Running and Your Health

By Tim Noakes, MD

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    George Sheehan was one of the first people to dare suggest that most runners do not actually run to be healthy. Accordingly, he proposed that runners be classified into one of three groups-joggers, racers, and runners-on the basis of their motivations for running (Sheehan 1978b).
    Joggers, Sheehan contended, are the physically reborn who preach the gospel of jogging for health and longevity. They will bore anyone incautious enough to ask with evangelical details of how jogging saved their lives. And as they begin to discuss the evidence that exercise increases longevity and protects against coronary heart disease (with names like Morris and Paffenbarger tripping off their tongues as if they were the jogger's nearest and dearest friends), they will be inspecting you carefully, looking for those telltale signs indicating your need for physical reform.
    Fortunately for all of us, most joggers grow up. As joggers mature, they begin to realize that the passions that motivate people to become healthy are the same as those that transform the jogger first into a racer and then finally into a runner. Sooner or later, the jogging bore may find that jogging has become boring. The exercise prescription that has made the body healthy has failed to do anything for the mind. The mental challenge to start exercising and become healthy has gone. It is time to move on-to enter a race.
    As soon as joggers mail their first race entry forms, they become racers and enter a new world. The racer, you see, no longer has any concern for health. The sole concern is performance, with the desire to run faster. Every training session, every waking moment, is concerned with what will make the legs run farther in less time. As the racer's expectations can never be satisfied, it is not possible to train sufficiently, or race enough. The result is that if there indeed are any medical dangers associated with jogging, they occur almost exclusively among the racers.

    Sheehan suggests that running competitively (racing) does for the mind what jogging does for the body. The race provides the fear, the excitement, the physical challenge from which our modern, repetitive, unchallenging nine-to-five lives have sheltered us.

    Ultimately, the jogger/racer may evolve into a runner who is unconcerned about the health aspects of running and whose psyche no longer needs the challenge of the race. The runner runs to meditate, to create, and to become whole. Sheehan writes: "Running is finally seeing everything in perspective. . . . Running is the fusion of body, mind and soul in that beautiful relaxation that joggers and racers find so difficult to achieve" (1978b, p. 287).

    With this introduction, let us discuss the real and perceived medical problems associated with running in general and racing in particular.

Gymboss Timers


    Most people who develop constriction of the bronchial airways during exercise are aware that they suffer from asthma and are under medical treatment for this condition. For this reason, I will not discuss this topic in detail but will cover it briefly along with exercise and lung cancer risks, and respiratory infections, including rhinorrhea (athlete's nose), pulmonary edema, and the phenomenon of the "second wind."

Exercise-Induced Asthma

    In essence, the bronchial airways of asthmatics are especially sensitive to a number of stimuli, including, for example, cold air, infections, cigarette smoke and other pollutants, and various allergic stimuli (such as house dust, animal dander, and certain foods). When exposed to these stimuli, the muscles lining the respiratory airways go into spasm, causing severe narrowing of the small air passages. This narrowing acts like a ball valve, allowing air to enter the lung but preventing its escape during normal exhalation. Thus, during an attack, the asthmatic has great trouble exhaling and the lungs become progressively more distended by trapped air, causing progressive respiratory distress.

The important practical points about asthma and its management are as follows.

    ◘    The condition must be treated by a medical practitioner.
    ◘    The vast majority of asthmatic symptoms can be adequately controlled, if not completely eliminated, by the use of appropriate medication (Hansen-Flasschen 1998). However, some of these medications contain substances that are banned by the International Olympic Committee (IOC). Thus, if you are an elite athlete who is likely to undergo doping control during competition, you must ensure that you use only those drugs that are cleared by the lOC for use during competition.
    ◘    Far from avoiding sport, asthmatics, especially children, should be encouraged to be as active as possible in sport, not only because the exercise will frequently reduce the amount of medication they need to control symptoms (King et al. 1989) but also because of the psychological benefits of participating in an activity. Running, however, is not the exercise of choice for asthmatics. For reasons that are not entirely clear, running is more likely to produce asthmatic attack than is, for example, swimming. If the asthma is well controlled, however, running can be encouraged.
    ◘    Despite the value that regular physical activity has for children with asthma (King et al. 1989), it is also clear that asthma is more common in elite athletes, especially endurance athletes, such as long-distance runners (Helenius et al. 1997) and cross-country skiers (Wilber et al. 2000), as well as power athletes (Nystad et al. 2000), than it is in the general population. Women are particularly at risk (Nystad et al. 2000). Risk rises with increased hours of training per week and is greatest in the group that trains the most (about 20 hours per week; Nystad et al. 2000). These findings invite the hypothesis that strenuous physical training is a risk factor for the development of asthma.
    Nystad et al. (2000) speculate that three factors may contribute to the higher incidence of asthma in athletes:
    1. Repeated damage from over stimulation of the mechanisms that protect against dry air-induced damage to the linings of the respiratory airways (repeated injury may lead to chronic inflammation)
    2. Recurrent infections that may be more common in athletes who train intensively
    3. Increased exposure to environmental factors, including air pollutants, that may increase the risk of developing asthma

Lung Cancer
    The risk of developing lung cancer, a condition usually associated with cigarette smoking, is substantially reduced in physically active men (Wannamethee et al. 1993; Lee and Paffenbarger 1994; Thune and Lund 1997), although no effect was found in women (Thune and Lund 1997).

