KEY POINTS

• Sickle cell trait is an inherited condition of the oxygencarrying protein, hemoglobin, in red blood cells. This genetic trait is generally benign, but during maximal exercise, the oxygen levels in muscles can decrease sufficiently to cause some of the red cells to change from the normal disk shape to a crescent or sickle shape. These sickled red cells can block blood vessels in muscles, kidneys, and other organs and can pose a grave risk for some athletes exercising all-out.
• In the past 6 1/2 years alone, exertional sickling has killed nine athletes, including five college football players. Death is caused by complications of a sudden and extreme breakdown of muscle tissue: cardiac arrhythmias and/or acute kidney failure.
• Sickling can begin in 2-3 minutes of sustained, maximal exertion, such as wind sprints in football or running laps in basketball. The harder and faster the athlete goes, the earlier and greater the sickling.
• The exertional sickling setting and syndrome are unique and can easily be differentiated from heatstroke or heat cramping. Sickling risk is increased by anything that increases the difficulty of the exercise, for example, hot weather, dehydration, high altitude, or asthma.
• Screening and precautions for sickle cell trait can prevent deaths from exertional sickling and enable sickle-trait athletes to thrive in their sports.

INTRODUCTION

Sickle cell trait is common and generally benign. More than 3 million Americans have sickle trait and almost all live healthy, normal lives. Yet for some athletes, sickle trait can pose a grave problem – a problem that can even cause death.  Understanding sickle cell trait is vital to athletes, coaches, and athletic trainers because sickling injuries are preventable with screening and proper precautions.

The sickle gene is common in people of African heritage; it produces a variant of hemoglobin, the oxygen-carrying protein of the red blood cell. Over the millennia, carrying one sickle gene–sickle cell trait–fended off death from malaria, leaving one in 12 African-Americans (versus one in 2,000 to one in 10,000 white Americans) with sickle trait. Athletes with sickle trait inherit one gene for normal hemoglobin and one gene for sickle hemoglobin (hemoglobin S). If oxygen in tissues falls to low levels, the red cells carrying the hemoglobin S can change from the usual disk shape to a crescent or sickle shape. These sickled red cells can clog blood vessels, impairing delivery of oxygen and removal of harmful metabolites, resulting in severe damage to the involved tissues.

In the past four decades, sickling has killed up to a dozen college football players during training and many more military recruits and others in boot camps (Eichner, 1993). In the past 6 1/2 years alone, sickling has killed nine athletes: five college football players, two high school athletes (including one basketball player), and two 12-year-olds training for football. Other recent non-fatal cases exist as well. In a review of sudden nontraumatic sports deaths over a decade in high school and college athletes, sickling-associated rhabdomyolysis (accumulation in the blood of myoglobin, potassium, and other substances from damaged muscle fibers) accounted for seven (5%) of 136 well-studied deaths (Van Camp et al., 1995).

The focus of this article is on sickling in sports, but the initial reports of sickling collapse and death – and the seminal field and laboratory research on the problem – come from the U.S. military.

RESEARCH REVIEW

Exertional Sickling Collapse: Military Experience

Fatal sickling collapse was first described in 1970, in a report of sudden deaths in four of about 4,000 black recruits (about 0.1%) during one year of Army basic combat training at Fort Bliss, Texas, altitude 4,060 feet (Jones et al., 1970). The discussion in that report begins, "That sickle cell trait can, under certain circumstances, be fatal is generally not appreciated." From 1970 to 1974, four similar collapses (with one death) in Air Force recruits and cadets with sickle trait – two of the collapses at an altitude of only 661 feet - increased the alarm and resulted in the temporary barring of applicants with sickle trait from the Air Force Academy (Koppes et al., 1977). These four were the only recruits, among thousands of trainees seen at two military bases, hospitalized for exertional rhabdomyolysis, for kidney failure caused by the accumulation of myoglobin in the kidney blood supply, and for widespread clotting of blood throughout the body (disseminated intravascular coagulation or DIC). All needed early dialysis for kidney failure; one died of heart failure associated with excessive accumulation of potassium in the blood (hyperkalemia). The illness followed vigorous exercise: two were running 1-2 miles and two were on an obstacle course. The weather was not stressful, and no case was tied to heatstroke.

