Review Article

Sports Medicine 8 (3): 139-153. 1989 0112-1642/89/0009-0139/$07.50/0 © ADIS Press Limited All rights reserved. SPORT2197A

The Effects of Exercise on Coronary Heart Disease Risk Factors in Children Paul Vaccaro and Anthony D. Mahon Exercise Science Laboratory, University of Maryland, College Park, Maryland, USA

Contents

Summary ....................................... ............. .. ..... ......................................................................... 139 I. Coronary Heart Disease: A Paediatric Problem ................................................................. 140 1.I Family History of Heart Disease .......................................... ............................... .......... 142 1.2 Blood Lipids ............................... ....... ............... .......... ..................................................... 142 1.3 Obesity ............... ....................... .................................................................................... ... 142 1.4 Hypertension ............... ......... ... ..... ...................... ............................................................. 144 1.5 Smoking ........... .......... ............................ ............................................ ..................... ......... 144 1.6 Diabetes Mellitus ................. ................... .. ........ ........... ... ....... .......................... ............... 144 1.7 Stress .................................................................. .......................................... ... ................. 144 2. The Effects of Physical Activity on CHD Risk Factors in Adults ................................... 144 3. The Effects of Physical Activity on CHD Risk Factors in Children ............................... 146 3.1 Obesity and Blood Lipids ............................... ..................... ........ .................................. 146 3.2 Blood Pressure .............................................................. ........................ ........................... 148 3.3 Smoking ........... ........... .................................. ................. .......................... ..... ................... 148 3.4 Diabetes ....... .. .......................... ............ ....... ......................................................... ............ 149 4. Conclusions ................................... ................... ....... .................................... ........................... 149

Summary

Coronary heart disease (CHD) is now recognised as a paediatric problem despite the fact that clinical symptoms of this disease do not become apparent until much later in life. Epidemiological studies of risk factors in children have now been conducted. These studies suggest that the risk factors for cardiovascular disease in adults. which include a family history of heart disease, elevated blood lipids (serum cholesterol and triglycerides), obesity, hypertension, smoking, diabetes mellitus and inadequate physical activity, can be identified in children. Several investigators have reported the existence of one or more risk factors in more than 50% of the children they have examined. It is now clear that we can detect most children who are potentially at risk for CHD. The notion ortracking' some of the most common CHD risk factors in children has been used in several studies. Results from this type of research indicate that children who are at the extreme end of the distribution and have high levels of blood pressure, adverse lipid levels and are obese will continue to exhibit these coronary risk factors as they grow. The research completed at present does not answer the question of whether children who exhibit a coronary-prone risk factor profile will exhibit this same profile at an age when one is most likely to develop the clinical manifestations of CH D. It does make sense, however, to identify those children who may be at risk for developing premature CHD and

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to initiate safe interventions such as behaviour modification. changes in diet and increases in physical activity. These have all been shown to alter risk factors which are associated with increased relative risk of CHD in adults. It should be noted that in adults regular aerobic exercise often may alter all risk factors for CHD. including hypertension and diabetes. Whether regular aerobic exercise will induce similar changes in children is not fully understood.

Coronary heart disease (CHD) due to atherosclerosis remains one of the leading causes of disability and death in industrialised nations. It accounts for more deaths annually than any other disease in the United States. It ranks first in terms of Social Security disability. In direct health care costs and lost wages, it costs the United States in the vicinity of $US60 billion per year (Lipid Research Clinics Program 1984). There has been, however, a decline in CHD mortality for all major sex and race groups since 1968 (Stamler 1978). While this trend has not even put a dent in the catastrophic losses which accompany CHD, it does reflect, at least in part, the outcome of preventative measures which have emerged following the isolation of factors known to be associated with an increased risk of developing atherosclerosis (Castelli et al. 1977; Heldenberg et al. 1979; Kannel 1976; Kannel et al. 1971; Keys 1975; Kolata & Marx 1976; Morrison et al. 1978; Stamber et al. 1979; Stamler 1973; Streja et al. 1978; Webber et al. 1983a). Observational epidemiological studies have established a list of CHD risk factors in adults which identify individuals who are susceptible to premature development of CHD. These include: a family history of heart disease, elevated blood lipids (serum cholesterol and triglycerides), obesity, hypertension, smoking, diabetes mellitus, stress, and inadequate physical activity. There is uncertainty about the relationship the risk factors have to each other and which factors are most important. It does seem that elevated blood lipids may accompany several of the other predictors. Health professionals are now faced with the challenge of establishing methods of intervention which will have significant effects in reducing one"s disposition to CHD, a disease whose origin