Respiratory Infections
    The high incidence of the symptoms of respiratory infections in competitive runners in the week following major competitions (Nieman 1994) was discussed in chapter 10. The reason for the high incidence of these symptoms is unknown but may be related to two factors. The first is trauma to the membranes of the respiratory passages caused by sustained high levels of ventilation. Such damage will be exacerbated if the environmental temperatures are low. The second is exercise and diet-induced (Kono et al. 1988) impairment of the body's resistance to infection owing to alterations in the function of the immune system (Lewicki et al. 1987; Nieman, Berk, et a11989; Nieman, Johanssen, et al. 1989; Berk et al. 1990; Mackinnon and Jenkins 1993; Nieman 1995; Pedersen and Hoffman-Goetz 2000) or of the cilia in the respiratory tree that clear the airways of mucous and bacteria (Milns et al. 1995). However, there is growing evidence that these symptoms cannot be due to infections since they occur too soon (28 to 48 hours) after exercise, whereas the normal incubation period for viral infections is three to five days longer. Thus, trauma-induced inflammation is the more likely mechanism causing symptoms of respiratory infection.
    Regardless of the mechanism, you need to remember that you are at high risk of respiratory tract inflammation, allergy, or infection when you race competitively, especially in cold conditions. After such races, be extremely wary of starting training too soon. Remember that these symptoms always mean that you have done too much and are in need of rest, not more training. I continue to be amazed at the number of athletes who are ignorant of this basic fact and who continue to train through illness either before or after competition, and who are unable to understand why they perform so poorly for as long as they continue to train. Only when they stop training and rest will they have any chance of again performing to their potential.
    When should an athlete with a respiratory or other infection compete again? The most comprehensive advice I could find is that followed by the Swedish cross-country skiers, who are particularly prone to respiratory infections because they train and compete in very cold temperatures. Because they train in the cold, they are also more likely to suffer bronchoconstriction (asthma) if they exercise with respiratory infections, and they are at increased risk of developing asthma in the long term, particularly if they suffer frequent respiratory infections.
    Swedish cross-country skiers receive the following advice, equally applicable to runners (Bergh 1982):
    ** Never train hard and never race when you have an infection or are otherwise in poor health. If possible, seek the advice of a physician.
    ** Do not train or compete if you have a fever, a sore throat, or a bad cold or if you have just been vaccinated (within 3 to 7 days).
    ** You can continue training but should not train hard or compete if you have recently been ill, have a light (head) cold, or have a slightly blocked or runny nose with no fever or sore throat. Do not resume training until you are completely well and consult your physician. If you have a cold or other contagious condition, do not train, race, or go to training camps with other athletes.
    ** To race when you are not completely well is misguided loyalty to your teammates, club, or organization and leaders. Racing when you are ill can have serious consequences, as you may risk your health or your life.
    Runners are frequently unwilling to take antibiotics to treat their infections because of their fear that antibiotics will jeopardize their performances. In fact, it is the infection that jeopardizes running and indicates that runners have overtrained. Antibiotics have not been shown to affect performance adversely (Kuipers et al. 1980).
    Nasal secretions are increased during exercise (Stanford and Stanford 1988), possibly due to the increased humidification of the inhaled air. The effect is reversed relatively quickly after the cessation of exercise. This condition could possibly also be part of an allergic response.

Pulmonary Edema
    Fluid may accumulate in the lungs (a condition known as pulmonary edema) of healthy athletes if the heart fails temporarily, as reported in two Comrades ultramarathon runners (McKechnie et al. 1979); if there is marked fluid overload caused by excessive fluid consumption before (Weiler-Ravell et al. 1995) or during exercise (Noakes 1993); or if the athlete is treated inappropriately with excessive volumes of intravenous fluids after exercise for the wrong reasons (for example, the treatment of cramps; Noakes 1998a) or, even more inappropriately, for an unrecognized heart attack after ultramarathon running (Noakes et al. 1977), the symptoms of which were ascribed to the "dehydration myth."
    The fluid content of the lungs increases transiently after prolonged exercise (Caillaud et al. 1995), and this reduces the capacity of the lungs to transfer gasses. The cause and significance of this finding is unknown.

Second Wind
    The second wind is one of the more interesting and least understood phenomena in exercise physiology. It is defined as the subjective sensation of reduced breathlessness (dyspnea) that comes on after a few minutes of hard exercise.
    Perhaps one of the first references to this phenomenon comes from Webster. He suggested without any experimental justification that
When the second wind, that feeling of renewed energy that the runner experiences, comes on, a certain alkaline substance, created or multiplied in the blood by the process of training, begins to neutralize the acidity that has been produced by exercise activity running on into the beginning of fatigue. (Webster 1948, p. 119)
    The only scientific studies of the second wind are those of Scharf, Bark, et al. (1984) and Scharf, Bye, et al. (1984), who showed that, at the onset of the second wind, there was a change in the function of the muscles of inspiration. Specifically, there was a reduction in the number of muscle fibers recruited, indicating that the contractility of the inspiratory muscles, particularly the diaphragm, had increased. They suggest that a redistribution of blood flow to the diaphragm and stimulation of the contractility of the inspiratory muscles by adrenaline and other hormones could explain this change.
    They also suggest that the progressive breathlessness that develops during prolonged exercise may represent a reversal of the second wind-that is, a progressive failure of the contractility of the inspiratory muscles, requiring the recruitment of more muscle fiber, causing the subjective sensation of increasing breathlessness.

    Although the exact cause of coronary heart disease is unknown, certain known risk factors are associated with the disease. Therefore, the risk of developing the disease increases with the number of risk factors present. The most important risk factors include the following.
    ◙ Cigarette smoking. Smoking is one of the most powerful coronary risk factors and acts to increase the rate of development of coronary atherosclerosis (see chapter 5) by mechanisms as yet unknown. The most likely effect is a direct action of one or more constituents of cigarette smoke on endothelial and media cells in the arteries. The increased risk associated with cigarette smoking only abates about 15 years after stopping smoking (Robinson et al. 1989). It has been suggested that "smoking may be the gateway to an unhealthy lifestyle in general" (Prättäla et al. 1994) and that "about half of all regular cigarette smokers will eventually be killed by their habit" (Doll et al. 1994). On the other hand, smokers who are physically active have a 40% lower risk of heart attack than do smokers who are not active (Paffenbarger et al. 1978; Hedblad et al. 1997). Physically active smokers live longer than inactive smokers (Hedblad et al. 1997; Ferrucci et al. 1999) so that their further life expectancy at 65 or 75 is as good as, or perhaps marginally better than, that of sedentary nonsmokers (Ferrucci et al. 1999). Exercise also improves the maintenance of smoking cessation in women (Marcus et al. 1995).
    Elevated blood pressure (hypertension). Hypertension increases the risk of heart attack (and stroke). The accepted cutoff blood pressure, above which risk begins to rise more substantially, is 140/90 mmHg.
    ◙ Elevated blood cholesterol levels (hypercholesterolemia)-in particular, a , reduced ratio of high-density lipoprotein (HDL) to total cholesterol (Stampfer et al. 1991). Confirmation of these levels as direct cause of heart attack comes from studies showing that a new group of medications, the statins, lower blood cholesterol concentrations and reduce the risk of heart attack, even in those with "average" blood cholesterol concentrations, whether or not they already have diagnosed heart disease (Sacks et al. 1996).
    As is the case with all these risk factors, people who are physically active are at lower risk of developing coronary heart disease at any level of risk factor, including any blood cholesterol concentration (T.B. Harris et al. 1991). This means that exercise provides a measure of protection against coronary heart disease even in the presence of one or more coronary risk factors.
    The contention that low blood cholesterol levels may be undesirable because of an increased risk of cancer (Schatzkin, Hoover, et al. 1987) is not supported by other studies (Sherwin et al. 1987; K.M. Anderson et al. 1987). Hence, as is the case with systolic blood pressure, statistically speaking, the lower the blood cholesterol concentration (or the systolic blood pressure), the lower the risk of developing heart disease. But the risk for heart disease increases exponentially with rising blood cholesterol concentrations (or blood pressure). Thus, whereas small changes in those with high blood cholesterol concentrations (or markedly elevated blood pressures) substantially reduce the risk for heart disease, even quite large changes in the blood cholesterol concentrations or blood pressures of those who are already at low risk because their blood cholesterol concentrations (or blood pressures) are already low may produce a disappointingly small effect. Those who benefit from any intervention, be it increased physical activity or a lowering of blood cholesterol concentrations or blood pressure, are those who are at the greatest risk to begin with. Those who are most unhealthy stand to benefit the most; the very healthy benefit the least, because they are already at such low risk.
    Interestingly, the presence of the common coronary risk factors-hypertension, hypercholesterolemia, and obesity-is associated with poor endurance capacity in healthy, asymptomatic younger people (Abbott et al. 1989).

