Despite the increased attention football has received over growing concerns for the athlete’s health and safety, American football remains a vastly popular sport with participation numbers well over 3 million at the youth level, 1.1 million in high school, and more than 100,000 at higher levels in 2012 (29,3029,30). One of the largest risks inherent in playing football is the timing of the start of the season. The incidence of exertional heat illness (EHI) is correlated with the rise in ambient air temperature and humidity (4,174,17). These hot and humid conditions create significant risk to athletes, and despite improved understanding of the pathophysiology of heat illness, and its preventable nature, there continues to be an alarming trend of heat stroke fatalities in football players (22). While heat stroke is classified into two different types (classical and exertional), the primary focus of this review will be exertional type heat stroke, particularly as it relates to American football and its risk factors, management, and, most importantly, prevention (Table 1).
Since 1995, there have been at least 54 football player fatalities from heat stroke (42 in high school, nine in college, two in professional, and one in sandlot football). The incidence of morbidity and mortality has increased during this period, with the majority of deaths (61%) occurring over the last decade. (22). Cases of nonfatal heat illness are more difficult to estimate. There are multiple researchers who have utilized online injury surveillance data to calculate an incidence rate (IR) of nonfatal heat illness for high school football. Huffman et al. (18) noted an IR of five per 100,000 athlete-exposures (AE) in football over the 2005 to 2006 and 2006 to 2007 academic years (11 times higher than all other sports combined). When examining time lost (≥1 d of time lost from athletic activity) as a result of heat illness, Yard et al. (44) found similar rates for high school football (4.5 per 100,000 AE), which was 10 times higher than the average for the other eight sports examined. Kerr et al. (19) later expanded upon this data including 11 more sports and found 1.20 cases of EHI per 100,000 AE in all sports and 4.42 per 100,000 AE in high school football alone (more than 11 times greater than all other sports combined).
Pathophysiology and Thermoregulation
A variety of disorders fall within the category of heat illness and range from more mild to severe disease. Symptoms can include mild discomfort, cramps, edema, rash, and general physiological strain to, collapse, and possible mental status changes, multiorgan dysfunction, and death. Heat stroke is defined as marked hyperthermia with a core body temperature >40°C (104°F) and central nervous system (CNS) dysfunction. The marked hyperthermia may cause a systemic inflammatory response, which can impact the CNS and other vital organs, causing multiorgan dysfunction. It can be a result of hyperthermia primarily from environmental heat exposure (classical) and/or from an internal metabolic source of heat derived from strenuous exercise (exertional) (2,15,332,15,332,15,33).
The human body is designed to maintain homeostasis within a predefined temperature range. Thermoregulation is the process by which the body maintains this homeostasis while being exposed to differing internal and external stressors. Both classic and exertional heat stroke have the same essential component; somewhere along the thermoregulatory pathway, the dissipation of heat is either inhibited or overwhelmed. As heat enters the system, whether generated metabolically or absorbed from an external source, the body increases cardiac output and shunts blood away from the core to the skin. The skin is where critical thermoregulation occurs through conduction, convection, radiation, and, most importantly, evaporation which can dissipate up to 600 kcal of heat energy per hour (2,132,13). All of these mechanisms are important in heat loss and affected by both intrinsic (fitness level, hydration status, acclimatization, obesity, medications, and genetics) and extrinsic (environmental conditions, clothing/equipment worn, and activity level of athlete) factors (17,3317,33).
The pathophysiology of heat illness in football players can also manifest as exercise-induced hyperthermia. The authors have noted that temperature ranges can be very elevated during camp and can range from 99° to 103° but may vary depending on environmental and player-specific circumstances. Changes in temperature can be affected by many risk factors, but players are typically responsive to cooling modalities such as ice towels, hydration, removal of helmets, use of fans and shaded areas, and rest. Failure of these methods to improve the patients’ symptoms, continued rise of temperature, or changes in mental status should necessitate cold immersion therapy, administration of cold IV fluids, immediate medical evaluation, and removal of the player from practice and removal of pads, helmet, and uniform (9).
