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Objective: To present recommendations for the prevention, recognition, and treatment of exertional heat illnesses and to describe the relevant physiology of thermoregulation.
Background: Certified athletic trainers evaluate and treat heat-related injuries during athletic activity in “safe” and high-risk environments. While the recognition of heat illness has improved, the subtle signs and symptoms associated with heat illness are often overlooked, resulting in more serious problems for affected athletes. The recommendations presented here provide athletic trainers and allied health providers with an integrated scientific and practical approach to the prevention, recognition, and treatment of heat illnesses. These recommendations can be modified based on the environmental conditions of the site, the specific sport, and individual considerations to maximize safety and performance.
Recommendations: Certified athletic trainers and other allied health providers should use these recommendations to establish on-site emergency plans for their venues and athletes. The primary goal of athlete safety is addressed through the prevention and recognition of heat-related illnesses and a well-developed plan to evaluate and treat affected athletes. Even with a heat-illness prevention plan that includes medical screening, acclimatization, conditioning, environmental monitoring, and suitable practice adjustments, heat illness can and does occur. Athletic trainers and other allied health providers must be prepared to respond in an expedient manner to alleviate symptoms and minimize morbidity and mortality.
Heat illness is inherent to physical activity and its incidence increases with rising ambient temperature and relative humidity. Athletes who begin training in the late summer (eg, football, soccer, and cross-country athletes) experience exertional heat-related illness more often than athletes who begin training during the winter and spring.1–5 Although the hot conditions associated with late summer provide a simple explanation for this difference, we need to understand what makes certain athletes more susceptible and how these illnesses can be prevented.
This position statement provides recommendations that will enable certified athletic trainers (ATCs) and other allied health providers to (1) identify and implement preventive strategies that can reduce heat-related illnesses in sports, (2) characterize factors associated with the early detection of heat illness, (3) provide on-site first aid and emergency management of athletes with heat illnesses, (4) determine appropriate return-to-play procedures, (5) understand thermoregulation and physiologic responses to heat, and (6) recognize groups with special concerns related to heat exposure.
This position statement is organized as follows:
The traditional classification of heat illness defines 3 categories: heat cramps, heat exhaustion, and heat stroke.6–8 However, this classification scheme omits several other heat- and activity-related illnesses, including heat syncope and exertional hyponatremia. The signs and symptoms of the exertional heat illnesses are listed in Table Table11.
Heat illness is more likely in hot, humid weather but can occur in the absence of hot and humid conditions.
Exercise-associated muscle (heat) cramps represent a condition that presents during or after intense exercise sessions as an acute, painful, involuntary muscle contraction. Proposed causes include fluid deficiencies (dehydration), electrolyte imbalances, neuromuscular fatigue, or any combination of these factors.6,9–11,19
Heat syncope, or orthostatic dizziness, can occur when a person is exposed to high environmental temperatures.19 This condition is attributed to peripheral vasodilation, postural pooling of blood, diminished venous return, dehydration, reduction in cardiac output, and cerebral ischemia.10,19 Heat syncope usually occurs during the first 5 days of acclimatization, before the blood volume expands,12 or in persons with heart disease or those taking diuretics.10 It often occurs after standing for long periods of time, immediately after cessation of activity, or after rapid assumption of upright posture after resting or being seated.
