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Exertional Heat Illness during Training and Competition

2007; Lippincott Williams & Wilkins; Volume: 39; Issue: 3 Linguagem: Inglês

10.1249/mss.0b013e31802fa199

1530-0315

Lawrence E. Armstrong, Douglas J. Casa, Mindy Millard‐Stafford, Daniel S. Moran, Scott W. Pyne, William O. Roberts,

Climate Change and Health Impacts

SUMMARY Exertional heat illness can affect athletes during high-intensity or long-duration exercise and result in withdrawal from activity or collapse during or soon after activity. These maladies include exercise associated muscle cramping, heat exhaustion, or exertional heatstroke. While certain individuals are more prone to collapse from exhaustion in the heat (i.e., not acclimatized, using certain medications, dehydrated, or recently ill), exertional heatstroke (EHS) can affect seemingly healthy athletes even when the environment is relatively cool. EHS is defined as a rectal temperature greater than 40°C accompanied by symptoms or signs of organ system failure, most frequently central nervous system dysfunction. Early recognition and rapid cooling can reduce both the morbidity and mortality associated with EHS. The clinical changes associated with EHS can be subtle and easy to miss if coaches, medical personnel, and athletes do not maintain a high level of awareness and monitor at-risk athletes closely. Fatigue and exhaustion during exercise occur more rapidly as heat stress increases and are the most common causes of withdrawal from activity in hot conditions. When athletes collapse from exhaustion in hot conditions, the term heat exhaustion is often applied. In some cases, rectal temperature is the only discernable difference between severe heat exhaustion and EHS in on-site evaluations. Heat exhaustion will generally resolve with symptomatic care and oral fluid support. Exercise associated muscle cramping can occur with exhaustive work in any temperature range, but appears to be more prevalent in hot and humid conditions. Muscle cramping usually responds to rest and replacement of fluid and salt (sodium). Prevention strategies are essential to reducing the incidence of EHS, heat exhaustion, and exercise associated muscle cramping. INTRODUCTION This document replaces, in part, the 1996 Position Stand titled "Heat and Cold Illnesses during Distance Running" (9) and considers selected heat related medical conditions (EHS, heat exhaustion, and exercise associated muscle cramping) that may affect active people in warm or hot environments. These recommendations are intended to reduce the morbidity and mortality of exertional heat-related illness during physical activity, but individual physiologic responses to exercise and daily health status are variable, so compliance with these recommendations will not guarantee protection. Heat illness occurs world wide with prolonged intense activity in almost every venue (e.g., cycling, running races, American football, soccer). EHS (1,27,62,64,65,109,132,154,160,164) and heat exhaustion (54,71,149,150) occur most frequently in hot-humid conditions, but can occur in cool conditions, during intense or prolonged exercise (133). Heat exhaustion and exercise related muscle cramps do not typically involve excessive hyperthermia, but rather are a result of fatigue, body water and/or electrolyte depletion, and/or central regulatory changes that fail in the face of exhaustion. This document will address recognition, treatment, and incidence reduction for heat exhaustion, EHS, and exercise associated muscle cramping, but does not include anesthesia-induced malignant hyperthermia, sunburn, anhidrotic heat exhaustion, or sweat gland disorders that are classified in other disease categories, because these disorders may or may not involve exercise or be solely related to heat exposure. Hyponatremia also occurs more frequently during prolonged activity in hot conditions, but is usually associated with excessive fluid intake and is addressed in the ACSM Exercise and Fluid Replacement Position Stand. Evidence statements in this document are based on the strength of scientific evidence with regard to clinical outcomes. Because research ethics preclude the use of human subjects in the study of EHS and other exertional heat illnesses, this document employs the following criteria: A, recommendation based on consistent and good-quality patient- or subject-oriented evidence; B, recommendation based on inconsistent or limited-quality patient- or subject-oriented evidence; C, recommendation based on consensus, usual practice, opinion, disease-oriented evidence, or a case series for studies of diagnosis, treatment, prevention, or screening. General Background: Exhaustion, Hyperthermia, and Dehydration Exhaustion is a physiologic response to work defined as the inability to continue exercise and occurs with heavy exertion in all temperature ranges. As ambient temperature