Nowadays, the national sports culture is prevalent, which is good sense, but for competitive high-temperature sweat sports is good for health? The answer is no. Sports physical exertion, according to the temperature and humidity of the environment, can be brought into the formula to calculate the heat index, because the formula is quite complex, so the actual application is to check the table to assess the temperature and humidity of sports, the risk of sports. If overheating occurs during exercise in the condition of high core body temperature, in addition to showing extreme fatigue, the temperature of the blood also increases with the flow through the place will cause intracellular protein denaturation, blocking the metabolic path; high temperature will also directly harm the endothelium of blood vessels and cause diffuse intravascular coagulation, and affect the permeability of blood vessels. In addition, respiratory alkalosis caused by hyperventilation during exercise can make metabolic lactic acidosis more capable of directly harming cells, so acute renal tubular necrosis, liver shock, and gastrointestinal mucosal bleeding may occur. In extreme cases, the condition is called exertional pyrexia, or sports-type heat shock. Heat stroke, also known as heat shock and heat cramps, is a heat-induced dysregulation of the body’s thermoregulatory functions and excessive heat accumulation in the body, which leads to damage to the nervous organs. In the grading of heatstroke is severe heatstroke. The disease usually occurs in summer when high temperatures are accompanied by high humidity. This is because the continuous sweltering heat will cause the skin heat dissipation function to decrease, and infrared and ultraviolet rays can penetrate the skin directly to the deep inner layer of the muscle, the body heat can not be dissipated, then the heat gathered in the organs and muscle tissue, causing dry skin, muscle temperature, resulting in sweating, and then harm to the central nervous system. Subsequently, the function of all organs and tissues in the body is affected, and patients experience local muscle cramps, high fever, no sweating, dry mouth, coma, elevated blood pressure, cough, asthma, respiratory distress, and even respiratory failure, which is the most serious type of heat stroke. Physical activity or non-physical activity in high temperature conditions can trigger this severe heat stroke. Without timely and proper treatment, the mortality rate is as high as 40% to 50%. When you encounter hot weather, once you appear to be sweating profusely and in a trance, pay attention to cooling. If someone is unconscious in high temperature, the unconscious person should be immediately carried to a ventilated and cool place, pour cool water to reduce the body temperature of the unconscious person, and then continuously monitor the temperature changes, high fever of about 40 degrees Celsius continues to be sent immediately to an experienced hospital for liquid resuscitation treatment, never to be underestimated as ordinary heatstroke, delaying treatment time. Symptoms and signs of local muscle cramps, high fever, no sweating, dry mouth, coma, increased blood pressure, cough, asthma, respiratory distress, and even respiratory failure are the most serious type of heat stroke. It is also very rare to have hyperthermia vascular obstruction leading to muscle lysis. Muscle hypoxia rhabdomyolysis myocytes produce toxic substances that lead to kidney damage. It is important to distinguish between sunstroke and heatstroke, which is an acute illness caused by a purely physical cause of thermoregulatory dysfunction in the body. The brain and meninges are congested and hemorrhagic due to direct sunlight on the head, causing neurological dysfunction called heliotropic disease. Due to high external temperature and high humidity, resulting in heat production or heat absorption or heat dissipation is increased or reduced, and the body heat accumulation is called heat stroke. The clinical term is heat stroke. Sunstroke: Initially, mental depression, weakness of the limbs, gait instability, ataxia, gaze, protruding eyes, some sweating, with the progress of the disease, presenting cardiovascular motor center, respiratory center, thermoregulatory center disorders or even paralysis symptoms. Heart failure, venous stenosis, weak pulse, rapid respiration, rhythm disorders, Biot’s respiration or Chen-Schloss respiration, some body temperature rises, dry skin, little or no sweating, excitement, violent spasms or convulsions, and rapid death. Pyrexia: Most of the body temperature rises up to 40 ℃, mental depression, slow movement, unstable step-like, accelerated breathing, sweating all over the body, stop in the cool place, looking for water to drink, when the body temperature reaches 41 ℃, mental depression deepens, unstable standing, sometimes appear a short period of excitement and restlessness, rushing around, but soon turn to inhibition: sweating stops, skin temperature hot, breathing highly difficult, the number of frequent, nasal flaring, two ribs flapping or The body