Exercise (heat) exhaustion is the inability to continue exercise associated with any combination of heavy sweating, dehydration, sodium loss, and energy depletion. It occurs most frequently in hot, humid conditions. At its worst, it is difficult to distinguish from exertional heat stroke without measuring rectal temperature. Other signs and symptoms include pallor, persistent muscular cramps, urge to defecate, weakness, fainting, dizziness, headache, hyperventilation, nausea, anorexia, diarrhea, decreased urine output, and a body-core temperature that generally ranges between 36°C (97°F) and 40°C (104°F).6,9,10,13,19
Exertional heat stroke is an elevated core temperature (usually >40°C [104°F]) associated with signs of organ system failure due to hyperthermia. The central nervous system neurologic changes are often the first marker of exertional heat stroke. Exertional heat stroke occurs when the temperature regulation system is overwhelmed due to excessive endogenous heat production or inhibited heat loss in challenging environmental conditions20 and can progress to complete thermoregulatory system failure.19,21 This condition is life threatening and can be fatal unless promptly recognized and treated. Signs and symptoms include tachycardia, hypotension, sweating (although skin may be wet or dry at the time of collapse), hyperventilation, altered mental status, vomiting, diarrhea, seizures, and coma.6,10,14 The risk of morbidity and mortality is greater the longer an athlete's body temperature remains above 41°C (106°F) and is significantly reduced if body temperature is lowered rapidly.22–24
Unlike classic heat stroke, which typically involves prolonged heat exposure in infants, elderly persons, or unhealthy, sedentary adults in whom body heat-regulation mechanisms are inefficient,25–27 exertional heat stroke occurs during physical activity.28 The pathophysiology of exertional heat stroke is due to the overheating of organ tissues that may induce malfunction of the temperature-control center in the brain, circulatory failure, or endotoxemia (or a combination of these).29,30 Severe lactic acidosis (accumulation of lactic acid in the blood), hyperkalemia (excessive potassium in the blood), acute renal failure, rhabdomyolysis (destruction of skeletal muscle that may be associated with strenuous exercise), and disseminated intravascular coagulation (a bleeding disorder characterized by diffuse blood coagulation), among other medical conditions, may result from exertional heat stroke and often cause death.25
Exertional hyponatremia is a relatively rare condition defined as a serum-sodium level less than 130 mmol/L. Low serum-sodium levels usually occur when activity exceeds 4 hours.19 Two, often-additive mechanisms are proposed: an athlete ingests water or low-solute beverages well beyond sweat losses (also known as water intoxication), or an athlete's sweat sodium losses are not adequately replaced.15–18 The low blood-sodium levels are the result of a combination of excessive fluid intake and inappropriate body water retention in the water-intoxication model and insufficient fluid intake and inadequate sodium replacement in the latter. Ultimately, the intravascular and extracellular fluid has a lower solute load than the intracellular fluids, and water flows into the cells, producing intracellular swelling that causes potentially fatal neurologic and physiologic dysfunction. Affected athletes present with a combination of disorientation, altered mental status, headache, vomiting, lethargy, and swelling of the extremities (hands and feet), pulmonary edema, cerebral edema, and seizures. Exertional hyponatremia can result in death if not treated properly. This condition can be prevented by matching fluid intake with sweat and urine losses and by rehydrating with fluids that contain sufficient sodium.31,32
The National Athletic Trainers' Association (NATA) advocates the following prevention, recognition, and treatment strategies for exertional heat illnesses. These recommendations are presented to help ATCs and other allied health providers maximize health, safety, and sport performance as they relate to these illnesses. Athletes' individual responses to physiologic stimuli and environmental conditions vary widely. These recommendations do not guarantee full protection from heat-related illness but should decrease the risk during athletic participation. These recommendations should be considered by ATCs and allied health providers who work with athletes at risk for exertional heat illnesses to improve prevention strategies and ensure proper treatment.
In cases of exercise-associated muscle (heat) cramps or heat syncope, the ATC should discuss the athlete's case with the supervising physician. The cases of athletes with heat exhaustion who were not transferred to the physician's care should also be discussed with the physician. After exertional heat stroke or exertional hyponatremia, the athlete must be cleared by a physician before returning to athletic participation.92 The return to full activity should be gradual and monitored.8,87
To differentiate heat illnesses in athletes, ATCs and other on-site health care providers must be familiar with the signs and symptoms of each condition (see Table Table1).1). Other medical conditions (eg, asthma, status epilepticus, drug toxicities) may also present with similar signs and symptoms. It is important to realize, however, that an athlete with a heat illness will not exhibit all the signs and symptoms of a specific condition, increasing the need for diligent observation during athletic activity.
Athletic trainers and other health care providers should be sensitive to the following nonenvironmental risk factors, which could place athletes at risk for heat illness.
Dehydration Sweating, inadequate fluid intake, vomiting, diarrhea, certain medications,89,101–103 and alcohol104,105 or caffeine106 use can lead to fluid deficit. Body-weight change is the preferred method to monitor for dehydration in the field, but a clinical refractometer is another accurate method (specific gravity should be no more than 1.020).34,49,107–110 Dehydration can also be identified by monitoring urine color or body-weight changes before, during, and after a practice or an event and across successive days.53,54
The signs and symptoms of dehydration are thirst, general discomfort, flushed skin, weariness, cramps, apathy, dizziness, headache, vomiting, nausea, heat sensations on the head or neck, chills, decreased performance, and dyspnea.52 Water loss that is not regained by the next practice increases the risk for heat illness.110
Barriers to Evaporation Athletic equipment and rubber or plastic suits used for “weight loss” do not allow water vapor to pass through and inhibit evaporative, convective, and radiant heat loss.111,112 Participants who wear equipment that does not allow for heat dissipation are at an increased risk for heat illness.113 Helmets are also limiting because a significant amount of heat is dissipated through the head.
