E. Randy Eichner

National Athletic Trainers' Association Position Statement: Exertional Heat Illnesses.

OBJECTIVE To present best-practice recommendations for the prevention, recognition, and treatment of exertional heat illnesses (EHIs) and to describe the relevant physiology of thermoregulation. BACKGROUND Certified athletic trainers recognize and treat athletes with EHIs, often in high-risk environments. Although the proper recognition and successful treatment strategies are well documented, EHIs continue to plague athletes, and exertional heat stroke remains one of the leading causes of sudden death during sport. The recommendations presented in this document provide athletic trainers and allied health providers with an integrated scientific and clinically applicable approach to the prevention, recognition, treatment of, and return-to-activity guidelines for EHIs. These recommendations are given so that proper recognition and treatment can be accomplished in order to maximize the safety and performance of athletes. RECOMMENDATIONS Athletic trainers and other allied health care professionals should use these recommendations to establish onsite emergency action plans for their venues and athletes. The primary goal of athlete safety is addressed through the appropriate prevention strategies, proper recognition tactics, and effective treatment plans for EHIs. Athletic trainers and other allied health care professionals must be properly educated and prepared to respond in an expedient manner to alleviate symptoms and minimize the morbidity and mortality associated with these illnesses.

Sickle Cell Trait and Fatal Rhabdomyolysis in Football Training: A Case Study

We report the athletic, the clinical, and the pathological details of a case of fatal rhabdomyolysis during training in a college football player with sickle cell trait (SCT) who collapsed minutes after running 16 successive sprints of 100 yd each. The player, 19 yr old, African American, was apparently healthy when he took the field for the conditioning run. No exertional heat illness was present. After collapsing on-field, the player soon went into coma and developed fulminant rhabdomyolysis, profound lactic acidosis, acute myoglobinuric renal failure, refractory hyperkalemia, and disseminated intravascular coagulation. Despite intensive care in the hospital, he died about 15 h after admission, likely from a hyperkalemic cardiac arrhythmia; the terminal rhythm was pulseless electrical activity. The forensic autopsy confirmed that the cause of death was acute exertional rhabdomyolysis associated with SCT. Counting this case, at least 15 college football players with SCT have died from complications of exertional sickling, as have younger football players and other athletes. In SCT, maximal, sustained exercise evokes four forces that can foster sickling: hypoxemia, acidosis, hyperthermia, and red cell dehydration. The setting, the clinical and laboratory features, and the clinicopathological correlation here suggest that the fulminant rhabdomyolysis and its fatal sequelae were from exertional sickling. These data suggest that screening and simple precautions for SCT may be warranted to prevent tragedies like this and enable all athletes with SCT to thrive in their sports.

Sports anemia, iron supplements, and blood doping

1) Athletes tend to have lower hemoglobin concentrations than sedentary counterparts. This has been called sports anemia, a misnomer. 2) Sports anemia is a false anemia and a beneficial adaptation to aerobic exercise, caused by an expanded plasma volume that dilutes red blood cells. 3) Athletes, however, can also develop true anemia, most commonly caused by iron deficiency. True anemia curbs athletic performance, but nonanemic iron deficiency does not. 4) Iron supplements are useful for women endurance athletes who repeatedly develop iron deficiency anemia despite dietary advice. 5) Some endurance athletes today are blood doping by abusing recombinant human erythropoietin (rEPO). They risk dying to win.

Overtraining: Consequences and prevention

Overtraining refers to prolonged fatigue and reduced performance despite increased training. Its roots include muscle damage, cytokine actions, the acute phase response, improper nutrition, mood disturbances, and diverse consequences of stress hormone responses. The clinical features are varied, non-specific, anecdotal and legion. No single test is diagnostic. The best treatment is prevention, which means (1) balancing training and rest, (2) monitoring mood, fatigue, symptoms and performance, (3) reducing distress and (4) ensuring optimal nutrition, especially total energy and carbohydrate intake.

