Physical Activity and Health in younger adults (Kohrt et al. 1991). The inter- relationships of age, VO,max, and training status are evident when the loss in VO,max with age is compared for active and sedentary individuals (Figure 3-5). When the cardiorespiratory responses ofan older adult are compared with those of a young or middle- aged adult at the same absolute submaximal rate of work, stroke volume for an older person is generally lower and heart rate is higher from the attempt to maintain cardiac output. Because this attempt is generally insufficient, the A-VO, difference must increase to provide the same submaximal oxygen uptake (Raven and Mitchell 1980; Thompson and Dorsey 1986). Some researchers have shown, how- ever, that cardiac output can be maintained at both submaximal and maximal rates of work through a higher stroke volume in older adults (Rodeheffer et al. 1984). . The deterioration in physiological function nor- mally associated with aging is, in fact, caused by a combination of reduced physical activity and the aging process itself. By maintaining an active lifestyle, or by increasing levels of physical activ- ity if previously sedentary, older persons can maintain relatively high levels of cardiovascular and metabolic function, including VO,max (Kohrt etal. 1991), and of skeletal muscle function (Rogers and Evans 1993). For example, Fiatarone and col- leagues (1994) found an increase of 113 percent in the strength of elderly men and women (mean age of 87.1 years) following a 10-week training program of progressive resistance exercise. Cross-sectional thigh muscle area was increased, as was stair-climbing power, gait velocity, and level of spontaneous activ- ity. Increasing endurance and strength in the elderly contributes to their ability to live independently. Differences by Sex For the most part, women and men who participate in exercise training have similar responses in car- diovascular, respiratory, and metabolic function (providing that size and activity level are normal- ized). Relative increases inVO,max are equivalent Figure 3-5. Changes in VO, max with aging, comparing an active population and sedentary population (the figure also illustrates the expected increase in VO, max when a previously sedentary person begins an exercise program) 70> 60 — Active adults Reduction in activity c lus “aging” & 007 p Bing E s poe & 40 ~ Ne TTS aaa = Reduction in | Expected increase in VO, max” ~~ = _| activity plus | resulting from an exercise intervention ~~~ _ x 30 weight gain ~~. E Sedentary adults © _ Ss 20 10 - 0 ! I ! 20 30 40 50 60 70 80 Age (years) Adapted, by permission, from Buskirk ER, Hodgson JL. Federation Proceedings 1987. Physiologic Responses and Long-Term Adaptations to Exercise for women and men (Kohrt et al. 1991; Mitchell et al. 1992). Some evidence suggests that older women accomplish this increase in VO,max mainly through an increase in the A-VO, difference, whereas younger women and men have substantial increases in stroke volume, which increases maximal cardiac output (Spinaetal. 1993). With resistance training, women experience equivalent increases in strength (Rogers and Evans 1993; Holloway and Baechle 1990), although they gain less fat-free mass due to less muscle hypertrophy. Several sex differences have been noted in the acute response to exercise. At the same absolute rate of exercise, women have a higher heart rate response than men, primarily because of a lower stroke volume. This lower stroke volume is a func- tion of smaller heart size and smaller blood volume. In addition, women have less potential to increase the A-VO, difference because of lower hemoglobin content. Those differences, in addition to greater fat mass, result in a lower VO,max in women, even when normalized for size and level of training (Lewis, Kamon, Hodgson 1986). Conclusions 1. Physical activity has numerous beneficial physi- ologic effects. Most widely appreciated are its effects on the cardiovascular and musculo- skeletal systems, but benefits on the functioning of metabolic, endocrine, and immune systems are also considerable. WV . Many of the beneficial effects of exercise train- ing—from both endurance and resistance ac- tivities—diminish within 2 weeks if physical activity is substantially reduced, and effects disappear within 2 to 8 months if physical activity is not resumed. 3. People of all ages, both male and female, undergo beneficial physiologic adaptations to physical activity. Research Needs l. Explore individual variations in response to exercise. 77 2. Better characterize mechanisms through which the musculoskeletal system responds differen- tially to endurance and resistance exercise. 3. Better characterize the mechanisms by which physical activity reduces the risk of cardiovascular disease, hypertension, and non-insulin- dependent diabetes mellitus. 4. Determine the minimal and optimal amount of exercise for disease prevention. 5. Better characterize beneficial activity profiles for people with disabilities. References Abernethy PJ, Thayer R, Taylor AW. Acute and chronic responses of skeletal muscle to endurance and sprint exercise: a review. Sports Medicine 1990;,10:365-389. American College of Sports Medicine. Position stand: physical activity, physical fitness, and hypertension. Medicine and Science in Sports and Exercise 1993;25:i-x. Armstrong RB, Warren GL, Warren JA. Mechanisms of exercise-induced muscle fibre injury. Sports Medicine 1991512:184-207. Bar-Or O. Pediatric sports medicine for the practitioner: from physiologic principles to clinical applications. New York: Springer-Verlag, 1983. Birk TJ. Poliomyelitis and the post-polio syndrome: exer- cise capacities and adaptations—current research, fu- ture directions, and widespread applicability. Medicine and Science in Sports and Exercise 1993;25:466—472. Blomqvist CG, Saltin B. Cardiovascular adaptations to physical training. Annual Review of Physiology 1983;45:169-189. Bloomfield SA, Coyle EF. Bed rest, detraining, and reten- tion of training-induced adaptation. In: Durstine JL, King AC, Painter PL, Roitman JL, Zwiren LD, editors. ACSM'’s resource manual for guidelines for exercise test- ing and prescription. 2nd ed. Philadelphia: Lea and Febiger, 1993:115-128. Buskirk ER, Hodgson JL. Age and aerobic power: the rate of change in men and women. Federation Proceedings 1987;46:1824-1829. Chesnut CH III. Bone mass and exercise. American Journal of Medicine 1993;95(5A Suppl):34S—36S. Physical Activity and Health Coyle EF. Cardiovascular function during exercise: neural control factors. Sports Science Exchange 1991;4:1-6. Davis GM. Exercise capacity of individuals with para- plegia. Medicine and Science in Sports and Exercise 1993,25:423-432. Doubt TJ. Physiology of exercise in the cold. Sports Medicine 1991;11:367-381. Drinkwater BL. Physical activity, fitness, and osteoporosis. In: Bouchard C, Shephard RJ, Stephens T, editors. Physical activity, fitness, and health: international proceed- ings and consensus statement. Champaign, IL: Human Kinetics, 1994:724-736. Fagard RH, Tipton CM. Physical activity, fitness, and hypertension. In: Bouchard C, Shephard RJ, Stephens T, editors. Physical activity, fitness, and health: international proceedings and consensus statement. Champaign, IL: Human Kinetics, 1994:633-655. Farrell PA, Wilmore JH, Coyle EF, Billing JE, Costill DL. Plasma lactate accumulation and distance running performance. Medicine and Science in Sports 1979;11: 338-344. Fernhall B. Physical fitness and exercise training of indi- viduals with mental retardation. Medicine and Science in Sports and Exercise 1993;25:442-450. Fiatarone MA, O'Neill EF, Ryan ND, Clements KM, Solares GR, Nelson ME, etal. Exercise training and nutritional supplementation for physical frailty in very elderly people. New England Journal of Medicine 1994, 330:1769-1775. Figoni SF. Exercise responses and quadriplegia. Medicine and Science in Sports and Exercise 1993;25:433-—441. Fleck SJ, Kraemer WJ. Designing resistance training pro- grams. Champaign, IL: Human Kinetics, 1987:264. Fulco CS, Cymerman A. Human performance and acute hypoxia. In: Pandolf KB, Sawka MN, Gonzalez RR, editors. Human performance physiology and environ- mental medicine at terrestrial extremes. Indianapolis: Benchmark Press, 1988:467-495. George KP, Wolfe LA, Burggraf GW. The “athletic heart syndrome”: a critical review. Sports Medicine 1991;11:300-331. , Gledhill N, Cox D, Jamnik R. Endurance athletes’ stroke volume does not plateau: major advantage is diastolic function. Medicine and Science in Sports and Exercise 1994;26:1116-1121. Gonyea WJ, Sale DG, Gonyea FB, Mikesky A. Exercise- induced increases in muscle fiber number. European Journal of Applied Physiology 1986;55:137-141. 