Increased Body Mass Index (Thick Fat Layer or Small Surface Area) Obese individuals are at an increased risk for heat illness because the fat layer decreases heat loss.118 Obese persons are less efficient and have a greater metabolic heat production during exercise. Conversely, muscle-bound individuals have increased metabolic heat production and a lower ratio of surface area to mass, contributing to a decreased ability to dissipate heat.119–121
Wet-Bulb Globe Temperature on Previous Day and Night When the WBGT is high to extreme (see Table Table3),3), the risk of heat-related problems is greater the next day; this appears to be one of the best predictors of heat illness.121 Athletes who sleep in cool or air-conditioned quarters are at less risk.
Poor Physical Condition Individuals who are untrained are more susceptible to heat illness than are trained athletes. As the
O2max of an individual improves, the ability to withstand heat stress improves independent of acclimatization and heat adaptation.122 High-intensity work can easily produce 1000 kcal/h and elevate the core temperature of at-risk individuals (those who are unfit, overweight, or unacclimatized) to dangerous levels within 20 to 30 minutes.123
Excessive or Dark-Colored Clothing or Equipment Excessive clothing or equipment decreases the ability to thermoregulate, and dark-colored clothing or equipment may cause a greater absorption of heat from the environment. Both should be avoided.113
Overzealousness Overzealous athletes are at a higher risk for heat illness because they override the normal behavioral adaptations to heat and decrease the likelihood of subtle cues being recognized.
Medications and Drugs Athletes who take certain medications or drugs, particularly medications with a dehydrating effect, are at an increased risk for a heat illness.101–106,125–136 Alcohol, caffeine, and theophylline at certain doses are mild diuretics.106,137,138 Caffeine is found in coffee, tea, soft drinks, chocolate, and several over-the-counter and prescription medications.139 Theophylline is found mostly in tea and anti-asthma medications.140
Electrolyte Imbalance Electrolyte imbalances do not usually occur in trained, acclimatized individuals who engage in physical activity and eat a normal diet.141 Most sodium and chloride losses in athletes occur through the urine, but athletes who sweat heavily, are salty sweaters, or are not heat acclimatized can lose significant amounts of sodium during activity.142 Electrolyte imbalances often contribute to heat illness in older athletes who use diuretics.143,144
The following predisposing medical conditions add to the risk of heat illness.
Malignant Hyperthermia Malignant hyperthermia is caused by an autosomal dominant trait that causes muscle rigidity, resulting in elevation of body temperature due to the accelerated metabolic rate in the skeletal muscle.145–147
Neuroleptic Malignant Syndrome Neuroleptic malignant syndrome is associated with the use of neuroleptic agents and antipsychotic drugs and an unexpected idiopathic increase in core temperature during exercise.148–151
When the environmental temperature is above skin temperature, athletes begin to absorb heat from the environment and depend entirely on evaporation for heat loss.113,158,159 High relative humidity inhibits heat loss from the body through evaporation.61
The environmental factors that influence the risk of heat illness include the ambient air temperature, relative humidity (amount of water vapor in the air), air motion, and the amount of radiant heat from the sun or other sources.2,9,41 The relative risk of heat illness can be calculated using the WBGT equation.2,43,50,69,77,160,161 Using the WBGT index to modify activity in high-risk settings has virtually eliminated heat-stroke deaths in United States Marine Corps recruits.159 Wet-bulb globe temperature is calculated using the wet-bulb (wb), dry-bulb (db), and black-globe (bg) temperature with the following equation49,62,85,162,163:
When there is no radiant heat load, Tdb = Tbg, and the equation is reduced62 to
This equation is used to estimate risk as outlined in Table Table33.13,40,50,61,85 This index was determined for athletes wearing a T-shirt and light pants.158 The WBGT calculation can be performed using information obtained from electronic devices42 or the local meteorologic service, but conversion tables for relative humidity and Tdb are needed to calculate the wet-bulb temperature.50,162 The predictive value from the meteorologic service is not as accurate as site-specific data for representing local heat load but will suffice in most situations. When WBGT measures are not possible, environmental heat stress can be estimated using a sling psychrometer (see Figures Figures1,1, ,22).
Several recommendations have been published for distance running, but these can also be applied to other continuous activity sports. The Canadian Track and Field Association recommended that a distance race should be cancelled if the WBGT is greater than 26.7°C (80°F).39 The American College of Sports Medicine guidelines from 1996 recommended that a race should be delayed or rescheduled when the WBGT is greater than 27.8°C (82°F).31,72,73 In some instances, the event will go on regardless of the WBGT; ATCs should then have an increased level of suspicion for heat stroke and focus on hydration, emergency supplies, and detection of exertional heat illnesses.