Sickle cell trait associated with sudden death in competitive athletes

Sickle cell trait (SCT; hemoglobin AS) occurs in 8% of African Americans and although typically benign has been associated with sudden death in military recruits during intense physical activity. However, the role of SCT in the deaths of trained athletes is less well documented or acknowledged. The 31-year United States Sudden Death in Athletes Registry was interrogated to determine the frequency, epidemiology, and clinical profile of SCT-related death in a large population of competitive athletes. Of 2,462 athlete deaths, 23 (0.9% overall, 3.3% of African Americans) occurred in association with SCT: ages 12 to 22 years, 21 male (91%), and all African Americans. SCT diagnosis was made by solubility testing (n = 13) and/or hemoglobin electrophoresis (n = 16). Most victims competed in college (n = 17) and in football (n = 19). Of 271 African American football deaths in the registry, 7% (1 in 14) were known to be associated with SCT. Each athlete experienced distinctive noninstantaneous collapse with gradual deterioration over several minutes associated with vigorous or exhaustive physical exertion, usually during conditioning drills (n = 22) and typically early in the training season. Ambient temperatures were ≥80°F in 20 patients (87%), with most events in southern or border states during the summer and autumn (n = 17 [74%]). In conclusion, SCT can be associated with largely unpredictable sudden collapse and death and apparent predilection for African American college football players during conditioning. Understanding the risks, mechanisms, and event triggers of SCT may allow lifesaving alterations in training methods to be implemented.

The role of sodium in 'heat cramping'.

Abstract‘Heat cramping’ is defined here as severe, spreading, sustained, sharply painful muscle contractions that can sideline athletes. Not all cramps are alike, but three lines of evidence suggest heat cramping is caused by ‘salty sweating’, specifically by the triad of salt loss, fluid loss and muscle fatigue. The first line of evidence is historical. Dating back 100 years, heat cramping in industrial workers was alleviated by saline, and in a self-experiment, salt depletion provoked muscle cramping. The second line of evidence is from field studies of athletes. In tennis and football alike, heat-crampers tend to be salty sweaters. Some evidence also suggests that triathletes who cramp may lose more salt during the race than peers who do not cramp. The third line of evidence is practical experience with therapy and prevention. Intravenous saline can reverse heat cramping, and more salt in the diet and in sports drinks can help prevent heat cramping. For heat cramping, the solution is saline.

Blood doping : infusions, erythropoietin and artificial blood.

As science marches on, athletes and coaches march close behind. Researchers have long been interested in how red cell mass and blood volume affect exercise capacity. Interest in blood doping soared after the 1968 Mexico City Olympics. Studies in the 1970s and 1980s suggested that transfusing red cells could speed endurance performance. Diverse athletes of the time were accused of blood doping. In the late 1980s, recombinant human erythropoietin (EPO) began to supplant transfusion for doping. EPO use is a suspect in nearly 20 deaths in 4 years in European cyclists. In the 1998 Tour de France, a team was ejected for using EPO and six other teams quit the race. The beat goes on; in recent years, diverse endurance and sprint athletes have been caught or accused of using EPO. Tests to detect EPO are improving but are not yet foolproof. As EPO tests improve, blood transfusion is back in vogue and some athletes may have infused artificial blood. Tests for detecting artificial blood also exist, but it seems it will take widespread, year-round, unannounced, out-of-competition testing and stern penalties to deter blood doping.

Hyponatremia of exercise

ConclusionsThere is little doubt that proper hydration benefits physiologic function, performance, and health. There is also little doubt that excessive drinking can create a potentially lifethreatening situation. It appears that excessive fluid intake is the primary cause in most cases of hyponatremia in athletes. Hyponatremia can be prevented by educating athletes about proper hydration practices and adequate sodium intake.

Immunology and exercise: Physiology, Pathophysiology, and Implications for HIV Infection

This article covers the latest information on the immunologic changes of exercise as well as the effects of regular exercise on persons infected with HIV and the exercise recommendations for HIV-infected athletes. Included are discussions about psychoneuroimmunology and exercise-associated changes in immunity.

Heat cramps in sports.

Heat cramps were described as early as 1878 in men working in extreme heat in gold mines in Nevada (1). The term is still used today to describe the severe, spreading, sustained, sharply painful muscle contractions that can sideline athletes. It seems to describe the extreme end of the spectrum of exercise-associated muscle cramps (EAMC), in that cramping solely from fatigue tends to be milder, briefer, and more localized (2). Common in summer football (and seen even in ‘‘winter football,’’ such as the New York Giants players cramping in their Super Bowl win in February 2008), heat cramps also can strike in tennis and in distance cycling and running, especially in tropical triathlons. They also can occur in soccer and in beach volleyball, in point guards in basketball tournaments, and in pitchers in hot, humid baseball games. Paradoxically, heat cramps can even occur at the end of cross-country ski races and in ice hockey goalies late in long games. This suggests that even if the ‘‘macroclimate’’ is cold, the ‘‘microclimate,’’ of the hockey goalie, for example, can become too hot for too long. Pearl: Heat cramps could better be termed ‘‘sweat cramps,’’ in that salt (sodium chloride) loss via heavy sweating is a key culprit.