increases beyond 20°C (68°F) and heat stress rises, the time to exhaustion decreases (58). From a clinical perspective it is difficult to distinguish athletes with exhaustion in cool conditions from those who collapse in hot conditions. Exercise that must be stopped due to exhaustion is likely triggered by some combination of hyperthermia-induced reduction of peripheral muscle activation due to decreased central activation (brain fatigue) (110,118), hydration level, peripheral effect of hyperthermia on muscle fatigue, depletion of energy stores, electrolyte imbalance, and/or other factors. Some combination of central, spinal cord, and peripheral responses to hyperthermia factor into the etiology of withdrawal or collapse from exhaustion during activity; the exact mechanisms have yet to be explained (90,114-116,171). The exercise-related exhaustion that occurs in hot conditions may be an extension of this phenomenon, but it is more pronounced, because depletion of energy stores occurs faster in hotter conditions, especially when athletes are not acclimatized to exercise in the heat (71). When physiologic exhaustion results in collapse, the clinical syndrome is often referred to as heat exhaustion. In both hot and cool environments, postexercise collapse also may be due to postural hypotension rather than heat exhaustion and postural changes usually resolve with leg elevation and rest in less than 30 min. There are several variables that affect exhaustion in athletes including duration and intensity of exercise, environmental conditions, acclimatization to exercise-heat stress, innate work capacity (V˙O2max), physical conditioning, hydration status, and personal factors like medications, supplements, sleep, and recent illness. In human studies of exercise time to exhaustion at a fixed exercise load, both individuals and groups show a decrease in exercise capacity (time to exhaustion) and an increase in perceived exertion as environmental temperature and/or relative humidity increase and/or as total body water decreases. The combined effects of heat stress and dehydration reduce exercise capacity and performance to a greater degree than either alone. Compared to more moderate conditions, an athlete in hot conditions must either slow the pace to avoid collapse or maintain the pace and risk collapse before the task is completed. Evidence statement. Dehydration reduces endurance exercise performance, decreases time to exhaustion, increases heat storage (11,12,16,41,57,141). Evidence category A. Exertional hyperthermia, defined as a core body temperature above 40°C (104°F) (71,85,86,149,150), occurs during athletic or recreational activity and is influenced by exercise intensity, environmental conditions, clothing, equipment, and individual factors. Hyperthermia occurs during exercise when muscle-generated heat accumulates faster than heat dissipates via increased sweating and skin blood flow (3). Heat production during intense exercise is 15-20 times greater than at rest, and can raise core body temperature by 1°C (1.8°F) every 5 min if no heat is removed from the body (105). Prolonged hyperthermia may lead to EHS, a life-threatening condition with a high mortality rate if not promptly recognized and treated with body cooling. The removal of body heat is controlled by central nervous system (CNS) centers in the hypothalamus and spinal cord, and peripheral centers in the skin and organs. Heat flow to maintain a functional core temperature requires a temperature gradient from the body core to the body shell. If the skin temperature remains constant, the gradient increases as the core temperature increases during exercise, augmenting heat removal. If the shell or skin temperature also rises during exercise, as a result of either the environment or internal heat production, the core to skin gradient may be lost (i.e., reducing heat dissipation) and the core temperature increases. Wide variations of heat tolerance exist among athletes. The extent to which elevated body temperature below 40°C diminishes exercise performance and contributes to heat exhaustion (110) is unknown, but there is considerable attrition from exercise when rectal temperatures reach 39-40°C (144). In controlled laboratory studies, precooling the body will extend the time to exhaustion and preheating will shorten the time to exhaustion, but in both circumstances athletes tend to terminate exercise due to fatigue at a rectal temperature of about 40°C (104°F) (61). In recent years, the importance of hyperthermia in fatigue and collapse has been investigated. These studies have shown that the brain temperature is always higher than core temperature and heat removal is decreased in the hyperthermic brain compared to control (119). Also, as brain temperature increases from 37 to 40°C during exercise, cerebral blood flow and maximal voluntary muscular force output decrease with concurrent changes in brain