has not been isolated. Hypertension and diabetes many times require medication, but most of the other risk factors can be improved by behaviour modification, changes in diet and increases in physical activity levels. There is ample evidence which suggests that regular exercise alone may alter all risk factors for CHD, including hypertension and diabetes (Linder & Durant 1982). Interest in the effects of regular exercise on health is increasing since it is now recognised that physical activity may be an ideal non-pharmacological means of promoting well ness. The main questions being asked concern themselves with the possible benefits of exercise in reducing the incidence of CHD. Does chronic exercise protect one from CHD? If it does, what type of exercise provides the most protection? How much exercise is necessary? What are the physiological and biocpemical changes which take place to induce protection against CHD? Does regular exercise in children reduce the incidence of heart disease due to atherosclerosis in adults? In the remainder of this review we discuss the fact that CHD disease is in reality a paediatric disease. We review the risk factors for CHD and emphasise that most of them are common in children. For the purpose of this review, all individuals up to 18 years of age are considered children. The notion that the early years of life may be the best time for positive intervention for many risk factors are discussed. Special emphasis is given to the use of regular exercise as a possible means of diminishing a predisposition to CHD.

1. Coronary Heart Disease: A Paediatric Problem Coronary heart disease is now recognised as a paediatric problem despite the fact that clinical symptoms of this disease do not become apparent

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until much later in life (Kannel & Dawber 1972). Evidence from autopsy studies indicates that atherosclerosis begins early in childhood (Klotz & Manning 1911; Strong & McGill 1969; Zeek 1930; Zinserling 1925). Fatty streaks are found in the aortas of many children less than 3 years of age and in almost all children who are more than 3 years old (McGill et al. 1963; Strong & McGill 1969; Strong et al. 1972). The presence of fatty streaks in the coronary arteries is rare prior to age 10 years, but beyond this age fatty streaks in the coronary arteries of children occur in escalating numbers. By age 20, most people have evidence of fatty streaks in the coronary arteries (McGill et al. 1963; Strong & McGill 1969; Strong et al. 1972; Velican & Velican 1979, 1980). Some further support for this latter notion can be found in the work of Enos et al. (1953) and McNamara et al. (1971). Enos et al. (1953) demonstrated that 77% of autopsied Korean War casualties, with a mean age of 22 years, had advanced atherosclerotic lesions. McNamara et al. (1971) reported that 45% of the Vietnam War casualties exhibited evidence of coronary heart disease. Others have reported similar findings in groups of comparable young men (Mason 1963; Rigal et al. 1960). It should be noted that there are no longitudinal studies that show that the presence of fatty streaks in children are a good predictor of premature cardiovascular disease later in life. There is no question, however, that the fatty streaks do precede the formation of a fibrous plaque which leads to an atherosclerotic lesion and CHD and its complications such as angina pectoris, peripheral vascular disease, myocardial infarction, cerebral infarction and sudden death. These data suggest that atherosclerosis begins early in life. This stimulated interest in examining CHD risk factors in children. Multiple epidemiological studies of risk factors in children have now been conducted (Gilliam et al. 1977; Lauer et al. 1975; Mjos et al. 1977; Morrison et al. 1978; Morrison et al. 1980; Wilmore & McNamara 1974). These studies suggest that the risk factors for cardiovascular disease can be identified in children. Several investigators have reported the existence of one or more risk factors in more than 50% of the

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children they have examined (Gilliam et al. 1977; Wilmore & McNamara 1974). It is now clear that we can detect most children who are potentially at risk for CHD. In recent years the notion of 'tracking' some of the most common CHD risk factors has been employed in several investigations (Berenson 1980a,b; Boulton 1981; Costello et al. 1983; Cresanta et al. 1983; Laskarzewski 1979; Linder & Durant 1982; Voller & Strong 1981; Webber et al. 1983a,b). This mode of investigation uses the idea that a biological trait assessed at one time may be indicative of this same trait at a later time. It is a measure of the tendency of an individual to maintain a rank relative to her or his peers through time (Webber et al. I 983b). Results from this type of research indicate that children who are at the extreme end of the distribution and have high levels of blood pressure, adverse lipid levels and are obese will continue to exhibit these coronary risk factors as they grow (Laskarzewski 1979; Voller & Strong 1981; Webber et al. 1983a). Many of these risk factors for CHD are influenced by environmental and/or behaviour-lifestyle parameters. Behaviour patterns, which begin at home under parental or guardian influence in most instances, remain stable throughout life and are modified to a degree in the school setting. To illustrate this point it is known that one's eating habits, exercise habits, and smoking habits are established early in life and remain relatively stable from that point on in time. A question which still remains unanswered is whether children who exhibit an adverse CHD risk factor profile will exhibit this same profile at an age when one is most likely to develop the clinical manifestations of CHD. As has been mentioned previously, preliminary tracking studies lend credence to the hypothesis that a child who has multiple CHD risk factors will be at a higher risk for atherosclerosis or hypertension than one who has no risk factors. However, to answer this question definitively would require longitudinal observations beginning in childhood and extending over a lifetime. We have absolute confidence that such observations would show whether CHD risk factors identified early in life do cause increased