Three more military cases–virtually identical, and all fatal–were reported between 1974 and 1985. All three men collapsed after running 2-3 miles and all died from complications of acute exertional rhabdomyolysis and kidney failure.

A noted epidemiological study in 1987 strengthened the link between sickle cell trait and sudden death during physical training. Of all deaths that occurred among two million enlisted recruits during basic training in the U.S. Armed Forces over the five years from 1977 through 1981, the risk of sudden unexplained death in black recruits with sickle trait was 28 times higher than in black recruits without sickle trait and 40 times higher than in all other recruits (Kark et al., 1987).

On further analysis, the relative risk of exercise-related death in sickle trait, unexplained by pre-existing disease, was set at 30 times higher than in recruits without sickle trait. The risk of death for recruits increased with age, an 8-fold increase from age 17-18 to age 28-29. The risk plummeted, however, for career military after basic training. This observation led military researchers to speculate that the risk of exercise-related death in sickle trait is largely confined to a time of intense conditioning to unaccustomed exercise or a sustained event at a performance level for which the individual is unprepared (Kark & Ward, 1994).

Analysis also clarified the type of death. Most collapses occurred as recruits tried to run 1-3 miles. Of 40 military deaths or near-deaths from sickling collapse, some had features of exertional heat illness (but not heatstroke) and others were sudden cardiac death from arrhythmia. But most deaths were not sudden – occurred hours to a day or two after the collapse – and were from complications of extreme rhabdomyolysis, including muscle compartment syndromes (breakdown of swollen muscles confined by surrounding tough connective tissue) and myoglobinuric kidney failure. Indeed, acidosis and hyperkalemia from explosive rhabdomyolysis may have caused the arrhythmic sudden cardiac deaths. So the main cause of death in sickling collapse is fulminant exertional rhabdomyolysis, a risk that rises 200-fold in recruits with sickle trait (Gardner & Kark, 1994).

Physiology and Pathophysiology

Exercise physiology helps explain why extreme exertion in sickle trait can cause explosive exertional rhabdomyolysis. In sickle trait, vigorous exercise can evoke sickling that can have grave consequences. For decades, the concept was that, except in the medulla of the kidney, sickle-trait red cells "never sickle in live people" or that sickle trait "is innocuous" because no sickling occurs until blood oxygen saturation falls below 40%, a level not reached until red cells reach the venous exits of the tissue capillaries (Eaton & Hofrichter, 1987). This notion, however, fails to fathom the major metabolic changes of intense exercise – and their consequences.

When young men cycle to exhaustion in five minutes, for example, striking acidosis and low blood oxygen levels can occur: the femoral venous blood pH can fall to 7.15, the oxygen saturation to 19% (Hartley et al., 1973). With the same exercise at 4,000 m, blood oxygen saturation can fall as low as 11% (Hartley et al., 1973). When sprint-trained men run on a treadmill at a speed that exhausts them in one minute, femoralartery blood lactate levels soar and pH falls to 7.07 (Medbo & Sejersted, 1985). And when athletic men cycle or run to exhaustion in 1-2 minutes, arterialized capillary blood shows lactate levels up to 32 mM, bicarbonate levels down to 3 mEq/L, and blood pH values as low as 6.8 (Osnes & Harmansen, 1972). In addition to these extreme metabolic stresses, blood perfusing exercising muscles is exposed to excessive temperatures and to a hyperosmotic environment (partly from breakdown of large molecules of glycogen to multiple molecules of lactate) that moves water from red cells into the tissue fluids, thereby dehydrating the red cells (Eichner, 1993).

So in sickle trait, strenuous exercise evokes four forces that foster sickling. The acidosis and high tissue temperatures "shift to the right" the oxygen dissociation curve, displacing more oxygen from hemoglobin S. Dehydration of red cells increases the concentration of hemoglobin S. And a severe decline in blood oxygen because of extreme muscle demand for oxygen completes the sickling foursome.

