[Paleopsych] SW: On Disease in Marathon Runners
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Medical Biology: On Disease in Marathon Runners
http://scienceweek.com/2005/sw050715-5.htm
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
--------------------------------
Related Material:
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
--------------------------------
Related Material:
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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