Using ingestible thermistors, the authors have monitored football players for over a decade during summer training. This has enabled minimally invasive remote monitoring of a large number of players and has given the authors a great deal of clinical experience in observing the normal reactions of football players to extreme heat, the rigors of training camp, and exercise-induced hyperthermia. While ingestible thermistors can provide a good deal of insight into core body temperature, their cost, a requirement to take them up to 2 h before practice to reach the small gut, and concerns regarding magnetic resonance imaging, which could be needed if an injury occurs, and potential reactions to the thermistor limit their general use.
The greatest risk for EHS exists when the wet bulb globe temperature (WBGT) exceeds 28°C (82°F) during high-intensity exercise and/or strenuous exercise that lasts longer than 1 h as outlined (Table 2). EHS also can occur in cool (8°C to 18°C (45°F to 65°F)) to moderate (18°C to 28°C (65°F to 82°F)) environments. The authors have noted core body temperatures as >102°F in high school, collegiate, and professional football players even with ambient temperatures in the 70°F to 72°F range, which suggests that individual variations in susceptibility may be due to differing levels of fitness, heat acclimatization, or other temporary factors like viral illness or medications (15,1615,16).
Preparticipation hydration status has been shown to have effects on both core temperature regulation and performance, effects that are exaggerated when activity is performed in the heat (31,3731,37). Sweat rates in athletes have frequently been observed to exceed 2.0 L·h−1 (1,13,141,13,141,13,14). Godek et al. (13,1413,14) has examined the hydration status of football players in several studies. Body weight (BW), urine samples, and blood samples have been assessed, which have shown severe dehydration and sodium depletion during the first week of two-a-day practices. Football players were unable to maintain BW over the entire 8-d period and were not successful in defending plasma volume during the first few days. The largest contributor to dehydration, sweating, consistently exceeded 30 g·min−1 (1.8 kg·h−1) in American football players, regardless of environmental conditions or equipment worn. This resulted in mean daily sweat losses of more than 9 L (13,1413,14). When fluid deficits exceed 3% to 5% of BW, sweat production and skin blood flow begin to decline, reducing heat dissipation (2). Water deficits of 6% to 10% of BW may occur in hot weather, with or without clinically significant losses of sodium (2). Adequate replenishment of both fluids and electrolytes was challenging even with an unlimited supply of a common fluid replacement drink with added electrolytes. Adequate fluid replenishment is even more challenging in high school and college football where supplies and staffing are more limited, and education on appropriate hydration strategies is more challenging (10,11,3110,11,3110,11,31).
An additional consideration must be given to the possibility of hyponatremia, which can result from excessive hydration in this population. This can lead to significant medical comorbidities and must be distinguished from heat illness in the athlete at risk. Exertional hyponatremia is defined by serum sodium levels 130 mmol·L−1 and may present with a clinical appearance similar to heat stroke, with mental status changes and an altered level of consciousness (17). Exertional hyponatremia is distinguished from heat illness by a normal core body temperature and may present similarly to heat illness with lethargy (nausea, malaise, vomiting), and its symptomatology may lead athletes to paradoxically hydrate even more (13). Risk factors for hyponatremia somewhat differ from those for heat stroke and may include football players who have a high availability of fluids. At least one death in football has been attributed to exertional hyponatremia, and this must be in the differential diagnosis of heat illness. Severe hyponatremia (serum sodium, 120 mmol·L−1) can precipitate seizures, coma, and death. Treatment of the condition is beyond the scope of the current article but may begin with oral sodium solutions if mild and progresses to intravenous hypertonic saline for severe cases and inpatient management (17).
Run times have been closely associated with V˙O2max and thus are a measure of cardiovascular fitness (26). One study examined 1.5-mile run times in Marine Corps recruits and noted an independent increase in risk of EHI in those whose run times were >12 min (12).
