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Marathon Maladies
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     Patriots' Day, a Massachusetts holiday commemorating the Revolutionary War Battles of Lexington and Concord, is also the date of the annual Boston Marathon, a 42-km footrace. It was first run in 1897, one year after members of the Boston Athletic Association returned from the reincarnation of the Olympic Games in Greece.

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    As traditional as the marathon itself is the use of the event for research and of its runners as research subjects. In the second year of its existence, two physicians, Harold Williams and Horace D. Arnold, examined urine specimens from some of the runners and noted urinary casts and proteinuria — findings that would later be known as "athletic pseudonephritis."1 Clarence DeMar, a legendary Boston runner, won the marathon an incredible seven times. His total would probably have been higher had he not been advised against competing by a physician who detected what was undoubtedly an innocent flow murmur produced by DeMar's augmented cardiac stroke volume. DeMar was also a subject in studies performed by the noted Boston cardiologist Paul Dudley White, who had a lifelong interest in the marathon and had studied the heart rate of Boston participants in the 1915 and 1916 races. When DeMar died of colon cancer in 1958, White arranged for an autopsy on the already embalmed body. A report in 19612 presented results from both White's earlier studies of DeMar and the autopsy, which showed that the diameter of DeMar's coronary arteries was approximately two to three times that in normal adults. White, a great advocate of exercise who often rode his bicycle to work, was a big fan of the marathon and, ironically, first recognized his own heart disease because of angina that developed as he jogged over to the race venue to watch David McKenzie of New Zealand win the 1967 race.

    Research interest in marathon participants during the first decades of the 20th century was driven by concern for their health. Little was known about cardiac adaptations to endurance exercise, and what was known was determined by auscultation and the use of the "trained finger" for palpation and percussion. Hallmarks of an athlete's heart such as bradycardia, cardiac enlargement, and innocent flow murmurs, were, in the view of the clinicians of the day, possible signs of pathologic heart block, cardiomyopathy, and valvular obstruction. It was not until 1942 that White used electrocardiography to record markedly slow, but normal, sinus bradycardia in athletes. According to Tom Derderian, author of a history of the Boston Marathon,3 marathoners were the test pilots and astronauts of their time, running where none had run before — and possibly risking their health in the process. Concerns about the health of athletes ultimately abated with the growing understanding that these cardiac changes were normal physiological adaptations and that physical activity conferred multiple health benefits.

    In actuality, marathoning is a reasonably safe sport, with less than one death per 50,000 participants. Deaths that occur during less extreme physical activity and in previously healthy persons are usually caused by cardiac disease — predominantly, congenital problems such as hypertrophic cardiomyopathy or coronary anomalies in young athletes and atherosclerotic coronary artery disease in persons older than 35 years of age.

    Nontraumatic causes of death among marathoners and ultramarathoners, military recruits, and persons who labor in hot and humid conditions are more varied; historically, they have included heat stroke and exertional rhabdomyolysis. These conditions are mitigated by adequate hydration, and preventive efforts have led to widespread recommendations for aggressive fluid consumption during endurance events such as marathons. These recommendations stemmed from the argument that because thirst may not be a precise indicator of the state of the plasma volume, fixed (and large) quantities of fluids should be consumed by athletes during endurance events, regardless of fitness level, body size, and known amount or composition of sweat loss.

    However in 1981, during the 90-km Comrades Ultramarathon in South Africa, two cases of hyponatremia developed; they were later reported by Timothy Noakes in a runners' magazine called South African Runner. Although there has been vigorous debate about the relative importance of fluid overload as compared with sodium loss due to sweating in the development of hyponatremia in runners, an extensive literature has accumulated over the past 20 years documenting that the primary cause is water intake in excess of sodium loss. The relative importance of water loss and sodium loss depends on the type and duration of the race, weather conditions, and the rates of these losses (as well as the rate of replacement of water and sodium), which may vary widely among athletes.