temperature reaches 42℃, and the patient is in a state of shock. When the body temperature reaches 42 ℃, the state of coma, loss of consciousness, limbs scratching, shallow breathing, rhythm is uneven, the pulse is weak does not feel in the hand, conjunctival cyanosis, blood thick, foaming at the mouth, death in a spasm attack. Heat stroke is fatal heat stroke, the main clinical manifestations are high body core temperature (40 ℃ ~ 47 ℃), dry skin heat and central nervous system abnormalities, such as inattention, memory loss, delirium, convulsions, coma, etc. Severe patients can develop multi-organ dysfunction syndrome (MODS). Epidemiological data show that during a summer heat wave (temperature 32°C, duration ≥ 3 d) attack, the incidence of heat stroke in urban residents of the United States is 176/100,000~265/100,000 people, while the incidence of heat stroke in Saudi Arabia, which is located in the tropics and subtropics, can be as high as 250/100,000 people; with global warming and the annual increase in the frequency and intensity of heat wave attacks, active preparation to deal with With global warming and the increasing frequency and intensity of heat wave attacks, it is important to actively prepare for sudden heat injury events. The body maintains a dynamic balance between heat production and heat dissipation thermoregulation through the synergistic effects of the cardiovascular system, skin, sweat glands and internal organs under the regulation of the central nervous system and endocrine. Under heat stress or exercise, a small increase in blood temperature (< 1℃) can stimulate the skin thermoreceptors or central thermoreceptors to excite the heat dissipation center, and the body can promote heat dissipation and maintain normal body temperature by enhancing the activity of the sympathetic diastolic system in the skin and other mechanisms to distribute blood to the periphery, increase skin blood flow (up to 6~8 L/min), and increase sweat gland secretion. The evaporation of sweat is the main way for the body to dissipate heat in a hot environment, and the temperature gradient generated by sweat evaporation is closely related to the body’s heat dissipation effect. The evaporation of sweat is influenced by the temperature (Ta), air humidity (Tw) and airflow (V), among which the relative humidity (RH) is particularly important. If the relative humidity is too high, the dew point temperature rises, sweat secretion is greater than evaporation, and the body loses more water but does not play the role of evaporation and heat dissipation (ineffective sweat secretion), which may cause heat accumulation and thermoregulation tension. If the body’s heat load exceeds the body’s ability to dissipate heat, it can directly damage the thermoregulatory center, leading to thermoregulatory dysfunction and shock. The morbidity and mortality rate of pyrexia is approximately 50%, and 7%-14% of survivors suffer permanent central nervous system damage, which is directly related to the duration, degree, and rate of elevated body temperature and local circulatory changes. The cytotoxic effects of hyperthermia can cause extensive cellular degeneration, necrosis, and hemorrhage, with brain tissue damage being the most severe. In rats resuscitated with iced saline, the survival time after heat stroke was significantly longer in the jugular vein retrograde infusion group compared with the femoral vein retrograde infusion group; heating the carotid artery of isolated rabbits induced vascular smooth muscle contraction, and the degree of contraction was proportional to the heating temperature, suggesting that high brain tissue temperature and low perfusion of brain tissue under heat stress may be the causative factors of heat stroke. The results suggest that hyperthermia and hypoperfusion of brain tissue under heat stress may be causative factors of heat stroke. The corresponding changes in circulatory dynamics under thermoregulation are important for maintaining normal body temperature. Dysfunction of the cutaneous sympathetic vasodilator/sympathetic vasoconstrictor system (e.g., in menopausal women, type II diabetics, etc.), or dysregulation of the pressure-sensing reflexes of the cutaneous vasculature, or increased body temperature with limited compensatory cardiac output (e.g., due to disorders of hydrometabolism, cardiovascular disease, or drugs), may lead to thermoregulatory dysfunction in heat-stressed or physically active individuals (endogenous hyperthermia). Disturbances in thermoregulatory function and reduced heat resistance of the body can cause heat stress to develop into pyrexia. Heat accumulation in the body increases cardiac output and ventilation per minute, dilates peripheral vascular beds, and reduces visceral perfusion, which may cause acute pathological changes in the body, such as dehydration, circulatory failure, hypoxemia, and intestinal bacterial translocation. Dehydration is the most common causative factor of exertional pyrexia, and every 1% of body mass dehydrated in a state of strong physical activity can cause a rise in body core temperature of 