While it is agreed that simply living or working in hotter environments helps acclimatize individuals and offer some protection towards heat stroke, there is research to show that intense physical training in cooler environments can improve exercise heat tolerance while having the added benefit of conferring less risk of heat illness during training itself (36). The greatest improvements in heat tolerance seem to come from intensive interval or continuous training at an intensity greater than 50% of V˙O2max for 8 to 12 wk. It has been recommended that an athlete’s V˙O2max be increased by 15% to 20% to have the greatest effect. Utilization of proper physical training appears to produce about 50% of the total adjustment resulting from heat acclimatization, and those with increased physical fitness have greater retention of this acclimatization (36).
Given the role physical fitness plays in the risk for heat-related illness, one could expect the more obese younger football players (who have not had the physical training) to be at greater risk of heat illness (15,1615,16).
While increased body mass index (BMI) as an index for obesity has generally been accepted as an independent risk factor, it appears to be an effect that acts apart from cardiovascular fitness. Higher heat production during exercise (increased energy demands) and reduced ability to dissipate heat due to lower ratio of surface area to body mass have been suggested as additional factors to explain increased susceptibility to EHI (5). Gardner et al. (12) noted that in Marine recruits, a BMI >22 kg·m−2 and longer run times were both independent risk factors; however, when combined, the risk for EHI was even greater. Only one-fifth (18%) of the male recruits met both of these criteria, but they accounted for nearly half (47%) of the EHI during the 12-wk basic training course (12).
Gardner et al. (12) also summarized the results of two other studies involving Army recruits. Recruits with the highest attack rates of EHI had BMI >30 kg·m−2 (about 2% of the recruit population) (39). Fatal heat stroke was also 10 times more likely to occur in those who were greater than 40 lb overweight compared with those who were greater than 10 lb underweight (38). While increased size can provide a competitive advantage in football, these data and the fact that nearly all past heat stroke fatalities in football have been in linemen suggest increased risk for athletes at these positions.
Heat acclimatization involves multiple adaptations within the body system that can be protective when performing occupational or athletic activities in the heat. It can be obtained simply by living or working in a warmer climate throughout life or by successively increasing the amount of work performed in a hot environment. There have been multiple studies published emphasizing greater risk of heat illness in those individuals not previously exposed to warmer climates (15,1615,16).
Vandentorren et al. (41) examined excess death rates in French cities located in both northern and southern climates of France following a major heat wave in August 2003. They noted that cities located in the more northern climates of France had higher excess death rates than those cities in the more southern (warmer) climates despite similar peak temperatures. The heat wave represented a larger aberration of the normal temperature in the more northern cities (41).
A similar association was found by Carter et al. (8) in a 22-year epidemiological study of exertional heat injury in U.S. Army soldiers. Greater rates of hospitalizations and heat strokes occurred among recruits from northern states than those from southern states (incidence density ratio, 1.69 [95% confidence interval, 1.42–1.90]). Also, 44% of the heat illness cases occurred in recruits who had 1 year or less of military service (6). The authors feel that this underscores the importance of acclimatization in freshman/rookie football players who are moving to a more intense training environment and perhaps relocating to a warmer climate.
A period of 7 to 10 d is necessary to adequately prepare for intense physical activity, given environmental conditions and equipment considerations. Tripp et al. (40) noted in a population of high school football players that the highest rate of EHI was during August. Practices in August that exceeded the recommended 3 h were associated with a greater risk of heat illnesses. Athletes that practice for longer than 3 h during August were 9.84 times more likely to experience heat illness than those who practice for <3 h. In their study, acclimatization precautions were employed but compliance regarding practice length was not consistent. Despite guidelines from the state that no practice should exceed 3 h during the acclimatization period, 13.7% of practices lasted greater than 3 h and 6.5% were longer than 4 h. This noncompliance is consistent with another recent study suggesting that as few as 39.7% of high school football programs studied complied with single practices lasting less than 3 h during the acclimatization period (20). They further noted that 73.7% (42/57) of the EHI events were during a period that was regarded as high or extreme risk by the American College of Sports Medicine (ACSM) guidelines (32,37,4432,37,4432,37,44). In addition, of the 28 practices in the study that lasted longer than the recommended 3 h, 27 (96.4%) of them took place in high- or extreme-risk conditions (40).
