Chin Leong Lim

The ingestible telemetric body core temperature sensor: a review of validity and exercise applications

An ingestible telemetric temperature sensor for measuring body core temperature (Tc) 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 (Tintestinal), oesophageal temperature (Toesophageal) and rectal temperature (Trectal) 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 Tintestinal and Toesophageal is suggested to meet our delimitation for an acceptable level of agreement (ie, systematic bias <0.1°C and 95% LoA within ±0.4°C). The agreement between Tintestinal and Trectal shows a significant systematic bias >0.1°C, although the 95% LoA is acceptable. Tintestinal responds less rapidly than Toesophageal at the start or cessation of exercise or to a change in exercise intensity, but more rapidly than Trectal. 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 Tc in 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 Tc and shows excellent utility for ambulatory field-based applications.

The Roles of Exercise-Induced Immune System Disturbances in the Pathology of Heat Stroke The Dual Pathway Model of Heat Stroke

Heat stroke is a life-threatening condition that can be fatal if not appropriately managed. Although heat stroke has been recognised as a medical condition for centuries, a universally accepted definition of heat stroke is lacking and the pathology of heat stroke is not fully understood. Information derived from autopsy reports and the clinical presentation of patients with heat stroke indicates that hyperthermia, septicaemia, central nervous system impairment and cardiovascular failure play important roles in the pathology of heat stroke. The current models of heat stroke advocate that heat stroke is triggered by hyperthermia but is driven by endotoxaemia. Endotoxaemia triggers the systemic inflammatory response, which can lead to systemic coagulation and haemorrhage, necrosis, cell death and multi-organ failure. However, the current heat stroke models cannot fully explain the discrepancies in high core temperature (Tc) as a trigger of heat stroke within and between individuals. Research on the concept of critical Tc as a limitation to endurance exercise implies that a high Tc may function as a signal to trigger the protective mechanisms against heat stroke. Athletes undergoing a period of intense training are subjected to a variety of immune and gastrointestinal (GI) disturbances. The immune disturbances include the suppression of immune cells and their functions, suppression of cell-mediated immunity, translocation of lipopolysaccharide (LPS), suppression of anti-LPS antibodies, increased macrophage activity due to muscle tissue damage, and increased concentration of circulating inflammatory and pyrogenic cytokines. Common symptoms of exercise-induced GI disturbances include diarrhoea, vomiting, gastrointestinal bleeding, and cramps, which may increase gut-related LPS translocation.This article discusses the current evidence that supports the argument that these exercise-induced immune and GI disturbances may contribute to the development of endotoxaemia and heat stroke. When endotoxaemia can be tolerated or prevented, continuing exercise and heat exposure will elevate Tc to a higher level (>42°C), where heat stroke may occur through the direct thermal effects of heat on organ tissues and cells. We also discuss the evidence suggesting that heat stroke may occur through endotoxaemia (heat sepsis), the primary pathway of heat stroke, or hyperthermia, the secondary pathway of heat stroke. The existence of these two pathways of heat stroke and the contribution of exercise-induced immune and GI disturbances in the primary pathway of heat stroke are illustrated in the dual pathway model of heat stroke. This model of heat stroke suggests that prolonged intense exercise suppresses anti-LPS mechanisms, and promotes inflammatory and pyrogenic activities in the pathway of heat stroke.

Systemic Inflammation Mediates the Effects of Endotoxemia in the Mechanisms of Heat Stroke

Heat stroke is triggered by heat, but is driven by endotoxemia and the downstream effects of systemic inflammation, acute phase response and the pyrogenic response. Whereas heat stroke and its related fatality commonly occur at core temperature (Tc) >40°C, healthy individuals have tolerated Tc 40°C-42°C without symptoms of heat stroke, suggesting that besides hyperthermia, there are other factors that can also cause heat stroke. The “Dual-pathway model (DPM)” suggests that heat stroke is triggered by the endotoxemia pathway at Tc up to ~ 42°C and independently, by heat toxicity at Tc >42°C. The second pathway in the DPM is based on evidence showing that cytoskeletal structures start to disintegrate at ambient temperature >41.5°C. Since most exertional stroke cases occur at Tc <42°C, the endotoxemia pathway, and not heat, might be the primary cause of heat stroke in the active population. Current evidence suggests that exercising under a poor state of health and a compromised immune system may also cause heat stroke, independent from the effects of hyperthermia. Strategies to prevent heat stroke should put equal emphasis on maintaining a good state of health and immune function. The current practice of focusing primarily on heat strain and hydration to prevent heat stroke may not have comprehensively addressed the pathophysiology of heat stroke and may explain why heat stroke continues to occur after more than 2000 years.