    Elevated blood concentrations of fibrinogen (Kannel et al. 1987; Ridker 1999), high-sensitivity C-reactive protein, and homocysteine (Ridker 1999). Blood fibrinogen levels are lowest in those who are the most physically active (Connelly et al. 1992; Ernst 1993) and are reduced by physical training (Meade 1995). Furthermore, the concentration of tissue plasminogen activator, whose function is the opposite of fibrinogen, rises with increasing levels of physical activity (Eliasson et al. 1996).
    Whereas elevated blood fibrinogen concentrations increase the risk of heart disease, it is the combination of an elevated high-sensitivity C-reactive protein concentration with a low ratio of total cholesterol to HDL cholesterol that is really important. Hence, this combination is associated with a fivefold increased risk of heart attack, compared to a threefold increased risk if the blood cholesterol ratio is considered alone (Ridker 1999).
    Blood C-reactive protein concentrations are an indirect marker of inflammatory processes in the body (Strachan et al. 1984); the finding that their elevated concentrations in blood can predict risk of future heart attack invites the hypothesis that inflammation is involved in, or may indeed cause, coronary artery atherosclerosis (Ridker et al. 1998). lf this is correct, it may explain why the long-term use of the anti-inflammatory drug aspirin is so effective in reducing the risk of further heart attacks in those with coronary heart disease (lSIS2 Collaborative Group 1988).
    ◙ Lower social class. Risk rises appreciably with decreasing social class (Lapidus and Bengtsson 1986; Wing et al. 1987). This is due, at least in part, to an increasing prevalence of the classic coronary risk factors-cigarette smoking, elevated blood cholesterol concentrations, increasing body mass index, and elevated blood pressure-in the lower socioeconomic classes (Shewry et al. 1992).
    European ancestry. There are also ethnic differences in the incidence of the disease, which is highest in North Americans and Europeans and lowest in Africans and those living in less developed countries. Part of the effect may be due to differences in diet and physical activity patterns. Life expectancy is also less in people living in less developed countries, most especially in African, South American, and Asian countries that have been engulfed by the HIV / AIDS epidemic. Coronary heart disease is a disease of aging and will therefore be less common in populations dying at younger ages from other causes.
    ◙ Male gender. Males are more prone to heart disease than are females. This effect is probably related to the presence of testosterone and other androgenic hormones that are present in low concentrations in women. Some also believe that body iron stores may be related to the risk of heart attack (Salonen et al. 1992; J.L. Sullivan 1992; Roest et al. 1999; Salonen et al. 1999). In line with this theory, the monthly loss of iron through menstruation may offer women increased protection against coronary heart disease. Furthermore, physical activity also reduces body iron stores (Lakka et al. 1994) and serum ferritin concentrations (pate et al. 1993), the latter being a measure of body iron reserves.
    Women lose their relative protection from heart disease following menopause, after which they have low or absent blood estrogen concentrations. lf estrogen protects women from heart disease before menopause, then estrogen therapy after menopause should reduce their subsequent risk of developing this condition. At present, there is uncertainty whether estrogen replacement therapy initiated after menopause can prevent or delay the development of coronary heart disease (NabeI2000) but definitive studies-the Women's Health Initiative and the Raloxifenen Use for the Heart (RUTH) trial-are currently in progress.
    ◙ Family history of heart disease. People who have a close family history of heart disease, either in grandparents, parents, uncles, aunts, or siblings, are at increased risk. When such relatives have died from heart disease before the age of 45, it suggests that the family may carry the genes for very high blood cholesterol levels, displaying the so-called familial hypercholesterolemia. Members of families with a history of early deaths from heart attack should consult their doctors and have their blood cholesterol levels and blood pressures monitored.
    Certain disease states, such as diabetes. Diabetes is one of the most malignant chronic diseases, with a long-term prognosis little better than that of many of the cancers. Arterial damage is a cardinal feature of diabetes that substantially increases the incidence of heart attack, stroke, peripheral vascular disease, and kidney failure, all due to arterial disease.
    ◙ Short stature and early aging. The reason people of short stature (under 1. 7 m) should be at increased risk of heart disease is unknown (Herbert et al. 1993). Men, but not women, who show early signs of aging, including graying hair, frontal baldness, and facial wrinkling, are at increased risk of heart attack (Schnohr et al. 1995).
    Male- ("apple-," or abdominal-) type obesity. In the male form of obesity, there is excess accumulation of body fat in the abdominal organs, giving the typical beer belly. This type of obesity is associated with multiple metabolic abnormalities, including hypercholesterolemia, glucose intolerance, high blood insulin concentrations, and hypertension, so-called Syndrome X. As a result of this clustering of risk factors, people with this form of obesity are at increased risk of developing heart disease (Despres et al. 1990; Avery 1991).
    ◙ Increased body mass index with high waist-to-hip-circumference ratios. Nonsmoking white American men with a body mass index, calculated as weight in kilograms divided by height in square meters, between 23.5 and 24.9 kg per meter have the lowest mortality from death from all causes (Calle et al. 1999). The effect is less apparent in African-Americans. In women, the optimum body mass index is between 22.0 and 23.4 kg per meter. Similar findings have been reported in the Dutch.
    The waist-to-hip-circumference ratio may be a better predictor of death from all causes (Folsom et al. 1993), perhaps because it provides a more accurate measure of the amount of fat stored in the abdominal organs. It is believed that fat stored at that site is more closely linked to the risk of disease than is fat stored at other sites (Peiris et al. 1989).
    Interestingly, patterns of body fatness are established already at age 25 (Voorrips et al. 1992). Furthermore, even quite high levels of physical fitness (running more than 64 km per week) cannot prevent a remorseless increase in body mass index (approximately 0.5 kg per meter per decade) and waist-to-hip-circumference ratio (1.9 cm per decade) with advancing age (P.T. Williams 1997). Nevertheless, those who run the most have the most favorable body mass indexes and waist-to-hip ratios, in part because they have the most favorable ratios at all younger ages.
    P.T. Williams (1997) suggests that this progressive accumulation of body fat may be caused by an age-related decline in blood testosterone concentrations since the administration of testosterone to middle-aged men reduces their waist to-hip circumference ratios (Rebuffe-Scrive et al. 1991). He calculates that, to maintain the same body mass index with increasing age, runners would need to increase their training distance by 23 km per week each decade. This would mean that an athlete running 64 km per week at age 30 would need to more than double his weekly training distance to 133 km per week at age 60 and to 156 km per week at age 70, a physical impossibility at that age (chapter 11).
    ◙ Inappropriate alcohol intake. The intake of moderate amounts of alcohol, especially wine (Grømbræk et al. 1995), is associated with a reduced mortality from all causes, including heart attack and strokes in middle-aged to elderly men and women (Rimm et al. 1991; Thun et al. 1997; Berger et at. 1999; Sacco et al. 1999). The protective mechanisms remain uncertain, as does the exact amount of alcohol that is protective. In general, optimum benefits are achieved with no more than one to two drinks per day (Thun et al. 1997; Berger et al. 1999; Sacco et al. 1999). Whereas wine appears to be especially effective ( Grømbræk et al. 1995), the protective value of beer and other spirits is less well established. The protective effect of alcohol is greatest in those who metabolize alcohol the most slowly because they have a particular allele of the enzyme alcohol dehydrogenase 3 (ADH3; Hines et al. 2001). People with that genotype also had the highest blood HDL-cholesterol concentrations.
    However, the beneficial effect of appropriate alcohol consumption on mortality is quite small and does not compensate for the very much (twofold) increased risk associated with cigarette smoking. Hence, combining moderate alcohol consumption with smoking, a common practice, will not nullify the detrimental effects of smoking on the arteries and heart. Furthermore, alcohol consumption at younger ages is associated with increased mortality from trauma and other conditions, including poisoning (Rehm et al. 1993), and it presumably increases the probability that alcoholism will develop in those with the brain disorder that predisposes to the condition (Nestler and Aghajanian 1997; Leshner 1997).
    The evolutionary origins of human alcohol consumption and alcoholism have been traced by Dudley (2000). He proposes that fruit-eating (frugivorous) birds and mammals, including the human ancestors, may have learned to identify the smell and taste of ethanol in decaying fruit as a marker of energy-dense foods. As a result, alcohol-seeking behavior may have evolved in mammals, including humans, as a spur for nutritional reward. Since ethanol is infrequently available in the wild, alcoholism in those animals with any genetic predisposition is unlikely to occur. But the widespread availability of alcohol in modern society will inevitably convert an evolutionary, beneficial alcohol-seeking behavior in animals to alcoholism in some humans with a genetic predisposition once they are exposed to alcohol.
    ◙ Hostile personality type. Persons with the so-called type-A personality originally defined by Meyer Friedman and Ray Rosenman (1959) possess three characteristics: they are highly competitive and ambitious; they speak rapidly and interrupt others frequently; and they are seized by anger and hostility with uncommon frequency. In short, they are unable to sit back and relax but are consumed by hostility, haste, impatience, and competitiveness. The traditional belief has been that such people have a greater risk of developing coronary heart disease than do people without these characteristics, the so-called type B personalities. It is suggested that, of the three personality characteristics, it is the tendency of the type-A personality to hostility that explains the increased risk of heart disease (R. B. Williams 1987).
    But even hostility is not the best description of the dangerous personality characteristic. Rather, it appears that a mistrust of others, cynicism, is the toxic element in the type-A personality that explains this apparent increased susceptibility to coronary artery disease. The type-A person at risk of heart disease exhibits an absence of trust in the basic goodness of others, believing them to be mean, selfish, and undependable. Tutko (Cimons 1988) has suggested that there are two subsets of the type-A person: the type-A-hostile and the type-A-controlled. He argues that the type-A-hostile is the classic type-A person whose actions are motivated by hostility and anger. In contrast, the type-A-controlled is motivated "by excitement and reward, by the challenge of what he is doing. He's like a kid in a candy store. When he wants more, it's because he loves what he is doing" (Cimons 1988, p. 46). Furthermore, it has been found that middle-aged men who are without symptoms of heart disease but who express hostility are more likely to have silent coronary atherosclerosis than those without such hostility (Barefoot et al. 1994)..
    Another study (Ragland and Brand 1988) suggests that, at least after an initial heart attack, the risk of sudden death or heart attack is lower in type-A than in type-B people. Thus, the degree to which the type-A personality characteristics contribute to an increased risk of coronary heart disease remains controversial. Interestingly, owners of pets have an enhanced survival after heart attack (Friedman et al. 1982) and lower blood pressures and blood cholesterol and triglyceride concentrations (W. P. Anderson et al. 1992). Perhaps pet owners are likely to have less-hostile personalities, or else pets may moderate the hostility of their owners.

