[Paleopsych] SW: On Disease in Marathon Runners

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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
    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
    Related Material:
    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
    Related Material:
    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
    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.
    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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