78 Gordon NF, Kohl HW III, Pollock ML, Vaandrager H, Gibbons LW, Blair SN. Cardiovascular safety of maximal strength testing in healthy adults. American Journal of Cardiology 1995;76:851-853. Graves JE, Pollock ML, Leggett.SH, Braith RW, Carpenter DM, Bishop LE. Effect of reduced training frequency on muscular strength. International Journal of Sports Medicine 1988;9:316-319. Green HJ, Jones LL, Painter DC. Effects of short-term training on cardiac function during prolonged exer- cise. Medicine and Science in Sports and Exercise 1990;22:488-493. Grover RF, Weil JV, Reeves JT. Cardiovascular adaptation to exercise at high altitude. Exercise and Sport Sciences Reviews 1986;14:269-302. Hickson RC. Skeletal muscle cytochrome c and myoglo- bin, endurance, and frequency of training. Journal of Applied Physiology 1981,51:746-749. Hickson RC, Foster C, Pollock ML, Galassi TM, Rich S. Reduced training intensities and loss of aerobic power, endurance, and cardiac growth. Journal of Applied Physiology 1985;58:492-499. Hickson RC, Rosenkoetter MA. Reduced training fre- quencies and maintenance of increased aerobic power. Medicine and Science in Sports and Exercise 1981;13: 13-16. Hoffman-Goetz L, Pedersen BK. Exercise and the immune system: a model of the stress response? Immunology Today 1994;15:382-387. Holloway JB, Baechle TR. Strength training for female athletes: a review of selected aspects. Sports Medicine 1990;9:216~-228. Isea JE, Piepoli M, Adamopoulos S, Pannarale G, Sleight P, Coats AJS. Time course of haemodynamic changes after maximal exercise. European Journal of Clinical Investigation 1994,24:824-829. Jacobs I, Martineau L, Vallerand AL. Thermoregulatory thermogenesis in humans during cold stress. Exercise and Sport Sciences Reviews 1994;22:221-250. Jolesz F, Sreter FA. Development, innervation, and activity— pattern induced changes in skeletal muscle. Annual Review of Physiology 1981;43:531-552. Jorgensen CR, Gobel FL, Taylor HL, Wang Y. Myocardial blood flow and oxygen consumption during exercise. Annals of the New York Academy of Sciences 1977;301: 213-223. Physiologic Responses and Long-Term Adaptations to Exercise Kannus P, Jozsa L, Renstrém P, Jarvinen M, Kvist M, Lehto M, et al. The effects of training, immobiliza-— tion, and remobilization on musculoskeletal tissue. Scandinavian Journal of Medicine and Science in Sports 1992;2:100-118. Keast D, Cameron K, Morton AR. Exercise and the im- mune response. Sports Medicine 1988;5:248-267. Kiens B, Essen-Gustavsson B, Christensen NJ, Saltin B. Skeletal muscle substrate utilization during submaximal exercise in man: effect of endurance training. Journal of Physiology 1993;469:459-478. Kohrt WM, Malley MT, Coggan AR, Spina RJ, Ogawa T, Ehsani AA, etal. Effects of gender, age, and fitness level on response of VO, max to training in 60-71 yr olds. Journal of Applied Physiology 1991;71:2004-2011. Krahenbuhl GS, Skinner JS, Kohrt WM. Developmental aspects of maximal aerobic power in children. Exercise and Sport Sciences Reviews 1985;13:503-538. Lewis DA, Kamon E, Hodgson JL. Physiological differ- ences between genders: implications for sports condi- tioning. Sports Medicine 1986;3:357-369. Lipman RL, Raskin P, Love T, Triebwasser J, Lecocq FR, Schnure JJ. Glucose intolerance during decreased physical activity in man. Diabetes 1972;21:101-107. MacIntyre DL, Reid WD, McKenzie DC. Delayed muscle soreness: the inflammatory response to muscle injury and its clinical implications. Sports Medicine 1995,;20: 24-40. Marcus ML. The coronary circulation in health and disease. New York: McGraw Hill, 1983. Mitchell JH, Tate C, Raven P, Cobb F, Kraus W, Moreadith R, et al. Acute response and chronic adaptation to exercise in women. Medicine and Science in Sports and Exercise 1992;24(6 Suppl):S258-S265. Montain SJ, Coyle EF. Influence of graded dehydration on hyperthermia and cardiovascular drift during exercise. Journal of Applied Physiology 1992;73:1340-1350. Neufer PD, Costill DL, Fielding RA, Flynn MG, Kirwan JP. Effect of reduced training on muscular strength and endurance in competitive swimmers. Medicine and Science in Sports and Exercise 1987;19:486-490. Newsholme EA, Parry-Billings M. Effects of exercise on the immune system. In: Bouchard C, Shephard RJ, Stephens T, editors. Physical activity, fitness, and health: interna- tional proceedings and consensus statement. Champaign, IL: Human Kinetics, 1994:451-455. 79 Nieman DC. Exercise, infection, and immunity. Interna- tional Journal of Sports Medicine 1994,15(3 Suppl): $131-SI41. Pedersen BK, Ullum H. NK cell response to physical activity: possible mechanisms of action. Medicine and Science in Sports and Exercise 1994,26:140-146. Ponichtera-Mulcare JA. Exercise and multiple sclerosis. Medicine and Science in Sports and Exercise 1993;25: 451-465. Raven PB, Mitchell J. The effect of aging on the cardiovas- cular response to dynamic and static exercise. In: Weisfeldt ML, editor. The aging heart. New York: Raven Press, 1980:269-296.. Reichlin S$. Neuroendocrinology. In: Wilson JD, Foster DW, editors. Williams’ textbook of endocrinology. 8th ed. Philadelphia: W.B. Saunders, 1992:201. Rodeheffer RJ; Gerstenblith G, Becker LC, Fleg JL, Weisfeldt ML, Lakatta EG. Exercise cardiac output is maintained with advancing age in healthy human subjects: cardiac dilatation and increased stroke volume compensate for a diminished heart rate. Circulation 1984;69:203-213. Rogers MA, Evans WJ. Changes in skeletal muscle with aging: effects of exercise training. Exercise and Sport Sciences Reviews 1993:21:65-102. Rowell LB. Human cardiovascular control. New York: Oxford University Press, 1993. Rowell LB. Human circulation regulation during physical stress. New York: Oxford University Press, 1986. Saltin B, Blomqvist G, Mitchell JH, Johnson RL, Wildenthal K, Chapman CB. Response to exercise after bed rest and after training: a longitudinal study of adaptive changes in oxygen transport and body composition. Circulation 1968;38(Suppl 7):1-78. Saltin B, Rowell LB. Functional adaptations to physical activity and inactivity. Federation Proceedings 1980;39: 1506-1513. Scruggs KD, Martin NB, Broeder CE, Hofman Z, Thomas EL, Wambsgans KC, et al. Stroke volume during submaximal exercise in endurance-trained normo- tensive subjects and in untrained hypertensive sub- jects with beta blockade (propranolol and pindolol). American Journal of Cardiology 1991;67:416-421. Seals DR, Hagberg JM, Spina RJ, Rogers MA, Schechtman KB, Ehsani AA. Enhanced left ventricular perfor- mance in endurance trained older men. Circulation 1994,89:198—205. Physical Activity and Health Shephard RJ. Aerobic fitness and health. Champaign, IL: Human Kinetics, 1994. Shephard RJ. Metabolic adaptations to exercise in the cold: an update. Sports Medicine 1993;16:266-289. Shephard RJ, Shek PN. Cancer, immune function, and physical activity. Canadian Journal of Applied Physiology 1995;20:1-25. Sjéstrém M, Lexell J, Eriksson A, Taylor CC. Evidence of fibre hyperplasia in human skeletal muscles from healthy young men? A left-right comparison of the fibre number in whole anterior tibialis muscles. Euro- pean Journal of Applied Physiology 1991,62:301-304. Spina RJ, Ogawa T, Miller TR, Kohrt WM, Ehsani AA. Effect of exercise training on left ventricular perfor- mance in older women free of cardiopulmonary dis- ease. American Journal of Cardiology 1993;71:99-104. - Svedenhag J, Henriksson J, Sylvén C. Dissociation of training effects on skeletal muscle mitochondrial en- zymes and myoglobin in man. Acta Physiologica Scandinavica 1983,117:213-218. Terjung RL. Muscle adaptations to aerobic training. Sports Science Exchange 1995:8:1—4. Thompson PD, Dorsey DL. The heart of the masters athlete. In: Sutton JR, Brock RM, editors. Sports medi- cine for the mature athlete. Indianapolis: Benchmark Press, 1986:309-318. 