How much physical activity is good for health?

ANNUAL REVIEWS Annu. Rev. Publ. Health. Copyright

© 1992

1992. 13:99-126

Further

Quick links to online content

by Annual Reviews Inc. All rights reserved

HOW MUCH PHYSICAL ACTIVITY

Annu. Rev. Public. Health. 1992.13:99-126. Downloaded from www.annualreviews.org by Ryerson University on 03/20/13. For personal use only.

IS GOOD FOR HEALTH? S. N. Blair, H. W. Kohl, and N. F. Gordon Divisions of Epidemiology and Exercise Physiology, Institute for Aerobics Research, Dallas, Texas 75230

R. S. P affenbarger, Jr. Division o f Epidemiology, Stan ford University School of Medicine, Stan ford, California 95305 KEY WORDS:

physical fitness, cardiovascular disease, cancer, diabetes mellitus , musculoskeletal system

INTRODUCTION

Physical A ctivity from Prehistory to the Presen t Remains of our early, human-like ancestors, Australopithecus afarensis, have been dated as 3.5-3.8 million years old. Nearly 4 million years of evolution of the human family, Hominidae, produced modem humans, H. sapiens, by approximately 35,000 years ago (71). The earliest hominids were scavengers; but, by about I million years ago, hunting and gathering was firmly es tablished as a way of life for human beings. A hunting and gathering lifestyle involves high energy expenditure for several days a week, with peak bouts of strenuous physical activity (26, 93). The next major change in human sociocultural development was the domestication of p lants and animals and the rise of agriculture, which oc curred only 10,000 years ago. Industrialization advances over the past 200 years led to further urbanization and the rise of the middle-class. But, even during this period, most individuals had relatively high energy expenditures compared with those of society at the end of the twentieth century. Human energy expenditure requirements have declined over the twentieth century, a trend that has apparently accelerated during the technological e ra 99

0163-7525/92/0501-0000$02.00


100

BLAIR ET AL

following World War II (92). Increased automotive transportation, wide spread adoption of sedentary activities, and labor-saving devices are major contributors to the decline in energy expenditure by individuals. The metabol ic energy demands of previously strenuous jobs, such as working as a longshoreman or coal miner, are much lower today than in the past because of containerization, mechanization, and automation. Humans evolved to be active animals and may not be able to adapt well to the modem sedentary lifestyle. This point is well stated by Eaton et al (27): "From a genetic standpoint, humans living today are Stone Age hunter gatherers displaced through time to a world that differs from that for which our genetic constitution was selected." This teleological argument of human genetic selection and the need for physical activity does not prove that activity is necessary for health, but it may serve as a useful launching point for the review and discussion that follows.

Development of Exercise Scien ce The scientific study of exercise is a recent development (62) . Physiologists in the latter part of the nineteenth century began to use exercise to perturb body systems to understand physiological functioning better. Indeed, three exercise physiologists, Meyerhof (muscle metabolism) and Krogh, and Hill (physiolo gy of exercise), have been awarded the Nobel prize for their research (74). Over the past 70 years, hundreds of studies have documented the type and extent of changes with physical training that occur in skeletal muscle, the circulatory system, pulmonary function, the heart and vascular system, and endocrine function. These studies have been done in the young and the elderly , in men and women, with different training protocols, and under varying environmental conditions. The earlier studies typically had small samples, frequently lacked control groups, were short-term, and had other design flaws. These shortcomings have been overcome in studies over the past 10-20 years. Systematic studies on the health effects of physical activity are more recent, primarily confined to the past 30-40 years. Morris et al (75-77) are generally credited with a leading role in formulating the modem physical activity coronary heart disease hypothesis with their studies on London transport workers and, later, on British civil servants.

Definition s Several key terms, central to the purpose of this chapter, need to be defined. We adopt the definitions of Caspersen et al (17) for physical activity, ex ercise, and physical fitness: 1. Physical activity : Any bodily movement produced by skeletal muscles that

results in energy expenditure.

PHYSICAL ACTIVITY AND HEALTH

101


2 . Exercise: Planned, structured , and repetitive bodily movement done to improve or maintain one or more components of physical fitness. 3. Physical fitness: A set of attributes that people have or achieve that relates to the ability to perform physical activity. The physical fitness component that has been most frequently studied for an association to health is aerobic power or , as it is measured in the physiology laboratory , maximal oxygen uptake. This attribute is also called cardiovascu lar, cardiorespiratory, or endurance fitness. Unless otherwise specified, we use the term physical fitness to refer to aerobic power. The other major term that needs to be defined is health. In this chapter, we take a broad view of health, one that not only includes freedom from disease, but also the ability to achieve activities of daily living. Disease endpoints are frequently used in studies of physical activity. For our purposes , however, the definition of health goes beyond freedom from clinical disease to include a focus on functional capability or functional health status. This latter characteristic includes avoidance of functional disability , but also extends to higher levels of functional capability. One of the most well-documented effects of regular physical activity is a higher level of physical fitness. This permits a higher level of functional ability to participate in a wide array of life's activities with ease and enjoyment. The active and fit person is not likely to become fatigued by the routine activities of daily living and has a greater capacity to meet emergencies or par ticipate in vigorous recreational activities.

Purpose of th is Chapter This chapter reviews existing clinical exercise studies and population-based investigations of physical activity and physical health. We concentrate on potential preventive etiologic associations , with little emphasis on therapeutic effects of physical activity on health and disease. We integrate the findings from these two research fronts, point out agreements and disagreements, and summarize the results to assess how much physical activity is required for health. The descr iptive epidemiology of physical activity in the United States and the public health burden of a sedentary lifestyle is discussed , and public health recommendations for physical activity and physical fitness are pre sented. CLINICAL EXERCISE STUDIES

Exercise an d Physical Fitn ess Exercise-trained individuals have higher levels of physical fitness , and the relation between activity and fitness was probably known in antiquity. Athletes and soldiers have long been trained to improve their capacity for performance. Carefully done studies to quantify the training required to

102

BLAIR ET AL


produce an improvement in fitness are a recent phenomenon ; in 1957, Kar vonen et al (55) published one of the first of these studies. Dozens of studies over the past 35 years focused attention on three principles of exercise prescription: intensity, frequency, and duration (5). INTENSITY For the past several decades, the generally held view is that there is a minimum exercise intensity required to stimulate an improvement in physical fitness. The American College of Sports Medicine ( A C S M) was the first scientific organization to publish official statements on exercise prescrip tion. Their 1975 textbook set 70% of maximal oxygen uptake as the minimum recommended exercise intensity for improving physical fitness (4). Subse quent studies lowered recommendations for the intensity threshold, and the third edition of the A C S M book in 1986 (3) recommended a minimum exercise intensity of 50%. The 1991 fourth edition (2) recommends moderate exercise, defined as exercise between 40-60% of maximal capacity, as appropriate for many persons. A 1990 A C S M position stand states that "persons with a low fitness level can achieve a significant training effect with . . . 40-50%" of capacity (5). An alternate hypothesis to a threshold level of intensity is that the response to exercise training is primarily, if not ex clusively, dependent upon the total energy expended in exercise and not intensity. This distinction is important and needs additional clarification. If a minimum intensity threshold exists, it probably varies depending upon the initial fitness level of the participant, the duration of the exercise session, the length of the training period, and perhaps other individual characteristics of the person undergoing training. DURATION The A C S M recommends 20-60 minutes of continuous aerobic activity for each exercise session (2, 5). There is an interrelationship between intensity and duration in their impact on fitness change. Low intensity activity must be sustained longer than high intensity activity to have the same effect on improvement in aerobic power. Again, the total energy expenditure of the exercise session is likely the critical determining factor for fitness change. Investigators have challenged the belief that continuous aerobic activity is necessary to achieve a training effect. A recent study addresses the issue by comparing two different training regimens (21). One group trained five days per week with one 30-minute session per day. A second group trained five days per week with three lO-minute sessions per day. Improvements in physical fitness after eight weeks of training were similar, thus suggesting that the accumulation of activity over the course of the day can produce a training effect. FREQUENCY The A C S M recommends partICIpation in exercise training three to five days per week (2, 5). Most studies show little change in physical


103

fitness if exercise is done less than three days per week, unless the exercise is quite strenuous. And, exercising more than five days per week does not result in greater improvement in fitness than training five days per week (5).


Physiological Effects of A cute and Chron ic Exercise The potential beneficial effects of acute and chronic exercise on physical fitness and health have been intensely investigated in recent years. Existing laboratory and clinical studies have documented a broad array of physiologic benefits, including metabolic, hormonal, and cardiovascular adjustments that are evident at rest, as well as during and followirig both maximal and submaximal exertion (14). Acute and chronic exercise also reduce anxiety and depression and positively impact other psychological characteristics of both normal persons and those with clinical disorders (99). In this section, we focus only on those key physiological benefits that have been hypothesized to contribute toward a reduced risk for mortality, especially from cardiovascular

disease and cancer. IMPROVEMENT OF BALANCE BETWEEN MYOCARDIAL OXYGEN DEMAND AND SUPPLY The myocardial oxygen requirement during exercise is de termined by a variety of factors, the most important of which are reflected by the rate-pressure product (that is, the product of the heart rate and systolic blood pressure) (2). Because the rate-pressure product increases linearly during graded exercise, so too does the myocardial oxygen demand. Follow ing exercise training, the rate-pressure product elicited by a given submaximal exercise intensity is usually substantially attenuated (117). This enables a specific physical activity to be performed with a lessened myocardial oxygen demand and, therefore, a reduced r isk for myocardial ischemia. Currently, there is no direct evidence that exercise conditioning induces the formation of coronary collaterals in humans, and this issue will probably not be resolved until more sophisticated techniques for assessing coronary col lateralization are developed and utilized in clinical exercise training studies (56). However, there is now preliminary evidence that exercise training may indeed enhance myocardial oxygen delivery and/or utilization (29, 56). ECCENTRIC VENTRICULAR HYPERTROPHY Myocardial hyper trophy is an adaptive mechanism that develops in response to increased hemodynamic loading of the heart. Depending on the specific nature o f the hemodynamic loading, the resultant increase in cardiac mass is associated with characteristic alterations in the volume of the cardiac cavities and in the thickness of their walls. As an adaptive response to volume overloading of the left ventricle, dynamic exercise training often produces an increase in left ventricular wall thickness and, to a greater degree, chamber size. This so-called eccentric hypertrophy is believed to be associated with an increase in myocyte vascular-