Multiple authors have sought to understand the physiology behind heat acclimatization (2,18,212,18,212,18,21). Knochel (21) described several physiological adaptations as a result of training that can be protective against heat illness; some of these include increased plasma volume and cardiac output, activation of renin-angiotensin-aldosterone system, salt conservation by kidneys and sweat glands, and a higher threshold before exertional rhabdomyolysis occurs. Presently, the majority of National Football League (NFL) teams do utilize urine-specific gravity testing to assess hydration during training camp and 10 teams utilize ingestible thermistors to assess players’ body temperatures during camp (18).
Others (Genetics, Medications, and Sleep)
Genetics appears to also play a role in heat acclimatization. One area of genetic research has focused around genes that encode for heat shock proteins (HSP). Research performed on rats by Yang et al. (43) has suggested that previous exposure to heat upregulates the expression of HSP-72 in various vital organs and actually attenuates arterial hypotension, cerebral ischemia, and neuronal damage exhibited in heat stroke. Additional genetic risk factors may include athletes who are noted to have sickle cell trait (Table 2). During times of stress with exercise, however, they can be predisposed to sickling of their red blood cells. Several reports of increased risk of sudden death in athletes with sickle cell trait have been reported. Some of these deaths have been related to exertional heat stroke. Dehydration, extreme heat, and exercise at high altitudes have been shown to be risk factors related to these events (17).
A variety of classes of medications and nutritional supplements have been implicated in contributing to heat illness. Many of these medications may be taken by athletes to improve their performance or to treat common medical conditions. The common mechanism by which these medications contribute to heat illness is either increased heat production or decreasing the ability to dissipate heat, or they may inhibit the body’s natural response to dehydration or heat illness. Stimulant medications (i.e., amphetamines, ephedra, thyroid agonists) may cause increased heat production. Anticholinergic medications (i.e., antihistamine, antidepressant, and antipsychotic medications) may decrease sweat production. Medications that affect the cardiovascular system (i.e., antihypertensive medication, diuretics) may inhibit natural cardioprotective responses to dehydration and heat illness. The team medical staff should be aware of any athletes taking medications or supplements (17). While a full review on the implications of pretraining supplements is outside the scope of this article, medications and drugs, which have been implicated in heat illness, are summarized in Table 2 (17,2517,25). Oh and Henning (35) published a case report of EHS in a highly trained and experienced infantry solider near the end of a 12-mile march. He was reportedly well acclimatized, having successfully completed three similar marches in the previous month and well hydrated (consumed 3 L of water of the 3-h march). Near the end, he collapsed, was disoriented, had a rectal temperature of 41°C, and had multiple laboratory abnormalities consistent with multiorgan dysfunction. In addition to peripheral vasoconstriction, it is postulated that ephedra may have a thermogenic effect by activation of dopamine receptors (35,4535,45).
Sleep deprivation has been shown to have some association with increased risk for heat illness. Given the current understanding of the role endotoxin plays in the pathophysiology of heat stroke, observing the physiological response to endotoxin itself has some utility (23,4323,43). Lapshina and Ekimova (23) were able to clearly demonstrate that sleep-deprived pigeons injected with endotoxin had shorter time to onset of fever, higher brain temperature, increased muscle contractility (producing more metabolic heat), and delayed recovery of normal somatic function compared with those of controls. Other studies assessing the effects of sleep deprivation have shown greater concentrations of proinflammatory markers in the serum and decreased maximum oxygen intake. These factors could lead to an exaggeration of the normal immune response to vigorous exercise (42).