80 Tipton CM. Exercise, training, and hypertension: an update. Exercise and Sport Sciences Reviews 1991.19: 447-505. Tipton CM, Vailas AC. Bone and connective tissue adap- tations to physical activity. In: Bouchard C, Shephard RJ, Stephens T, Sutton JR, McPherson BD, editors. Exercise, fitness, and health: a consensus of current knowl- edge. Champaign, IL: Human Kinetics, 1990:331-344. Toner MM, McArdle WD. Physiological adjustments of man to the cold. In: Pandolf KB, Sawka MN, Gonzalez RR, editors. Human performance physiology and envi- ronmental medicine at terrestrial extremes. Indianapolis: Benchmark Press, 1988:361-399. Turley KR, McBride PJ, Wilmore JH. Resting metabolic rate measured after subjects spent the night at home vs at a clinic. American Journal of Clinical Nutrition 1993;58:141-144. Wilmore JH, Costill DL. Physiology of sport and exercise. Champaign, IL: Human Kinetics, 1994. Woods JA, Davis JM. Exercise, monocyte/macrophage function, and cancer. Medicine and Science in Sports and Exercise 1994;26:147-—157. CHAPTER 4 THE Errects OF PHysiCAL ACTIVITY ON HEALTH AND DISEASE Contents Introduction . 85 Overall Mortality Ln eee eee eee tee eee eee beeen eens 85 Conclusions 2.0... ee ee eee eee ence cece scenes 87 Cardiovascular Diseases .. 0.0.0.0 000 cece eee eee eee 87 Cardiovascular Diseases Combined .............00 0000 cc cece cece cnet eens 87 Coronary Heart Disease .... 0.2.20... 0c ee tte eens 87 CVD Risk Factors in Children ..... 2.000000. ccc eee 91 Stroke ee eee eee eee e bene been eeee 102 High Blood Pressure ......... Dee eee ee ee ee ev ew eee ee eyes shee eee saves 103 Biologic Plausibility 2.2... cece ett eens 110 Atherosclerosis 2... 00.0. cence eect eee n ees 110 Plasma Lipid/Lipoprotein Profile .......... 0.0.00 c eee 111 Blood Pressure... 0... ence cece ebb bebe een eeaes lll Ischemia 2.0... nee e ene ecb eee e teenie eee 111 Thrombosis . 0.0.0.0... eee ee eee ee eee eas 112 Arrhythmia 2.0... ete teens 112 Conclusions 2.0.0... ee ence eee ete n eee ees 112 Cancer eee eee eee beeen eee e neces 112 Colorectal Cancer 2... tte ee ete teen eee 113 Colon Cancer 0.0... cece nent teen ens 113 Rectal Cancer 2.0... cece cece eben ee eben nes 116 Hormone-Dependent Cancers in Women ............. 00.00. c cece eee 116 Breast Cancer 20... eee eee ee eee eee eens 117 Contents, continued Cancers in Men .... 6... eee cee ence ee eect eteeeered 121 Prostate Cancer 2.1... 00. e eect eeeeeeenaes 121 Testicular Cancer 2.0.0... ieee nce ete een eee eee 124 Other Site-Specific Cancers ©. 0.0... cece cece e ence cence eens 124 Biologic Plausibility 2.00.0... lec cee cece cence cece eens 124 Conclusions 2.2... 0. ccc cee teen cent e eee eeneeees 124 Non-Insulin-Dependent Diabetes Mellitus .........0.0.000 00.000 e eee ee ec eee eee. 125 Physical Activityand NIDDM ..............0 00000 c cece cece ee ceneeseee ees 125 Biologic Plausibility ©2000... 0. ec c cee eeee Serre 128 Conclusions ©... 0.0 cece ee eee eeeneeeeteenes 129 Osteoarthritis 2... e etc c cnet eet eeneeseeeens 129 Physical Activity in Persons with Arthritis ...........00.0.00 0000 ccc ceecccceeeuee 129 Biologic Plausibility 22.002. .ccecce eect e cece eee, 130 Conclusions ............... ee tence eee eee ae 130 Osteoporosis . 2.0... ce cece cen b bebe eee e cee eeenees 130 Biologic Plausibility 2.6... e cece eee eeeeees 131 Physical Activity and the Prevention of Fractures and Falling ..................... 132 Conclusions 2.20... 2c ccc eee n eee e ete teeeeeees 132 SC 133 Physical Activity and Obesity ........00 200.0000 c cece eee ec eeeeeseceeeeey 133 Biologic Plausibility ©... 0.0. c eee e cece eeeee, 134 Conclusions ... 2... cece cent e ete n ee netebeeenes 135 Mental Health .. 222.0 c nee e ett e eee ceeeeeee. 135 Physical Activity and Mental Health .........0.0.0.00 000 0c cece cceceeeecceeeey 136 Biologic Plausibility 2.02... e cece ecebevns 141 Conclusions ©1000... eee n cece tee t eevee eeeeees 141 Health-Related Quality of Life 2.0.0... ccc ccc cece ce eeeeeeeee 141 Conclusions Contents, continued Adverse Effects of Physical Activity ....... 00... eee 142 Types of Adverse Effects ©... 0.0.00 e ee eees 142 Musculoskeletal Injuries... 2.0.0.0... eee eee c ene eees 142 Metabolic Abnormalities 0.2.0... 0. cece eee een 143 Hematologic and Body Organ Abnormalities ......................... Sees 143 Hazards 2.0... cc tet eee nee beens 143 Infectious, Allergic, and Inflammatory Conditions .........................005. 143 Cardiac Events 2.00... 00. ccc eee cece cr enn bene eens 143 Occurrence of Adverse Effects 2.0.0... 0... cee e eens 144 Conclusions ..... 6... teen t nent neeees 144 Nature of the Activity/Health Relationship ............00...0. 0000 cccceeeeeeeeee 144 Causality . 2... ccc ene c eben eee neeeneeenes 144 Population Burden of Sedentary Living .............. 00. cee eee ccc eee eee ee 145 6 146 Conclusions .............. bee v eve e teen ete eevee teeeevevereerneees 148 Chapter Summary .. 2... cece eee cence ne eeees 149 Conclusions 20... 0... cence eee cece e cece cece eee 149 Research Needs ... 2... cece eee n eee e eee eens 150 References CHAPTER 4 THe Errects OF PHysiICAL ACTIVITY ON Introduction his chapter examines the relationship of physi- cal activity and cardiorespiratory fitness to a variety of health problems. The primary focus is on diseases and conditions for which sufficient data exist to evaluate an association with physical activity, the strength of such relationships, and their potential biologic mechanisms. Because most of the research to date has addressed the health effects of endurance- type physical activity (involving repetitive use of large muscle groups, such as in walking and bicy- cling), this chapter focuses on that type of activity. Unless otherwise specified, the term physical activity should be understood to refer to endurance-type physical activity. Less well studied are the health effects of resistance-type physical activity (i.e., that which develops muscular strength); when this type of physical activity is discussed, it is specified as such. Much of the research summarized is based on studies having only white men as participants; it remains to be clarified whether the relationships described here are the same for women, racial and ethnic minority groups, and people with disabilities. Physical activity is difficult to measure directly. Three types of physical activity measures have been used in observational studies over the last 40 years. Most studies have relied on self-reported level of physical activity, as recalled by people prompted by a questionnaire or interview. A more objectively measured characteristic is cardiorespiratory fitness (also referred to as cardiorespiratory endurance) which is measured by aerobic power (see Chapter 2 for more information on measurement issues). Some studies have relied on occupation to classify people according to how likely they were to be physically active at work. HEALTH AND DISEASE Epidemiologic studies of physical activity and health have compared the activity levels of people who have or develop diseases and those who do not. Cohort studies follow populations