exercise intensity, but more rapidly than T_rectal. When using this technology, care should be taken to ensure adequate control over sensor calibration and data correction, timing of ingestion and electromagnetic interference. The ingestible sensor has been applied successfully in numerous sport and occupational applications such as the continuous measurement of T_cin deep sea saturation divers, distance runners and soldiers undertaking sustained military training exercises. It is concluded that the ingestible telemetric temperature sensor represents a valid index of T_cand shows excellent utility for ambulatory field-based applications.

To the race and wore an ambulatory Tc data recorder and HR monitor during the race. Pre- to postrace changes in nude body mass quantified fluid balance. Results: Environmental wet bulb globe temperature averaged 26.5°C. All runners finished the race asymptomatic of heat illness in a mean ± SD (range) time of 118 ± 13 (105-146) min, corresponding to an average running speed of 10.8 ± 1.1 (8.6-12.0) km×h−1. All runners recorded peak Tc > 39°C; 56% (N = 10) > 40°C; and 11% (N = 2) > 41°C. Peak Tc was 40.1 ± 0.7 (39.3-41.7) °C at 86 ± 36 (13-130) min, with Tc 39.9 ± 0.8 (38.3-41.7) °C at race finish. The magnitude of Tc response was unrelated (P > 0.05) to running time or fluid balance (e.g., fluid intake, % dehydration). Cumulative heat strain index was 2790 ± 1112 (1046-5144) units at race finish. Conclusion: Ingestible telemetric temperature sensors demonstrated utility for continuous measurement of Tc during mass-participation running. Successful application of this technology has highlighted the magnitude and durationof Tc elevation that runners will voluntarily achieve during mass-participation distance races in heat and high humidity without medical consequence....

Weather factors are widely studied for their effects on indicating dengue incidence trends. However, these studies have been limited due to the complex epidemiology of dengue, which involves dynamic interplay of multiple factors such as herd immunity within a population, distinct serotypes of the virus, environmental factors and intervention programs. In this study, we investigate the impact of weather factors on dengue in Singapore, considering the disease epidemiology and profile of virus serotypes. A Poisson regression combined with Distributed Lag Non-linear Model (DLNM) was used to evaluate and compare the impact of weekly Absolute Humidity (AH) and other weather factors (mean temperature, minimum temperature, maximum temperature, rainfall, relative humidity and wind speed) on dengue incidence from 2001 to 2009. The same analysis was also performed on three sub-periods, defined by predominant circulating serotypes. The performance of DLNM regression models were then evaluated through the Akaike's Information Criterion. From the correlation and DLNM regression modeling analyses of the studied period, AH was found to be a better predictor for modeling dengue incidence than the other unique weather variables. Whilst mean temperature (MeanT) also showed significant correlation with dengue incidence, the relationship between AH or MeanT and dengue incidence, however, varied in the three sub-periods. Our results showed that AH had a more stable impact on dengue incidence than temperature when virological factors were taken into consideration. AH appeared to be the most consistent factor in modeling dengue incidence in Singapore. Considering the changes in dominant serotypes, the improvements in vector control programs and the inconsistent weather patterns observed in the sub-periods, the impact of weather on dengue is modulated by these other factors. Future studies on the impact of climate change on dengue need to take all the other contributing factors into consideration in order to make meaningful public policy recommendations. As dengue virus transmission is through a human-to-mosquito-to-human cycle, the influence of meteorological factors on dengue is likely to be associated with their impact on mosquito populations and behavior. Other than the influence of weather factors, the shift of dominant serotypes and pre-emptive measures taken against dengue vectors may possibly affect the dengue transmission trend. In this study, we investigate the impact of weather factors on dengue in tropical Singapore, taking into consideration the disease epidemiology and profile of virus serotypes. We found that absolute humidity, as a composite index of mean temperature and relative humidity, is a more stable and better predictor for modeling dengue incidence than the other unique weather variables when virological factors are taken into consideration. This research suggests that absolute humidity needs to be considered together with all the other contributing factors in order to make meaningful public policy recommendations for dengue control.

Heat stroke (HS) is an ancient illness dating back more than 2000 years and continues to be a health threat and to cause fatality during physical exertion, especially in military personnel, fire-fighters, athletes, and outdoor laborers. The current paradigm in the pathophysiology and prevention of HS focuses predominantly on heat as the primary trigger and driver of HS, which has not changed significantly for centuries. However, pathological and clinical reports from HS victims and research evidence from animal and human studies support the notion that heat alone does not fully explain the pathophysiology of HS and that HS may also be triggered and driven by heat- and exercise-induced endotoxemia. Exposure to heat and exercise stresses independently promote the translocation of lipopolysaccharides (LPS) from gram-negative bacteria in the gut to blood in the circulatory system. Blood concentration of LPS can increase to a threshold that triggers the systemic inflammatory response, leading to the downstream ramifications of cellular and organ damage with sepsis as the end point i.e., heat sepsis. The dual pathway model (DPM) of HS proposed that HS is triggered by two independent pathways sequentially along the core temperature continuum of >40 °C. HS is triggered by heat sepsis at Tc < 42 °C and by the heat toxicity at Tc > 42 °C, where the direct effects of heat alone can cause cellular and organ damage. Therefore, heat sepsis precedes heat toxicity in the pathophysiology of HS.

The international community has recognized global warming as an impending catastrophe that poses significant threat to life on earth. In response, the signatories of the Paris Agreement (2015) have committed to limit the increase in global mean temperature to <1.5 °C from pre-industry period, which is defined as 1850–1890. Considering that the protection of human life is a central focus in the Paris Agreement, the naturally endowed properties of the human body to protect itself from environmental extremes should form the core of an integrated and multifaceted solution against global warming. Scholars believe that heat and thermoregulation played important roles in the evolution of life and continue to be a central mechanism that allows humans to explore, labor and live in extreme conditions. However, the international effort against global warming has focused primarily on protecting the environment and on the reduction of greenhouse gases by changing human behavior, industrial practices and government policies, with limited consideration given to the nature and design of the human thermoregulatory system. Global warming is projected to challenge the limits of human thermoregulation, which can be enhanced by complementing innate human thermo-plasticity with the appropriate behavioral changes and technological innovations. Therefore, the primary aim of this review is to discuss the fundamental concepts and physiology of human thermoregulation as the underlying bases for human adaptation to global warming. Potential strategies to extend human tolerance against environmental heat through behavioral adaptations and technological innovations will also be discussed. An important behavioral adaptation postulated by this review is that sleep/wake cycles would gravitate towards a sub-nocturnal pattern, especially for outdoor activities, to avoid the heat in the day. Technologically, the current concept of air conditioning the space in the room would likely steer towards the concept of targeted body surface cooling. The current review was conducted using materials that were derived from PubMed search engine and the personal library of the author. The PubMed search was conducted using combinations of keywords that are related to the theme and topics in the respective sections of the review. The final set of articles selected were considered “state of the art,” based on their contributions to the strength of scientific evidence and novelty in the domain knowledge on human thermoregulation and global warming.