Medications, history, and review of these risk factors for heat illness are important topics to cover prior to the season starting, whether it is organized by team physicians during preseason physical examinations or by individual providers performing sports physical examinations at the high school level.
Football-Specific Risk Factors
Given the overwhelming incidence of heat illness in football compared with that in other sports, it is important to think about “football-specific” risk factors as well. High school football can be a particularly dangerous time when young athletes are asked to perform at higher levels physically, thus experiencing symptoms of more significant fatigue, muscle soreness, and nausea. Some players may be completely new to sports, such as football players trying out for their first team. Adolescents at this age may have significant peer and internal pressure to perform, and cultural components of football may dissuade some from appropriate hydration (15–17,20,32,40,4415–17,20,32,40,4415–17,20,32,40,4415–17,20,32,40,4415–17,20,32,40,4415–17,20,32,40,4415–17,20,32,40,44). Additionally, as discussed, lack of access to cooling modalities and education regarding hydration also may contribute to heat illness (28).
Nearly all cases of heat illness in football occur during the first week of training camp (16,1716,17). There are a multitude of reasons for this, not the least of which is the ambient conditions at this time of year (16,17,4016,17,4016,17,40). In addition, football players (particularly at the younger levels) may arrive in suboptimal physical condition and unprepared to stress themselves in the heat (15–17,3215–17,3215–17,3215–17,32). The availability of trained sideline staff, protective equipment worn, competitive advantage of being overweight, and practice length (such as “two-a-days”) are all risks inherent to football as well.
The football-specific risk for exertional heat stroke does appear to differ among the different levels of football. There are a multitude of possibilities to explain this. While NFL camps no longer hold two-a-day full pad practices, this is still commonplace among many high school and colleges across the nation (40). In addition, NFL athletes are more likely to maintain physical fitness in the off-season whether through personal trainers or through the motivation of needing to perform at such high level in an intensively competitive environment. The resources available for NFL teams also dwarf most high school and colleges comparatively. Numerous trained sideline personnel, cooling devices, increased access to hydration, and overall better preparedness at the NFL level is likely largely responsible for why only two of the last 54 heat stroke fatalities (and none since 2001) have been at the NFL level (22).
Management and Prevention
While the biggest key to management of EHI is prevention, cases will inevitably occur, and if the proper actions are carried out swiftly, fatalities from heat stroke can be prevented. Assessing the different risk levels among the varying athletes can help the medical staff focus their attention on higher risk players.
It is important to remember that the two diagnostic criteria for EHI are marked hyperthermia with a core body temperature >40°C (104°F) and CNS dysfunction. Athletes experiencing EHI may demonstrate performance deficits and cognitive deficits, which are imperative to determine for optimal management. They may slow down, cramp, make more mistakes in their routines, become nauseated, dizzy, or irritable, and may or may not physically collapse. When these things are identified, time is of the utmost importance, as is having certain tools and equipment available. The athlete should be immediately removed from play to a shaded or cool environment. Excess clothing and equipment should be removed, and rectal temperature must be obtained (33). 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. Oral temperature measurements also are affected by hyperventilation, swallowing, ingestion of cold liquids, and face fanning. At the time of collapse, systolic blood pressure <100 mm Hg, tachycardia, hyperventilation, and a shock-like appearance (i.e., sweaty, cool skin) are common. Appropriate management of hemodynamic status is important, as these athletes may require cold IV fluids, and a systemic response may make blood pressure difficult to maintain. Immediate and uninterrupted cooling can be the difference between life and death, and ice water immersion has become the gold standard. Lowering the core body temperature to less than 40°C (104°F) within 30 min should be the primary goal of EHS treatment (7–97–97–9). Immersion ice tubs can be