forward in time to observe how physical activity habits affect disease occurrence or death. In case-control studies, groups of persons who have disease and separate groups of people who do not have disease are asked to recall their previous physical activity. Cross-sectional stud- ies assess the association between physical activity and disease at the same point in time. Clinical trials, on the other hand, attempt to alter physical activity patterns and then assess whether disease occurrence is modified as a result. Results from epidemiologic studies can be used to estimate the relative magnitude or strength of an association between physical activity and a health outcome. Two such measures used in this chapter are risk ratio (RR) and odds ratio (OR). For these measures, an estimate of 1.0 indicates no association, when the risk of disease is equivalent in the two groups being compared. RR or OR estimates greater than 1.0 indicate an increase in risk; those less than 1.0 indicate a decreased risk. Confidence intervals (Cl) reported with estimates of association indicate the precision of the estimate, as well as its statistical significance. When the CI range includes 1.0, the effect is considered likely to have occurred by chance, therefore the estimate of association is not consid- ered statistically significantly different from the null value of 1.0. Overall Mortality Persons with moderate to high levels of physical activity or cardiorespiratory fitness have a lower mortality rate than those with sedentary habits or Physical Activity and Health low cardiorespiratory fitness. For example, com- pared with people who are most active, sedentary people experience between a 1.2-fold to a 2-fold increased risk of dying during the follow-up interval (Slattery and Jacobs 1988; Slattery, Jacobs, Nichaman 1989: Leon and Connett 1991; Stender et al. 1993; Sandvik et al. 1993; Chang-Claude and Frentzel- Beyme 1993; Kaplan et al. 1987; Arraiz, Wigle, Mao 1992; Paffenbarger et al: 1993). Associations are generally stronger for measured cardiorespiratory fitness than for reported physical activity (Blair, Kohl, Paffenbarger 1989). Blair, Kohl, and Barlow (1993) showed that low levels of cardio- respiratory fitness were strongly associated with overall mortality for both women (RR = 5.35; 95% Cl, 2.44-11.73) and men (RR = 3.16; 95% CI, 1.92- 5.20). The association with physical inactivity was weaker for men (RR = 1.70; 95% CI, 1.06-2.74), and there was no association for women (RR = 0.95; 95% Cl, 0.54-1.70). : Though cardiorespiratory fitness may be the better indicator of regular physical activity, the level of reported physical activity has been associated with reduced all-cause mortality. Paffenbarger, Lee, and Leung (1994) evaluated several types of recalled activity (walking, stair climbing, all sports, moderate- level sports, and total energy expended in activity per week) as predictors of all-cause mortality among male Harvard alumni. Among these men, the relative risk of death within the follow-up period was reduced to 0.67 with walking 15 or more kilometers per week (reference group, <5 kilometers/week), to 0.75 with climbing 55 or more flights of stairs per week (refer- ence group, < 20 flights/week), to 0.63 with involve- ment in moderate sports (reference group, no involvement), and to 0.47 with 3 or more hours of moderate sports activities per week (reference group, <1 hour/week). Mostimportantly, there wasa signifi- cant trend of decreasing risk of death across increas- ing categories of distance walked, flights of stairs climbed, and degree of intensity of sports play. Researchers have also examined age-specific ef- fects of different levels of physical activity on all- - cause mortality. Kaplan and colleagues (1987) have shown that physical activity level has an effect on death rates among both older and younger persons. Data from a study of 9,484 Seventh-Day Adventist men aged 30 years or older in 1958 who were 86 followed through 1985 indicated that both moderate and intense levels of activity reduced overall risk of death even late in life (Lindsted, Tonstad, Kuzma 1991). Both moderate and vigorous levels of activity were equally protective at age 50 years. The protec- tive effect of high levels of activity lasted only until age 70 , but the protective effect for moderate activity lasted beyond age 80. The studies cited thus far in this section assessed physical activity or cardiorespiratory fitness at baseline only and then followed up for mortality. A stronger test for a causal relationship is to examine the effect that changing from lower to higher levels of physical activity or cardiorespiratory fitness has on subsequent mortality. Two large studies provide such evidence. Among middle-aged Harvard male alumni who were sedentary in 1962 or 1966, those who took up moderately intense sports activity dur- ing the study’s 11 years of follow-up hada 23 percent lower death rate (RR = 0.77; 95% Cl, 0.58-0.96) than those who remained sedentary (Paffenbarger et al. 1993). (By comparison, men who quit smoking during the interval had a 41 percent decrease in death rate [RR = 0.59; 95% Cl, 0.43-0.80].) Men 45-84 years of age who took up moderately intense sports extended their longevity on average by 0.72 years; added years of life were observed in all age groups, including men 75-84 years of age (Paffenbarger et al. 1993). Similar reductions in death rates with increases in cardiorespiratory fitness were reported for men in the Aerobics Center Longitudinal Study. Blair and colleagues (1995) reporteda reduction in death rates among healthy men (aged 20-82 years) who im- proved their initially low levels of cardiorespiratory fitness. The men performed two maximal exercise tests an average of 4.8 years apart; follow-up for mortality after the second test occurred an average of 4.7 years later. Among men in the bottom fifth of the cardiorespiratory fitness distribution, those who improved to at least a moderate fitness level had a 44 percent lower death rate than their peers who re- mained in the bottom fifth (RR = 0.56; 95% Cl, 0.41- 0.75). After multivariate adjustment, those who became fit had a significant 64 percent reduction in their relative mortality rate. In comparison, men who stopped smoking reduced their adjusted RR by about 50 percent. Conclusions The data reviewed here suggest that regular physical activity and higher cardiorespiratory fitness decrease overall mortality rates in a dose-response fashion. Whereas most studies of physical activity and health address specific diseases and health conditions, the studies in this chapter provide more insight into the biologic mechanisms by which mortality rate reduc- tion occurs. Cardiovascular Diseases Despite a progressive decline since the late 1960s, cardiovascular diseases (CVDs), including coronary heart disease (CHD) and stroke, remain major causes of death, disability, and health care expenditures in the United States (NCHS 1994: Gillum 1994). In 1992, more than 860,000 deaths in the United States were attributed to heart disease and stroke (DHHS 1994). High blood pressure, a major risk factor for CVD, affects about 50 million Americans (National Institutes of Health [NIH] 1993), including an esti- mated 2.8 million children and adolescents 6-17 years of age (Task Force on Blood Pressure Control in Children 1987). The prevalence of CVD increases with age and is higher among African Americans than whites. The majority of population-based research in the area of physical activity and health has focused on some aspect of CVD. Cardiovascular Diseases Combined Most of the reported studies relating physical activity to CVD have reported CVD mortality as an endpoint; two also reported on nonfatal disease, and one re- ported on CVD hospitalization (Table 4-1). Seven cohort studies evaluated the association between level of physical activity and