104

BLAIR ET AL


ity that is commensurate with the degree of hypertrophy of the myocytes themselves and thereby improves myocardial function and assures myocyte health (123). Left ventricular function is a principal determinant of the risk of mortality following an acute myocardial i nfarction. Because persons with eccentric hypertrophy could suffer relatively less impairment in left ventricular function for a given amount of myocardial damage, Ekelund et al (31) have hypothe sized that they may be better able to survive an acute myocardial infarction. Noakes et al (81) have shown that the exercise-trained rat heart has a reduced propensity for ventricular fibrillation during normoxia, hypoxia, and acute regional myocardial ischemia. They have further demonstrated that exercise training i ncreases the ventricular fibrillation threshold of the previously infarcted isolated rat heart before and after the onset of reinfarction (96). These findings imply that regular exercise, before or after an acute myocardial infarction, may act directly on the myocardium to enhance its resista nce to lethal ventricul ar arrhythmias. Although human studies are needed to substantiate this hypothesis, it is compatible with the finding of metaanalyses, which demonstrate that cardiac rehabilitation protects against mortality (which is mostly related to lethal ventricular arrhythmias) rather than reinfarctio n (82, 83), and epidemiologic studies, which link a physically active lifestyle with a reduced risk for sudde n cardiac death (76, 84). REDUCED RISK FOR LETHAL VENTRICULAR ARRHYTHMIAS

FAVORABLE EFFECT ON BLOOD COAGULABILITY Total occlusion of a coronary artery as a result of thrombus formation at the site of a n atheroscle rotic stenosis is believed to be the final precipitating event in more than 90% of acute myocardial i nfarctions. Although conflicting findings have been reported and additional research is st ill needed, exercise traini ng is thought to reduce the adhesiveness and aggregability of blood platelets (30, 101). Moreover, whereas physical inactivity appears to decrease fibrinolysis, ex ercise traini ng tends to moderately augment it (30), which would improve the body's ability to dissolve thrombi if they form. IMPROVED PLASMA LIPIDS AND LIPOPROTEINS Table 1 presents a sum mary of the effect of acute a nd chronic exercise on plasma lipids a nd lipoproteins. Of these benefits, perhaps the most relevant is the increase in high density lipoprotein (HDL)-cholesterol. Generally, a single bout of mod erate-to-Iong duration aerobic exercise evokes a 4-6 mg/dl i ncrease in the HD L-cholesterol levels of men and women (4 1). Recent studies by Hughes et al (51, 52) further suggest that although exercise i ntensity does not appear to be a significant modifier of the acute impact of aerobic exercise on HDL cholesterol levels in men, exercise duration does. In their study, the i ncrease

PHYSICAL ACTIVITY AND HEALTH Table 1

Results of studies investigating the relationship between aerobic

105

ex

ercise training and lipoprotein levels·, b


Total Cholesterol

Cross-sectional

Longitudinal

exercise

studies

studies

t

t

�

t

�

t

VLDL

t

LDL

t

HDL

t

t

t

t

t

t

Total eholesterol/HDL

-->

Studies of acute

a t t

=

generally, a decrease has been found; t

t t

�

=

�

t

generally, an increase has been found;

generally, no change or a decrease has been found, bReproduced with pennission from Ref. 41. =

in serum HDL-cholesterol levels at 24 hours after a bout of exercise per formed at an oxygen uptake of 20% below the anaerobic threshold was greater when the exercise duration was 45 minutes, as compared with 30 minutes (52), Likewise, although not all studies are in agreement, results generally show a 5- 15% increase in plasma HDL-cholesterol levels following chronic ex ercise training (41), In men, such increases appear to be directly related to both the intensity of exercise and total quantity of weekly energy expenditure (126), In women, recent research conducted at the Institute for Aerobics Research suggests that moderate intensity exercise training performed at approximately 55% of the maximal heart rate may be as effective in increas ing HDL-cholesterol levels as higher intensity exercise training (25), REDUCED RISK FOR HYPERTENSION AND LOWERING OF HIGH BLOOD PRESSURE Epidemiologic studies have documented a reduced risk for the development of hypertension in physically active persons (42), Several stud ies have also demonstrated that the blood pressures of hypertensive patients are reduced for one to three hours following a single 30-45 minute bout of aerobic exercise (42), Moreover, a recent metaanalysis of 25 longitudinal studies has confirmed the efficacy of aerobic exercise training in lowering elevated systolic and diastolic blood pressures (43), The average sample-size weighted reductions in resting systolic and diastolic blood pressures in this metaanalysis were 10.8 and 8.2 mmHg, respectively. Interestingly, in the studies included in the metaanalysis, moderate-intensity exercise appeared to be just as effective-if not more so--than higher-intensity exercise . ENHANCED INSULIN SENSITIVITY Findings from the Framingham study indicate that the incidence of cardiovascular disease among individuals with


106

BLAIR ET AL

diabetes mellitus is approximately two to three times higher than that in normoglycemic individuals (53). Recent research has further shown that insulin enhances the proliferation of arterial smooth-muscle cells and stimu lates lipogenesis in arterial tissue (34). Not surprisingly, hyperinsulinemia has also been linked to an accentuated risk for acute myocardial infarction, even in nondiabetic men (24). Acutely, a single bout of submaximal aerobic exercise enhances insulin sensitivity in skeletal muscle and other tissues . Therefore, such exercise often results in a decline in the blood glucose levels of patients with insulin dependent or noninsulin dependent diabetes mellitus ( 122). This exercise induced improvement in glucose metabolism may persist from hours to days and is thought to be modulated by an increase in the cell membrane glucose transporter number, as well as an increase in the intrinsic activity of these transporters (59). With chronic exercise training, glycemic control also improves in persons with noninsulin-dependent and, to a lesser degree, insulin-dependent diabetes (122). However, as is partly the case with plasma lipoproteins and blood pressure, it is unclear whether such improvements are largely due to the cumulative effects of the individual acute bouts of exercise, rather than a training-mediated change in fitness per se (122). REDUCTION OF OBESITY AND IMPROVEMENT IN BODY FAT DISTRIBU

Caloric restriction through dieting, in combination with caloric ex penditure through regular exercise, appears to be the most effective means of preventing obesity and maintaining an ideal body weight. This approach, as compared with dieting alone, better preserves lean body mass and may possibly be linked to favorable chronic changes in resting metabolic rate (35, 94, 120). Regular exercise may also be associated with benefits in terms of both maintenance and stability of weight loss (57). Recent studies have shown that many of the adverse consequences of obesity may be more closely coupled to the distribution of body fat than to the amount of body fat (8). Indeed, individuals with more fat on the trunk, especially intraabdominal fat, are at increased risk of death when compared with individuals who are equally fat, but whose fat is predominantly on the extremities (8). Although additional studies are needed, regular exercise appears capable of evoking favorable changes in body fat distribution (23). Indeed, preliminary exercise-training studies suggest a preferential mobiliza tion of trunk subcutaneous fat as compared with peripheral subcutaneous fat (23). TION

ENHANCEMENT OF IMMUNOLOGIC FUNCTION In view of existing evidence that physical activity decreases the risks of colon cancer (especially in men) and breast and reproductive cancer in women, together with the recognized



107

importance of the immune system in the body's defense against neoplasia, it is understandable why the immunology of exercise is currently an active area of research (15, 1 08). Although both acute and chronic exercise have been associated with potentially beneficial immunologic consequences, the hypoth esis that an exercise-induced enhancement of immunosurveillance contributes to a decreased cancer risk is currently controversial and in need of consider able future research. Indeed, many experts now believe that the mechanism by which regular physical activity may protect against certain types of cancer is nonimmunologic in nature ( 15, 108). Such nonimmunologic mechanisms are thought to include a reduction in intestinal transit time, in the case of colon cancer (61), and hormonal alterations (for example , decreased estrogen levels and consequently less end-organ stimulation), in the case of breast and reproductive cancers (15, 1 08).