useful, but players must be carefully monitored to avoid injury from being completely submerged. Additionally, rapid vasodilation after immersion can lead to vagal episodes and must be guarded against (27,3327,33). Temperature should be assessed every 5 to 10 min, and once the core temperature has been cooled to 101°F to 102°F, the athlete should be removed from cooling to avoid overcooling (3). If the athlete has persistent core temperature elevations, hypotension, or tachycardia or exhibits signs or symptoms of disrupted mental status, the local emergency medical system should be activated; however, cooling should not be interrupted. Miller et al. (27) evaluated cooling players in full uniform versus cooling with players with uniforms removed. They noted that removing equipment may not be necessary before cold water immersion in athletes with EHS because cooling rates of athletes with hyperthermia wearing full uniforms were well above minimally acceptable cooling rates (i.e., >0.08°C per minute). Additionally, wearing the full uniform after immersion did not result in more overcooling than wearing the control uniform (27). If managed quickly and appropriately, most cases on the spectrum of heat illness that occur in football players will respond to cooling and athletes can return to play when all symptoms have resolved (typically within 24 to 48 h) (34). Cooling and removal of uniforms must take into account other comorbid factors, including the size of the player, and medical issues that may be ongoing in the management of the player with EHI (27). Athletes who do not respond to cooling modalities should be assessed for other risk factors, and workup should include consideration of other diagnoses, and Emergency Medical Services (EMS) should be activated to allow for continued treatment and observation. There are no evidence-based guidelines describing the return to play criterion. Finally, it is important to consider any medical comorbidities and other factors as well as the players’ history before determining when the player is safe to return to play.
Initial assessments at how well high schools across the nation are doing at implementing EHI prevention strategies have demonstrated that greater implementation of effective prevention measures is needed (20,2420,24). In 2009, the National Athletic Trainers’ Association (NATA) published “preseason heat acclimatization guidelines” to reduce the risk of EHI by gradually introducing equipment, exercise duration, and exercise intensity across a 14-d period to help athletes adjust to the environment (8). This was the first comprehensive set of preseason heat acclimatization guidelines with a specific timeline for high school sports programs (Table 4). Kerr et al. (20) assessed how closely these guidelines are being followed by surveying more than 1,100 certified athletic trainers (ATC) nationwide. ATC demonstrated an average overall compliance 10.4/17 NATA-IATF guidelines (standard deviation, 3.2); 29 ATC (2.5%) reported compliance with all 17 guidelines. Guidelines with the lowest compliance were as follows: “single practice days consisted of practice no more than 3 h in length” (39.7%) and “during days 3 to 5 of acclimatization, only helmets and shoulder pads should be worn” (39.0%) (20). Programs in states with mandated guidelines had higher levels of compliance with guidelines and greater prevalence of EHI prevention strategies.
Despite the vast body of research published on EHI and heat stroke and the improved efforts at the NFL level, there is an upward trend in EHI-associated fatalities per year in high school football players. For multiple reasons, football players appear to be at high risk for morbidity and mortality from heat stroke, and continued efforts need to be focused on education, improving access to monitoring and cooling modalities, and mandated guidelines for implementing EHI prevention strategies.
The authors declare no conflicts of interest and do not have any financial disclosures.
1. Armstrong LE, Casa DJ, Millard-Stafford M, et al. American College of Sports Medicine position stand: exertional heat illness during training and competition. Med. Sci. Sports Exerc.
2007; 39: 556–72.
2. Armstrong LE, Costill DL, Fink WJ. Influence of diuretic-induced dehydration on competitive running performance. Med. Sci. Sports Exerc.
1985; 17: 456–61.
3. Armstrong LE, Hubbard RW, Jones BH, Daniels JT. Preparing Alberto Salazar for the heat of the 1984 Olympic marathon. Phys. Sportsmed.
1986; 14: 73–81.
4. Armstrong LE, Maresh CM, Gabaree CV, et al. Thermal and circulatory responses during exercise: effects of hypohydration, dehydration, and water intake. J. Appl. Physiol.