Exactly where the change in red cell shape from disk to sickle occurs is debated. Most red cells traverse the capillary circulation in about one second. It is argued that for sickle-trait red cells the "delay time" to sickling, even at zero percent oxygen saturation, is slightly longer than one second, so even with extremely low blood oxygen levels, the red cells would escape the microcirculation before they sickle. In other words, any sickling that occurs must be in the veins, where it is "harmless" because any sickled cells will revert to normal shape as they take up oxygen in the lungs.

Two flaws weaken this hypothesis. First, red-cell dehydration makes normally nonadherent sickle-trait cells adhere to vascular endothelium, so some may linger in the microvasculature and sickle there (Hebbel, 1991). Second, even if most of the sickling occurs in veins leaving exercising muscles, some sickle cells fail to revert to normal in the lungs. Indeed, in an early study, when fi ve black men with sickle trait performed vigorous leg cycling, nearly 1% of red cells in venous blood from the arm were sickle cells (Ramirez et al., 1976). So sickle cells likely accumulate in the blood during strenuous exercise and are pumped to the working muscles where they can "logjam" the microcirculation and cause rapid ischemic breakdown of muscles – acute, severe rhabdomyolysis. Exercise studies support this hypothesis.

Exercise Laboratory Studies: Military

Exercise research on military recruits confirms sickling in blood draining exercising muscles. Fifteen sickle-trait men did two brief, maximal arm-cranking exercise tests, one at 1,270 m and one at a simulated 4,000 m (Martin et al., 1989). Sickle cells were counted in venous blood draining the arms. At 1,270 m, exercise evoked a mean of 2.3% sickle cells; at 4,000 m, this increased to 8.5%. One recruit, exercising maximally at 4,000 m (28% oxygen saturation), had 25% sickle cells in venous blood from exercising muscles.

A second military study published in abstract form shows that sickle cells can accumulate in the arterial circulation (Weisman et al., 1988a). Recruits with sickle trait exercised to near exhaustion on a cycle ergometer, once at sea level and again at a simulated 4,000 m. Sickle cells were counted at peak exercise in venous blood from the forearm. Such cells likely sickled in the exercising lower limbs and traversed not only the lungs but also another capillary bed, that of the (resting) forearm. At sea level, sickle cells in forearm blood reached only about 1%. But at 4,000 m, sickle cells rose to a mean of 9% and a maximum in one man of 28%. This strongly suggests that as exercise stress increases and blood oxygen declines, athletes with sickle trait will steadily accumulate sickle cells that are pumped to the heart, brain, and muscles.

In a third military study, men with sickle trait, cycling hard at 4,000 m, developed more symptoms than control men (Weisman et al., 1988b). Symptoms included headache or dizziness, leg cramps, chest pain, and/or pain in the left upper quadrant of the abdomen. Symptoms developed in more men who had sickle trait (9 of 30) than in control men (2 of 28). Left upper quadrant pain, likely from sickling in the spleen, occurred only in men (3 of 30) with sickle trait. For sickle-trait athletes, the implications of these studies are obvious.

Exercise Laboratory Studies: Civilian

Civilian studies complement the military studies. A 2004 study by Bergeron et al. suggests that dehydration can compound sickling during exercise. Two men with sickle trait walked briskly for 45 minutes in the heat, once while drinking fluids (1 L, to offset sweat losses) and once without fluids. Without fluids to offset dehydration, sickling (in forearm venous blood) increased steadily to peaks of 3.5% and 5.5%, respectively. In this relatively mild exercise bout, no sickling was evident when fluids were consumed (Bergeron et al.,2004).

Several studies keyed on small groups of sickle-trait subjects versus controls performing various anaerobic and/or aerobic exercises (Bile et al., 1996, 1998; Freund et al., 1995; Gozal et al., 1992; Sara et al., 2003). In general, performance differences between groups were not detected or were small and mixed. In other words, most of these studies suggest that subjects with sickle trait have normal exercise ability. Small differences observed in blood lactate accumulation or removal–lactate either higher or, more commonly, lower in sickletrait subjects – may be from imperfect matching of groups for fitness.