Summary of Clinical Exercise Studies Clinical studies confirm that exercise influences many bodily systems and functions. Several possibly healthful effects of exercise have been identified. Some of these effects are acute responses to a single bout of exercise; others result from chronic training adaptations. EPIDEMIOLOGICAL STUDIES OF ACTIVITY OR FITNESS AND HEALTH

Cardiov ascular Diseases Increased risk of cardiovascular diseases caused by sedentary lifestyle has been evaluated in more epidemiological studies than for all other disease endpoints combined, and coronary heart disease (CHD) is by far the most frequently studied of the cardiovascular diseases. Numerous review papers are available on the risk of C HD associated with sedentary habits; in 1987, Powell et al (97) published one of the most comprehensive of these papers. As it has been established that sedentary habits are causally related to increased risk of C HD, we will not review this topic in detail. HYPERTENSION Cross-sectional studies show lower blood pressures in ac tive and fit persons, compared with their unfit and sedentary peers (19, 40). The magnitude of differences in blood pressure across activity or fitness groups is modest, typically less than 10 mm Hg for systolic pressure and 5 mm Hg for diastolic pressure. This association appears to be independent of potential confounding variables, such as body fat, alcohol intake, family history of hypertension, and age. However, activity does not seem to normal ize the blood pressure in all hypertensive persons (43). One prospective epidemiological study evaluated change in physical fitness in relation to change in blood pressure ( 10). A total of 753 middle-aged men


108

BLAIR ET AL

were followed for an average of 1.6 years, with physical f itness assessed at baseline and fo llow-up examinations by max imal exercise treadmill test ing. Increases in f itness and decreases in body we ight were assoc iated w ith decreases in systolic and d iastolic blood pressures. The assoc iat ion between f itness change and blood pressure change disappeared in mult ip le regress ion models when change in body we ight was added. Thus, the effect of fitness change on b lood pressure was largely med iated by changes in we ight. There are two prospect ive stud ies on sedentary hab its or low levels of phys ical fitness on r isk of developing physician-d iagnosed hypertens ion. Both studies followed large groups [14,998 Harvard alumni (90) and 4820 men and 1219 women from the Cooper Clinic ( 1 1)] for up to 12 years. A ll study partic ipants were free of d iagnosed hypertension at base line. The risk of developing physician-diagnosed hypertens ion dur ing follow-up was increased by 35% in sedentary as compared with act ive a lunm i, and by 52% in unfit as compared with f it Cooper Clin ic patients. These results were not due to confounding by such factors as age, smok ing habit, family history of hypertension, or body compos ition. STROKE There are only a few epidemiological reports on physical activ ity or f itness and inc idence of stroke, and the f in dings are equ ivocal. Results of these stud ies are d isplayed in Table 2. A problem in interpreting these data is that most studies do not distinguish between hemorrhagic and nonhemorrhag ic (thromboembolic) stroke. We may reasonably expect that physical activity or fitness could have an impact on nonhemorrhagic stroke, as this d isease seems to have a s im ilar pathogenetic mechanism as that ascribed to C HD, and act ivity and f itness are inverse ly re lated to C HD. Activ ity and f itness m ight affect risk of hemorrhagic stroke indirectly v ia an assoc iat ion w ith blood pressure, but the associat ion, if present, would likely be weak. Stroke in c idence in the Harvard alumni study shows a strong inverse gradient across le isure t ime physical activ ity in kilocalories per week (86). Job-re lated activ ity shows a V-shaped re lat ionship with stroke among Italian railroad workers. Workers in both sedentary and heavy activity categor ies have an e levated relative risk of 2.2 compared w ith workers in the moderate activity group (73). We cons ider the possible relationsh ip between activity or fitness and stroke to be likely, but not established. As evidenced by Table 2, problems in further interpretation stem from varying def in it ions of phys ica l activ ity (occu pational/leisure t ime, lifet ime versus po int estimate), outcome, and differ ences in popUlat ions under study. PERIPHERAL VASCULAR DISEASE If an act ive and fit way of l ife reduces the r isk of atherosc lerotic coronary disease, it m ight a lso affect peripheral atherosclerotic d isease. Investigators from the Framingham Heart Study ex amined the 14-year inc idence of periphera l artery disease by physical activ ity


109

index at basel ine in men aged 35-64 years (54). Bivar iate and mult ivar iate analyses showed no relationship between activ ity and peripheral artery d is ease.


Cancer Nearly 70 years ago, investigators noted that death rates from cancer among men class ified by occupational ass ignment were inversely related to energy expend iture from muscular activity (18, 109). More recently, ev idence has accumulated that physical activ ity may protect against colon, but not rectal, cancer (1, 38, 39, 61, 95, 107, 110, 121, 125, 127). Physical activ ity assessment at a s ingle t ime may not reflect activ ity over the long term, and long-term activ ity may be important for d iseases such as cancer, which has a long development stage. Two points of activ ity assess ment (1962 or 1966 and 1977) were obta ined in 17,148 Harvard alumni who were followed prospectively for colon and rectum cancer occurrence by 1988 (67). H igher levels of phys ical act iv ity, which were evaluated by us ing e ither assessment taken alone, were not associated w ith colon cancer r isk. However, alumni who were highly active (energy expenditure of 2500 or more kcal per week) at both assessments had half the risk of developing colon cancer as those who were inactive (less than 1000 kcal per week) at both assessments. Thus, e ither cons istently h igher levels of activity are necessary to protect against colon cancer, or combining two assessments increases the prec ision of the phys ical activity measurement. No evidence was found that higher levels of activ ity protected aga inst rectum cancer. Clinical and laboratory stud ies have suggested a role of testosterone in the development of prostate cancer. Exercise may have phys iolog ic affects on sex hormone production and ut il izat ion. Accordingly, these same Harvard alumni were followed for the inc idence of this cancer in the same 26-year per iod (68). Although men who were h ighly active (expend ing 4000 or more kcal per week at both assessments) were at reduced risk of prostate cancer, there was no grad ient response of protect ion at lower levels of energy expend iture, and these f ind ings need to be repeated. In l ike fashion, observat ions suggest ing a lower risk of breast cancer among women athletes as compared w ith nonathletes (36) are based on small num bers and must be interpreted cautiously. Further, this particular study is based on interv iews w ith women who have survived breast cancer, and select ion or survival biases cannot be ruled out in interpret ing the f ind ings. Phys ical fitness, as assessed by maximal exercise tolerance on a treadmill test, is inversely assoc iated w ith cancer mortality in the Aerobics Center Longitud inal Study (12). There were 64 cancer deaths in 1 0,224 men and 18 cancer deaths in 3 120 women who were followed for an average of e ight years (total of 110,482 person-years of observation). Age-adjusted cancer death rates per 10,000 person-years of observation across low, moderate, and h igh


Table 2

Summary of studies assessing the relationship between physical activity and stroke

Study (ref.)

Population

Definition of Exposure

Definition of Stroke

Result

Comments

Paffenbarger &

>50,000 male college

Participation in varsity

Death due to stroke

Inverse association

Twofold higher rate of stroke

Williams (88)

alumni survivors'

college athletics

(hemorrhagic and

among non-varsity athletes; no

age range 30 -70

(yes/no)

occlusive) (n

confounding assessment

=

171)

years Kannel & Sor lie (54)

1 909 men aged 35-64

Physical activity index

Cerebrovascular accident

Inverse association

No statistically significant associa

at fourth biennial

based on hours/day

examination, Fram

at specific activity

systolic BP, serum cholesterol,

ingham; 1 4-year

intensity

glucose intolerance, cigarette

(n

=

87)

tion after controlling for age,

follow-up

habit, and left ventricular hypertrophy

Salonen et al (105)

3829 women and 41 10

Physical activity at

Cerebral stroke ICD-8

Eastern Finnish men

work and during lei-

430-437 morbidity and

aged 30-59 years;

sure time low/high

mortality (n

approximately 7-year

=

Inverse association Women: leisure

71

men and 56 women)

Men:

time work work

follow-up

Statistically significant RR ( 1 .6, 95% CI

=

1 . 1-2.5) for men

and women ( 1 .7, 95% CI = 1 . 1-2.7) who were inactive at work . No significant association

Null association

for leisure time physical activ

Men:

leisure

ity, multivariate adjustment for

time

age, serum cholesterol , diastolic BP, body mass index, and tobacco habit

Herman et al (49)

132 hospital-based

Physical activity dur-

Rapidly developed clin-

Inverse association

Statistically significant association

stroke cases and 239

ing leisure time

ical signs of focal or

(compared with the least active

age/sex matched

(greatest portion of

global disturbance of

category) with an apparent

controls; Dutch men

one's lifetime) rang-

cerebral function last-

dose-response across increasing

and women aged

ing from little to

ing more than 24

levels of physical activity. Ad

40-74 years

regular-heavy

hours or leading to

justed for a variety of possible

death, with no appar-

confounders . Relative odds (rel

ent cause other than

ative to lowest activity cate

vascular origin

gory): light, 0.72 (95% CI

=

0.37- 1 . 42); heavy, 0.41 (95% CI = 0.21-0. 84)


Paffenbarger et al (86)

16,936 male college alumni entering col-

Physical activity index (kcallwk) estimated

Fatal stroke (n

==

Inverse association

103)

Statistically significant association after adjustment for age, ciga-

lege between 1 9 1 6

from reports of

rette habit, and physician-

and 1 950 followed

stairs climbed, city

diagnosed hypertension, dose-

from 1 962-1 978

blocks walked, and

response gradient across physi-

sports-play each

cal activity index

week Lapidus & Bengtsson (66)

1462 Swedish women


aged 38-60, follow-

work and during lei-

up between 1 968

sure hours, lifetime

and 1 98 1

Fatal and nonfatal stroke (n

==

Inverse association

Statistically significant association for work and leisure physical

13)

activity in past year. No statis-

and during previous

tical association for measures of

years

lifetime exposure during work and leisure

Menotti & Seccareccia (73)

99,029 male Italian

Job classification of

Fatal stroke (n

==

1 87)

"U" association

Lowest stroke death rate in "mod-

railroad employees aged 40-59 years,

physical activity at work (heavy, mod-

erate" physical activity category. No control for confound-

followed for five

erate, and sedentary)

ing influences

years Menotti et al (72)

8287 men aged 40-59

Job classification of

in six of seven

physical activity at

countries from

work (heavy, mod-

seven-country study;

erate , and sedentary)

Null association

Fatal stroke

No association after statistical adjustment for risk factors

20-year follow-up Harmsen et al (45)

7495 Swedish men aged 47-55 years at baseline and followed an average of ll . 8 years

Note: CI == confidence interval


Fatal stroke (n

==

230)

Null association

No association after adjustment for

work and leisure

a variety of risk factors. Rela-

hours

tive odds

==

(inactive versus all

others) 1 .2, 95% CI

==

0 . 8- 1 . 8


112

BLAIR ET AL

phys ical f itness categories were 20, 7, and 5 in men and 16, 10, and 1 in women, and these trends are statistically s ignificant. The number of deaths in this study is relatively small at this t ime and prec ludes an evaluation of the assoc iation of f itness with site-spec ific cancer deaths. All patients in the analysis were apparently healthy at base line; persons with a h istory or ev i dence of several chronic d iseases were excluded. However, some ind iv iduals probably had subclinical cancer a lready present at baseline. Undetected d is ease could cause lass itude and inactive hab its and result in lower f itness levels. Thus, some of the associat ion between fitness and cancer mortality may have been due to cancer, thus causing low f itness. However, the inverse grad ient of cancer mortality across fitness groups is strik ing and ind icates a need for additional research.