1997; 82: 2028–35.
5. Binkley HM, Beckett J, Casa DJ, Kleiner DM, Plummer PE. National Athletic Trainers’ Association position statement: exertional heat illnesses. J. Athl. Train.
2002; 37: 329–43.
6. Bouchama A, Knochel JP. Heat stroke. N. Engl. J. Med.
2002; 346: 1978–88.
7. Buskirk ER, Lundegren H, Magnusson L. Heat acclimatization patterns in obese and lean individuals. Ann. N. Y. Acad. Sci.
1965; 131: 637–53.
8. Carter R, Cheuvront SN, Williams JO, et al. Epidemiology of hospitalizations and deaths from heat illness in soldiers. Med. Sci. Sports Exerc.
2005; 37: 1338–44.
9. Casa DJ, Stearns RL, Lopez RM, et al. Influence of hydration on physiological function and performance during trail running in the heat. J. Athl. Train.
2010; 45: 147–56.
10. Casa DJ, Csillan D, Inter-Association Task Force for Preseason Secondary School Athletics Participants, et al. Preseason heat-acclimatization guidelines for secondary school athletics. J. Athl. Train.
2009; 44: 332–3.
11. Casa DJ, McDermott BP, Lee EC, et al. Cold water immersion: the gold standard for exertional heatstroke treatment. Exerc. Sport Sci. Rev.
2007; 35: 141–9.
12. Fortney SM, Nadel ER, Wenger CB, Bove JR. Effect of blood volume on sweating rate and body fluids in exercising humans. J. Appl. Physiol. Respir. Environ. Exerc. Physiol.
1981; 51: 1594–600.
13. Fortney SM, Wenger CB, Bove JR, Nadel ER. Effect of hyperosmolality on control of blood flow and sweating. J. Appl. Physiol. Respir. Environ. Exerc. Physiol.
1984; 57: 1688–95.
14. Gardner JW, Kark JA, Karnei K, et al. Risk factors predicting exertional heat illness in male Marine Corps recruits. Med. Sci. Sports Exerc.
1996; 28: 939–44.
15. Godek SF, Bartolozzi AR, Godek JJ. Sweat rate and fluid turnover in American football players compared with runners in a hot and humid environment. Br. J. Sports Med.
2005; 39: 205–11.
16. Godek SF, Godek JJ, Bartolozzi AR. Hydration status in college football players during consecutive days of twice-a-day preseason practices. Am. J. Sports Med.
2005; 33: 843–51.
17. Grundstein A, Ramseyer C, Zhao F, et al. A retrospective analysis of American football hyperthermia deaths in the United States. Int. J. Biometeorol.
2012; 56: 11–20.
18. Grundstein A, Cooper E, Ferrara M, Knox JA. The geography of extreme heat hazards for American football players. Appl.Geogr.
2014; 46: 53–60.
19. Howe AS, Boden BP. Heat-related illness in athletes. Am. J. Sports Med
. 2007; 35: 1384–95.
20. Huffman EA, Yard EE, Fields SK, Collins CL, Comstock RD. Epidemiology of rare injuries and conditions among United States high school athletes during the 2005–2006 and 2006–2007 school years. J. Athl. Train.
2008; 43: 624–30.
21. Kerr ZY, Casa DJ, Marshall SW, Comstock RD. Epidemiology of exertional heat illness among U.S. high school athletes. Am. J. Sports Med.
2014; 42: 70–7.
22. Kerr ZY, Marshall SW, Comstock RD, Casa DJ. Implementing exertional heat illness prevention strategies in US high school football. Med. Sci. Sports Exerc.
2014; 46: 124–30.
23. Knochel JP. Catastrophic medical events with exhaustive exercise: “white collar rhabdomyolysis”. Kidney Int.
1990; 38: 709–19.
24. Kucera KL, Klossner D, Colgate B, Cantu R. Annual Survey of Football Injury Research: 1931–2014
. Chapel Hill (NC): National Center for Catastrophic Sports Injuries, 2014, pp. 1–36.