    ◙ Depression. Men who are depressed are at an increased risk of developing heart disease (Hippisley-Cox et al. 1998).
    ◙ Chronic infection with chlamydia pneumoniae. In contrast to the more accepted theory-that coronary heart disease occurs as the result of arterial damage caused by the interaction of cholesterol, elevated blood pressure, and inflammation-is the "germ theory," which holds that the arterial damage results from chronic infection with as yet unidentified viruses or bacteria. An early study found that patients with acute heart attack were more likely to have evidence of recent or longstanding infection with the bacterium chlamydia pneumoniae (Saikku et al. 1988). This organism was subsequently isolated from the atheromatous coronary artery plaques of patients dying from coronary heart disease (Kuo et al. 1993; Ramirez 1996). More recently, Strachan et al. (1999) found that people with elevated 1gA antibodies to chlamydia pneumoniae had increased mortality, mainly from fatal heart attack, over a 13 year period. They suggest that treatment for this infection may improve survival in people with coronary heart disease.

Lack of Physical Activity
    Six researchers have contributed significantly to our understanding of the relationship between activity level and coronary heart disease. Jeremy Morris, Ralph Paffenbarger, David Siscovick, Ken Cooper, Steven Blair, and Urho Kujaala and their colleagues concluded separately that those who actively exercise are less likely to suffer from coronary heart disease.

Morris' Studies
    One of the first studies to suggest that physical inactivity may be an important risk factor for coronary artery disease was reported in 1953 by Jeremy Morris and his associates at the London School of Tropical Medicine (J. N. Morris et al. 1953). They found that conductors on the London Transport system had a 30% lower incidence of heart disease than did the sedentary bus drivers. A similarly favorable result was found for mail carriers when compared to less active postal clerks, who performed sedentary work.
    However, subsequent analysis suggested that fat, heavy-smoking, high-blood-cholesterol people likely to develop heart disease chose sedentary occupations, while thin nonsmokers with low blood cholesterol levels chose active occupations (J. N. Morris et al. 1956; Oliver 1967). This finding suggests that physical activity at work was not the sole determinant of heart attack among higher or lower risk groups.