Thermoregulation is a complex interaction among the central nervous system (CNS), the cardiovascular system, and the skin to maintain a body-core temperature of 37°C.9,43,51,164 The CNS temperature-regulation center is located in the hypothalamus and is the site where the core temperature setpoint is determined.9,43,82,158,164–166 The hypothalamus receives information regarding body-core and shell temperatures from peripheral skin receptors and the circulating blood; body-core temperature is regulated through an open-ended feedback loop similar to that in a home thermostat system.158,165,167,168 Body responses for heat regulation include cutaneous vasodilation, increased sweating, increased heart rate, and increased respiratory rate.38,43,51,164,165
Body-core temperature is determined by metabolic heat production and the transfer of body heat to and from the surrounding environment using the following heat-production and heat-storage equation166,167:
where S is the amount of stored heat, M is the metabolic heat production, R is the heat gained or lost by radiation, K is the conductive heat lost or gained, Cv is the convective heat lost or gained, and E is the evaporative heat lost.
Basal metabolic heat production fasting and at absolute rest is approximately 60 to 70 kcal/h for an average adult, with 50% of the heat produced by the internal organs. Metabolic heat produced by intense exercise may approach 1000 kcal/h,51,164 with greater than 90% of the heat resulting from muscle metabolism.9,40,42,166
Evaporation Heat transfers via the vaporization of sweat § and is the most efficient means of heat loss.51,158,169 The evaporation of sweat from the skin depends on the water saturation of the air and the velocity of the moving air.170–172 The effectiveness of this evaporation for heat loss from the body diminishes rapidly when the relative humidity is greater than 60%.9,20,164
Cognitive performance and associated CNS functions deteriorate when brain temperature rises. Signs and symptoms include dizziness, confusion, behavior changes, coordination difficulties, decreased physical performance, and collapse due to hyperthermia.168,173 The residual effects of elevated brain temperature depend on the duration of the hyperthermia. Heat stroke rarely leads to permanent neurologic deficits51; however, some sporadic symptoms of frontal headache and sleep disturbances have been noted for up to 4 months.168,174,175 When permanent CNS damage occurs, it is associated with cerebellar changes, including ataxia, marked dysarthria, and dysmetria.174
Heat acclimatization is the physiologic response produced by repeated exposures to hot environments in which the capacity to withstand heat stress is improved.14,43,75,176,177 Physiologic responses to heat stress are summarized in Table Table4.4. Exercise heat exposure produces progressive changes in thermoregulation that involve sweating, skin circulation, thermoregulatory setpoint, cardiovascular alterations, and endocrine adjustments.29,43,178 Individual differences affect the onset and decay of acclimatization.29,45,179 The rate of acclimatization is related to aerobic conditioning and fitness; more conditioned athletes acclimatize more quickly.43,45,180 The acclimatization process begins with heat exposure and is reasonably protective after 7 to 14 days, but maximum acclimatization may take 2 to 3 months.45,181,182 Heat acclimatization diminishes by day 6 when heat stress is no longer present.180,183 Fluid replacement improves the induction and effect of heat acclimatization.184–187 Extra salt in the diet during the first few days of heat exposure also improves acclimatization; this can be accomplished by encouraging the athlete to eat salty foods and to use the salt shaker liberally during meals.