25. Lapshina KV, Ekimova IV. Effects of sleep deprivation on measures of the febrile reaction and the recovery of somatovisceral functions and sleep in endotoxemia. Neurosci. Behav. Physiol.
2010; 40: 381–8.
26. Luke AC, Bergeron MF, Roberts WO. Heat injury prevention practices in high school football. Clin. J. Sport Med.
2007; 17: 488–93.
27. Martinez M, Davenport L, Saussy J, Martinez J. Drug-associated heat stroke. South Med. J.
2002; 95: 799–802.
28. Mello RP, Murphy MM, Vogel JA. Relationship between a two mile run for time and maximal oxygen uptake. J. Appl. Sport Sci. Res.
1988; 2: 9–12.
29. Miller KC, Swartz EE, Long BC. Cold-water immersion for hyperthermic humans wearing American football uniforms. J. Athl. Train.
2015; 50: 792–9.
30. Nadel ER, Fortney SM, Wenger CB. Effect of hydration state on circulatory and thermal regulations. J. Appl. Physiol.
1980; 49: 715–21.
31. National Collegiate Athletic Association Web site [Internet]. Probability of going pro methodology. Available from: http://www.ncaa.org
. Accessed 2014 Mar 11.
32. National Federation of State High School Association Web site [Internet]. Participation data. Available from: http://www.nfhs.org
. Accessed 2014 Mar 10.
33. Noonan B, Bancroft RW, Dines JS, Bedi A. Heat- and cold-induced injuries in athletes: evaluation and management. J. Am. Acad. Orthop. Surg.
2012; 20: 744–54.
34. O’Connor FG, Casa DJ, Bergeron MF, et al. American College of Sports Medicine roundtable on exertional heat stroke — return to duty/return to play: conference proceedings. Curr. Sports Med. Rep.
2010; 9: 314–21.
35. Oh RC, Henning JS. Exertional heatstroke in an infantry soldier taking ephedra-containing dietary supplements. Mil. Med.
2003; 168: 429–30.
36. Pandolf KB. Effects of physical training and cardiorespiratory physical fitness on exercise-heat tolerance: recent observations. Med. Sci. Sports
. 1979; 11: 60–5.
37. Sawka MN, Francesconi RP, Young AJ, Pandolf KB. Influence of hydration level and body fluids on exercise performance in the heat. JAMA
. 1984; 252: 1165–9.
38. Schickele E. Environment and fatal heat stroke. An analysis of 157 cases occuring in the Army in the U.S. during World War II. Mil. Surg.
1947; 100: 235–56.
39. Stallones RA, Gauld RL, Dodge HJ, Lammers TF. An epidemiological study of heat injury in army recruits. AMA Arch. Ind. Health
. 1957; 15: 455–65.
40. Tripp BL, Eberman LE, Smith MS. Exertional heat illnesses and environmental conditions during high school football practices. Am. J. Sports Med
. 2015; 43: 2490–5.
41. Vandentorren S, Suzan F, Medina S, et al. Mortality in 13 French cities during the August 2003 heat wave. Am. J. Public Health
. 2004; 94: 1518–20.
42. Walsh NP, Gleeson M, Pyne DB, et al. Position statement. Part 2: maintaining immune health. Exerc. Immunol. Rev.
2011; 17: 64–103.
43. Yang YL, Lu KT, Tsay HJ, Lin CH, Lin MT. Heat shock protein expression protects against death following exposure to heatstroke in rats. Neurosci. Lett.
1998; 252: 9–12.
44. Yard EE, Gilchrist J, Haileyesus T, et al. Heat illness among high school athletes — United States, 2005–2009. J. Safety Res.
2010; 41: 471–4.
45. Yeo TP. Heat stroke: a comprehensive review. AACN Clin. Issues
. 2004; 15: 280–93.