the risk of total CVD (Kannel and Sorlie 1979; Paffenbarger et al. 1984; Kannel et al. 1986; Lindsted, Tonstad, Kuzma 1991; Arraiz, Wigle, Mao 1992; Sherman etal. 1994; LaCroix et al. 1996). All relied on a single point-in-time estimate of physical activity, in some cases assessed as long as 26 years before the end of the observational period, and four had follow-up periods of > 14 years. Four of the seven studies found both an inverse association and a dose-response gradient between level of physical activity and risk of CVD outcome (Kannel and Sorlie 1979; Paffenbarger et al. 1984; The Effects of Physical Activity on Health and Disease 87 Kannel et al. 1986; LaCroix et al. 1996). One study among men found an inverse association among the moderately active group but less of an effect in the vigorously active group (Lindsted, Tonstad, Kuzma 1991). One study of women 50-74 years of age found no relationship of physical activity with CVD mor- tality (Sherman et al. 1994). Five large cohort studies have related cardiores- piratory fitness to the risk of CVD mortality (Arraiz, Wigle, Mao 1992; Ekelund et al. 1988; Blair, Kohl, Paffenbarger 1989; Sandvik et al. 1993; Blair et al. 1995), but only one provided a separate analysis for women (Blair, Kohl, Paffenbarger 1989). Each of these studies demonstrated an inverse dose-response relationship between level of cardiorespiratory fit- ness and CVD mortality. Three of the five studies relied on a maximal or near-maximal exercise test to estimate cardiorespiratory fitness. One study (Blair et al. 1995) demonstrated that men with low cardio- respiratory fitness who became fit had a lower risk of CVD mortality than men who remained unfit. Taken together, these major cohort studies indi- cate that low levels of physical activity or cardiores- piratory fitness increase risk of CVD mortality. Findings seem to be more consistent for studies of cardiorespiratory fitness, perhaps because of its greater precision of measurement, than for those of reported physical activity. The demonstrated dose- response relationship indicates that the benefit de- rived from physical activity occurs at moderate levels of physical activity or cardiorespiratory fitness and increases with increasing levels of physical activity or higher levels of fitness. Coronary Heart Disease Numerous studies have examined the relationship between physical activity and CHD asa specific CVD outcome. Reviews of the epidemiologic literature (Powell et al. 1987; Berlin and Colditz 1990; Blair 1994) have concluded that physical activity is strongly and inversely related to CHD risk. Although physical exertion may transiently increase the risk of an acute coronary event among persons with advanced coro- nary atherosclerosis, particularly among those who do not exercise regularly (Mittleman et al. 1993, Willich et al. 1993; Siscovick et al. 1984), physically active people have a substantially lower overall risk for major coronary events. Physical Activity and Health Table 4-1. Population-based studies of association of physical activity or cardiorespiratory fitness with total cardiovascular diseases Study Physical activity Kannel and Sorlie (1979) Paffenbarger et al. (1984) Kannel et al. (1986) Lindsted, Tonstad, Kuzma (1991) Arraiz, Wigle, Mao (1992) Sherman et al. (1994) LaCroix et al. (1996) Population 1,909 Framingham (MA) men and 2,311 women aged 35-64 years at 14-year follow-up 16,936 US male college alumni who entered college between 1916 and 1950; followed from 1962-1978 1,166 Framingham (MA) men aged 45-64 years; 24-year follow-up 9,484 Seventh-Day Adventist men aged 2 30 years; 26-year | follow-up Stratified probability sample of Canadians aged 30-69 years, conducted in 1978- 1979; 7-year follow-up 1,404 Framingham (MA) women aged 50-74 years; 16-year follow-up 1,645 HMO members age 2 65 years; 4.2-year average follow-up Cardiorespiratory fitness Ekelund et al. (1988) Blair et al. (1989) 3,106 North American men aged 30-69 years; 8.5-year average follow-up 10,244 men and 3,120 women aged = 20 years; 8.1-year average. follow-up Definition of physical activity or cardiorespiratory fitness Physical activity index based on hours per day spent at activity-specific intensity Physical activity index estimated from reports of stairs climbed, city blocks walked, and sports played each week Physical activity index based on hours per day at activity-specific intensity; occupational physical activity classified by physical demand of work Self-report to single physical activity question Physical activity index summarizing frequency, intensity, and duration of leisure-time activity and household chores Physical activity index based on hours per day spent at activity- specific intensity Hours of walking per week Submaximal aerobic capacity estimated from exercise test Maximal aerobic capacity estimated by exercise test 88 Definition of cardiovascular disease CVD fatal and nonfatal in men (n = 140 deaths, n = 435 total cases) and women (n = 101 deaths) Death due to CVD (n = 640) Death due to CVD (n = 325) Death due to CVD (ICD-8 410-458) (n = 410) Death due to CVD (n = 256) CVD incidence (n = 994) and mortality (n = 303) CVD hospitalization (ICD-9 390-448) (n = 359) Death due to CVD (ICD-8 390-458) (n = 45) Death due to CVD (ICD-9 390-448) in men (n = 66) and women (n = 7} The Effects of Physical Activity on Health and Disease Main findings Inverse association between physical activity index and CVD mortality for both men and women Inverse association; relative to highest category (2,000+ kcal/week), relative risk estimates were 1.28 and 1.84, respectively Inverse association; for physical activity. index, age-adjusted RR relative to high activity category = 1.62 for low activity, 1.30 for moderate; for occupational activity, age-adjusted RR relative to heavy physical demand category = 1.34 for sedentary, 1.26 for light, 1.09 for medium Inverse association relative to inactive group; moderately active RR = 0.79 (95% Cl, 0.58-1.07), highly active RR = 1.02 (95% Cl,0.66-1.58) Null association across categories of physical activity index Null association across quartiles of physical activity index Inverse association; compared with walking 4 hrs/week, RR = 0.90 (95% Cl 0.69-1.17) for walking 1-4 hrs/week; RR = 0.73 (95% Cl 0.55—0.96) for walking > 4 hrs/week Inverse association; adjusted risk estimate of 2.7-fold increased risk of CVD death for a 35 beat/min increase in heart rate for stage II of exercise test Inverse association; for men, age-adjusted RR for lowest 20% compared with upper 40% = 7.9; for middle 40% = 2.5; for women, 9.2 and 3.6 Dose response’ Yes Yes Yes No No No Yes Yes Yes 89 Adjustment for confounders and other comments Control for several confounding variables; Statistical significance only for men after multivariate adjustment Significant dose-response after adjusting for age, smoking, and hypertension prevalence Inverse association constant across all analyses; inverse association maintained after multivariate analyses No statistical significance after controlling for sociodemographic variables, BMI, and dietary pattern Point estimates adjusted for age, BMI, sex, and smoking No statistical significance after controlling for several clinical and sociodemographic confounding variables Multivariate analysis adjusted for age, sex, functional status, BMI, smoking, chronic illnesses, and alcohol Extensive control for clinical and sociodemographic confounding influences Significant linear dose-response association; adjusted for age Physical Activity and Health Table 4-1. Continued Definition of physical activity Definition of Study Population or cardiorespiratory fitness cardiovascular disease Arraiz, Wigle, Stratified probability Submaximal aerobic capacity Death due to CVD Mao (1992) sample of Canadians estimated from home step test (n = 37) aged 30-69 years, conducted in 1978- 1979; 7-year