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ScienceWeek
MEDICAL BIOLOGY: ON DISEASE IN MARATHON RUNNERS
The following points are made by B.D. Levine and P.D. Thompson (New Engl. J. Med. 2005 352:1516):
1) 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 1961 [2] 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.
2) 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.
3) 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.
4) 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.
5) 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.[3-5]
1. Williams H, Arnold HD. The effects of violent and prolonged muscular exercise upon the heart. Phila Med J 1899;3:1233-9
2. 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
3. Derderian T. The Boston Marathon: the first century of the world's premier running event. Champaign, Ill.: Human Kinetics, 1996
4. Casa D. Proper hydration for distance running -- identifying individual fluid needs. Indianapolis: USA Track & Field, 2003.
5. 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
New Engl. J. Med. http://www.nejm.org
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ANTHROPOLOGY: ENDURANCE RUNNING AND HUMAN EVOLUTION
The following points are made by D.M. Bramble and D.E. Lieberman (Nature 2004 432:345):
1) Most research on the evolution of human locomotion has focused on walking. There are a few indications that the earliest-known hominids were bipeds[1,2], and there is abundant fossil evidence that australopithecines habitually walked by at least 4.4 million years (Myr) ago[3,4]. Many researchers interpret the evolution of an essentially modern human-like body shape, first apparent in early Homo erectus, as evidence for improved walking performance in more open habitats that came at the expense of retained adaptations in the australopithecine postcranium for arboreal locomotion [5].
2) Although the biomechanics of running, the other human gait, is well studied, only a few researchers have considered whether running was a mode of locomotion that influenced human evolution. This lack of attention is largely because humans are mediocre runners in several respects. Even elite human sprinters are comparatively slow, capable of sustaining maximum speeds of only 10.2 m/s for less than 15 s. In contrast, mammalian cursorial specialists such as horses, greyhounds, and pronghorn antelopes can maintain maximum galloping speeds of 15-20 m/s for several minutes. Moreover, running is more costly for humans than for most mammals, demanding roughly twice as much metabolic energy per distance travelled than is typical for a mammal of equal body mass. Finally, human runners are less manoeuvrable and lack many structural modifications characteristic of most quadrupedal cursors such as elongate digitigrade feet and short proximal limb segments.
3) However, although humans are comparatively poor sprinters, they also engage in a different type of running, endurance running (ER), defined as running many kilometers over extended time periods using aerobic metabolism. Although not extensively studied in non-humans, ER is unique to humans among primates, and uncommon among quadrupedal mammals other than social carnivores (such as dogs and hyenas) and migratory ungulates (such as wildebeest and horses).
4) In summary: Striding bipedalism is a key derived behavior of hominids that possibly originated soon after the divergence of the chimpanzee and human lineages. Although bipedal gaits include walking and running, running is generally considered to have played no major role in human evolution because humans, like apes, are poor sprinters compared to most quadrupeds. The authors assess how well humans perform at sustained long-distance running, and review the physiological and anatomical bases of endurance running capabilities in humans and other mammals. Judged by several criteria, humans perform remarkably well at endurance running, thanks to a diverse array of features, many of which leave traces in the skeleton. The fossil evidence of these features suggests that endurance running is a derived capability of the genus Homo, originating about 2 million years ago, and may have been instrumental in the evolution of the human body form.