Diabetes (NIDDM) Non insulin-dependent diabetes mellitus ( NIDDM), which affects 10- 12 million persons age 20 years or older, is a complex disorder characterized by increased insulin resistance and impaired insulin secretion. This disorder leads to increased risk of mor tality from C HD and to other vascular complications, such as periph eral vascular d isease, kidney disease, and blindness (22, 28, 80). Along with proper control of body weight and a prudent diet, physical activity is commonly advocated in the management of NIDDM (50, 80, 106, 128), but it has been little studied in the prevention or deferment of this disease. Certain indirect lines of evidence support the contention that physical activity lowers risk of NIDDM. For example, physically active societies have less NIDDM than more sedentary societies (7, 26, 124) ; as populations have become less active, the incidence of th is d isease has increased steadily. Physical activity increases insulin sensitivity (103, 112), and regular endurance exerc ise induces we ight loss and positive changes in glucose metabolism (59, 100). Physical activity has also been in versely associated with the prevalence of diabetes in several cross-sectional studies (37, 58, 78, 116). D irect evidence of a protective role of physical activ ity aga inst NIDDM has been demonstrated in a prospective study of Univers ity of Pennsylvan ia a lumni (47, 89). By us ing mail quest ionna ires, contemporary physical act iv ity patterns and other life-style hab its were examined in relation to the incidence of NIDDM in 5990 men; the disease deve loped in 202 of these men in 15 years of follow-up. Le isure-t ime physical activity, expressed as k ilocalories (kcal) in walking, sta ir climbing, and recreational act ivit ies, was inverse ly re lated to the de ve lopment of NIDDM. Incidence rates dec lined as energy expend iture in creased from less than 500 to 3500 or more per week. For each 500 kcal increment in energy expenditure, d iabetes was reduced by about 6%, and this inverse relat ionship persisted when body compos it ion, we ight ga in s ince college, h istory of hypertension, and parental h istory of d iabetes were consid-


113


ered. The protective effect of physical activity was strongest with moderate to v igorous sports play. The effect was also strong in individuals considered at higher r isk of NIDDM because they were overweight-for-height or hyperten s ive, or had parental h istory of diabetes. This study among college alumni supports the concept that prevent ion or delay of NIDDM may be achieved by increasing overall activ ity and that v igorous activ it ies (swimming, br isk cycling, running, etc.) may induce a stronger effect than more moderate activ it ies.

Osteoarthritis Osteoarthr itis is a major public health problem in the United States (79), and Some investigators are concerned that vigorous exerc ise may increase r isk of the disease developing. The t itle of a recent editorial in the Journal ofInternal Medicine, "Jogging-for a healthy heart and worn-out hips?," expresses a COmmon concern that exerc ise may increase the r isk of osteoarthritis (32). Cross-sectional studies show no differences in the prevalence of osteoarthrit is between runners and control subjects (64, 91). A two-year follow-up study by Lane et al (63) also shows sim ilar progress ion rates for osteoarthrit is in runners and controls. A preliminary analysis of data from the Aerobics Center Long itudina l Study shows no increase in osteoarthr itis of the h ip or knee across levels of exposure to runn ing (13). The s ix-year inc idence of osteoarthr itis in a group of 1039 women and 4429 men was higher in older and more obese subjects. But, the inc idence was not h igher in subjects who had run more miles in their lifetimes, had been running for more years, and had run more m iles in the year before the beginning of the study. Although select ion/protection compe t it ion cannot be unraveled in these early data, ava ilable indications are that running and jogg ing are not assoc iated with an increased r isk of osteoarthr itis of the hip or knee.

Osteoporosis Osteoporosis, and the associated fracture r isk, are major public health prob lems, espec ially for older indiv iduals. Peak bone mass is attained early in life, probably by the second or third decade (lll). A gradual decline in bone m ineral density occurs throughout m iddle-age and is markedly accelerated in women after menopause, especially during the first f ive postmenopausa l years (1 1 1). Numerous studies on the relation of phys ical act ivity to bone m ineral density have been conducted over the past several years. Two reviews (Il l, l l9) prov ide an excellent summary of these reports. The current research supports a few general conclus ions. Clearly, bone responds to the physical stress of exercise. Regular physical activ ity is likely to boost peak bone mass in young women, probably slows the decline in bone m ineral dens ity in m iddle-aged and older women, and may increase bone


114

BLAIR ET AL

mineral density in patients with established osteoporosis (111). Much addi tional research is needed to clarify the specific type and amount of exercise that most efficaciously promotes bone health at various stages of life. There is a paucity of studies of men, and this void also needs to be addressed. It is not clear how physical activity and other proven or suspected effective in terventions, such as calcium supplementation and estrogen replacement ther apy, might interact to promote or maintain bone health. Regular physical activity may provide benefits beyond a direct impact on bone mineral density. Active individuals have greater muscle mass and are stronger, which might reduce the risk of falling and protect against fractures when falls occur. Sorock et al (113) report a reduced risk of fracture (relative risk 0.41 in men and 0.76 in women) in active individuals when compared with sedentary ones. =

Musculoskeletal Disability Musculoskeletal disorders are common, especially in older individuals. These disorders may contribute to inability to perform routine activities or to risk of falling. The high prevalence of relative disability in older persons is man ifested by problems with walking, doing household chores. and accomplish ing personal activities (20). Falls are a major health problem for the elderly. The etiology of falling is complex, and multiple factors are identified as possible causes; but, limitations in musculoskeletal function, such as low levels of muscle strength, balance, and flexibility, may be contributors (118). Runners report fewer limitations in routine activities and lower levels of disability than control subjects (65). Muscle dysfunction and problems with mobility are strongly associated with low levels of muscular strength (33). Furthermore, even elderly individuals (8�96 years) improve muscle strength with an eight-week, weight training program (33); in fact, average gains in strength of 175% were noted. Increases in strength were also associated with objective improvements in mobility tests. At present, data are limited, and more studies, including intervention trials, are needed to evaluate the possible impact of increased physical activity on the incidence of musculoskeletal disorders. However, older persons in par ticular are clearly likely to suffer relative disability, decreased function, falls, and specific musculoskeletal disorders; some of these problems may be due to a progressive loss of musculoskeletal function caused by decades of sedentary living habits. Future work should focus on quantifying levels of activity and fitness required to prevent dysfunction and on appropriate and acceptable intervention programs to restore function.

Summary of Epidemiological Studies Most of the general public and many health professionals believe that regular exercise is an important health habit. For the past two decades, exercise scientists have promoted a scientific DOSE-RESPONSE RELATIONSHIP



115

approach to exercise prescription that specifies exercise intensity, duration, and frequency (2-5). These recommendations are based on numerous con trolled trials of exercise training that have characterized the shape of the dose-response relationship of exercise to short-term improvements in physical fitness. The exercise prescription emphasizes relatively vigorous, large mus cle activity for at least 20 minutes at a minimum of three times per week. This dose of exercise was adopted by the Surgeon General of the United States for the 1990 health objectives (98). Many public education campaigns, books, and articles have presented the exercise prescription approach as advice to the public. We believe that these activities have led both the public and health professionals to adopt a dichotomous view of exercise. That is, unless a person achieves the specified exercise prescription, there are no benefits or responses to the training program. In our opinion, this is an incorrect view, especially in terms of the health effects of physical activity. The relation between various levels of physical activity or physical fitness to mortality from five recent prospective studies is presented in Figure 1. These studies indicate that there is a gradient of risk across activity or fitness levels and that moderate levels of activity or fitness are associated with important and clinically significant reductions in risk. This observation op poses the widely believed threshold concept, which asserts that there is no benefit from physical activity until the exercise prescription level is reached and that there are further improvements across higher levels of exercise. Figure 2 illustrates an idealized benefit curve (solid line) across activity or fitness levels based on current studies, and a second hypothetical curve (dotted line) that probably represents the prevailing opinion of the public and health professionals. The dose-response relationship indicated by the five studies is good news for sedentary individuals. They can have hope that a moderate physical activity program is likely to yield some important health benefits. The public health message should be "Doing some physical activity is better than doing none at all." That is, a little is better than none, and, to a degree, more is better than less. The moderate level of physical fitness that is associated with much lower death rates than the low fitness level in the Aerobics Center Longitudinal Study ( 12) can be achieved with relatively little activity. A brisk, two-mile walk in 30-40 minutes (3-4/mph) taken on most days would be sufficient to produce the moderate fitness level defined in the study. A recent randomized clinical trial suggests that three ten-minute walks over the course of the day have about the same impact on physical fitness as one 30-minute walk (2 1). Thus, exercise recommendations can emphasize the accumulation of 30 minutes of walking (or the energy expenditure equivalent in some other activity) over the day as sufficient to have important health and functional benefits. This approach may be less intimidating and easier to follow than the prescription of a continuous exercise session and should be

116

BLAIR ET AL


A

B

Tartlla

01 Lelau,...tiru Ptly,ical Activity

D

c

2.0 .,..-----,

1.0

0.0

...

n••

,...

KIIoc.tor...'.... 'n

E

....

.

F

MEN

I_ ...

..

a-u

�C............I"

Wodar.'.

PhniCai Fit....

Figure 1

...

....

phy�" actlwlty

C••gar".

WOMEN

I

....

......... c..pIN

Phyek:aI 'ItnMa

Rates for coronary heart disease, cardiovascular disease, or all-cause mortality are

plotted on the vertical axis. The horizontal axis indicates exposure to various levels of physical activity or physical fitness. The figure is constructed from data taken from five prospective epidemiological studies: A (69); B (75); C (87); D (31); E and F (12). The rates in the different panels cannot be compared directly because' of different methodology, endpoints, and study populations.