wave activity and perceived exertion (110,118). Brain hyperthermia may explain why some exercising individuals collapse with exhaustion, while others are able to override central nervous system controls and push themselves to continue exercising strenuously and develop life-threatening EHS. It is not unusual for some athletes to experience prolonged hyperthermia without noticeable medical impairment, especially during competition. Elevated rectal temperatures up to 41.9°C (107.4°F) have been noted in soccer players, American football lineman, road runners, and marathoners who show no symptoms or signs of heat related physical changes (21,42,46,98,125,129,130,132,161,165,176). This is significant because some athletes tolerate rectal temperatures well above the widely accepted threshold for EHS of >40°C without obvious clinical sequelae (71,85,86,104,149,150). Dehydration occurs during prolonged exercise, more rapidly in hot environments when participants lose considerably more sweat than can be replaced by fluid intake (3,72,126). When fluid deficits exceed 3-5% of body weight, sweat production and skin blood flow begin to decline (19) reducing heat dissipation. Water deficits of 6-10% of body weight occur in hot weather, with or without clinically significant losses of sodium (Na+) and chloride (Cl−) (25,45,71,100,102,155,173) and reduce exercise tolerance by decreasing cardiac output, sweat production, and skin and muscle blood flow (12,41,57,71,101,141,142). Dehydration may be either a direct (i.e., heat exhaustion, exercise associated muscle cramps) or indirect (i.e., heatstroke) factor in heat illness (10). Excessive sweating also results in salt loss, which has been implicated in exercise associated muscle cramps and in salt loss hyponatremia during long-duration (>8 h) endurance events in the heat. In one study illustrating the cumulative affects of heat stress, a male soldier (32 yr, 180 cm, 110.47 kg, 41.4 mL·kg−1·min−1) participating in monitored, multiday, high-intensity exercise regimen at 41.2°C (106.0°F), 39% RH was asymptomatic with a postexercise rectal temperature of 38.3-38.9°C on days 3-7 (16). From the morning of day 5 to day 8, he lost 5.4 kg of body weight (4.8%) and had an increase of baseline heart rate, skin temperature and rectal temperature during days 6 and 7. On day 8, he developed heat exhaustion with unusual fatigue, muscular weakness, abdominal cramps, and vomiting with a rectal temperature of 39.6°C (103.3°F). His blood endorphin and cortisol levels were 6 and 2 times greater, respectively, than the other study subjects on day 8, indicating severe exercise-heat intolerance. Thirteen other males who maintained body weight near their prestudy baseline completed this protocol without incident. Because day-to-day dehydration affects heat tolerance, physical signs and hydration status should be monitored to reduce the incidence of heat exhaustion in hot environments. When humans exercise near maximal levels, splanchnic and skin blood flow decrease as skeletal muscle blood flow increases to provide plasma glucose, remove heat, and remove metabolic products from working muscles (70). As the central controls for blood flow distribution fatigue due to a core temperature increase, the loss of compensatory splanchnic and skin vasoconstriction results in reduction of the total vascular resistance and worsens cardiac insufficiency (71,84). The loss of splanchnic vasoconstriction during exhaustion has been reproduced in a laboratory rat model and supports the assertion that loss of splanchnic vasoconstriction plays a role in heat exhaustion in athletes (70,73,84). This mechanism partially explains why exertional collapse is less likely to occur in cool environments, where cool, vasoconstricted skin helps maintain both cardiac filling and mean arterial pressure, and prolongs the time to exhaustion. How EHS and heat exhaustion evolve, and in what sequence, are not completely understood (106). Some athletes tolerate hot conditions, dehydration, and hyperthermia well and are seemingly unaffected, while others discontinue activity in relatively less stressful conditions. The path that leads to EHS has been assumed to pass through heat exhaustion, however anecdotal and case study data seem to refute that notion as EHS can occur in relatively fresh athletes who develop symptomatic hyperthermia in 30-60 min of road racing in hot, humid conditions with no real signs of dehydration or heat exhaustion. If these athletes have heat exhaustion, then the duration and transition must be very short. Heat exhaustion should be protective for athletes in that, once exercise is stopped, the risk of developing exertional heat stroke is reduced because exercise-induced metabolic heat production decreases and heat dissipation to the environment increases. A program of prudent exercise in the heat along with acclimatization, improved cardiorespiratory physical fitness, and