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CHD in adults. For the time being it does seem prudent to identify those children who may be at risk for developing premature CHD and initiate safe interventions which certainly would harm no one and could possibly reduce the incidence of CHD. l.l Family History of Heart Disease While it is often impossible to divorce the influence of environment from that offamily history, there is no doubt that heredity is in and of itself a most ·important risk factor for CHD. Risk factors in children are generally higher if their parents' risks are greater (Feinleib et al. 1976; Glueck et al. 1974; Ibsen et al. 1982; Linder & Durant 1982; Montoye 1986). If a child has a first degree relative who has had a myocardial infarction before 55 years of age, the likelihood that this child will develop CHD is increased considerably (Nora 1980a; Nora et al. 1980b). On the other hand, in countries where the incidence of CHD is low, children exhibit positive risk profiles which correspond to this reduced incidence of atherosclerosis. For example, the Pima and Tarahumara Indians, who both have low levels of CHD, also exhibit low levels of total cholesterol in both adults and children (Connor et al. 1978; Savage et al. 1976). Several other studies have also shown that risk factors for CHD show a distinct parent-child clustering (Glueck 1980; Glueck et al. 1974; Heldenberg 1979; Mayer 1968; Morrison et al. 1978, 1980; Stamber et al. 1979; Streja et al. 1978). A promising way to identitY children who may be at risk for CHD as adults is to identitY high risk families and then assess coronary risk factors in children from these families. This identification technique may in the long run be the easiest way to detect children who may be highly susceptible. 1.2 Blood Lipids Epidemiological studies in adults have provided convincing information that elevated total plasma cholesterol levels place an individual at increased risk for CHD (Castelli et al. 1977; Kannel et al. 1971; American Heart Association 1980). It is now

recognised that the relationship between total plasma cholesterol and CHD is not simple. Blood lipids are insoluble in blood plasma and must combine with protein molecules to be transported. This combination of lipid with protein is called a lipoprotein. There are 3 major categories of lipoprotein-cholesterol complexes which have been classified according to size and density. There is high density lipoprotein (HDL), low density lipoprotein (LDL) and very low density lipoprotein (VLDL) cholesterol. Each of these complexes has been shown to be either directly or inversely related to the incidence of CHD. In adults it is now recognised that there is a positive association between CHD and elevated levels of LDL cholesterol (American Heart Association 1980; Castelli et al. 1977; Kannel et al. 1971). More recently an inverse relationship between HDL cholesterol and CHD has been established, and HDL cholesterol is now regarded as having a protective effect against CHD (American Heart Association 1980; Castelli et al. 1977). It is thought to be responsible for carrying cholesterol from peripheral tissues including the arterial walls back to the liver where it is metabolised and excreted (Miller 1978). Although plasma triglycerides and VLDL cholesterol show a positive association with CHD, their importance as independent risk factors has not been as firmly established (Castelli et al. 1977; Kannel et al. 1971). Some investigators have also suggested that the ratio of HDL cholesterol to total cholesterol and the ratio of LDL to HDL cholesterol may be more important determinants of the risks of developing CHD than total, LDL or HDL cholesterol levels utilised as independent predictors of CHD (Adner & Castelli 1980; American Heart Association 1980; Durant et al. 1983). The use of specific apolipoprotein profiles as CHD risk factors has also been suggested by recent investigations, although it should be noted that virtually no data for these parameters are available on children (American Health Foundation 1979; Macek et al. 1985).

1.3 Obesity The age at which obesity in childhood becomes indicative of obesity in adulthood has not been identified. It does seem, however, that obesity in