Very recent laboratory exercise studies suggest microcirculatory problems in sickle trait. For example, sickle-trait subjects have more rigid red blood cells at rest and a longer-lasting rise in certain vascular cell-adhesion molecules with exercise (Connes et al., 2006c; Monchanin et al., 2006). In constant strenuous cycling exercise for nine minutes, sickle-trait subjects, compared to controls, are not limited initially but are prone to exercise intolerance and lower aerobic capacity thereafter (Connes et al., 2006a). Also, when sickle-trait subjects do five 6-second maximal anaerobic cycling sprints, performance is normal on the first sprint but falls off faster (than in controls) during repeated sprinting (Connes et al., 2006b). These results tend to jibe with field studies in Africa that suggest sickle-trait runners gravitate to shorter distances (Marlin et al., 2005).

Field Studies in Africa

Observational studies in Africa find that sickle-trait runners fare better in sprints than in longer races - and struggle at altitude. For example, among 129 champion runners in Ivory Coast, 13 (10%) had sickle trait. These 13 runners won 33 titles, but only one was in a race of 800 m or more. The other 32 wins were all in races of 400 m or less (Le Gallais et al.,1991). A similar field study found sickle-trait runners underrepresented among top finishers in an Abidjan semi-marathon (Le Gallais et al., 1994). In a rugged distance race, the Mount Cameroon Ascent, among runners of the Bakoueri tribe, where winning confers social status, sickle-trait runners were underrepresented in general and underperformed in the high-altitude stretches (Thiriet et al., 1994). These observations, along with the laboratory studies above, suggest that sickle trait can limit performance not only at altitude but also in any all-out running that approaches or exceeds 800 m. This is borne out by observations in American college football players.

Exertional Sickling Collapse: College Football

The first sickling death in football was in 1974, a black defensive back from Florida who collapsed two years in a row on the first day of practice at altitude (5,118 feet) at the University of Colorado (Eichner, 1993). The first year, he survived. The second year, aiming to finish the first conditioning sprint

Up to 13 college football players have died after sickling in training, and although in some the proximate cause of death has been debated (and litigated), the setting and syndrome in most are similar (Table 1).

TABLE 1. Deaths after sickling collapse in college football.

The features of the sickling collapse syndrome are unique, but are not yet widely recognized (Rosenthal & Parker, 1992). Take the above Tennessee case (2000), for example. On the first day of summer practice, this second-year defensive back passed a physical examination. At 5-feet 11-inches and 190 pounds, he was the picture of health. He had kept fit all summer. One hour after passing the physical, he took the field for the conditioning test. He wore shorts and T-shirt. The field temperature was in the mid-80s, the humidity low by local standards. He breezed through the first two-thirds of the test, two series of five 60-yard sprints, 600 yards total. He collapsed late in the last third of the test – he ran less than 900 yards total.

The player was taken to a nearby hospital, where he soon died. Lacking a core temperature, the coroner attributed the death to heatstroke. The evidence points instead to exertional sickling and acute rhabdomyolysis. The coroner was unaware the victim had sickle cell trait (Eichner, 2000).

Sickling Situations

Sickling collapse is not limited to college football training. It has killed or nearly killed several college or high school basketball players (two were female athletes) in training, typically when "running for time," such as repeated sprints up and down the basketball court ("suicide runs") or laps on a track or a 3-mile run (Eichner, 1993, 2000). A sickle-trait runner collapsed two years in a row at the end of cross-country races. He survived severe rhabdomyolysis and renal failure (Helzlsouer et al., 1983). A medical student in Chicago barely survived a sickling collapse after jogging a vigorous mile for the first time in years; he was lucky that he collapsed very near the hospital (Eichner, 1993). Sickling has killed firefighters in training (Wirthwein et al., 2001) and men captured by police after chase and struggle (Mercy et al., 1990; Thogmartin,1998).