reasonable fluid replacement during exercise reduce the risk and incidence of both problems. Evidence statement. Exertional heatstroke (EHS) is defined in the field by rectal temperature >40°C at collapse and by central nervous system changes. Evidence category B. EXERTIONAL HEAT ILLNESSES Exertional Heatstroke Etiology. Exertional heatstroke (EHS) is defined by hyperthermia (core body temperature >40°C) associated with central nervous system disturbances and multiple organ system failure. When the metabolic heat produced by muscle during activity outpaces body heat transfer to the surroundings, the core temperature rises to levels that disrupt organ function. Almost all EHS patients exhibit sweat-soaked and pale skin at the time of collapse, as opposed to the dry, hot, and flushed skin that is described in the presentation of non-exertion-related (classic) heatstroke (162). Predisposing factors. Although strenuous exercise in a hot-humid environment, lack of heat acclimatization, and poor physical fitness are widely accepted as the primary factors leading to EHS, even highly trained and heat-acclimatized athletes develop EHS while exercising at a high intensity if heat dissipation is inadequate relative to metabolic heat production (18,34,71). The greatest risk for EHS exists when the wet bulb globe temperature (WBGT) exceeds 28°C (82°F) (20,81,156) during high-intensity exercise (>75% V˙O2max) and/or strenuous exercise that lasts longer than 1 h as outlined below in "Monitoring the Environment." EHS also can occur in cool (8-18°C [45-65°F]) to moderate (18-28°C [65-82°F]) environments (14,56,132,133), suggesting that individual variations in susceptibility (14,22,55,56,66) may be due to inadequate physical fitness, incomplete heat acclimatization, or other temporary factors like viral illness or medications (81,133). Evidence statement. Ten to 14 days of exercise training in the heat will improve heat acclimatization and reduce the risk of EHS. Evidence category C. The risk of EHS rises substantially when athletes experience multiple stressors such as a sudden increase in physical training, lengthy initial exposure to heat, vapor barrier protective clothing, sleep deprivation (14), inadequate hydration, and poor nutrition. The cumulative effect of heat exposure on previous days raises the risk of EHS, especially if the ambient temperature remains elevated overnight (14,168). Over-the-counter drugs and nutritional supplements containing ephedrine, synephrine, ma huang and other sympathomimetic compounds may increase heat production (23,121), but require verification as a cause of hyperthermia by controlled laboratory studies or field trials. Appropriate fluid ingestion before and during exercise minimizes dehydration and reduces the rate at which core body temperature rises (46,60). However, hyperthermia may occur in the absence of significant dehydration when a fast pace or high-intensity exercise generates more metabolic heat than the body can remove (18,34,165). Skin disease (i.e., miliaria rubra), sunburn, alcohol use, drug abuse (i.e., ecstasy), antidepressant medications (69), obesity, age >40 yr, genetic predisposition to malignant hyperthermia, and a history of heat illness also have been linked to an increased risk of EHS in athletes (14,55,85,150). Athletes should not exercise in a hot environment if they have a fever, respiratory infection, diarrhea, or vomiting (14,81). A study of 179 heat casualties at a 14-km race over 9 yr showed that 23% reported a recent gastrointestinal or respiratory illness (128). A similar study of 10 military patients with EHS reported that three had a fever and six recalled at least one warning sign of impending illness prior to collapse (14). In American football, EHS usually occurs during the initial 4 d of preseason practice, which for most players takes place during the hottest and most humid time of the summer when athletes are the least fit. This emphasizes the importance of gradually introducing activity to induce acclimatization, carefully monitoring changes in behavior or performance during practices, and selectively modifying exercise (i.e., intensity, duration, rest periods) in high-risk conditions. Three factors may influence the early season EHS risk in American football players: (a) failure of coaches to adjust the intensity of the practice to the current environmental conditions, following the advice of the sports medicine staff; (b) unfit and unacclimatized players practicing intensely in the heat; and (c) vapor barrier equipment introduced before acclimatization. One study of 10 EHS cases (14) reported that eight incidents occurred during group running at a 12.1-13.8 km·h−1 pace in environmental temperatures of ≥25°C (77°F), suggesting that some host factor altered exercise-heat tolerance on the day that EHS occurred. Heat tolerance is often less in individuals who have the lowest maximal aerobic