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later childhood and adolescence may be an excellent predictor of obesity in adulthood (Abraham & Nordsieck 1960; Aristimuno et al. 1984; Hueneman et al. 1974; Kelly et al. 1984; Nutrition Committee Canadian Paediatric Society 1983; RollandCachera et al. 1984; Stark et al. 1981). Since adult obesity and its many consequences are related to weight problems occurring during childhood and adolescence, identification and preventive measures should be considered as early in life as possible. The aetiology of childhood obesity is complex. Heredity is regarded as a contributing factor in the development of childhood obesity. Neuroendocrine and metabolic disturbances contribute significantly to one's propensity for fatness. Environmental factors such as cultural background, socioeconomic status, nutrition (overeating) and physical activity have also been identified as causes of childhood obesity. Overeating and physical inactivity have been implicated as the leading causes of the early onset of obesity (Gilliam & MacConnie 1984). It is impossible to influence heredity factors and difficult to separate hereditary factors from environmental factors when probing for causes of obesity. It does seem that the only viable means to influence the onset of childhood obesity is to alter family life style. To say the least, this is an extremely difficult task which is often impossible to carry out. This notion takes on added significance when one recognises the fact that childhood is the time when people establish eating and physical activity habits (Brownell 1984). Some studies have reported that obese children actually take in fewer calories per unit of bodyweight than non-obese children (Johnson et al. 1956). Hueneman et al. (1974), Saris et al. (1980), and Waxman & Stunkard (1980), on the other hand, have reported that obese boys consume more calories than non-obese boys. At first glance one would find the data which supports the premise that obese children consume fewer calories than non-obese children paradoxical. Closer inspection of these studies reveals the fact that in all instances the non-obese children expended more calories per unit of bodyweight per day than their obese counterparts. This latter finding is supported by several

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others (Ishiko et al. 1968; Parizkova 1974; and Stefanski et al. 1959). It seems safe to say that fat children are less active than lean children. Obesity should be considered an important risk factor for cardiovascular disease in children (Linder & Durant 1982; Mayer 1968; Pate & Blair 1978). It is important to control since it is related to other CHD risk factors such as hypertension, hypercholesteraemia, hyperglycaemia, and hyperuricaemia and it is highly correlated with adult obesity (Linder & Durant 1982; Pate & Blair 1978). In adults, hypertension is clearly related to obesity, with both parameters producing an elevated risk for congestive heart failure and stroke. Weight loss alone has been shown to be an effective measure for reducing and controlling high blood pressure (Craddock 1978). Excess caloric intake also produces abnormal plasma lipid and lipoprotein concentrations. Total cholesterol levels are increased since the liver increases its synthesis of serum cholesterol. LDL cholesterol is typically elevated and HDL cholesterol is reduced in the obese individual (Pollock et al. 1984). VLDL cholesterol production also increases due to its increased production by the liver. This always accompanies elevations in triglyceride levels. These adverse lipid profiles are indicative of a person who is at high risk for CHD. Weight reduction has been shown to be effective in normalising these values. The composition of the diet is also important for controlling bodyweight in children. It has also been associated with lipid and lipoprotein levels, hypertension, and diabetes mellitus. Some studies on adults have reported a linear relationship between dietary intake of saturated fatty acid and plasma cholesterol (Linder & Durant 1982). This has not been extensively investigated in children and the level of dietary cholesterol which produces adverse lipid profiles in children has not been clearly identified. The negative effects of consuming excessive sodium, sugar, and calories on hypertension and diabetes are more clear cut (Linder & Durant 1982). While many questions with regard to the paediatric diet cannot be definitively answered at present, the importance of dietary inter-

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vention programmes in conjunction with physical activity for controlling obesity cannot be denied. 1.4 Hypertension A major risk factor associated with CHD is hypertension. In 1980 it was estimated that 37 million Americans had this disease (American Heart Association 1982). In adults, it appears that as blood pressure rises from normal levels there is a concomitant rise in the incidence of CHD and death. Observations from Berenson et al. (1978) illustrate that blood pressure levels in children and adolescents are good predictors of adult blood pressure behaviour. It appears that essential hypertension may begin early in life and that detection and treatment of possible blood pressure abnormalities at young ages is important. Linder and Durant (1982) suggest that hypertension at a young age when combined with a family history of high blood pressure represents a legitimate risk factor for cardiovascular disease. There is still, however, no evidence which can directly link CHD or death to elevated blood pressure levels in children. Despite this it does seem prudent to detect hypertension as early in life as possible and then to treat this disease before considerable organ damage occurs. 1.5 Smoking

It is known that smoking is an important health hazard in the United States, where mortality from all causes of death is 2 times higher in smokers than in non-smokers (Pollock et al. 1984). In particular, high levels of smoking are associated with an increase in the incidence of lung cancer and an increase in the incidence of CHD. Recent estimates suggest that one-third of all adolescents in the United States now smoke (Smoking and Health 1979). The percentage of young smokers in Germany, Norway, and Czechoslavakia is also alarmingly high (Bell et al. 1986). Adults who smoke generally acquire this habit in adolescence (Nora 1980b). It is also known that the number of years of smoking and the amount of tobacco smoked are

positively related to CHD (Strong 1977). Smoking should be considered an important CHD risk factor in children. 1.6 Diabetes Mellitus It has been suggested that diabetic men are at twice the risk of non-diabetic men for CHD and that diabetic women are at 3 times greater risk than non-diabetic women for CHD (Kannel & McGee 1979). Based on this information it is important to identify the diabetic as early in life as possible in hopes of intervening in a manner which would reduce the likelihood of CHD. It should be noted that the pathogenesis of CHD in diabetics is not fully understood. Despite this it seems reasonable to conclude that early insulin treatment may help prevent hyperlipaemia and obesity, 2 known risk factors for CHD. This may possibly help prevent adult onset cardiovascular disease (Larsson 1984; Sterky et al. 1963). I. 7 Stress