follow-up Sandvik et al. 1,960 Norwegian men Maximal aerobic capacity Death due to CVD (1993) aged 40-59 years; estimated by exercise test (n = 144) average 16-year follow-up / Blair et al. 9,777 US men aged Maximal aerobic capacity Death due to CVD (1995) 20-82 years with 2 estimated by exercise test (ICD-9 390-449.9) evaluations; 5.1-year average follow-up Thirty-six studies examining the relationship of physical activity level to risk of CHD have been published since 1953 (Table 4-2). Studies published before 1978 predominantly classified physical activ- ity level by job title or occupational activities. Studies thereafter usually defined activity level by recall of leisure-time activity or by such activity combined with occupational activity. These later studies were also able to control statistically for many potentially confounding variables in addition to age. Most of these studies focused on men in the age ranges associated with increasing risk of CHD (30-75 years), only four included women. Although in several stud- ies, CHD mortality was the sole outcome variable, most included both fatal and nonfatal disease. All but one (Morris et al. 1973) were cohort studies; lengths of follow-up from baseline assessment ranged from 4 to 25 years. All studies related a single baseline estimate of physical activity level to risk of CHD during the follow-up period. Some study populations have had more than one follow-up assessment for CHD. For example, three follow-up assessments (at 10, 12, and.23 years) have been reported for men in the Honolulu Heart Pro- gram (Yano, Reed, McGee 1984; Donahue etal. 1988, Rodriguez et al. 1994). Each represented follow-up further removed from the original determination of physical activity. Thus, the diminishing effect seen over time might indicate changing patterns of physical 90 (n = 87) activity—and thereby a lessening of validity of the original physical activity classification (Table 4-2). Oddly, in the 12-year follow-up, the reduction in CHD risk observed among both active middle-aged men (RR = 0.7) and active older men (RR = 0.4) when compared with their least active counterparts was not diminished by bivariate adjustment for serum cholesterol, body mass index (BMI), or blood pressure (Donahue et al. 1988). In the 23-year follow-up, however, the reduction in CHD risk among active men (RR = 0.8) was greatly diminished by simultaneous adjustment for serum cholesterol, BMI, blood pressure, and diabetes (RR = 0.95), leading the authors to conclude that the beneficial effect of physical activity on CHD risk is likely mediated by the beneficial effect of physical activity on these other factors (Rodriguez et al. 1994). These reports thus illustrate not only the problem oflengthy follow-up without repeated assessments of physical activity but also the problem of lack of uniformity in adjustment for potential confounding factors, as well as the underlying, thorny problem of adjustment for multiple factors that may be in the causal pathway between physical activity and disease. Studies have in fact varied greatly in the extent to which they have controlled for potential confounding and in the factors selected for adjustment. Although early studies were not designed to dem- onstrate a dose-response gradient between physical The Effects of Physical Activity on Health and Disease Dose Adjustment for confounders Main findings response” and other comments Inverse association; relative to highest fitness No Point estimates adjusted for age, BMI, sex, and level, persons in “moderate” and “low” smoking categories had risks of 0.8 (95% Cl, 0.1-7.6) and 5.4 (95% Cl, 1.9-15.9), respectively Inverse association; relative to men in lowest Yes Extensive control for confounding influences fitness quartile, multivariate adjusted RR in quartiles 2, 3, and 4 were 0.59, 0.45, and 0.41, respectively Inverse association; relative to men who Yes For each minute of improvement in exercise test remained unfit (lowest 20% of distribution), those who improved had an age-adjusted RR of 0.48 (95% Cl, 0.31-0.74) time, adjusted CVD mortality risk was reduced 8.6% Abbreviations: BMI = body mass index (wt [kg] /ht (ml? ); CVD = cardiovascular disease; Cl = confidence interval; HMO = health maintenance organization; ICD = international Classification of Diseases (8 and 9 refer to editions); RR = telative risk. ‘A dose-response relationship requires more than 2 levels of comparison. In this column, “NA” means that there were only 2 levels of comparison; “No” means that there were more than 2 levels but no dose-response gradient was found; “Yes” means that there were more than 2 levels and a dose-response gradient was found. activity level and CHD, most found an inverse asso- ciation: more active persons were found to be at lower risk of CHD than their more sedentary coun- terparts. Of the 17 recent studies that found an inverse relationship and were able to examine dose- response relationships, 13 (76 percent) demonstrated an inverse dose-response gradient between level of physical activity and risk of CHD, whereas 2 showed a dose-response gradient only for some subgroups. The relationship between cardiorespiratory fit- ness and risk of CHD was examined in seven cohort studies (follow-up range, 4-20 years). All but two (Lie, Mundal, Erikssen 1985; Erikssen 1986) used estimates of aerobic power based on submaximal exercise testing. None of these studies included women. Similar to the studies of physical activity and CHD, these all related a single baseline assess- ment of cardiorespiratory fitness to risk of CHD during the follow-up period. Most controlled statis- tically for possible confounding variables. Allseven ‘studies showed an inverse association between cardiorespiratory fitness and CHD. Of the six studies that had more than two categories of cardio- respiratory fitness, all demonstrated an inverse dose-response gradient. 91 Two recent meta-analyses of studies of physical activity and CHD have included independent scoring for the quality of the methods used in each study (Powell et al. 1987; Berlin and Colditz 1990). Both concluded that studies with higher-quality scores tended to show higher relative risk estimates than those with lower-quality scores. In the Berlin and Colditz quantitative meta-analysis, the pooled rela- tive risk for CHD—comparing risk for the lowest level of physical activity with risk for the highest level— was 1.8 among the studies judged to be of higher quality. In contrast, the pooled relative risk for the studies with low-quality scores was in the null range. CVD Risk Factors in Children Because CHD is rare in children, the cardiovascular effects of physical activity in children are assessed through the relationship of physical activity with CHD risk factors such as elevated low-density lipo- protein cholesterol (LDL-C), lowered high-density lipoprotein cholesterol (HDL-C), and elevated blood pressure. The presence of CHD risk factors in chil- dren is of concern because of evidence that athero- sclerosis begins in childhood (Stary 1989), that presence of CHD in adults is related to elevated blood Physical Activity and Health Table 4-2. Population-based studies of association of physical activity or cardiorespiratory fitness with coronary heart disease Study Physical activity Morris et al. (1953) Morris and Crawford (1958) Taylor et al. (1962) Kahn (1963) Morris et al. (1966) Cassel et al. (1971) Morris et al. (1973) Brunner et al. (1974) Population 31,000 male employees of London Transport Executive aged 35-64 years 3,731 case necropsy studies (decedents aged 45-70 years) conducted in Scotland, England, and Wales 191,609 US white male railroad industry employees aged 40-64 years . 