    In an attempt to exclude the possibility that people at increased risk of heart attack choose sedentary occupations, Morris' group next studied 16,882 British civil servants, all of whom were involved in sedentary occupations and who were quite similar in respect of their coronary risk factors. This group was then subdivided on the basis of whether they performed vigorous exercise in their leisure time. Vigorous exercise was classified as swimming, tennis, hill climbing, running, jogging, mountain walking, or fast cycling, but these authors did not quantify how often or for how long the required activity had to be.
    The heart attack rate in the vigorously active group was one-third of that in the less active group (J. N. Morris et al. 1973). Furthermore, vigorous exercise in leisure time even offered a measure of protection for smokers and for those with high blood pressure, but, for obvious reasons, these subgroups had a higher heart attack rate than did nonsmoking, vigorously active civil servants whose blood pressures were normal (Chave et al. 1978). A subsequent study (J. N. Morris et al. 1980) confirmed that physical activity provided a degree of protection even for fat civil servants of small stature who smoked or who had high blood pressure, diabetes, or even chest pain. Furthermore, whereas the heart attack rate in the active group stayed the same between the ages of 40 and 60 years, the rate in the inactive group more than doubled during those years.
    J. N. Morris and colleagues (1980) concluded that "vigorous exercise is a natural defense of the body with a protective effect on the ageing heart against ischemia [a reduced blood flow usually caused by progressive atherosclerotic narrowing of the coronary arteries] and its consequences" (J. N. Morris et al. 1980, p. 1207). Vigorous activities included participation in sports and games such as running and jogging, cycling, rugby, squash, badminton, tennis, football, boxing, swimming, hockey, and rowing as well as recreational activities such as aerobics, calisthenics, hill climbing, and gardening (digging, tree-felling) at least twice a week.
In contrast, participation in non-vigorous activities, including walking, golf, dancing, and table tennis, provided no beneficial effect, even in those who walked up to 7 hours per week.

Paffenbarger's Studies
    The next outstanding studies in this field are those by Ralph Paffenbarger and his colleagues (Paffenbarger and Hale 1975; Paffenbarger et al. 1977; 1978; 1983; 1984a and b; 1986; 1993; 1994; Lee and Paffenbarger 1992; 1994; 1998; Sasco et al. 1992; Helmrich et al. 1991). Paffenbarger is an experienced ultramarathon runner, having completed the grueling Western States Hundred-Miler (a mountain race through the Sierra Nevada mountains of northern California) on five occasions, as well as the Comrades and the Two Oceans Marathons in South Africa. He is currently emeritus professor of epidemiology at the Stanford University School of Medicine and has written his own book incorporating his research findings and advice on exercise for optimum health and a longer life (Paffenbarger and Olsen 1996). American sports journalist James Fixx wrote an excellent review of Ralph Paffenbarger and his work in his Second Book of Running (Fixx 1980) in a chapter entitled, "Is Running Really Good for Us?"
    Indeed, it is a sad paradox that Fixx was one of the few journalists to grasp the complexities encountered by scientific studies attempting to measure the cardiovascular benefits of running. His subsequent sudden death during exercise was sadly seen by many as proof that exercise could not be good for anyone, and Fixx's own meticulous reporting of Paffenbarger's research (Fixx 1980) was forgotten in the rush to incriminate jogging as the cause of his death. But Fixx was never under any illusion that running could prevent heart disease absolutely, for he wrote to the effect that, although strange to believe, runners also die.
    In the early 1950s, Paffenbarger chose to study two populations: people who were vigorously active in their occupations (the San Francisco Longshoremen Study: Paffenbarger and Hale 1975; Paffenbarger et al. 1977; 1984a) or in their leisure time (the Harvard Graduate Study: Paffenbarger et al. 1978; 1983; 1984a; 1986; 1991; 1993; 1994; Lee and Paffenbarger 1992; 1994; 1998; Sesso et al. 2000; Paffenbarger and Lee 1997). As the finding from both studies are complementary, only the Harvard Graduate Study will be considered in detail. The special value offered by the Harvard alumni study was that excellent medical data had been collected years earlier, when the alumni were students at Harvard. This made it possible for Paffenbarger to begin a study on subjects whose medical histories were known for up to 40 years previously, staring in 1916. He was therefore able to start a project that covered the life span of his experimental subjects and that would provide significant information in his own lifetime.
    In the Harvard study, Paffenbarger et al. (1978) graded leisure-time activity according to the following classification: 10 stairs climbed every working day each week = 118 kJ per week; one city block walked every working day each week = 235 kJ per week; participation in light sports = 21 kJ per minute; participation in vigorous exercise = 42 kJ per minute.
    Using this classification, they found (Paffenbarger et al. 1984a) that men who reported climbing 50 or more steps each working day had a 20% lower risk of suffering a heart attack than men who climbed less; those who walked five or more blocks daily were at 21 % lower risk than those who walked less; and those who reported vigorous sporting activity in leisure time had a 27% lower risk than those who did not exercise vigorously. Participation in light sporting activity did not influence cardiac risk.
    When total leisure-time physical activity was calculated, it was found that risk of a first heart attack fell with increasing leisure-time physical activity and was 39% lower in those expending more than 8400 kJ of energy in leisure-time exercise each week (figure 15.1).


Calculating Weekly Kilojoule Expenditure
    Runners wanting to calculate their weekly kilojoule energy expenditure to estimate their likely health benefits according to the Paffenbarger studies can do so by referring to figure 15.2. This figure shows that the kilojoule energy expenditure per kilogram of body weight (y-axis on the right) increases linearly with increasing running speed.
    To calculate your total energy expenditure during a particular exercise session, you need to know your body weight, the duration of exercise, and your average running speed. An 80-kg runner whose average running speed is 10 km per hour (6:00 per km) expends approximately 0.83 kJ per kg per minute, or 66 kJ per minute, during exercise. To expend more than 8400 kJ of energy per week, the value shown by Paffenbarger et al. (1984a) to be associated with a 39% reduction in heart attack risk, this runner would need to run at that speed for 8400 + 66 minutes (that is, 127 minutes) per week. Similarly, a 50-kg runner whose average training speed is 16 km per hour (3:45 per km) expends approximately 1.14 kJ per kg per minute (57 kJ per minute) and would need to run 147 minutes per week at that speed to achieve the same total energy expenditure.

    Certain heart rate monitors, including the Polar OwnCal watch, calculate energy expenditure during exercise on the basis of the athlete's mass and heart rate. This calculation is possible because, when a large number of people are studied, there is a linear relationship between energy expenditure and heart rate. Hence, the measured heart rates during exercise can be converted to an estimated energy expenditure in kilojoules or calories.
    However, there is a large interindividual variability in this relationship, so that the actual kilojoule value calculated by the watch may be either too high or too low. Therefore, the real value of these calculations is not in the precise accuracy of the numbers that they provide but rather in the trends that they identify. Thus, measuring energy expenditure on a weekly basis during training enables us to estimate how we compare to the Paffenbarger data (figure 15.1) and can provide an added (health) incentive to maintaining higher levels of physical activity on a weekly, annual, and lifetime basis.