The harder and faster athletes go, the earlier and greater the sickling. That is why sickle collapse occurs sooner (at a shorter distance) in top college football players sprinting all out (their "drop zone" is often 800-1,200 m, see Table 1) than in military recruits trying to run 1-3 miles. Sickling can begin in only 2-3 minutes of sustained sprinting – or in any other sustained all-out exertion - and sickling can soon increase to grave levels if the symptomatic athlete tries to exceed his limits or is urged by the coach to push beyond pain and weakness. Any cramping, struggling, or collapse in a sickle-trait athlete must be considered sickling--a medical emergency--until proved otherwise.

The degree of exertional sickling also seems to vary with the percentage of hemoglobin S in each red cell. Typically in sickle trait, each red cell has about 40% S and 60% A (normal) hemoglobin. But if the athlete co-inherits a trait for alpha thalassemia, for instance, this reduces the amount of hemoglobin S in each red cell to less than 30%, and the tendency to sickle is milder (Kark, 1994; Monchanin et al., 2005). Conversely, if the athlete co-inherits hemoglobin E trait, as in the recent sickling death of a Florida boy in a youth football league (Graham, 2006), the amount of hemoglobin S may exceed 60% and the tendency to sickle is greater. Surely other unknown conditions–some inborn, some not–shape the chance and severity of sickling in individual athletes. We need more research here.

Heat and dehydration increase sickling, mainly because they make the drill more difficult and drive the blood oxygen lower. Exercise-induced asthma and the thin air of altitude also increase sickling because of lower blood oxygen.

Differential Diagnosis

Sickling collapse has been confused with heat cramping, eat exhaustion, and heatstroke. The most telling symptom of sickling collapse is increasing pain and weakness in the working muscles, especially the legs, buttocks, and/or low back, usually during sprinting. The athlete may call the pain "cramping," but it is unique. Sickling pain is unlike that of heat cramping or "burning" muscles from middle-distance racing (Eichner, 2000). Sickling pain is from insufficient blood flow to working muscles – ischemic pain. Quickly, the blood-starved muscles fail to support the athlete. Knowing which athletes have sickle trait avoids possible confusion over "cramping" – any cramping should be considered sickling until proved otherwise.

Unlike in heatstroke, sickling athletes may be on-field only briefly, sprinting as little as 800-1,200 meters, early in training, often on the first or second day of preseason workouts. Sickling can occur during repeated running up hills, ramps, or stairs, or even during extreme weight-lifting. Sickling collapse can occur if the tempo increases late in one-hour football drills, including "mat drills" in the winter. At the end of a long, hot football practice, if the players run sprints or "gassers" with insufficient breathers, sickling can begin in 800 meters or less. Sickling can even occur rarely during the play of the game, for example, when a running back is in almost constant action during a long, frantic drive downfield. Unlike in many cardiac collapses, especially those from ventricular fibrillation, sickling athletes can still talk when they hit the ground, even though they are gravely ill.

In general, players who have had both heat cramping and sickling can tell the difference between the two syndromes.

Five differences:

1) Heat cramping often has an early warning sign. Hours or minutes before the athlete suffers heat cramping, he may see or feel twitching or twinges in tired muscles, those destined to cramp. The athlete who knows heat cramps will tell you, "They are about to come on." In contrast, sickling usually hits suddenly, with no early warning.

2) The pain is different. Heat cramping pain is an excruciating pain of sustained, full contraction of muscles, a "lockup." Sickling pain is milder, an ischemic pain from working muscles robbed of blood supply, like the pain of intermittent claudication when leg arteries are narrowed by atherosclerosis.

3) What stops the athlete is different. With heat cramping, athletes "hobble to a halt" – the fully contracted muscles no longer work. With sickling, athletes "slump to a stop" - the legs become "weak and wobbly" and no longer hold them up.