2,240 Postal Service employees in the Washington, D.C., Post Office between 1906 and 1940; followed” through December 1961 667 London bus conductors and drivers aged 30-69 years; 5-year follow-up 3,009 male residents of Evans County, Georgia, aged over 40 years in 1960-1962; 7.25-year average follow-up British male executive grade civil servants aged 40-60 years; 232 heart attack case- patients and 428 matched controls . 5,288 male and 5,229 female residents of 58 Israeli kibbutzim aged 40-69 years; 15-year follow-up Definition of physical activity or cardiorespiratory fitness Occupational classification of job duties: sedentary drivers and active conductors Physical activity at work defined by coding of last known job title before death (light, active, heavy) Physical activity at work defined by job title for clerks, switchmen, and section men Physical activity at work defined by job title for clerks and carriers Occupational classification of job duties as sedentary drivers and active conductors Occupational classification of job duties as active or sedentary 48-hour recall of leisure-time physical activities; activities defined as capable of reaching 7.5 kcal/min were defined as vigorous Work types classified as sedentary or nonsedentary 92 Definition of coronary heart disease First clinical episode of CHD Necropsy evaluation of IMF among persons dying from noncoronary causes Death due to arteriosclerotic disease (ICD 420, 422) in 1955-1956 Death due to CHD Incidence of CHD (n = 47) Incidence of CHD (n = 337) First CHD attack (fatal and nonfatal) Fatal and nonfatal CHD, males (n = 281) and females (n = 70) The Effects of Physical Activity on Health and Disease Main findings inverse association; relative to men whose main job responsibility was driving buses, conductors had an age-adjusted risk of first coronary episode of 0.70 Inverse association; RR for IMF for persons in light occupations was 1.97 relative to heavy group; active group rate was intermediate Inverse association; RR for arteriosclerotic disease among clerks was 2.03 relative to that for section men; risk estimate for switchmen was 1.46 Inverse and null associations; among employees classified by their original occupational category, the age-adjusted risk for CHD death for clerks relative to carriers was 1.26 Inverse association; age-adjusted risk of CHD incidence among drivers was 1.8 relative to that for conductors Inverse association; age-adjusted risk of CHD among sedentary, nonfarm occupations relative to that for active nonfarm occupations was 1.8 Inverse association; RR estimate for first attack among vigorous group = 0.33 compared with nonvigorous group Inverse association; risk for CHD incidence among those engaged in sedentary work compared with that for nonsedentary peers was 2.52 for men and 3.28 for women Dose response’ NA Yes Yes NA NA NA NA NA Adjustment for confounders and other comments No control for confounding; results were similar in subgroup of men who died of CHD-associated conditions No control for confounding; one of few pathology studies No control for confounding; specific analyses were consistent with overall results No control for confounding; extensive efforts made to consider and evaluate job transfers Medical evaluation data used to control for confounding variables Data also available on black residents; comparisons between sedentary and active occupations not possible Only study to analyze 48-hour recall of leisure-time physical activity (5-minute intervals) No differences in serum cholesterol and body weight between groups 93 Physical Activity and Health Table 4-2. Continued Definition of physical activity ‘or cardiorespiratory fitness Definition of coronary heart disease Study Population Paffenbarger and 6,351 San Francisco Hale (1975) Bay Area longshoremen aged 35-74 years; followed for 22 years, from 1951 to death or to age 75 3,686 San Francisco Bay Area longshoremen aged 35-74 years; followed for 22 years, from 1951 to death or to age 75 Paffenbarger et al. (1977) Rosenman, Bawol, 2,065 white male San Oscherwitz Francisco Bay Area (1977) federal employees aged 35-59 years; 4-year follow-up Chave et al. 3,591 British male (1978) executive-grade civil servants aged 40-64 years; 8.5-year average follow-up from 1968 to 1970 Paffenbarger, 16,936 Harvard male Wing, Hyde alumni aged 35-74 (1978) years; followed up for 6-10 years Morris et al. 17,944 British male (1980) executive grade civil servants aged 40-64 years; 8.5-year average follow-up from 1968 to 1970 - Salonen et al. 3,829 women and (1982) 4,110 men aged. 30-59 years from Eastern Finland; 7-year follow-up Pomrehn et al. (1982) 61,922 deaths from 1964-1978 among lowa men aged 20 to 64 years Work-years according to required energy output: heavy (5.2-7.5 kcal/min), moderate (2.4-5.0 kcal/min), and light (1.5-2.0 kcal/min) Work-years according to required energy output: high (5.2-7.5 kcal/min), intermediate (2.4-5.0 kcal/min), and light (1.5~2.0 kcal/min) Occupational physical activity; estimated caloric expenditure for work and nonwork activity 48-hour leisure-time physical activity recall; activities capable of reaching 7.5 kcal/min defined as vigorous Physical activity index based on self-report of stairs climbed, blocks walked, and strenuous sports play 48-hour recall of leisure-time physical activities; activities defined as capable of reaching 7.5 kcal/min were defined as vigorous Dichotomous assessment of occupational and leisure-time physical activity (low/high) Occupational classification; farmers vs. nonfarmers 94 CHD death (ICD-7 420) (n = 598) CHD death (ICD-7 420) (n = 395) Fatal and nonfatal CHD (n = 65) Fatal and nonfatal first CHD attack (n = 268) Fatal and nonfatal first heart attack (n = 572) Fatal and nonfatal first heart attack (n =1,138) Fatal acute ischemic heart disease (ICD-8, 410-41 2) - (n = 89 men and 14 women) and acute myocardial infarction (ICD-8, 410-411) (n = 210 men and 63 women) Death from ischemic heart disease The Effects of Physical Activity on Health and Disease Main findings Inverse association; relative to heavy category, age-adjusted RR of CHD death was 1.70 in moderate and 1.80 in light categories Inverse association overall, inverse for younger birth cohorts and null for older cohorts; relative to high category, age-adjusted RRs of CHD death were 1.8 in intermediate and 1.60 in light categories Null association Inverse association; risk of CHD attack among men reporting nonvigorous exercise relative to men reporting vigorous exercise was 2.2 Inverse association; age-adjusted RR of first heart attack for men who expended fewer than 2,000 kcal/week was 1.64 compared with men who expended 2,000 or more kcal/week inverse association; age-adjusted risk of CHD attack among men reporting nonvigorous exercise relative to those reporting vigorous exercise was 2.2 Inverse association; RR of acute myocardial infarction for men and women with low levels of physical activity at work = 1.5 (90% Cl, 1.2-2.0) for men and 2.4 (90% CI, 1.5—3.7) for women Farm men had significantly less mortality than expected from the experience in the general population of lowa men (SMR = 0.89) Dose response’ Yes No/Yes No NA Yes NA NA NA Adjustment for confounders and other comments No control for confounding variables; efforts made to evaluate job changes in the cohort over time Dose response noted in age-adjusted rates only for two younger groups; two older groups exhibited no association Relatively short-term follow-up Preliminary report of further data of Morris et al. 1980 History of athleticism not associated with lower risk unless there was also current energy expenditure Increased risk similar for fatal and nonfatal attacks No associations with leisure-time physical activity; extensive adjustment for confounding No adjustment for confounding 95 Physical Activity and Health Table 4-2. Study Garcia-Palmieri et al. (1982) Paffenbarger et al. (1984) Yano, Reed, McGee (1984) Menotti and Seccareccia (1985) Kannel et al. (1986) Lapidus and Bengtsson (1986) Leon et al. (1987) Pekkanen et al. (1987) ‘Sobolski et