    The Harvard Graduate Study has also produced a number of other important findings, including the following.
    ◙ A leisure-time energy expenditure of less than 8400 kJ per week was as strong a risk factor for a first heart attack as were those other well-established heart attack-risk factors (smoking, high blood pressure, and high blood cholesterol levels). Thus, on the basis of this study, physical inactivity must now be considered to be as important a risk factor for heart disease as the other three risk factors, an opinion that has since received universal support (Powell et al. 1987; Fletcher et al. 1992; Bijnen et al. 1994). It has been subsequently shown that alumni expending more than 8400 kJ per week have a 20% lower risk of developing all forms of coronary heart disease (Sesso et al. 2000), regardless of the duration of their exercise bouts. Hence, equal benefit could be achieved by longer bouts of lower-intensity effort or shorter bouts of more intensive exercise, provided the weekly energy expenditure exceeded 8400 kJ (Lee et al. 2000).
    Only Harvard graduates who remained active after graduation were protected from heart attack. The genetic athletes who won fame and glory on the Harvard sports fields in their college days had a reduced heart attack rate only if they continued to exercise vigorously in the years following their graduation. This suggests strongly that it is continued exercise for life, not genetic ability, that is associated with a subsequent reduction in heart attack risk. More recent findings suggest that, if anything, the health of the former university athletes tends to deteriorate more rapidly with age than that of those who were not athletic at university. This is possibly because the body type of the university athlete proficient in power sports, such as football and baseball, is more likely to be mesomorphic (muscular). Mesomorphy is not associated with longevity or good health in later life (Sheehan 1973), perhaps because mesomorphs may have a higher proportion of Type II fast-twitch muscle fibers. Power athletes with a higher proportion of Type II muscle fibers are at greater risk of developing coronary heart disease than are endurance athletes (Lean and Han 1998; Kujala et al. 2000), perhaps because they have more coronary risk factors, including lower blood levels of the protective HDL cholesterol (Tikkanen et al. 1991; 1996). 

    Exercise offered protection even in the face of other coronary risk factors (Paffenbarger et al. 1978; Sesso et al. 2000). Thus, Harvard graduates who were short in stature, had a parental history of heart attack or hypertension, smoked, were overweight, had high blood pressure, or had a history of diabetes or stroke were still at a 50% lower risk of heart attack if they expended more than 8400 kJ energy per week in leisure-time activities than were alumni with the same risk factors who did not exercise. Figure 15.3 compares the risk of developing a heart attack in smokers and nonsmokers who differ in their amounts of habitual physical activity. The highest risk (relative risk of 1.00) is found in those who smoke more than 10 cigarettes per day and who are not sufficiently physically active, expending less than 500 kJ per week in physical activity (column D). In contrast, those nonsmokers who are the most active (column C) have the lowest risk (relative risk of 0.25), indicating a 75% lower risk of heart attack than inactive nonsmokers. However, it is worth noting that physically active smokers (column I) have a relative risk of heart attack of about 0.5, which is even slightly lower than that of inactive nonsmokers (column A). Therefore, the risk of heart attack is no higher in physically active smokers than in physically inactive nonsmokers. This occurs because cigarette smoking and physical inactivity are equivalent risk factors for heart disease. The avoidance of both risk factors produces the most favorable result (column C).

    ◙ Alumni who reported vigorous leisure-time exercise had a lower risk of fatal heart attack at all levels of total weekly energy expenditure (figure 15.1). Thus, additional benefit seemed to be gained by including vigorous exercise in the exercise sessions. Lee and Paffenbarger's more recent study (1994) found that vigorous but not non-vigorous exercise was inversely related to mortality.
    Those graduates who had suffered a heart attack but who reported 8400 or more kJ per week of leisure-time energy expenditure had a 29% lower heart attack fatality rate than did those graduates who had also suffered heart attacks but who did not exercise as vigorously.
    Vigorously active graduates had a 27% lower risk of developing high blood pressure than did less active alumni (Paffenbarger et al. 1983). The heavier the graduate, the greater the degree to which exercise reduced the risk of developing hypertension (figure 15.4). Even high rates of total energy expenditure in activities of low intensity were not protective. Rather, protection was present only in those who included moderately vigorous activities, such as tennis, cycling, swimming, or running (Paffenbarger and Lee 1997).

    Paffenbarger et al. (1984a) calculated that if five risk factors for heart attack (physical inactivity, cigarette smoking, obesity, high blood pressure, and a family history of heart attack) were removed from all the Harvard alumni, the risk of heart attack would be reduced by 67%.
    Paffenbarger and his colleagues (1986) have shown that the longevity of alumni who exercised vigorously for life is increased. Thus, graduates who continued to expend more than 8400 kJ per week in leisure-time physical activity from the age of 35 years onward enjoyed a two-and-a-half year gain in life expectancy (figure 15.5). Those who began vigorous exercise only after 50 years had a one-to-two-year extension in longevity. A number of other studies support this conclusion that lifelong physical activity probably increases longevity by one to two years (Pekkanen et al. 1987; Heyden and Fodor 1988).

    Paffenbarger's study group has now lived sufficiently long for the effect of recent changes in physical activity patterns to be evaluated. Indeed, this information provides one of the strongest tests of the general hypothesis that physical activity reduces the risk of heart disease. If recent changes in physical activity do not produce changes in line with the findings described, there might be a serious flaw in these findings.
    Fortunately, Harvard alumni who increased their levels of habitual physical exercise to more than 8400 kJ (2000 kcal) per week sometime between 1977 and 1985 reduced their heart attack risk by 26% (Paffenbarger et al. 1993), identical to the reduction enjoyed by those who had always exercised at that level. They also increased their longevity by up to one year. These effects were equivalent to those achieved by stopping smoking. In contrast, the heart attack risk of alumni who stopped regular vigorous exercise increased by 20%. This detrimental effect was greater than the effect of taking up smoking. Hence, an important conclusion from that study was that it is never too late to start exercising. Equally, it is never a good time to stop.
    The effects of changes in body weight on mortality from all causes and from coronary heart disease and cancer were evaluated (Lee and Paffenbarger 1992). Those alumni who remained weight-stable for life were at the lowest risk of mortality from all causes and from heart disease, whereas those who either lost or gained more than 5 kg were at the greatest risk. Lesser amounts of weight loss or weight gain were associated with intermediate risks. Changes in weight did not alter the risk of developing cancer.
    A sister study performed on alumni from the University of Pennsylvania showed that for each additional 2100 kJ per week of energy expenditure, the risk of developing non-insulin-dependent diabetes fell by 6% (Helmrich et al. 1991). Female alumni in that study were also at lower risk of developing breast cancer if they were physically active (Sesso et al. 1998).
    Alumni who had a body mass index greater than 26 kg per m but who expended more than 10,460 kJ per week had a significantly lower risk of colon cancer. In addition, physical activity did not influence the risk of colon cancer in alumni with lower body mass indexes (Paffenbarger et al. 1994). Highly active alumni also had a significantly lower risk of lung cancer. Risks of rectal, prostatic, or pancreatic cancers were not influenced by physical activity.
    Risk of stroke was reduced in alumni who expended more than 4200 kJ per week and fell further in those expending 8400 to 12,596 kJ per week (Lee and Paffenbarger 1998). However, no further reduction occurred with greater weekly energy expenditure. As in the previous studies, activities of light intensity did not reduce risk further.
    Physically active alumni were at a reduced risk of depression but not of suicide (Paffenbarger et al. 1994). The earliest publications of the Harvard Graduate Study focused on factors predicting risk of suicide (Paffenbarger and Asnes 1966), a condition for which this population were at greater risk than most Americans.
    The risk of Parkinson's disease was also slightly reduced in physically active alumni (Sasco et al. 1992).