015 ℃ to 020 ℃. Intractable hypoxemia and sudden circulatory failure are often the key to the rapid progression of systemic inflammatory response syndrome (SIRS), acute respiratory distress syndrome (ARDS), severe systemic infections (systemic infections with combined organ dysfunction) to multi-organ dysfunction syndrome and death. Internal tissues and organs such as the intestine are in a state of ischemia and hypoxia, which stimulates the release of inflammatory mediators such as oxygen free radicals, which can induce, participate in, and aggravate inflammatory reactions and mucosal damage. Therefore, the body should be rehydrated in a timely manner under the condition of elevated body temperature, hyper-metabolism and massive sweating, and avoid or reduce exposure to high temperature and high humidity to maintain water and electrolyte balance and adequate evaporation of sweat from the body to maintain normal body temperature regulation and blood circulation and other physiological functions. The repeated effect of thermal stimulation can make the body’s adaptation to heat stress enhanced, i.e., heat habituation, which is manifested by the enhanced compensatory capacity of the cardiovascular system for high temperature, the reduced effect of strong physical activity on heart rate, blood pressure, and body core temperature, and the increased cardiac output; the increased activity of renin angiotensin aldosterone system (RAAS), which improves the body’s heat habituation capacity by reducing metabolic heat production and regulating water-electricity balance and other mechanisms; plasma The volume of blood plasma expands and blood dilution is rapid and significant, avoiding hypokalemia and other water and electrolyte disorders caused by high temperature exercise; sweat secretion increases while sodium content decreases, sweat surface tension decreases, sweat distribution is uniform, and the effective evaporation rate increases; promoting the adjustment of circulating blood volume and reestablishing the normal distribution of body fluids; glomerular filtration rate increases, and the resistance to rhabdomyolysis caused by strong physical activity is enhanced; the decrease in skin temperature is significantly lower than that of The decrease of skin temperature is significantly lower than the decrease of body core temperature, which increases the thermal gradient and facilitates heat dissipation, etc. The body’s glycogen synthesis increases, the rate of gluconeogenesis and glycolysis decreases, energy consumption decreases, savings increases, and heat production decreases. Heat training can also reduce metabolic heat production through fat metabolism and mitochondrial oxidative phosphorylation, thus playing a protective role in the body. Cytokines (CK) are closely related to the pathogenesis of heat exhaustion. The synthesis and secretion of CK increases under heat stress, and plays an important role in mediating and regulating the inflammatory response, tissue damage and repair associated with heat stress. Among them, anti-inflammatory CKs such as interleukin (IL)4, IL10 and tumor necrosis factor soluble receptor can alleviate the symptoms of fever and increased leukocyte count, stimulate the hypothalamic pituitary adrenal system, activate leukocytes and vascular endothelial cells, thus defending against tissue damage and promoting repair. IL6 has multi-directional bioefficacy under heat stress, which can alleviate local and systemic inflammatory responses through mechanisms such as controlling the level of pro-inflammatory cytokines, promoting hepatocyte synthesis of acute phase reactive proteins, thereby inhibiting excessive tissue damage by protein hydrolases, and enhancing the body’s ability to resist infection, hemorrhage and injury. Heat stress response simultaneously stimulates the release of pro-inflammatory cytokines, such as tumor necrosis factor (TNF) and IL1β, from inflammatory cells, such as macrophages, granulocytes, lymphocytes and endothelial cells, releasing a large number of inflammatory mediators, which is greater than the counteracting effect of endogenous anti-inflammatory mediators, forming a cascade amplification reaction mediated by inflammatory mediators, leading to systemic inflammatory response syndrome or even multi organ dysfunction syndrome. Studies of CK and chemotactic cytokines in patients with exertional heat stroke (EXHS) have shown that proinflammatory cytokines (IL1β, TNFα, IL6, etc.), CK of helper T cells (TH) TH1 (INFγ, IL2R, etc.), monocyte chemotactic protein 1, and RANTES are significantly increased in the acute phase of exertional heat stroke.CK or simplified acute physiology score ( The levels of SAPS did not correlate with the degree of hyperthermia, but the levels of IL6, INFγ, IL2R, and MCP1 were positively correlated with SAPS and can be used as reference indicators to assess the severity of exertional pyrexia disease in the acute phase. The upregulation of IL6 gene expression levels in myocytes (but not monocytes) in the acute phase of the organism’s response to strong physical activity may suggest