Emotional stress has been suggested as a risk for CHD (Freidman & Rosenman 1974). Coronaryprone behaviour or Type A behaviour is characterised by competitive drive, hurrying, preoccupation with deadlines and excessive aggressiveness. Type B or non-coronary-prone behaviour, which is opposite of Type A behaviour, is associated with one-half the coronary risk of Type A behaviour (Nora et al. \980). It is extremely difficult to quantify Type A behaviour in adults and even more difficult to assess this parameter in a growing child. Its usefulness as a risk factor is therefore questioned by some (Pollock et al. 1984). Linder and Durant (1982) have suggested that the manner in which a child handles psychological, social and environmental stress may be more indicative of risk for CHD than merely the quantity of stress factors a child experiences.

2. The Effects of Physical Activity on CHD Risk Factors in Adults If a person increases their physical activity level or engages in exercise on a regular basis will they lower their risk for developing CHD? The ideal

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study to answer this would require a controlled clinical trial of a large population of infants who are assigned to either a sedentary or an active lifestyle. These subjects would then be closely monitored on a periodic basis for approximately 65 years. In this manner a complete answer to this question would be possible. It is unlikely that such a study will ever be conducted due to the many economic and logistic constraints inherent in such a research design. A number of adult epidemiology population studies have utilised indirect lines of inquiry to investigate the relationship between physical activity and cardiovascular disease and have reported that increased physical activity levels are associated with a lower incidence of heart disease (Brunner et al. 1974; Kagan et al. 1976; McDonough et al. 1965; Paffenbarger & Hale 1975; Paffenbarger et al. 1977, 1978; Taylor et al. 1962). In these studies the prevalence of CHD was contrasted between active and inactive populations. Frequently exercise or physical activity levels were related to angina pectoris, myocardial infarction or CHD death. A limitation to these studies in many instances was the lack of quantification of physical activity which was often determined by physical activity scales. Other studies in adults also indicate that exercise and increased physical activity levels can positively influence several of the risk factors for CHD. For example, cardiorespiratory endurance training which produces increases in Y02max has been shown to be associated with more favourable levels of relative bodyweight (Montoye 1975; Oscai 1973; Pollock 1973). This is of considerable importance when one considers that being overweight is associated with hypertension, hyperglycaemia, hypercholesteraemia, and hyperuraemia (Montoye 1975; Montoye et al. 1976; Stamler 1973; Tyroler et al. 1975). This same type of physical exercise has been shown to have a positive influence on plasma lipids and lipoproteins. Both cross-sectional studies of well-trained endurance athletes and longitudinal studies which have demonstrated improvements in aerobic capacity in individuals before and after a period oflong term endurance exercise suggest that

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long term aerobic exercise increases the levels of HDL cholesterol and decreases the levels of total cholesterol, triglycerides, LDL and VLDL cholesterol, the ratio oftotal to HDL cholesterol and the ratio ofLDL to HDL cholesterol (Wood & Haskell 1979). Although there are some inconsistencies in the studies in adults, hypertension appears to respond well to regular endurance exercise (Boyer & Kasch 1970; Choquette et al. 1973; Garrett et al. 1966; Johnson & Grover 1967). It should be noted that regular aerobic exercise in individuals with normal blood pressure does not result in any further lowering of blood pressure (Pollock et al. 1984). Endurance training in hypertensive individuals does, however, in many instances lower both systolic and diastolic blood pressures (Boyer & Kasch 1970; Brunner et al. 1974; Choquette & Ferguson 1973; Garrett et al. 1966). The mechanisms by which exercise training exerts this normalising effect have not been clearly identified. Cigarette smoking has been shown to increase systolic blood pressure and to reduce the ability to perform sustained work (McHenry et al. 1977). Despite this there appears to be little association between physical activity and cigarette smoking (Paffenbarger et al. 1977; Williams et al. 1980). Often, however, individuals who smoke and then adopt a lifestyle which incorporates physical activity on a regular basis are able to withdraw from a dependency on tobacco (Pollock et al. 1984). In fact, many smoking cessation programmes utilise this principle and incorporate physical activity as a substitute behaviour for smoking. The efficacy of this technique has not yet been established. For many years physical activity has been recommended in the treatment of diabetes mellitus (Errebo-Knudsen 1948; Montoye et al. 1977). In most instances diabetic control appears to improve with a programme of regular exercise (Lawrence 1926; Marble et al. 1971). In summary, there is accumulating evidence which suggests that regular aerobic exercise which increases cardiorespiratory capacity positively affects many risk factors related to CHD. Much less