Cumulative dehydration develops insidiously over several days and is typically observed during the first few days of a season during practice sessions or in tournament competition. Cumulative dehydration can be detected by monitoring daily prepractice and postpractice weights. Even though a small decrease in body weight (less than 1%) may not have a detrimental effect on the individual, the cumulative effect of a 1% fluid loss per day occurring over several days will create an increased risk for heat illness and a decrease in performance.110
During intense exercise in the heat, sweat rates can be 1 to 2.5 L/h (about 1 to 2.25 kilograms [2 to 5 pounds] of body weight per hour) or more, resulting in dehydration. Unfortunately, the volume of fluid that most athletes drink voluntarily during exercise replaces only about 50% of body-fluid losses.188 Ideally, rehydration involves drinking at a rate sufficient to replace all of the water lost through sweating and urination.60,77 If the athlete is not able to drink at this rate, he or she should drink the maximum tolerated. Use caution to ensure that athletes do not overhydrate and put themselves at risk for the development of hyponatremia. However, hydration before an event is essential to help decrease the incidence of heat illnesses. For more information on this topic, see the “National Athletic Trainers' Association Position Statement: Fluid Replacement in Athletes.”52
The fastest way to decrease body-core temperature is immersion of the trunk and extremities into a pool or tub filled with cold water (between 1°C [35°F] and 15°C [59°F]).39,88,91,97 Conditions that have been associated with immersion therapy include shivering and peripheral vasoconstriction; however, the potential for these should not deter the medical staff from using immersion therapy for rapid cooling. Shivering can be prevented if the athlete is removed from the water once rectal temperature reaches 38.3°C to 38.9°C (101°F to 102°F). Peripheral vasoconstriction may occur, but the powerful cooling potential of immersion outweighs any potential concerns. Cardiogenic shock has also been a proposed consequence of immersion therapy, but this connection has not been proven in cooling heat-stroke patients.39 Cold-water immersion therapy was associated with a zero percent fatality rate in 252 cases of exertional heat stroke in the military.89 Other forms of cooling (water spray; ice packs covering the body; ice packs on axillae, groin, and neck; or blowing air) decrease body-core temperature at a slower rate compared with cold-water immersion.97 If immersion cooling is not being used, cooling with ice bags should be directed to as much of the body as possible, especially the major vessels in the armpit, groin, and neck regions (and likely the hands and feet), and cold towels may be applied to the head and trunk because these areas have been demonstrated on thermography173,189 to have the most rapid heat loss.
Most research related to heat illness has been performed on normal, healthy adults. Child athletes, older athletes, and athletes with spinal-cord injuries have been studied less frequently. The following are suggestions for special populations or those with special conditions.
Exercise in hot environments and heat tolerance are affected by many physiologic factors in children. These include decreased sweat gland activity,190 higher skin temperatures,191–193 decreased cardiac output (increased heart rate and lower stroke volume) due to increased peripheral circulation,194 decreased exercise economy,195 decreased ability to acclimatize to heat (slower and takes longer),192 smaller body size (issues related to body surface-to-mass ratio), maturational differences,190 and predisposing conditions (obesity, hypohydration, childhood illnesses, and other disease states).190,192,196
As sport participation for athletes with spinal-cord injuries increases from beginner to elite levels, understanding the disability,209,210 training methods, and causes of heat injury will help make competition safer.211 For example, the abilities to regulate heart rate, circulate the blood volume, produce sweat, and transfer heat to the surface vary with the level and severity of the spinal-cord lesion.208,212–218
After an episode of heat stroke, the athlete may experience impaired thermoregulation, persistent CNS dysfunction,221,222 hepatic insufficiency, and renal insufficiency.39,223 For persons with exertional heat stroke and associated multisystem tissue damage, the rate of recovery is highly individualized, ranging up to more than 1 year.8,86,221 In one study, 9 of 10 patients exhibited normal heat-acclimatization responses, thermoregulation, whole-body sodium and potassium balance, sweat-gland function, and blood values about 2 months after the heat stroke.8 Transient or persistent heat intolerance was found in a small percentage of patients.83 For some athletes, a history of exertional heat stroke increases the chance of experiencing subsequent episodes.39
An athlete who experiences heat stroke may have compromised heat tolerance and heat acclimatization after physician clearance.35,224,225 Decreased heat tolerance may affect 15% to 20% of persons after a heat stroke-related collapse,226,227 and in a few individuals, decreased heat tolerance has persisted up to 5 years.35,224,228 Additional heat stress may reduce the athlete's ability to train and compete due to impaired cardiovascular and thermoregulatory responses.115,228–230
After recovery from an episode of heat stroke or hyponatremia, an athlete's physical activity should be restricted8,86 and the gradual return to sport individualized by his or her physician. The athlete should be monitored on a daily basis by the ATC during exercise.86 During the return-to-exercise phase, an athlete may experience some detraining and deconditioning not directly related to the heat exposure.8,86 Evaluate the athlete over time to determine whether there has been a complete recovery of exercise and heat tolerance.8,86
Athletic trainers and other allied health providers must be able to differentiate exercise-associated muscle (heat) cramps, heat syncope, exercise (heat) exhaustion, exertional heat stroke, and exertional hyponatremia in athletes.
This position statement outlines the NATA's current recommendations to reduce the incidence, improve the recognition, and optimize treatment of heat illness in athletes. Education and increased awareness will help to reduce both the frequency and the severity of heat illness in athletes.
This pronouncement was reviewed for the NATA by the Pronouncements Committee, Edward R. Eichner, MD, FACSM, and William O. Roberts, MD, MS, FACSM. T. Kyle Eubanks, MA, ATC, and Paul C. Miller, PhD, provided assistance in the preparation of the manuscript.