References (abridged):
1. Haile-Selassie, Y. Late Miocene hominids from the Middle Awash, Ethiopia. Nature 412, 178-181 (2001)
2. Galik, Y. et al. External and internal morphology of the BAR 1002'00 Orrorin tugenensis femur. Science 305, 1450-1453 (2004)
3. Ward, C. V. Interpreting the posture and locomotion of Australopithecus afarensis: where do we stand? Yb. Physical Anthropol. 35, 185-215 (2002)
4. Aiello, L. & Dean, M. C. An Introduction to Human Evolutionary Anatomy (Academic, London, 1990)
5. Rose, M. D. in Origine(s) de la BipÚdie chez les Hominides (eds Coppens, Y. & Senut, B.) 37-49 (CNRS, Paris, 1991)
Nature http://www.nature.com/nature
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MEDICAL BIOLOGY: DOPING AND ATHLETIC PERFORMANCE
The following points are made by Timothy D. Noakes (New Engl. J. Med. 2004 351:847):
1) Is it possible for the "natural" athlete who competes without chemical assistance to achieve record-breaking performances in sports requiring strength, power, speed, or endurance? Because doping tests are infrequently positive in international sports, it has been widely believed that the answer is yes -- and that few athletes competing in major sporting events, including the Olympic Games and the Tour de France, use performance-enhancing drugs. But multiple sources of evidence, including personal testimony(1,2) and an ever-increasing incidence of doping scandals, suggest the opposite: that widespread use of performance-enhancing drugs has fundamentally distorted the upper range of human athletic performance.(1,3-5) Unfortunately, a global code of silence has kept the problem hidden from public view.(4,5)
2) Drugs have been in sports for a long time. In the earliest modern Olympic Games, the drugs of choice included strychnine, heroin, cocaine, and morphine,(4) which were probably more harmful than helpful. The first "effective" performance-enhancing drugs, the amphetamines, which were used widely by soldiers in the Second World War, crossed over into sports in the early 1950s.(4) These drugs -- nicknamed "la bomba" by Italian cyclists and "atoom" by Dutch cyclists -- minimize the uncomfortable sensations of fatigue during exercise. By setting a safe upper limit to the body's performance at peak exertion, these unpleasant sensations prevent bodily harm. The artificial manipulation of this limit by drugs places athletes at risk for uncontrolled overexertion.
3) The first cases of fatal heatstroke in athletes using atoom were reported in the 1960s. In the 1967 Tour de France, elite British cyclist Tom Simpson died on the steep ascent of Mont Ventoux, allegedly because of amphetamine abuse. The precise extent to which amphetamines enhance athletic performance is unknown, since, as with all performance-enhancing drugs, there are few modern studies quantifying their effects. The convenient absence of such information represents further evidence of a hidden problem. A popular opinion is that la bomba can turn the usual Tour de France domestique, or support rider, into a stage winner.
4) Since amphetamines must be present in the body to be effective, the sole method of avoiding the detection of their use during competition is to substitute a clean urine sample for the doped specimen. A multitude of innovative techniques have been developed to accomplish this swap.(2) Cortisone, a potent but legal performance-enhancing drug used to dampen inflammation, also reduces the discomfort of heavy daily training and competition and lifts the mood. It is also widely abused by professional cyclists.(2)
5) Testosterone propionate (Testoviron), the prototype of the anabolic steroids, the second major group of potent performance-enhancing drugs, was synthesized in 1936 and appeared in sport sometime after the 1948 Olympic Games. The subsequent synthesis of methandrostenolone (Dianabol) in the USin 1958 and oral chlordehydromethyltestosterone (Turinabol) in East Germany after 1966 marked the beginning of the "virilization" of modern sport.(4) By increasing muscle size, these drugs increase strength, power, and sprinting speed; they also alter mood and speed the rate of recovery, permitting more intensive training and hence superior training adaptation. For maximal effect, anabolic steroids are used in combination with other hormones that have similar activity, including insulin, growth hormone, and insulin-like growth factor. They have multiple side effects, some of which are serious, including premature death.
References:
1. Reiterer W. Positive -- an Australian Olympian reveals the inside story of drugs and sport. Sydney: Pan Macmillan Australia, 2000
2. Voet W. Breaking the chain: drugs and cycling; the true story. Fotheringham W, trans. London: Yellow Jersey, 2001
3. Franke WW, Berendonk B. Hormonal doping and androgenization of athletes: a secret program of the German Democratic Republic government. Clin Chem 1997;43:1262-1279
4. Hoberman JM. Mortal engines: the science of performance and the dehumanization of sport. New York: Free Press, 1992
5. Hoberman JM. How drug testing fails: the politics of doping control. In: Wilson W, Derse E, eds. Doping in elite sport: the politics of drugs in the Olympic movement. Champaign, Ill.: Human Kinetics, 2001:241-70
New Engl. J. Med. http://www.nejm.org
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