power (i.e., V˙O2max ≤ 40 mL·kg−1·min−1) (14,64,96). To maintain pace when running in a group, these less fit individuals must function at higher exercise intensities to maintain the group's pace and are likely to have higher rectal temperatures at the end of a run compared to individuals with a higher V˙O2max. Air flow and heat dissipation also are reduced for runners in a pack. More clinical and scientific reports of EHS involve males, and some hypotheses have been advanced (14). First, men may simply be in more EHS prone situations (i.e., military combat and American football). Second, men may be predisposed because of gender-specific hormonal, physiological, psychological, or morphological (i.e., muscle mass, body surface area-to-mass ratio) differences. Women, however, are not immune to the disorder, and the number of women who experience EHS may rise with the increased participation of women in strenuous sports. Evidence statement. The following conditions increase the risk of EHS: obesity, low physical fitness level, lack of heat acclimatization, dehydration, a previous history of EHS, sleep deprivation, sweat gland dysfunction, sunburn, viral illness, diarrhea, or certain medications. Evidence category B. Physical training, cardiorespiratory fitness, and heat acclimatization reduce the risk of EHS. Evidence category C. Pathophysiology. The underlying pathophysiology of EHS occurs when internal organ tissue temperatures rise above critical levels, cell membranes are damaged, and cell energy systems are disrupted, giving rise to a characteristic clinical syndrome (56,149). As a cell is heated beyond its thermal threshold (i.e., about 40°C), a cascade of events occurs that disrupts cell volume, metabolism, acid-base balance, and membrane permeability leading initially to cell and organ dysfunction and finally to cell death and organ failure (71,91,175). This complex cascade of events explains the variable onset of brain, cardiac, renal, gastrointestinal, hematologic, and muscle dysfunction among EHS patients. The extent of multisystem tissue morbidity and the mortality rate are directly related to the area in degree-minutes under the body core temperature vs. time graph and the length of time required to cool central organs to <40°C (14,20,47,48). Tissue thresholds and the duration of temperature elevation, rather than the peak core body temperature, determine the degree of injury (72). When cooling is rapidly initiated and both the body temperature and cognitive function return to the normal range within an hour of onset of symptoms, most EHS patients recover fully (47,48). EHS victims who are recognized and cooled immediately theoretically tolerate about 60°C·min (120°F·min; area under the cooling curve) above 40.5°C without lasting sequelae (see Fig. 1). Conversely, athletes with EHS who go unrecognized or are not cooled quickly, and have more than 60°C·min of temperature elevation above 40.5°C, tend to have increased morbidity and mortality. Outcomes of 20 "light" and 16 "severe" cases of EHS during military training (150) showed that coma was relatively brief in light cases when hyperthermia was limited to 145. The prognosis based on area under the cooling curve for the late intervention is poor. Cooling can be delayed when heat stoke is not recognized early in the evaluation or if the athlete is transported before cooling is initiated. The arrow marks the start of cooling at 10 min for early intervention and 50 min for late intervention.Hyperthermia of heart muscle tissue directly suppresses cardiac function, but the dysfunction is reversible with body cooling, as demonstrated by echocardiography (133). Cardiac tissue hyperthermia reduces cardiac output, oxygen delivery to tissues, and the vascular transport of heat from deep tissues to the skin. Cardiac insufficiency or failure associated with hyperthermia accelerates the elevation of core temperature and increases tissue hypoxia, metabolic acidosis and organ dysfunction. The concurrent heating of the brain begins a cascade of cerebral and hypothalamic failure that also accelerates cell death by disrupting the regulation of blood pressure and blood flow. Interestingly, direct hyperthermia-induced brain dysfunction may lead to collapse that can be "lifesaving," if stopping exercise allows the body to cool or the collapse triggers medical evaluation that leads to cooling therapy. Exercise stimulates increased blood flow to working muscle. During a maximal effort, for example, approximately 80-85% of maximal cardiac output is distributed to active muscle tissue (139). As core temperature increases during exercise, the thermoregulatory response increases peripheral vasodilatation and blood flow to the cutaneous vascular beds to augment body cooling. The brain also regulates blood pressure during exercise by decreasing blood flow to splanchnic organs. This decreased intestinal blood flow limits vascular heat