1 17

'0 -'" '" a:

co .�

a; o

Q) .s:: I-

Level of Physical Activity or Physical Fitness Figure 2 The solid line indicates change in risk across levels of activity of fitness; this line is idealized from published prospective studies. The dashed (upper) line indicates the relation of disease endpoints to level of activity or fitness on the assumption that the traditional exercise prescription is required to obtain health benefits and that higher levels of activity or fitness produce additional benefits, as indicated by the decline in risk beyond the threshold point.

considered for intervention programs (9, 46). A five-minute walk after break fast and before dinner, a ten-minute walk at lunchtime, and a few minutes of stair climbing spread across the day would result in the accumulation of a dose of activity that should improve health and function in previously sedentary and unfit individuals. METHODOLOGIC ISSUES IN POPULATION STUDIES OF PHYSICAL ACTIVITY

Design and methodological concerns are sometimes raised regarding the interpretation of data from epidemiological studies. In this section, we discuss the issues of bias and physical activity assessment. Bias Much has been written about bias in population studies, and most standard texts treat the topic thoroughly (48, 102). Epidemiological studies of physical activity, physical fitness, and health have been typically conducted in opportunistic cohorts, such as college alumni (86, 87, 90), preventive medicine clinic patients ( 1 1, 12), or high risk men (69). Frequently, results from such studies are questioned because of possible selection bias. Selection bias is not a major problem in these studies, however, because persons enrolled in such studies come under observation before knowledge of any outcome. As in most epidemiological investigations, care must be taken when

1 18

BLAIR ET AL


generalizing the results, and replications in other groups are needed. One possible bias in existing studies is that the sedentary or unfit subjects may be in those ca tegories because they may already have some disease, which in tum causes inactivity and concomitantly increases risk of death. Investigators have dealt with these problems by evaluating the relationship between activity or fitness to mortality in early and later follow-up intervals ( 1 2 , 7 5 , 87) , or by considering changes in classifications of work activity (84). Assessment Issues Efforts have been made to validate physical actIvIty assessment instruments used in popul ation studies (60, 104, 1 1 5) , but there are several important issues that need further attention. First is the temporality of the physical activity exposure , as it may be positioned in the etiologic pathway or constellation of diseases and disorders. All studies to date have typically relied on a single, point estimate of physical activity (or inactivity) as a measure of exposure . Earlier studies (77, 84, 85) assessed relative and absolute energy expenditure needs on the job, whereas the more recent studies focused on leisure-time physical activity (69 , 86, 87 , 90) . As in the study of dietary intake and disease, investigators have assumed that these point es timates of activity are correlated with the habitual, or lifetime, exposure to physical activity that is more plausibly in an etiologic pathway ; this assump tion has not yet been confirmed. The problem of misclassification of exposure to physical activity (either by a change in behavior during a follow-up period or by real assessment error) based on a single baseline measure is one that should serve to underestimate the true point estimate of risk . Thus, we may argue that any increased risk demonstrated with a single, point estimate of physical activity should only be strengthened with a more complete and accurate, and less variable, measure of physical activity e xposure. This has not often been demons trated ; a notable exception is the above-mentioned study of physical activity and colon cancer incidence (67). The second issue is that even if the assumption of a single, point-estimate of physical activity is etiologically valid, it is unknown how many days (or views) of assessment are necessary to build a picture of true habitual energy expenditure . As with dietary intake (70) , we can reasonably assume a certain degree of intraindividual variation in energy expenditure. Thus, how many assessment days are needed to minimize this intraindividual variation and provide unbiased estimates of physical activity habits? Such work has been done in the area of dietary intake (6, 70) , but nothing is yet available for energy expenditure. This problem relates to measurement error and subse quent misclassification of exposure in much the same way as was discussed above, and must be solved to provide more precise estimates of physical activity exposure . New approaches to physical activity assessment need to be developed to address these problems to approximate appropriate physiologic p arameters of interest in different populations better.


1 19

DESCRIPTIVE EPIDEMIOLOGY OF PHYSICAL ACTIVITY IN THE UNITED STATES


Physical A ctivity Within Demographic Groups The contributions of physical activity to a healthful lifestyle have received an increasing amount of emphasis over the past two or three d ecad es. Casual observation that adults are becoming more physically active can be supported by data from national surveys that show small increases in the percentage of individuals who are active and decreas es in the p ercentage who are sed entary ( 1 14). We are, however, not an active society; seven out of eleven of the Surgeon G eneral 's objectives for activity and fitness for 1990 were probably not achiev ed (98). Data from the 1985 National Health Interview Survey show that 25% of adult men and 30% of adult women were sedentary (no reported physical activity in the past month) ( 1 6). Another 30% of men and women w ere classified as irregularly active, and only 8% of the men and 7% of the women were exercising at the level recommended in the 1 990 objec tives. Physical activity levels generally were inversely related to age and directly related to educational level and income. Whites appeared to be somewhat more active than blacks and p ersons with race not specified .

P opulation A ttributable Risks of Low A ctivity and Fitn ess The epidemiological studies reviewed above support the inference that low levels of physical activity and physical fitness are strong and independent risk factors for cardiovascular, cancer, and all-cause mortality. The high preva lence of sedentary habits in the US thus leads to a high population attributable risk for sedentary lifestyle. Paffenbarger et al (87) calculate the population attributable risk for all-cause mortality for sedentary habits « 2000 kilocalor ies p er w eek in physical activity; approximately 60% of the Harvard alumni were at risk by this definition) to be 1 6%, compared with 6% for hyperten sion, 22% for cigarette smoking, and 5% for a positive family history of early parental death . Low physical fitness (l east fit quintile) in the A erobics Center Longitudinal Study was associated with population attributable risks of 9% in m en and 15% in women ( 1 2). These risk estimates were comparable to, or higher than, the estimates for other well established risk factors, such as cigarette smoking, elevated blood cholesterol or blood pressure, high fasting blood glucose, high body mass index, and a history of premature coronary heart disease death in a parent. Hahn et al (44) recently estimated the number of deaths attributed to several risk factors for nine chronic diseases. The estimates were based on published studies and death rat es in the US in 1986. The number of deaths attributed to sed entary habits [sedentary or irregularly active as described by Caspersen et al ( 1 6)] was 256,686. This number was exceeded by the estimates for

120

BLAIR ET AL

smoking (361,9 1 1) and obe sity (26 1 ,988), but wa s greater than the number s e st imated for elevated chole sterol (253, 1 94) or hypertension (225,962). Popula tion -a ttr ibutable r isk e stimates for sedentary habits and low physical f itness are h igh. Inactivity in the US appears to be a public health problem that is of comparable magnitude to c igarette smok ing, obe sity, high blood pres sure, and h igh blood cholesterol levels.


SUMMARY Research studies over the pa st several decade s confirm the health benefit s of regular physical activity, a concept wi th founda tion s in antiquity. The effects of activ ity on certain ind iv idual health cond it ions, the precise dose of activity that is requ ired for specif ic benefits, the role ( if any) of intensity of effor t, and the elucidation of b iological pathway s whereby act ivity contr ibute s to health are topics for further re search. Although details remain to be clarif ied, it is now clear that regular phy sical activity reduce s the r isk of morbid ity and mortality from several chronic d iseases and increases physical fitne ss, which leads to improved function. Table 3 outl ine s the relation ship of activ ity to several d isea se s , a judgment on the strength of the evidence, and a rough determination of the amount of re search extant. Re sult s from clinical e xercise stud ie s and epidemiolog ical inve stigations can be integrated into a consistent and coherent theory of healthful phy sical act ivity. However, some d ifferences between these two re search streams need to be reconciled. Exercise physiolo g ist s have generally recommedned relatively intensive activ ity and a formal approach to e xerc ise prescr iption . The epidem iological studie s sugge st a l inear dose-re spon se relation sh ip, at lea st up to a point, between phy sical activ ity and health and functional effect s. These data support publ ic health recommendation s d irected toward the most sedentary and unfit stratum of the population and empha size doing at lea st moderate physical activity. If this group of adults would accumulate 30 minutes of walking per day (or the equivalent energy expend iture in other activ it ies), they would receive cl inical ly signif icant health benef it s. An important point is that it does n9t matter what type of physical activ ity is performed : Sports, planned exerc ise, house hold or yard work, or occupational ta sk s are all beneficial. The key factor is total energy e xpend iture ; if that is constant, improvements in f itness and health w ill be comparable. There are probably 40 m illion adults in the U S whose sedentary habit s place them at considerably increased ri sk of morbidity and mortality from several di sea ses. The se same ind ividual s al so are more l ikely to have functional limitations, especially as they move into the later years of l ife. The sizable independent relative risk for impaired health in sedentary persons, and the large number at r isk, lead s to a substantial public health


121

Table 3 Summary results of studies investigating the relationship of physical activity or physical fitness to selected incidences of chronic diseases·,b

Disease

Number of

Trends across activity or fitness categories and strength

studies

of evidence

* **

! ! ! ! ! ! ! ! !

Obesity


Coronary artery disease

. **

Hypertension

**

Stroke Peripheral vascular disease

**

Cancer (all sites)

"

* **

breast

*

prostate

" "

Osteoarthritis Osteoporosis

*

•

-

! ! !

"

Non-insulin dependent diabetes

Musculoskeletal disability

! ! !

***

colon rectum

lung

-

"

� � -

**

! ! ! !