4) The physical findings are different. In heat cramping, one can see and feel large, rock-hard muscles in full contraction– and the athlete often is yelling in pain. It can take several people to stretch out the legs of a huge football player with major heat cramps in the thighs or hamstrings. With sickling, the exhausted player lies fairly still and complains little - except to say that his legs hurt and won’t hold him up- and the muscles look and feel normal.

5) The response is different. After 10 to 15 minutes sitting in a cold tub, drinking fluids and getting supplemental oxygen by face mask, the athlete with mild sickling "feels fine." This is likely because many sickle cells have reverted to normal as they regained oxygen. In contrast, major heat cramping often takes an hour or two to resolve, even in a player resting in the training room, being treated with stretching, massage, and intravenous fluids.

In short, although athletes and coaches tend to lump heat cramping and sickling as "cramping," the two syndromes are starkly different.

PRACTICAL MANAGEMENT POINTS FOR COACHES AND SPORTS HEALTH PROFESSIONALS

Screen all athletes -- It is vital to know which athletes have sickle trait. Although most states test at birth for hemoglobinopathies, most college athletes do not know their sickle-trait status. All it takes is inexpensive blood testing Informed athletes, coaches, and athletic trainers can prevent sickling deaths.

Acclimation -- Build up slowly in conditioning or lifting regimens. The harder and faster sickle-trait athletes work, the more likely they are to sickle. Slow the tempo of their training. Have supplemental oxygen ready for games at altitude. Encourage regular sleep. Control any asthma. Do not allow ill athletes to work out.

Modify drills -- No timed sprints or miles. No repeat sprints beyond 500 m total without a "breather." No all-out exertion of any type sustained 2-3 minutes without a breather. If repeat sprints ("gassers" or "trippers") are done at the end of practice, double or triple the rest time between sprints for sickle-trait athletes. If they can set their own pace, they usually do well. They will tell you, "If I can just catch my breath, I’ll do fine." During rest, sickle cells tend to revert to normal shape as they regain oxygen traversing the lungs.

Hydrate -- Dehydration fosters sickling (Bergeron et al.,2004). Make sure sickle-trait athletes stay hydrated. Modify work/rest cycles for the heat. After they have had a night’s sleep (without fluids) test to see if their urine is concentrated. Because of sickling in the medulla of the kidney, some sickletrait athletes – especially older athletes - lose the ability to concentrate urine so they excrete too much water (Kark,1994). This can increase the risk of dehydration.

Set the tone -- The sickle-trait athlete in particular should feel comfortable reporting unusual symptoms immediately. The coach should consider any struggling, cramping, or collapse as likely sickling and seek help fast.

Act fast -- A sickling collapse is a medical emergency. Check vital signs. Give oxygen by face mask. Cool the athlete, if necessary. If there is no improvement very quickly or if vital signs or alertness decline, call 911, attach an automatic emergency defibrillator, start an intravenous drip of normal saline, and get the athlete to the hospital quickly.

SUMMARY

Sickle cell trait can pose a grave risk for some athletes. In the past six years alone, exertional sickling has killed eight athletes, including four college football players. Exercisephysiology research, both military and civilian, shows how and why sickle red cells accumulate in the bloodstream of sickle-trait athletes in a variety of exercise bouts. Sickle cells can "logjam" blood vessels and cause collapse from ischemic rhabdomyolysis. Death can ensue from complications of explosive rhabdomyolysis: cardiac arrhythmias and/or acute myoglobinuric kidney failure. Sickling can begin in 2-3 minutes of any all-out exertion. Heat, dehydration, altitude, and asthma can worsen exertional sickling. This sickling syndrome is unique and can easily be distinguished from heatstroke or heat cramping. Sickling collapse is a medical emergency. Screening and precautions for sickle trait can prevent sickling collapse and enable sickle-trait athletes to thrive in their sports.

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Thogmartin J.R. (1998). Sudden death in police pursuit. J. Forensic Sci.43:1228-1231.

Van Camp, S. P., C. M. Bloor, F. O. Mueller, R. C. Cantu, and H. G. Olson (1995). Nontraumatic sports death in high school and college athletes. Med.Sci. Sports Exerc. 27:641-647.