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is known about the relationship between physical activity and risk factors for CHD in children

3. The Effects 0/ Physical Activity on CHD Risk Factors in Children Since it is now recognised that risk factors for CHD are readily detectable in children at very young ages, it seems logical that intervention strategies might be most effective in childhood before the development of atherosclerosis. As has just been mentioned, intervention strategies which stress increased levels of physical activity have been shown to reduce coronary heart disease risk factors in adults. There is some question with regard to whether the positive effects of exercise seen in adults will occur in children. For example, several authors have reported that regular exercise in children does not result in increases in the dimensional and functional components of the cardiorespiratory system (Bar-Or & Zwiren 1973; Mocellin & Wasmund 1973; Stewart & Gutin 1976; Yoshida 1980). Others however, have reported that regular exercise training in children will produce increases in both ventilatory threshold (Becker & Vaccaro 1983; Mahon & Vaccaro 1989) and V02max (Astrand et al. 1963; Brown et ai, 1972; Ekblom 1969; Kellet et al. 1978; Lussier & Buskirk 1977; Massicotte & MacNab 1974; Sundberg & Elovainio 1982; Vaccaro & Clarke 1978; Vaccaro et al. 1980). Vaccaro and Mahon (1987) in a recent review paper support the notion that regular aerobic exercise in children will produce significant improvements in cardiorespiratory capacity provided the exercise programme adheres to the guidelines established by the American College of Sports Medicine (1978) for intensity, frequency, and duration. They point out that physical activity programmes which do not appear to meet these criteria do not result in improvements in V02max beyond what one would expect to see with normal growth. This notion is supported by Rowland (1985). A question which remains unanswered, however, is at what age will the effects of regular exercise present themselves in children? The ef-

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fects of exercise as a means of reducing risk factors for CHD in children is under active investigation. 3.1 Obesity and Blood Lipids At the present time the question of whether obesity in infancy leads to obesity in adulthood is controversial (Committee on Nutrition of the Mother and Preschool Child 1978; Doyard et al. 1978; Richmond et al. 1983; Vobecky et al. 1983; Wolman 1984). As has been previously mentioned it does seem that obesity in later childhood and adolescence is a very good predictor of obesity in adulthood (Abraham & Nordsieck 1960; Aristimuno et al. 1984; Huenemann et al. 1974; Kelly et al. 1984; Nutrition Committee Canadian Paediatric Society 1983; Rolland-Cachera et al. 1984: Stark et al. 1981). This indicates that the later into adolescence one remains obese, the more likely they will remain this way as an adult. When one also considers the previously mentioned notion that adult obesity is associated with hypertension, hyperglycaemia, hypercholesteraemia and hyperuraemia, early exercise intervention strategies designed to reduce obesity in children may be warranted. The literature available at the present time indicates that obese children have a very low level of physical activity (Huenemann et al. 1974; Parizkova 1972; Shestowsky 1983). Cross-sectional studies which have compared lean and obese children with regard to activity levels, with few exceptions, indicate that fat children are less active than lean children (Ishiko et al. 1968; Johnson et al. 1956; Parizkova 1974; Saris et al. 1980; Stefanski et al. 1959). With this in mind a number of investigations have experimentally manipulated the amount of exercise in obese children to see what effects increased physical activity would have on obesity. The consensus from these studies is that an increase in physical activity will result in a reduction in fatness (Brownell & Kaye 1982; Bryant et aI. 1984; Dwyer et al. 1983; Fisher & Brown 1982; Parizkova et al. 1971; Thompson et al. 1982; Vlasek et al. 1983). It seems that a child's body fatness is inversely related to his/her propensity for per-