**

·Few studies, probably less than 5; ·"several studies, approximately 5-\0; """many

studies, more than 10,

b -> No apparent difference in disease rates across activity or fitness categories;

evidence of reduced disease rates across activity or fitness categories;

1 1

!

some

good evidence of

reduced disease rates across activity or fitness categories, control of potential confounders, good methods, some evidence of biological mechanisms;

1 1 1

excellent evidence of

reduced disease rates across activity or fitness categories, good control of potential confound ers, excellent methods, extensive evidence of biological mechanisms, relationship is consid ered causal,

burden . This problem de serve s continue d and increased attent ion by phy si c ian s and other health profe ssionals, scientist s , and the public health e s tablishment . ACKNOWLEDGMENTS We thank Laura Becker for p roviding secretarial support and Chris En smann and Shannon Jackson for a ssistance w ith the literature review. This work wa s supporte d in part by grant s fro m the National Institute s of Health (AG06945, AR39715, HL34174, CA44854). Literature Cited 1 . Albanes, D" Blair, A . , Taylor, P. R. 1 989. Physical activity and risk of can cer in the NHANES I population. Am. J. Public Health 79:744-50 2. Am. ColI. Sports Med. 1 99 1 . Guide lines for Exercise Testing and Prescrip tion . Philadelphia: Lea & Febiger. 3 14 pp. 4th ed.

3. Am. Coll. Sports Med. 1986. Guide lines for Exercise Testing and Prescrip tion . Philadelphia: Lea & Febiger. 179 pp. 3rd ed. 4. Am. Coll. Sports Med. 1 975. Guide lines for Graded Exercise Testing and Exercise Prescription . Philadelphia: Lea & Febiger. 1 1 6 pp.


122

BLAIR ET AL

5. Am. Coil. Sports Med. Position Stand. 1990. The recommended quantity and quality of exercise for developing and maintaining cardiorespiratory and mus cular fitness in healthy adults. Med. Sci. Sports Exerc. 22:265-74 6. Beaton, G. H . , Milner, J . , Corey, P. , McGuire, V. , Cousins, M . , et a!. 1979. Sources of variance in 24-hour dietary recall data: implications for nutrition study design and interpretation. Am. J. Clin. Nutr. 32:2546-59 7. Bjomtorp, P . , De Jounge, K. , Sjostrom, L . , Sullivan, L. 1970. The effect of physical training on insulin production in obesity. Metabolism 19:63 1-37 8. Bjomtorp, P . , Smith, U. , L(innroth, P. , eds. 1988. Health implications of re gional obesity. Acta Med. Scand. 723 ( Supp!. ) . 237 pp. 9. Blair, S. N . 1 99 1 . Living with Exercise . Dallas: American Health Publishing Company. 1 19 pp. 10. Blair, S. N . , Cooper, K . H . , Gibbons, L. W . , Gettman, L. R . , Lewis, S . , et a!. 1983. Changes in coronary heart disease risk factors associated with increased treadmill time in 753 men. Am. J. Epidemiol. 1 1 8:352-59 1 1 . Blair, S. N . , Goodyear, N. N . , Gib bons, L. W . , Cooper, K. H. 1984. Physical fitness and incidence of hyper tension in healthy normotensive men and women. 1. Am. Med. Assoc. 252:48790 1 2 . Blair, S. N . , Kohl, H. W. III, Paffen barger, R. S . Jr. , Clark, D . G . , Cooper, K. H . , et a!. 1989. Physical fitness and all-cause mortality: a prospective study of healthy men and women. 1. Am. Med. Assoc. 262:2395-2401 1 3 . Blair, S. N . , Kohl, H. W. III , Powell, K. E . , Caspersen, C. J . , Barlow, C . E. 1990. Running and incidence of osteoar thritis (abstract). Med. Sci. Sports Ex erc. 22(Suppl .):S 1 16 1 4 . Bouchard, C . , Shephard, R. J . , Ste phens, T . , Sutton, J . , McPherson, B . , eds. 1990. Exercise. Fitness and Health.

A Consensus of Current Knowledge.

Champaign: Human Kinetics . 720 pp. 1 5 . Calabrese, L. H. 1990. Exercise, immu nity, cancer and infection. See Ref. 14, pp. 567-79 1 6 . Caspersen, C. J . , Christenson, G. M . , Pollard, R. A. 1986. Status of the 1990 Physical Fitness and Exercise Objec tives-evidence from NHIS 1985. Public Health Rep. 1 0 1 :587-92 1 7 . Caspersen, C. J . , Powell, K. E. , Christ enson, G. M. 1985. Physical activity, exercise, and physical fitness: defini tions and distinctions for health-related

research. Public Health Rep. 100: 1 2631 1 8 . Cherry, T . 1922. A theory of cancer. Med. 1. Aust. 1 :425-38 1 9 . Cooper, K. H . , Pollock, M. L . , Martin, R. P . , White, S. R. 1976. Physical fit ness levels vs. selected coronary risk factors. 1. Am. Med. Assoc. 236: 1 6669 20. Comoni-Huntley, J . , Brock, D. B . , Ostfeld, A . M . , Taylor, 1 . 0 . , Wallace, R. B . , eds. 1986. Established Pop

ulations for Epidemiologic Studies of the Elderly. Bethseda: Nat!. Inst. Health.

428 pp. 2 1 . DeBusk, R. F . , Stenestrand, U . , Shee han, M . , Haskell, W. L. 1 990. Training effects of long versus short bouts of ex ercise in healthy subjects. Am. J. Car diol. 65: 1010-13 22. Defronso, R. A., Ferrannin, E . , Koivis to, V. 1983 . New concepts in the patho genesis and treatment of non-insulin dependent diabetes mellitus. Am. J. Med. 74(Suppl. I A):52-8 1 23. Despres, J.-P. , Tremblay, A . , Nadeau , A . , Bouchard, C. 1988. Physical train ing and changes in regional adipose tis sue distribution. Acta Med. Scand. 723(Suppl. ):205-1 2 24. Ducimetiere , P . , Eschwege, E . , Papoz, L . , Richard, J. L . , Claude , J. R . , et al. 1 980. Relationship of plasma insulin levels to the incidence of myocardial in farction and coronary heart disease mortality in a middle-aged population. Diabetologia 19:205-1 0 25 . Duncan, J . J . , Gordon, N . F. , Scott, C . B . , Vaandrager, K . , Rudling, K . , e t al. 1991 . Walking for cardiovascular fit ness--walking for health: how much is enough? (abstr.) Natl. Conf. Cholesterol

and High Blood Pressure Control program book, pp. 97-98

26. Eaton, S. B . , Konner, M . , Shostak, M . 1 9 8 8 . Stone agers i n the fast lane: chronic degenerative disease in evolu tionary perspective. Am. J. Med. 84: 739-49 27. Eaton, S . B . , Shostak, M . , Konner, M . 1 98 8 . The Paleolithic Prescription: A

Program of Diet and Exercise and a Design for Living. New York: Harper &

Row 28. Editorial: Type 2 Diabetes or NIDDM. Looking for a better name. 1989. Lancet i:588-91 29. Ehsani, A . , Heath, G . , Hagberg, J . , Burton, E . , Holloszy, J . 1 98 1 . Effects of 12 months of intense exercise training on ischemic ST-segment depression in patients with coronary artery disease. Circulation 64: 1 1 1 6-24

PHYSICAL ACTIVITY AND HEALTH E. 1986. Coagulability and rheology: hematologic benefits from ex ercise, fish, and aspirin: implications for athletes and nonathletes. Physician Sportsmed. 14: 102-10 3 1 . Ekelund, L . , Haskell, W. L . , Johnson, J. L . , Whaley, F. S . , Criqui, M. H. , et al. 1988. Physical fitness as a predictor of cardiovascular mortality in asympto matic North American men: the Lipid Research Clinics Mortality Follow-up Study. N. Engl. J. Med. 3 19:


30. Eichner,

1 379-84 32. Ernst, E. 1990. Jogging-for a healthy

heart and worn-out hips? J. Int. Med.

43. Hagberg, J. M. 1 990. Exercise, fitness, and hypertension. See Ref. 1 4 , pp. 45566 44. Hahn, R. A . , Teutsch, S. M . , Rothen berg , R . B . , Marks, J. S. 1990. Excess

deaths from nine chronic disease in the United States, 1986. J. Am. Med. Assoc.

264:2654-59 45. Hannsen, P. , Rosengren, A . , Tsipo gianni, A . , Wilhelmsen, L. 1990. Risk

factors for stroke in middle-aged men in Giiteburg, Sweden. Stroke 2 1 : 223-

29 46. Harris, S. S . , Caspersen, C. J . , De Friese, G. H . , Estes, H. JT. 1989.

Physical activity counseling for healthy adults as a primary preventive inter vention in the clinical setting: report for the US Preventive Services Task Force. J. Am. Med. Assoc. 261 :3590-

228:295-97 3 3 . Fiatarone, M. A . , Marks, E. C . , Ryan,

N. D . , Meredith, C. N . , Lipsitz, L. A . , e t a l . 1 990. High-intensity strength training in nonagenarians: effects on skeletal muscle. J. Am. Med. Assoc.

263:3029-34 34. Flodin, N. 1986. Atherosclerosis: an in

sulin-dependent disease? J. Am. Coli. Nutr. 5:417-27 35. Frey-Hewitt, B . , Vranizan, K. M . , Dreon, D. M . , Wood , P . D. 1990. The effect of weight loss by dieting and ex ercise on resting metabolic rate in over weight men. Int. J. Obes. 14:327-34 36. Frisch, R. E . , Wyshak, G . , Albright, N. L., Albright, T. E., Schiff, I., et al. 1985. Lower prevalence of breast cancer and cancers of the reproductive system among fonner college athletes compared to non-athletes. Br. J. Cancer 52:885-

98 47. Helmrick,

S. P . , Ragland, D. R . , Leung, R. W . , Paffenbarger, R. S . Jr. 1 99 1 . Physical activity and reduced occurrence of non-insulin-dependent di abetes mellitus. N. Engl. J. Med. 325:

1 47-52 48. Hennekens, C. H . , Buring, J. E. 1987.

49.