Weisman, I. M., R. J. Zeballos, and T. W. Martin (1988a). Role of severe inspiratory hypoxia during lower extremity exercise on antecubital venous sickling in sickle cell trait. Clin. Res. 36:422a (abstract).

Weisman, I. M., R. J. Zeballos, and T. W. Martin (1988b). The impact of inspiratory hypoxia simulating 4000 m on acute strenuous exercise performance in sickle cell trait. Am. Rev. Resp. Dis. 137:338a (abstract).

Wirthwein, D. P., S. D. Spotswood, J. J. Barnard, and J. A. Prahlow (2001). Death due to microvascular occlusion in sickle-cell trait following physical exertion. J. Forensic Sci. 46:399-401.

S U P P L E M E N T

DANGER LURKS FOR ATHLETES WITH SICKLE CELL TRAIT

In sickle trait, each red blood cell has about 60% normal hemoglobin and 40% sickle hemoglobin. In everyday life, sickle trait causes few or no problems. However, problems arise if oxygen in the bloodstream drops too low – as it can during sustained sprinting. During such activity, some red cells change from a normal disk shape to a quarter-moon shape – the "sickle" shape. This shape change is termed "sickling."

Exertional Sickling: Clinical Consequences

If many red cells sickle, they clump in a "log-jam" that clogs the blood vessel and cuts off blood flow to the muscles. This results in rhabdomyolysis – the breakdown of muscles. Acute, severe rhabdomyolysis can release enough lactic acid and potassium to sap the pumping power of the normal heart – even enough to cause fatal arrhythmia. In addition, it can release enough myoglobin, the oxygen-binding protein in muscle, to plug the kidneys and cause acute renal failure. So exertional sickling collapse is a medical emergency.

SICKLING SETTINGS IN SPORT: EXAMPLES

Football training

• Wind sprints early in practice
• Repeated runs up hills, ramps, or stairs
• "Gassers" at the end of practice
• Extreme weight-lifting bouts
• Intense drills and other spurts of exercise after 40-50 minutes of conditioning
• Rarely in the play of the game
• Normal red blood cell Sickled red blood cell

Basketball Training

• Running laps on a track
• Running timed distances
• "Suicide runs" on-court

Track athletes

• Running repeat hills
• Cross-country racing

WHAT TO DO ABOUT EXERTIONAL SICKLING

• Screen athletes during pre-conditioning medical exams -- It is vital to know which athletes have sickle trait.
• Acclimation -- Build up slowly in training. Slow tempo. Longer breathers. Control asthma. Supplemental oxygen for altitude. No workout if ill.
• Modify drills -- No timed sprints or miles. No sprints > 500 m. No all-out exertion of any type for 2-3 minutes without a breather. Adjust work/rest cycles for heat.
• Hydrate -- Ensure good hydration. Check overnight urine to ensure that kidneys can concentrate urine.
• Set the tone -- Athletes should report any unusual symptoms immediately. Coach should consider any struggling, cramping, or collapse as sickling.
• Act fast -- A sickling collapse is a medical emergency. Check vital signs. Give oxygen by face mask. Cool the athlete, if necessary. If there is no improvement very quickly or if vital signs or alertness decline, call 911, attach an automatic emergency defi brillator, start an IV, and get the athlete to the hospital quickly.

SUGGESTED ADDITIONAL RESOURCES

Bergeron, M.F., J. G. Cannon, E. L. Hall, and A. Kutlar (2004). Erythrocyte sickling during exercise and thermal stress. Clin. J. Sport Med. 14:354-356.

Browne, R. J., and Gillespie, C. A. (1993). Sickle cell trait: A risk factor for life-threatening rhabdomyolysis? Phys. Sportsmed. 21(6):80-88.

Dincer H.E., and T. Raza (2005). Compartment syndrome and fatal rhabdomyolysis in sickle cell trait. Wisconsin Med. J. 104:67-71.

Eichner, E.R. (1993). Sickle cell trait, heroic exercise, and fatal collapse. Phys. Sportsmed. 21(7):51-65