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forming endurance activities. This propensity can be determined via assessment of work capacity or V02max (Brownell & Kaye 1982; Bryant et al. 1984; Dwyer et al. 1983; Fisher & Brown 1982; Parizkova 1982; Thompson et al. 1982; Vlasek et al. 1983). This same relationship has been repeatedly exhibited in adults of both sexes (Wilmore 1982). In adults, obesity has been shown to be directly related to adverse plasma lipid and lipoprotein concentrations which usually accompany CHD (Pollock et al. 1984). Data supporting this relationship is beginning to emerge in children. Ylitalo (1984) compared obese and non-obese children (mean age = 11.4 years) following a 2-year conditioning programme which incorporated dietary control and physical training. The training consisted of three 30- to 60-minute sessions per week conducted at an intensity which ranged from 60 to 70% of maximum heart rate. Following this training regimen the non-obese children exhibited higher HDL cholesterol levels and a higher HDL to total cholesterol ratio than their obese counterparts. It should be noted that the confounding effects of diet were not adequately partitioned out in this study thus making it impossible to identify causative factors which contributed to the reported lipoprotein lipids differences between groups. Despite this shortcoming this study indicates that obesity can be linked to adverse lipid and lipoprotein concentrations at a relatively young age. Wenninger et al. (1980) and Srinivasian et al. (1978) have reported data which support the finding that obese children have a tendency toward lower HDL cholesterol values and higher LDL cholesterol values than nonobese children. Some studies have compared physically active children and adolescents with those who are less active. These authors generally reported little differences in total cholesterol across activity levels, but lower values for triglycerides in the active subjects (Thorland & Gilliam 1981; Valimaki et al. 1980; Wanne et al. 1984). This same cross-sectional approach has been employed to assess HDL, LDL and VLDL cholesterol and HDL to total cholesterol values across activity levels. Thorland and Gilliam (1981) found that highly active pre-

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adolescent males (8 to 10 years old) had higher HDL to total cholesterol ratios than did less active subjects. Wanne et al. (1984) supported this notion when contrasting serum lipids in 14- to 16-yearold trained, normally active and inactive children. They reported that trained males had higher HDL cholesterol concentrations and a higher HDL to total cholesterol ratio than did either normally active or inactive children. These authors were unable to demonstrate significant differences in lipid profiles when comparing females of the same ages who were also classified as trained, normally active and inactive. Valimaki (1980), on the other hand, did find significant differences between active and inactive females 11 to 13 years of age on these same parameters. While the data presented in these studies indicate that physical activity may positively affect lipids and lipoproteins in children, we must not lose sight of the fact that in each study the degree of physical activity of the children was assessed using inventories which may have a wide margin of error. To assess physical activity levels in adults using inventories is a difficult task. To do this in children, particularly young children, is even more difficult. There have been a few studies which have experimentally manipulated the amount of exercise children received in an attempt to assess the effects of physical activity on blood lipids. Linder et al. (1979) examined 103 Black children 7 to 15 years of age before and after a 4-week exercise programme of unspecified intensity and frequency. No significant changes in any blood lipids were detected. Whether significant training effects or weight changes occurred were not reported. In a followup study, Linder et al. (1983) examined the effects of a 4 day per week exercise programme on the lipoprotein lipid levels of 50 male volunteers, 11 to 17 years of age. The programme was conducted over an 8-week period. The exercise programme consisted of a 3-day per week walk/jog programme which required the subjects to alternate walking for 60 seconds with jogging 100m 20 times, during week 1, to alternating 7 repetitions of walking for 60 seconds and jogging 600m during week 8. The

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exercise intensity during jogging was 80% of the maximum pulse rate reached during a cycling physical working capacity test. On a fourth day subjects engaged in competitive soccer or rugby. The authors reported improvements in physical working capacity, no changes in body fatness and no changes in blood lipids. Gilliam and Burke (1978) and Savage et al. (1985) have reported favourable alterations in lipoprotein lipid profiles in children as a result of exercise training. Gilliam and Burke (1978) examined 14 girls 8 to 10 years old before and after a 6-week exercise programme. The girls exercised at an unknown intensity 40 minutes per day, 5 days per week. They demonstrated significant improvements in HDL cholesterol values and the ratio of HDL to total cholesterol with no changes in total cholesterol. No controls were used in this study and no evidence of a training effect was reported. Savage et al. (1985) reported improvements in V02max, no changes in dietary intake or bodyweight and significant increases in HDL cholesterol following an II-week training programme in 8-year-old boys. These subjects were involved in a walking/jogging/ running programme, 3 days per week. Distances covered per session ranged from 2.4km in week I to 4.8km in weeks 5 to 11. Exercise was performed at 75% of V02max. In this same study a group of 8-year-old boys who followed the same exercise programme, but performed it at only 40% of V02max did not demonstrate improvements in either V02max or HDL cholesterol levels. The results of these 4 studies (Gilliam & Burke 1978; Linder et al. 1979, 1983; Savage et al. 1985) summarise quite well the conflicting information on the effects that experimental manipulation of exercise has on blood lipids in children. At present it is impossible to isolate the effects of a regular exercise programme on the lipoprotein lipid levels of children. More studies which adequately control for percentage of body fat, dietary intake and intensity, frequency and duration of exercise are required before more definitive conclusions can be reached. It is essential to have this information on normal children before instituting studies on the effects of exercise in children with conditions such