a limitation of the initial trigger range of inflammation. The spread and loss of control of the systemic inflammatory response in heat stroke has many similarities to the development of a systemic infection response. ck can also act on the thermoregulatory system, shifting the tuning point upward, altering vascular tension and causing responses such as acute hypertension. The intestinal vascular permeability increases under heat stress, toxins and bacteria translocate into the blood, and the intestine may become the driving organ for the development of inflammation, pyrexia and multi-organ dysfunction syndrome. Studies on primates (monkeys) have shown that endotoxin can enter the blood from the intestine when the body nucleus temperature is passively increased to 40°C under high temperature and high humidity (Ta: 41°C, RH: 100%) environment, and the plasma endotoxin concentration is positively correlated with the body nucleus temperature, and the endotoxin concentration reaches the highest value at the body nucleus temperature of 43°C, while the heart rate and blood pressure drop sharply and circulatory failure occurs rapidly. In the same type of animals induced endotoxemia, the plasma endotoxin concentration was significantly lower in the anti-endotoxin antibody pretreatment group than in the control group during heat stress, while the survival time was significantly longer, suggesting that endotoxemia under heat stress is closely related to sudden circulatory failure. In contrast, lowering the somatic nucleus temperature (18℃~27℃) in endotoxemic rats could inhibit the release of inflammatory mediators from alveolar macrophages, induce the release of anti-inflammatory mediators, activate NFkB, and avoid the cascade amplification response mediated by inflammatory mediators. High temperature can lead to endothelial cell damage and the development of DIC. endothelium has an important role in maintaining normal vascular elasticity and permeability, regulating leukocyte motility, and maintaining the balance between pro- and anti-coagulation. The elevated levels of blood hereditary pseudohemophilic factor antigen, nitric oxide metabolites, and soluble E selectin in patients with pyrexia suggest that high temperature can lead to intravascular coagulation, enhance vascular permeability, and increase the expression of adhesion molecules on the cell surface and the shedding of their soluble forms. The pathogenesis of pyrexia is consistent with activation of the coagulation system: endotoxin, TNFα, and IL1 cause endothelial cells and monocytes to express tissue factor in large amounts, activating exogenous coagulation pathways and increasing thrombin synthesis; the levels of endogenous anticoagulant substances protein C (PC), protein S, and antithrombin III (ATIII) are significantly reduced, and thrombin-antithrombin complexes and soluble fibrin monomers appear, causing The activated coagulation system interacts with the inflammatory response through multiple links, and pro-inflammatory cytokines can inhibit the expression of endothelial cell protein C receptors and thrombin-regulated proteins and suppress the protein C pathway of anticoagulation. Heat stress can lead to hyperfibrinolysis, as evidenced by increased D-dimer levels and decreased fibrinogen levels. Lowering the nucleus temperature to the normal range inhibits fibrinolysis, but not activation of the coagulation system and further procoagulant reactions, similar to the pattern of coagulation-anticoagulation-fibrinolysis abnormalities in systemic infections. The cellular heat stress response is capable of synthesizing or increasing the synthesis of heat shock proteins (or stress proteins). Heat stress causes structural damage to proteins, exposing binding sites for heat shock proteins, and heat shock proteins bind to damaged proteins to release free heat shock transcription factors (HSF), initiating transcriptional synthesis of heat shock proteins. The increased heat shock proteins can help proteins fold, shift, maintain and degrade correctly, promoting repair and removal of damaged proteins and avoiding cellular damage from heat, ischemia and hypoxia, endotoxin , inflammatory cytokines, etc. Gene transcription or specific antibody levels block the synthesis of heat shock proteins, making cells less heat resistant and more sensitive. Endotoxin mediated the inflammatory response in both heat-stressed and non-heat-stressed (control) mice, but the healing time of endotoxemic mice in the heat-stressed group was significantly faster than that in the control group, suggesting that heat shock proteins may increase the tolerance to endotoxin and the speed of healing in mice. Heat-stressed mice alleviated the altered vascular permeability caused by endotoxin through mechanisms such as synthesis of heat shock protein 90 and were able to inhibit the release of the inflammatory mediator TNFα. Factors such as advanced age, absence of heat habituation, and genetic polymorphism may lead to abnormal expression or reduced levels of heat shock proteins, predisposing heat stress to the development of pyrexia.