Siscovick's Studies
    The third researcher who has made a significant contribution in this field is David Siscovick, a research cardiologist currently working at the University of North Carolina.
    Siscovick and colleagues (1982; 1984a; 1984b) collected detailed information on all people who died suddenly in Seattle, Washington, during a one-year period. Analysis of 145 sudden deaths in a group of people who were, to all intents and purposes, absolutely healthy right up to the moment they died showed that those who exercised vigorously on a regular basis had an overall risk of sudden death approximately two-thirds lower than that of the non-exercisers (figure 15.6; compare lines A and C). However, the risk of sudden death in the habitually exercising group increased acutely during exercise (vertical column D in figure 15.6). Thus, although habitual exercisers had a reduced risk of sudden death, that subset of exercisers with advanced heart disease who would ultimately die suddenly were more likely to die while they were exercising than when they were at rest.

    This finding explains why the sudden death of athletes usually occurs during exercise and also why such events do not prove that exercise is dangerous and should therefore be avoided. In fact, if the habitual exercisers were to stop exercising, their risk of sudden death would increase threefold, as shown in figure 15.6, since their incidence of cardiac arrest would rise from line A to line C, a 66% increase. This group (Lemaitre et al. 1999) has also shown that moderate physical activity, including walking for exercise or gardening, performed for more than 60 minutes per week was as effective as more vigorous or prolonged exercise in reducing the risk of sudden cardiac arrest.
    Therefore, the studies of Siscovick and colleagues confirm the finding that the risk of sudden death is reduced in people who exercise regularly. But they also show that there is an increased likelihood that those people who have heart disease in spite of their regular exercise will die during their exercise bouts. Interestingly, the degree of benefit is directly related to the higher the level of coronary risk; people who are at low risk of dying suddenly from coronary heart disease benefit less from vigorous physical exercise than do those who are at high risk either because of a family history of heart disease or because they are smokers who have other risk factors already described.
    As Siscovick et al. have stated, "Efforts to discourage clinically healthy people at risk of primary cardiac arrest from continuing to engage in vigorous exercise may be inappropriate" (1984b, p. 625). More recently, Siscovick et al. (1997) found that coronary risk factors and markers of sub-clinical (asymptomatic) heart disease fell with increasing intensities of leisure-time physical activity in men and women older than 65. They therefore concluded that the intensity of exercise undertaken in later life was an important determinant of benefit.

Exercise Versus Sudden Death
    If exercise has a protective role in heart disease, why is it that some athletes die suddenly during exercise? This is a question that the media, in particular, seem unable to resist. In an attempt to find an answer, I have looked at this phenomenon from a historical perspective.
    The marathon race itself commemorates the immortal run of an unknown soldier, fully armored and "hot from battle," to Athens. His mission was to inform the Greek capital that the invading Persians had been defeated on the plains of Marathon. Within seconds of delivering the joyous words, "Rejoice, rejoice, victory is ours," the messenger reportedly died. While this event was probably mythical (D. E. Martin et al. 1977), genuine tragedies have since been documented in actual marathon races.
    The Greek physician Galen was one of the first to express an opinion on the risk of exercise on the heart. He wrote, Athletes live a life quite contrary to the precepts of hygiene, and I regard their mode of living as a regime far more favorable to illness than to health. . . .
    While athletes are exercising their professions, their body remains in a dangerous condition but, when they give up their professions, they fall into a condition more parlous still; as a fact, some die shortly afterward; others live for some little time but do not arrive at old age (Hartley and Llewellyn 1939, p. 657).
    The first modern sport to attract a similar concern was rowing. In 1845, the seventh Oxford and Cambridge Boat Race was the first to be rowed on the current course on the Thames between Putney and Mortlake. No sooner had it moved to its longer course through the British capital than an irate letter written by one Frederick C. Skey, past president and Fellow of the Royal College of Surgeons, appeared in The Times of London, charging that "The University Boat Race as at present established is a national folly" (Hartley and Llewellyn 1939, p. 657). Skey claimed that rowing was bringing young men to an early grave. A scientific study published shortly afterward by John Morgan (1873), a Birmingham physician, proved that Skey was in error. Morgan showed that the life expectancy of university oarsmen was not reduced. If anything, it was slightly longer than that of the average Englishman of the period.
    The introduction of professional marathon running to the United States after the 1908 Olympic Games marathon (Martin and Glynn 1979) induced the following judgment:
    It is only the exceptional man who can safely undertake the running of 26 miles, and even for them the safety is comparative rather than absolute. The chances are that everyone of them weakens his heart and shortens his life, not only by the terrible strain of the race itself, but by the preliminary training, which produces muscular and vascular developments that become perilous instead of advantageous the moment a return to ordinary pursuits and habits puts an end to the need for them. (New York Times 1909)
    In 1968, this issue was revived in a letter that appeared in the Journal of the American Medical Association (Moorstein 1968), stating that all members of the 1948 Harvard rowing crew had since died "of various cardiac disease"-an assertion that was enthusiastically denied by these oarsmen, who reported that they were all alive and well (Quigley 1968).
    In the 1890s, North Americans suddenly discovered the bicycle, and medicine had another sport about which to express its alarm (M. M. Sherman 1983). Prospective cyclists were warned that prolonged bending over the handlebars could cause kyphosis bicyclistarum, or, in lay terms, cyclist's stoop or cyclist's spine. Then, too, there was cyclist's throat, caused by the inhalation of cold, dusty air, and cyclist's face, the determined grimace that indicated the excessive tension caused by riding a bicycle. The incidence of hernias and appendicitis were also said to be more common in cyclists, and these too were related to the cycling position. Manufacturers were urged to develop a cycle that could be pedaled in the upright position. Women who cycled, it was said, were especially prone to uterine prolapse and to distortion of the pelvic bones and hardening of the muscles of the pelvic floor, both of which would cause difficult labor, should they ever stop cycling long enough to become pregnant.
    Finally, of course, there was cyclist's heart. The working life of the heart was limited to only a certain number of heartbeats, these physicians asserted, and the faster heart rate during cycling would only waste these precious beats and, in so doing, lead to premature heart failure.
    One of the next references to the dangers of exercising on the heart was made in 1909 by five eminent British physicians who initiated a chain of correspondence in The Times of London by stating that "school and cross-country races exceeding one mile in distance were wholly unsuitable for boys under the age of 19, as the continued strain involved is apt to cause permanent injury to the heart and other organs" (Friend 1935; editorial 1938).
    Again, this view was easily refuted. From an analysis of 16,000 schoolboys covering a period of 20 years, Lempriere (1930) could find only two cases of sudden death during exercise that were not due to accidents. He concluded that "heart strain through exercise is practically unknown," a conclusion echoed by Sir Adolphe Abrahams (1930; 1951), who denounced the concept of the strained athletic heart. Instead Lempriere (1930) made this very significant observation: "The real risk lies in boys playing games or running after some minor illness, generally slight influenza, and in times of epidemics it is impossible to be sure that no unfit boy takes part."
    Running again became a medical cause célébre in the 1970s, as the popularity of the sport mushroomed. One of the first articles to question the safety of such activity reported that half of 59 sudden deaths occurred during or immediately after severe or moderate physical activity, especially jogging. The authors questioned "whether it is worth risking an instantaneous coronary death by indulging in an activity, the possible benefit of which. . . has yet to be proved" (Friedman et al. 1973, p 1327). They also considered "the possible lethal peril of violent exercise to [heart] disease patients" (Friedman et al. 1973, p. 1327).