exchange in the gut and promotes bowel tissue hyperthermia and ischemia. Gut cell membrane breakdown allows lipopolysaccharide fragments from intestinal gram-negative bacteria to leak into the systemic circulation, increasing the risk of endotoxic shock. Dehydration can accentuate these effects on the GI tract and speed the process. Rhabdomyolysis, the breakdown of muscle fibers, occurs in EHS as muscle tissue exceeds the critical temperature threshold of cell membranes (i.e., about 40°C). Although eccentric and concentric muscle overuse is a common cause of rhabdomyolysis, muscle membrane permeability increases due to hyperthermia and occurs earlier in exercise when the muscle tissues are hyperthermic (71,74). As heat decomposes cell membranes, myoglobin is released and may cause renal tubular toxicity and obstruction if renal blood flow is inadequate. Intracellular potassium is also released into the extracellular space, increasing serum levels and potentially inducing cardiac arrhythmias. Heating renal tissue above its critical threshold can directly suppress renal function and induce acute renal failure that is worsened by sustained hypotension, crystallization of myoglobin, disseminated intravascular coagulation, and the metabolic acidosis associated with exercise (31,70,153). Incidence. The incidence of EHS varies from event to event and increases with rising ambient temperature and relative humidity. Limited data exist regarding the incidence of EHS during athletic activities. While fatal outcomes are often reported in the press, there is limited reporting of non fatal EHS unless it involves high profile athletes. In most cases, fatal EHS is a rare event that strikes "at random" in sports like American football, especially during the initial four days of preseason conditioning, where the incidence of fatal EHS was about 1 in 350,000 participants from 1995 through 2002 (131). Fatal EHS in American football players often occurs when air temperature is 26-30°C (78-86°F) and relative humidity is 50-80% (87). EHS is observed more often during road racing and other activities that involve continuous, high-intensity exercise. The Twin Cities Marathon, which is run in cool conditions, averages <1 EHS per 10,000 finishers (136); this incidence rises as the WBGT rises. In contrast, one popular 11.5-km road race, staged in hot and humid summer conditions (WBGT 21-27°C), averages 10-20 EHS cases per 10,000 entrants (18,34). The same race course, run in cool conditions, had no cases of EHS (A Crago, M.D., personal communication). Such a high incidence burdens the medical care system and suggests that the summer event is not scheduled at the safest time for the runners. Recognition. Immediate recognition of EHS cases is paramount to survival (68). The appearance of signs and symptoms depends on the degree and duration of hyperthermia (14,48,71,81,150). The symptoms and signs are often nonspecific and include disorientation, confusion, dizziness, irrational or unusual behavior, inappropriate comments, irritability, headache, inability to walk, loss of balance and muscle function resulting in collapse, profound fatigue, hyperventilation, vomiting, diarrhea, delirium, seizures, or coma. Thus, any change of personality or performance should trigger an assessment for EHS, especially in hot-humid conditions. In collision sports like American football, EHS has been initially mistaken for concussion; among nonathletes, EHS also has been initially misdiagnosed as psychosis. A body core temperature estimate is vital to establishing an EHS diagnosis, and rectal temperature should be measured in any athlete who collapses or exhibits signs or symptoms consistent with EHS. Ear (aural canal or tympanic membrane), oral, skin over the temporal artery, and axillary temperature measurements should not be used to diagnose EHS because they are spuriously lowered by the temperature of air, skin, and liquids that contact the skin (18,134,135). Oral temperature measurements also are affected by hyperventilation, swallowing, ingestion of cold liquids, and face fanning (33,151). At the time of collapse, systolic blood pressure <100 mm Hg, tachycardia, hyperventilation, and a shocklike appearance (i.e., sweaty, cool skin) are common. Evidence statement. Ear (i.e., aural), oral, skin, temporal, and axillary temperature measurements should not be used to diagnose or distinguish EHS from exertional heat exhaustion. Evidence category B. Early symptoms of EHS include clumsiness, stumbling, headache, nausea, dizziness, apathy, confusion, and impairment of consciousness (71,85,149,161). Evidence category B. Treatment. EHS is a life-threatening medical emergency that requires immediate whole body cooling for a satisfactory outcome (14,44,48,72,82,85,120,132,149). Cooling should be initiated and, if there are no other life-threatening complications, completed on-site prior to evacuation to the hospita