91 3 7 . Frisch, R . E . , Wyshak, G . , Albright, T . E . , Albright, N. L . , Schiff, I. 1986.

50.

Lower prevalence of diabetes in female fonner college athletes compared to non athletes. Diabetes 35: 1 1 01-5 3 8 . Garabrant, D. H . , Peter, J . M . , Mack, T. M . , Bernstein, L. 1984. Job activity and colon cancer risk. Am. J. Epidemiol.

51.

1 19: 1005-14

52.

39. Gerhardsson, M . , Norell, S. E . , Kivir

anta, H . , Pedersen, N. L . , Ahlbom, A. 1986. Sedentary jobs and colon cancer. Am. J. Epidemiol. 123:775-80 40. Gibbons, L. W . , Blair, S. N . , Cooper, K. H . , Smith, M. 1983. Association be tween coronary heart disease risk factors and physical fitness in healthy adult women. Circulation 67:977-83 4 1 . Gordon, N. F. , Cooper, K. H. 1988. Controlling cholesterol levels through exercise. Compr. Ther. 14:52-57 42. Gordon, N. F. , Scott, C. B . , Wilkinson, W. J., Duncan, J. J . , Blair, S. N. 1 990. Exercise and mild essential hyperten sion. Recommendations for adults. Sports Med. 10:390-404

1 23

53.

Epidemiology in Medicine. Boston: lit tle Brown. 383 pp. Hennan, B . , Schmitz, P. I. M . , Leyten, A. C. M . , Van Luijk, J. H. , Frenken, C. W. G. M . , et al. 1983. Multivariate logistic analysis of risk factors for stroke in Tilburg, The Netherlands. Am. J. Epidemiol. 1 1 8:5 14-25 Horton, E. S. 1988. Role and manage ment of exercise in diabetes mellitus. Diabetes Care 1 1 :201- 1 1 Hughes, R. A . , Thorland, W. G. , Eyford, T. , Hood, T. 1990. The acute effects of exercise duration on serum lipoprotein metabolism. J. Sports Med. Phys. Fitness 30:37-44 Hughes, R. A . , Thorland, W. G . , Housh, T . J . , Johnson, G. o. 1 990. The effect of exercise intensity on serum lipoprotein responses. J. Sports Med. Phys . Fitness 30:254-60 Kannel, W. B . , McGee, D. 1979. Di abetes and cardiovascular disease: The Framingham Study . J. Am. Med. Assoc .

24 1 :2035-38 54. Kannel, W. B . , Sorlie, P. 1979. Some

health benefits of physical activity: the Framingham Study . Arch. Intern. Med.

1 39:857-61 55. Karvonen, M . , Kentala, K . , Mustala, O. 1957. The effects of training heart

rate: a longitudinal study. Ann. Med. Exp. Bioi. Fenn. 35:307-1 5 5 6 . Kavanagh, T. 1989. Does exercise im prove coronary collateralization? A new


124

BLAIR ET AL

look at an old belief. Physician Sports med. 17:96- 1 14 57. King, A. c . , Frey-Hewitt, B . , Dreon, D . M . , Wood, P. D. 1989. Diet vs. exercise in weight maintenance: the effects of minimal intervention strategies on long-term outcomes in men. Arch. Intern. Med. 1 49:2741-46 58. King, H . , Zimmet, P . , Raper, L. R . , Balkau, B. 1 984. Risk factors for dia betes in three Pacific populations. Am. J. Epidemiol. 1 1 9:396-409 59. King, P. , Hirshman, M . , Horton, E. D . , Horton, E. S . 1989. Glucose transport in skeletal muscle membrane vesicles from control and exercised rats. Am. J. Physi01. 257:C l 1 28-34 60. Kohl, H. W . , Blair, S. N . , Paffenbar ger, R. S . Jr. , Macera, C. A . , Kronen feld, J . 1. 1 988. A mail survey of physical activity habits as related to measured physical fitness. Am. 1. Epi demiol. 1 27:1 228-39 6 1 . Kohl, H. W . , LaPorte , R . E . , Blair, S . N . 1 988. Physical activity and cancer: an epidemiological perspective. Sports Med. 6:222-37 62. Koplan, 1. P . , Powell, K. E. 1984. Physicians and the Olympics. 1. Am. Med. Assoc. 252:529-30 63. Lane, N. E . , Bloch, D. A . , Hubert, H. B . , Jones, H . , Simpson, U . , et al. 1 990. Running, osteoarthritis, and bone den sity: initial 2-year longitudinal study . Am. J. Med. 88:452-59 64. Lane, N. E . , Bloch, D. A . , Jones, H. H . , Marshall , W . H . Jr. , Wood, P. D . , e t al. 1 986. Long-distance running, bone density, and osteoarthritis. J. Am. Med. Assoc. 255 : 1 147-5 1 65 . Lane, N. E . , Bloch, D. A . , Wood, P. D . , Fries, J. F. 1 987. Aging, long distance running, and the development of musculoskeletal disability: a Con trolled study. Am. J. Med. 82:772-80 66. Lapidus, L . , Bengtsson, C. 1986. Socioeconomic factors and physical activity in relation to cardiovascular dis ease and death. A 1 2-year follow-up of participants in a population study of women in Gothenburg, Sweden. Br. Heart J. 55:295-301 67. Lee, I.-M . , Paffenbarger, R. S. Jr. , Hsieh, C-c. 1 99 1 . Physical activity and risk of colorectal cancer among college alumni. J. Natl. Cancer Inst. In pre�s 68. Lee, I . -M . , Paffenbarger, R. S . Jr. , Hsieh, C-c. 1 99 1 . Physical activity and risk of prostatic cancer among college alumni. Am. J. Epidemiol. In press 69. Leon, A. S . , Connett, J . , Jacobs, D. R. Jr., Raurarnaa, R . 1987. Leisure-time physical activity levels and risk of

coronary heart disease and death: the Multiple Risk Factor Intervention Trial. J. Am. Med. Assoc. 258:2388-95 70. Liu, K . , Stamler, J . , Dyer, A . , Mc Keever, J. , McKeever, P. 1978. Statis tical methods to assess and minimize the role of intra-individual variability in obscuring the relationship between di etary lipids and serum cholesterol. J. Chron . Dis. 3 1 :399-4 1 8 7 1 . Malina, R: M . 1 988. Physical activity in early and modem populations: an evolu tionary view. In Physical Activity in Early and Modern Populations, ed. R . Malina, H . Eckert, 2 1 : 1- 1 2 . Cham paign: Human Kinetics. 1 14 pp. 72. Menotti, A . , Keys, A . , Blackburn, H . , Aravanis, c . , Dontas, A . , e t al. 1 990. Twenty-year stroke mortality and pre diction in twelve cohorts of the Seven Countries Study. Int. J. Epidemiol. 19:309- 1 5 73. Menotti , A . , Seccareccia, F. 1985. Physical activity at work and job responsibility as risk factors for fatal coronary heart disease and other causes of death. J. Epidemiol. Community Health 39:325-29 74. Montoye, H. J. 1 99 1 . Health, exercise and athletics: a millennium of observa tions-a century of research. Am. J. Hu man Bioi. In press 75. MOrris, J. N . , Clayton, D. G . , Everitt, M. G . , Semmence , A. M . , Burgess, E. H. 1990. Exercise in leisure time: coro nary attack and death rates. Br. Heart J. 63:325-34 76. Morris, J. N . , Everitt, M . , Pollard, R . , Chave, S . , Semmence, A . 1 980. Vigor ous exercise in leisure-time: protection against coronary heart disease. Lancet ii: 1 207-10 77 . Morris, J. N., Heady, J . A . , Raffle, P. A. B., Roberts, C . G . , Parks, J. W . 1953. Coronary heart disease and physi cal activity of work. Lancet ii: 1053- 1 1 20 78. Morsiani, M. 1989. Epidemiology and Screening of Diabetes. Boca Raton, F1a: CRC 79. Natl. Cent. Health Stat . , Collins, J. G. 1986. Prevalence of selected chronic conditions, United States, 1 979-8 1 . Vi tal and Health Statistics. Ser. 1 0 , No. 1 55 . DHHS Pub!. No. (PHS) 86- 1 583. Public Health Servo Washington, DC: GPO 80. Natl. Inst. Health. 1987. Consensus De velopment Conference statement on diet and exercise in non-insulin-dependent Diabetes Mellitus. Diabetes Care 10: 639-44 8 1 . Noakes, T . , Higginson, L . , Opie, L.


82.


83.

84.

85.

86.

87.

88.

89.

90.

91.

92.

93 .

1983. Physical training increases ven tricular fibrillation thresholds of isolated rat hearts during normoxia, hypoxia and regional ischemia. Circulation 67:25-30 O'Connor, G . , Buring, J . , Yusaf, S . , Goldhaber, S . Z. , Olmstead, E. M . , ct al. 1989. An overview of randomized trials of rehabilitation with exercise after myocardial infarction. Circulation 80: 234-44 aldridge, N. B . , Guyatt, G. H . , Fis cher, M . S . , Rimrn, A. A. 1988 . Car diac rehabilitation after myocardial infarction: combined experience ran domized clinical trials. J. Am. Med. Assoc. 260:945-50 Paffenbarger, R. S. Jr. , Hale, W. E. 1975. Work activity and coronary heart disease mortality. N. Engl. J. Med. 292:545-50 Paffenbarger, R. S. Jr. , Hale, W. E . , Brand, R . J . , Hyde, R. T. 1 977. Work energy level, personal characteristics, and fatal heart attack: a birth-cohort effect. Am. J. Epidemiol. 105:200-- 1 3 Paffenbarger, R . S . Jr. , Hyde, R . T., Wing, A. L., Steinmetz, C. H. 1984. A natural history of athleticism and car diovascular health. J. Am. Med. Assoc. 252:491-95 Paffenbarger, R. S. Jr. , Hyde, R. T . , Wing, A . L . , Hsieh, C-c. 1 986. Physi cal activity, all-cause mortality, and longevity of college alumni. N. Engl. J. Med. 3 14:605-13 Paffenbarger, R . S . Jr. , Williams , J. L. 1967. Chronic disease in former college students V. Early precursors of fatal stroke . Am. J. Public Health 57: 1 29099 Paffenbarger, R. S. Jr. , Wing, A. L. 1 973. Chronic disease in former college students XII. Early precursors of adult onset diabetes mellitus . Am. J. Epidemi01. 97 : 3 1 4-23 Paffenbarger, R. S. Jr. , Wing, A. L . , Hyde, R . T . , Jung, D . L . 1983. Physical activity and incidence of hypertension in college alumni. Am. J. Epidemiol. 1 17: 245-57 Panush, R. S . , Schmidt, C . , Caldwell, J. R . , Edwards, N. L . , Longley, S . , et al. 1986. Is running associated with de generative joint disease? J. Am. Med. Assoc. 255: 1 1 52-54 Park, R. J. 1989. Healthy, moral, and strong; educational views of exercise and athletics in 1 9th century America. In Fitness in American Culture; Images of Health, Sport, and the Body 1830-1940, ed. K. Grover, pp. 1 23-68. Amherst, Mass: Amherst Univ. Park, R. J. 1988 . How active were early

94.