Blair and Cooper's Studies
    Many regard the publication of Ken Cooper's classic book Aerobics (1968) as one of the greatest influences on the physical fitness boom that began in the 1970s.
    The influence of Cooper's book can possibly be ascribed to two factors. Cooper was the first to suggest that endurance-type (aerobic) activities were especially beneficial to health-until that time, most people believed that strength, not endurance, was the key to health. More important, Cooper devised a method (Cooper's aerobic points) of grading the amount of exercise performed and thereby assessing the relative health benefits you could expect from participating in different activities for different durations and at different intensities. In accordance with this method, the optimum amount of exercise needed to ensure good health were 30 points in one week. To achieve this you would, for example, need to walk 4.8 km five days per week; run 3.2 km five days per week; cycle 9.6 km five days per week; swim 900 m five days per week; or play handball, basketball, or squash for 40 minutes five days per week. Remarkably, these guidelines are not greatly different from the current activity guidelines of the American College of Sports Medicine (ACSM).
    Cooper's next significant contribution was to establish the Cooper Clinic in Dallas, Texas, for health screening and exercise prescription. By 1981, more than 13,000 medical evaluations and exercise prescriptions had been performed. Realizing that this information would be of great value if the health of the participants were to be followed into later life, Cooper initiated the Institute for Aerobics Research, housed in the grounds of the Cooper Clinic. He contracted epidemiologist Steven Blair to follow the future health of the Cooper Clinic patients, in much the same way that Morris and Paffenbarger followed their respective study populations.
    In 1989, Blair and his team reported that participants who were judged to be physically fit on the basis of their treadmill running performance at the initial screening test had lower mortality from all causes of death, from heart disease, and from cancer at specific sites, than did those who were judged unfit on their initial assessment. As in the studies of Morris and Paffenbarger, risk reduction occurred even in the presence of risk factors, so that those at high risk benefited the most from increased levels of physical fitness. Furthermore, sporting activity at high school or college was not associated with any alteration in risk (Brill et al. 1989).
    Subsequent studies from Blair's group have shown that fitness levels, measured as the number of minutes that subjects can continue to exercise during a progressive maximal exercise test to exhaustion, is inversely related to mortality from all causes and from coronary heart disease in men (Blair et al. 1996) and women (Blair et al. 1993; Blair et al. 1996). People who increased their fitness over a five-year period reduced their mortality risk by 44% (Blair et al. 1995). Members of the moderate-to-high fitness groups usually walked between 2 and 3 hours per week (Stofan et al. 1998), compatible with the current recommendation that 30 minutes of exercise on most days of the week is an optimum exercise dose for most people.
    Using the same population group, Wei et al. (1999) have also shown that sedentary, obese men are at a 2.6 times higher risk of developing coronary heart disease than are men of normal weight. But regular physical activity reduced risk independent of their levels of obesity, indicating that part of the increased risk for obese men results from an associated physical inactivity.
    Although it was not stated in their article (Wei et al. 1999), in other presentations by Blair and colleagues I have heard it suggested that physical activity normalizes coronary risk in the obese, in much the same way as it does in those who are smokers or who have high blood pressure (see figure 15.3).

Finnish Studies
    An unusual characteristic of the Finnish health care system is that all hospital discharges from both public and private hospitals are recorded on a central register. This makes it possible to determine diagnoses and associated medical costs in different Finnish groups, including former athletes.
    Using this technique, a series of studies have shown that Finnish former elite athletes have increased life expectancy (Sarna et al. 1993), which is greatest in endurance athletes (76 years), less in power athletes (72 years), and least in the matched reference group of healthy but non-elite athletic Finns (70 years). Former elite athletes also maintained healthier lifestyles for life. They remained physically active, were more likely to eat fruits and vegetables and to avoid vitamin supplements, and were less prone to taking up smoking or to consuming butter, high-fat milk, and alcohol (Fogelholm et al. 1994). Greater habitual physical activity and a lower smoking incidence could partly explain the greater life expectancy of those athletes.
    This group of former elite Finnish athletes also had a substantially lower risk of developing or dying from coronary heart disease or cancer, or of developing diabetes or hypertension (Kujala et al. 1994b; Sarna et al. 1997; Kujala et al. 1999; Kujala et al. 2000; Pukkala et al. 2000). However, endurance athletes had a greater reduction in the risk of developing coronary heart disease than did power athletes (Kujala et al. 2000), perhaps because endurance athletes participated more often in vigorous exercise after retiring from world-class competitive sport. In another study, mortality among the best Finnish weightlifters between 1977 and 1982 was 4.6 times higher than the expected rate for elite Finnish athletes, whereas elite Finnish weight lifters between 1920 and 1965 had a normal life expectancy (Sarna et al. 1993). The authors suggest that the increased use of anabolic steroids by power athletes after the 1970s might explain that phenomenon.
    Former athletes also had lower total blood cholesterol and higher HDL-cholesterol concentrations with a reduced oxidation of LDL-cholesterol (Kujala, Ahotupa, et al. 1996). Although their risk of developing knee but not hip (Kujala et al. 1999) osteoarthritis was marginally increased, they were less likely to develop occupational disabilities. As a result, those athletes made less use of hospital care, with the greatest reduction (29%) being achieved by the endurance athletes and the least (5%) by the power athletes.
    Kujala et al. (1998) have tried to establish the extent to which genetic factors alone might explain the superior health of former elite Finnish athletes. By studying pairs of Finnish twins in which one twin was more active than the other, they found that the more active twins had lower mortality rates despite having identical or very similar genetic material. Hence, in people with shared genetic material, physical activity reduces mortality rate from all causes of death.



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