as hyperlipidaemia to see if exercise can be used as a non-pharmacological means of treating this disease. 3.2 Blood Pressure There is a paucity of information with regard to the relationship of blood pressure and physical activity levels in children. That information which is available mirrors that in adults. Aerobic exercise training programmes have been found to produce little change in the blood pressure of children who were normotensive at the onset of training (Dwyer et al. 1983; Eriksson & Koch 1973; Linder et al. 1983; Pate & Blair 1978). Exceptions to this trend have been reported in obese children who have lost weight following a programme of diet and exercise and in children who were hypertensive at the onset of a diet and exercise regimen (Frank et al. 1982; McKenzie et al. 1984). In these instances reductions in blood pressure were seen following the specified intervention strategies. Unfortunately, the effects of exercise on blood pressure could not be isolated in either instance because the confounding effects of diet were not adequately controlled. Hagberg et al. (1983) examined 25 hypertensive adolescent children (mean age = 16) before and after an aerobic exercise training programme which lasted 6 months. The subjects exercised 3 days per week at an intensity of between 60 and 65% of V02max. The children demonstrated significant decreases in resting blood pressure without any significant changes in bodyweight. Dietary controls were not utilised in this study. Montoye (1986) recently summarised the results of several studies which related physical activity level to blood pressure in children. He concluded that once the effects of body fat are accounted for there appears to be only a slight negative relationship between resting blood pressure and physical fitness. Much more research in this area is needed before any firm conclusions can be reached. 3.3 Smoking Recent trends in the US show a continuously increasing prevalence of smoking in adolescent girls in spite of the educational efforts in the public

CHD Risk Factors in Children

schools and despite the repeated warnings of the Surgeon General (Smoking and Health 1979). There are few published data which relate smoking to physical activity levels in children (Bell et al. 1986; Montoye 1986). 3.4 Diabetes Non-insulin dependent diabetes is rare in children, but insulin-dependent diabetes mellitus (IDDM) is much more common and presents a significant problem in youth. It is one of the most common chronic disorders among children (Larsson 1984). The relationship of physical activity level to IODM is important to understand. Firstly, a number of diabetic youngsters are involved in regular physical activity, and secondly diabetes, which is often accompanied by an adverse lipid profile, is a potent risk indicator for CHD. The consequences of acute exercise in the young diabetic are fairly well understood; however, the long term effects of physical training in IDDM are not well known. Landt et al. (1985) have reported that 12 weeks of exercise training in children with insulindependent diabetes mellitus (IODM) results in improvements in ~02max, increased insulin sensitivity and no changes in glycohaemoglobin levels. They concluded that there was no improvement in overall glycaemic control. Larsson et al. (l964a,b) and Dahl-lorgenson et al. (1980), on the other hand, report that diabetic children who are physically active have lower glycohaemoglobin levels and a more stable metabolism than diabetic children who are more sedentary. There is a paucity of information on the effects of physical training on blood lipid profiles in children and adolescents with IDDM. Campaigne et al. (1985) reported that a 12-week aerobic exercise programme resulted in a significant decrease in LDL cholesterol levels with no corresponding changes in HDL cholesterol values. The fact that HDL cholesterol levels remained unchanged despite increases in V02max is somewhat surprising, since in adult IODM and non-diabetic subjects increased physical activity levels have been frequently accompanied by increases in HDL chol-

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esterollevels (Gunnarsson et al. 1982; Rainville & Vaccaro 1984; Wood & Haskell 1979). This is of particular interest because of the negative correlation between HDL cholesterol levels and CHD. We conclude that the relationship between blood lipids and physical activity levels in children and adolescents with IDDM is essentially unexplored.

4. Conclusions Multiple epidemiological studies suggest that risk factors for coronary heart disease can be identified early in life. Whether children who exhibit an adverse CHD risk factor profile will demonstrate an increased propensity for heart disease in adult life has not been fully answered. Preliminary 'tracking' studies lend credence to the notion that a child who has multiple CHD risk factors can be at a higher risk for atherosclerosis. Based on this information it seems prudent to identify those children who smoke, are under undue stress and exhibit characteristics such as elevated blood lipids, obesity, hypertension, and diabetes mellitus since these factors are associated with an increased incidence of CHD. Evidence is beginning to accumulate in the adult literature which suggests that regular aerobic exercise alone may alter all risk factors for CHD including hypertension and diabetes. Whether regular exercise will reduce the CHD risk of children requires further investigation.

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