    It has become clear that the hormonal and renal mechanisms that correct for water intoxication in athletes constitute physiologic responses, but they can be overwhelmed by the dilution that occurs when one drinks excessive amounts of water — an effect that may be compounded by reductions in renal blood flow and glomerular filtration during exercise. It is important to recognize that currently available "sports drinks" are not protective: most are hypotonic and provide far more water than salt. Similarly, the infusion of large volumes of hypotonic intravenous solution into athletes who have an exercise-associated collapse, especially if it is performed without knowledge of the serum sodium concentration (as it often is by emergency medical personnel who assume that dehydration is the culprit), may exacerbate the underlying pathophysiology and do more harm than good.

    Although it is common to see broad-based recommendations stating that vigorous hydration is essential for preventing heat-related illness arising from participation in any prolonged exercise in the heat, it is now well recognized that excess hydration can lead to hyponatremia — for instance, during military operations or during desert hikes. Indeed, hyponatremia became so common among backpackers in desert areas of national parks that emergency rescue workers in Grand Canyon National Park began to use a "point of care" device for rapid field assessment of the serum sodium concentration in order to detect hyponatremia in collapsed hikers. These devices remain in use and, given the frequency with which hyponatremia appears to develop even during relatively short events such as marathons, should be considered standard equipment in the medical tents for all endurance races that take place in hot environments.

    It should be emphasized that athletes of all types have been instructed that water consumption during exercise is necessary to prevent illness from heat and to maintain performance levels, which is undoubtedly true. However, it is also clear from the article by Almond et al. in this issue of the Journal (pages 1550–1556) that fixed, global recommendations for fluid replacement may not be optimal for individual athletes of different body types and with varying degrees of training and heat acclimatization, and varying rates of water and sodium loss. The fact that a slower pace during a race (and therefore a longer period when water can be consumed) seems to be a risk factor for this complication makes sense in the context of this discussion. The recommendation by Almond et al. that fluid-replacement schedules be individualized for athletes competing in such events is sensible and practical and should be considered seriously by all competitors.

    In fact, many organizations are beginning to revise their recommendations that fixed, large volumes of dilute fluids be consumed during athletic competition. For example, USA Track and Field, the national governing body for track-and-field sports in the United States, now suggests that athletes use thirst as their guide for fluid replacement. This major change in guidelines (from "stay ahead of your thirst" to "replace sweat loss") was released4 just before the 2003 Boston Marathon (the year after the one run by the participants studied by Almond et al.). Moreover, the International Olympic Committee Medical Commission has issued new recommendations regarding fluid intake during participation in sports that emphasize more limited fluid consumption in order to avoid weight gain; these recommendations were disseminated during the 2004 Olympic Games in Athens.5 Whether such changes have actually had an effect on the practices of individual athletes is unknown. Finally, an international consensus conference on exertional hyponatremia is convening in South Africa this spring and should contribute to the setting of new guidelines for fluid replacement during exercise — guidelines designed for the prevention of heat injury and the avoidance of the potentially devastating consequences of hyponatremia.

    The article by Almond et al. continues the long tradition of using the Boston Marathon as a research laboratory. Williams, Arnold, DeMar, and White would be proud to know that the tradition lives on.

    Source Information

    Dr. Levine is a professor of cardiology and the director of the Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, University of Texas Southwestern Medical Center at Dallas. Dr. Thompson is the director of the preventive cardiology program, Division of Preventive Cardiology, Hartford Hospital, Hartford, Conn.

    References

    Williams H, Arnold HD. The effects of violent and prolonged muscular exercise upon the heart. Phila Med J 1899;3:1233-9.

    Currens JH, White PD. Half a century of running: clinical, physiologic and autopsy findings in the case of Clarence DeMar ("Mr. Marathon"). Nord Hyg Tidskr 1961;265:988-993.

    Derderian T. The Boston Marathon: the first century of the world's premier running event. Champaign, Ill.: Human Kinetics, 1996.

    Casa D. Proper hydration for distance running — identifying individual fluid needs. Indianapolis: USA Track & Field, 2003. (Accessed March 24, 2005, at http://www.usatf.org/news/showRelease.asp?article=/news/releases/2003-04-19-2.xml.)

    Maughan RJ, Burke LM, Coyle EF, eds. Food, nutrition and sports performance II: the International Olympic Committee consensus on sports nutrition. New York: Taylor & Francis Group/ Routledge, 2004.(Benjamin D. Levine, M.D.,)