95.

96.

97.

98.

99.

100.

101.

102.

103 .

104.

1 05 .

125

populations? In Physical Activity in Ear ly and Modern Populations, ed. R . Malina, H. Eckert, 1 : 1 3-2 1 . Cham paign: Human Kinetics . 1 14 pp. Pavlou , K., Steffee, W . , Lerman, R. , Burrows, B. 1985. Effects of dieting and exercise on lean body mass, oxygen up take , and strength. Med. Sci. Sports Ex ere. 17:466-7 1 Peters, R. K . , Garabrant, D. H . , Yu, M . c . , Mack, T . M . 1989. A case-control study of occupational and dietary factors in colorectal cancer in young men by subsite . Cancer Res. 49:5459-68 Posel, D . , Noakes, T. , Kantor, P . , Lam bert, M . , Opie, L. H. 1989. Exercise training after experimental myocardial infarction increases the ventricular fibril lation threshold before and after the onset of reinfarction in the isolated rat heart. Circulation 80: 1 38-45 Powell, K. E. , Thompson, P. D . , Cas persen, C. J . , Kendrick, J. S. 1 987. Physical activity and the incidence of coronary heart disease. Annu. Rev. Public Health 8:253-87 Progress toward achieving the 1 990 National Objectives for Physical Fitness and Exercise. 1989. Morbid. Mortal. Wkly. Rept. 38:449-53 Raglin, J. S. 1990. Exercise and mental health. Beneficial and detrimental ef fects. Sports Med. 9:323-29 Rauramaa, R. 1984. Relationship of physical activity glucose tolerance and weight management. Prevo Med. 1 3:3746 Rauramaa, R . , Salonen, J. T . , Sep panen, K . , Salonen, R . , Veralainen , J. M . , et al. 1986. Inhibition of platelet aggregability by moderate-intensity physical exercise: a randomized clinical trial in overweight men. Circulation 74:939-44 Rothman, K. J . 1987. Modern Epidem iology. Boston: Little Brown. 358 pp. Ruderman, N . B . , Ganda, O. P . , Johan sen, K. 1978. The effect of physical training on glucose tolerance and plasma lipids in maturity-onset diabetes. Di abetes 28 (Suppl.):89-92 Sallis, J. F . , Haskell , W. L . , Wood, P. D . , Fortmann, S. P. , Rogers , T. , et al. 1985. Physical activity assessment methodology in the Five-City Project. Am. J. Epidemiol. 1 2 1 :91-106 Salonen, 1. T. , Puska, P. , Tuomilehto, 1. 1982. Physical activity and risk of myocardial infarction, cerebral stroke , and death: a longitudinal study in East ern Finland . Am. J. Epidemiol. 1 1 5: 526-37


126

BLAIR ET AL

106. Schneider, S. H . , Rudennan, N. B. 1986. Exercise and physical training and the treatment of diabetes mellitus. Com pro Ther. 12:49-56 107. Severson, R. K . , Nomura, A. M. Y . , Grove, J. S . , Stemmennann, G. N . 1 989. A prospective analysis o f physical activity and cancer. Am. J. Epidemiol. 130:522-29 108. Simon, H. B . 1990. Discussion: exer cise, immunity, cancer and infection. See Ref. 14, pp. 58 1-88 109. Sivertsen, I . , Dahlstrom, A. N. 1922. The relation of muscular activity to car cinoma. A preliminary report. J. Cancer Res. 6:365-78 1 10. Slattery , M. L . , Schumacher, M. c . , Smith, K. R . , West, D . W . , Abd Elghany, N. 1988. Physical activity, diet, and risk of colon cancer in Utah. Am. J. Epidemiol. 1 28:989-99 1 1 1 . Snow-Harter, C . , Marcus, R . 1 99 1 . Ex ercise, bone mineral density, and osteoporosis. In Exercise and Sport Sci ences Reviews, ed. J. O. Holloszy, 1 9:351-88. Baltimore: Williams & Wil

kins. 606 pp.

1 12 . Soman, V. R . , Veikko, K. A. , Deibert, D . , Feliz, P . , De Fronzo, R. 1979. In creased insulin sensitivity and insulin binding to monocytes after physical training. N. Engl. J. Med. 30 1 : 1 200-4 1 13 . Sorock, G. S . , Bush, T. L . , Golden, A. L . , Fried, L. P . , Breuer, B. et al. 1 988. Physical activity and fracture risk in a free-living elderly cohort. J. Gerontol. : Med. Sci. 43:M134--39 1 14 . Stephens, T. 1987. Secular trends in adult physical activity: exercise boom or bust? Res. Q. Exerc. Sport 58:94105 1 15 . Taylor, H. L . , Jacobs, D . R. Jr. , Schucker, B . , Knudsen, J . , Leon, A. S . , e t al. 1 978. A questionnaire for the assessment of leisure time physical ac tivities. J. Chron. Dis. 3 1 :74 1-55 1 16. Taylor, R . , Ram, P. , Zimmet, P. , Rap er, L. R . , Ringrose, H. 1 984. Physical activity and prevalence of diabetes in Melanesian and Indian men in Fiji. Di abetologia 27:578-82

1 17. Thompson, P. 1 988. The benefits and risks of exercise training in patients with chronic coronary artery disease. J. Am. Med. Assoc. 259 : 1537-40 1 1 8. Tinetti, M . E . , Speechley, M . , Ginter, S . F . 1 988. Risk factors for falls among elderly persons living in the community. N. Engl. J. Med. 3 1 9 : 1 701-7 1 19 . Tipton, C. M . , Vailas, A. C. 1 990. See Ref. 14, pp. 331-34 1 20. Van Dale, D . , Saris, W . , Ten Hoor, F. 1 990. Weight maintenance and resting metabolic rate 1 8-40 months after a diet exercise treatment. Int. J. Obes. 14: 347-59 1 2 1 . Vena, J. E . , Graham, S . , Zielezny, M . , Swanson, M . K . , Barnes, R . E . , Nolan, J. 1985. Lifetime occupational exercise and colon cancer. Am. J. Epidemiol. 1 22:357-65 1 22 . Vranic, M . , Wassennan, D. 1990. Ex ercise, fitness, and diabetes. See Ref. 1 4 , pp. 467-90 1 23 . Weber, J. R. 1 988. Left ventricular hypertrophy: its prime importance as a controllable risk factor. Am. Heart J. 1 16:272-79 124. West, K. M . 1978. Epidemiology of Di abetes and Its Vascular Lesions. New York: Elsevier. 579 pp. 1 25 . Whittemore , A. S . , Wu-Williams, A . H . , Lee, M . , Zheng, S . , Gallagher, R. P. 1990. Diet, physical activity, and colorectal cancer among Chinese in North American and China. J. Natl. Cancer [nst. 82:9 1 5-26 1 26. Wood, P . , Haskell, W . , Blair, S . , Wil liams, P. T . , Krauss, R. M . 1 983 . In creased exercise level and plasma lipo protein concentrations: a one-year, randomized controlled study in seden tary, middle-aged men. Metabolism 32: 3 1-39 1 27 . Wu, A. H . , Paganini-Hill, A . , Ross, R. K., Henderson, B . E. 1987. Alcohol, physical activity and other risk factors for colorectal cancer: a prospective study. Br. J. Cancer 55:687-94 1 28 . Zinman, B . , Vranic, M. 1985. Diabetes and exercise. Med. Clin. North Am. 69: 1 45-57

Rx exercise: physical activity is good medicine.

Psychiatric assessments: how much is too much?

How much therapy is too much? - extra.

How much is enough?

Forum: How much technology is too much?

Drugged driving: how much is too much?

How much is enough.

Tell me how much you move, I'll tell you how much you'll live. Editorial of the JONAFES I International Symposium of Physical Activity, Sport & Health.

How much physical therapy for patients with stroke?

Pay for quality: how much pay for how much quality?

Physical activity: can there be too much of a good thing?

Regular physical activity: a little is good, but is it good enough?

Physical Activity and Successful Aging: Even a Little Is Good.

Alcohol and fertility: how much is too much?

Obstructive sleep apnea: how much is too much?

Hair shedding in women: how much is too much?

Sepsis-associated renal salt wasting: how much is too much?

Bilateral supernumerary kidneys: how much is too much?

Ethics of administrative guidance: how much is too much?

Exercise and vascular function: how much is too much?

Physical Activity Is Key for Successful Aging-Reply: Even a Little Is Good.

How much evidence is required for a paradigm shift in mental health?

How much is Journal of Educational Evaluation for Health Professions promoted based on journal metrics?

Acute hospital care: how much activity is attributable to caring for patients with dementia?