al. (1987) Continued Population 8,793 Puerto Rican men aged 45-64 years; followed for up to 8.25 years 16,936 US male college alumni who entered college between 1916 and 1950; followed from 1962 to 1978 7,705 Hawaiian men of Japanese ancestry aged 45-68 years with no history of heart disease; 10-year follow-up 99,029 Italian male railroad employees aged 40-59 years; 5-year follow-up 1,166 Framingham (MA) men aged 45-64 years; 24-year follow-up 1,462 Swedish women aged 38-60 years; follow-up between 1968 and 1981 12,138 North American men at high risk for CHD, aged 35-57 years; 7-year average follow-up 636 apparently healthy Finnish men aged 45-64 years, followed for 20 years from 1964 baseline 2,109 Belgian men aged 40-55 years in 1976-1978; 5-year -follow-up Definition of physical activity or cardiorespiratory fitness Usual 24-hour physical activity index based on hours/day at specific intensity Physical activity index estimated from reports of stairs climbed, city blocks walked, and sports played each week Self-report of 24-hour habitual physical activity in 1965-1968 Occupational physical activity (heavy, moderate, sedentary) Physical activity index based on hours per day at activity-specific intensity; occupational physical activity classified by physical demand of work ~ Physical activity at work and during leisure hours, lifetime, and during previous years Leisure-time physical activity index: energy expenditure (minutes/week) Occupational and transport/ recreational physical activity (high or low) Occupational and leisure-time physical activity (4 categories each) 96 Definition of coronary heart disease CHD incidence other than angina pectoris (n = 335) Death due to CHD (n = 441) Incident cases of fatal and nonfatal CHD (n = 511) Fatal myocardial infarction (n = 614) Death due to CHD (n = 220) Nonfatal myocardial infarction and angina pectoris Fatal and nonfatal CHD (n = 781; 368 fatal) Death due to CHD (n = 106) Incident cases of fatal and nonfatal myocardial infarction and sudden death (n = 36) The Effects of Physical Activity on Health and Disease Main findings Inverse association; physical activity index was significantly related to lower risk of CHD in urban as well as rural men inverse association; relative to highest category of index (2,000+ kcal/week), risk estimates in next two lower categories were 1.28 and 1.84, respectively Inverse association; significant only for all CHD; no significant association for various subtypes Inverse association; relative to sedentary, men in moderate and heavy occupational activity had RRs of 0.97 and 0.64, respectively Inverse association; age-adjusted RR (relative to high category) = 1.38 (low), 1.21 (moderate); for occupational activity, age-adjusted RR (relative to heavy category) = 1.27 (sedentary), 1.22 (light), 0.99 (medium) Inverse association only for leisure-time physical activity; RR = 2.8 (95% Cl, 1.2- 6.5) comparing low leisure-time physical activity with all other categories Inverse association; multivariate adjusted risk estimate (relative to low activity tertile) was 0.90 (95% Cl, 0.76-1.06) for more active and 0.83 (95% Cl, 0.70-0.99) for most active Inverse association; adjusted RR for men in low physical activity group was 1.30 (p = 0.17) Null association for both leisure-time and occupational physical activity Dose response” Yes Yes NA Yes Yes NA Yes NA No Adjustment for confounders and other comments Significant inverse relationship for CHD after multivariate adjustment Significant dose-response after adjusting for age, smoking, and hypertension prevalence Adjusted for age, blood pressure, cholesterol, BMI, serum glucose, vital capacity, etc. Adjusted for age Inverse association constant across all analyses and maintained after controlling for multivariate confounding Adjusted for age Dose response for fatal and nonfatal cases combined but not for CHD death or sudden death separately Association limited to second half of follow-up period One of two studies to simultaneously evaluate associations of physical activity, fitness, and CHD 97 Physical Activity and Health Table 4-2. Study Donahue et al. (1988) Salonen et al. (1988) johansson et al. (1988) Slattery, Jacobs, Nichaman (1989) Morris et al. (1990) Lindsted, Tonstad, Kuzma (1991) Shaper and Wannamethee (1991) Seccareccia and Menotti (1992) Continued Population 7,644 Hawaiian men of Japanese ancestry aged 45-64 years with no history of heart disease; 12-year follow-up 15,088 Eastern Finnish men and women aged 30-59 years; 6-year follow-up 7,495 Goteburg men aged 47-55 years at entry; 11.8-year average follow-up 3,043 US male railroad employees; followed for 17-20 years 9,376 British male middle grade executives aged 45-64 years; 9.3-year average follow-up 9,484 Seventh-Day Adventist men aged 2 30 years; 26-year follow-up 7,735 British men aged 40-59 years; 8.5-year follow-up 1,712 men from Northern and Central italy, aged 40-59 years, initially examined in 1960; 25-year follow-up Definition of physical activity or cardiorespiratory fitness Self-report of 24-hour habitual physical activity in 1965-1968; 3-point scale defined by tertiles of distribution Self-reported leisure-time and occupational physical activity (4 levels collapsed into 2 categories each) Physical activity at work and physical activity during leisure time (4-point scale for each) Leisure-time physical activity index (kcal/week) Leisure-time physical activity reported over previous 4 weeks; energy expenditure values ascribed to reported activities Self-report to single physical activity question Self-report of physical activity at baseline; 6-point scale Occupational physical activity (self-report): sedentary, moderate, and heavy Definition of coronary heart disease Incident cases of fatal and nonfatal CHD (n = 444) Death due to CHD (ICD-8 410-414) (n = 102 90 men, 12 women) Incident cases of fatal and nonfatal CHD Death due to CHD (ICD-8 410-414) Fatal and nonfatal CHD (ICD-8 410-414) (n = 474) Ischemic heart disease mortality (ICD-8 410-414) (n = 1,351} Fatal and nonfatal heart attack (n = 488) Death due to CHD Hein, 4,999 Copenhagen Leisure-time physical activity Fatal myocardial Suadicani, men aged 40-59 years; (4-point scale) infarction Gyntelberg 17-year follow-up (ICD-8 410-414) (1992) from 1970/1971 (n = 266) 98 The Effects of Physical Activity on Health and Disease Main findings Inverse association; RR among active men relative to sedentary men was 0.69 (95% Cl, 0.53-0.88) for men aged 45-64 and 0.43 (95% CI, 0.19-0.99) for older men aged 65-74 Inverse association; occupational: adjusted RR among inactive was 1.3 (95% Cl, 1.1-1.6) relative to active; adjusted RR of CHD among leisure-time active was 1.2 (95% Cl, 1.0-1.5) Null association between physical activity at work and CHD risk; inverse association (not statistically significant) between leisure-time physical activity and CHD Inverse association; adjusted risk estimate (relative to highest physical activity category) was 1.28 for sedentary group (not statistically significant) Inverse association; age-adjusted RR for — 3 episodes per week of vigorous physical activity relative to sedentary group was 0.36 Null association; risk estimates of CHD death exhibited a U-shaped relationship with increasing physical activity levels Inverse association only for 2 activity levels; RR compared with sedentary for increasing physical activity levels: occasional 0.9 (95%CI, 0.5—-1.3), light 0.9 (95% Cl, 0.6-1.4), moderate 0.5 (95% Cl, 0.2~0.8), moderately vigorous 0.5 (95% Cl, 0.3-0.9), and vigorous 0.9 (95% Cl, 0.5-1.8) Inverse association; age-adjusted RR for moderate and heavy categories compared with that for sedentary group was 0.69 and 0.58, respectively Inverse association; relative to more active men (categories 2—4 of index), least active men had an adjusted RR of CHD of 1.59 (95% Cl, 1.14-2.21) Dose response’ Yes NA No Yes Yes No No Yes No 99 Adjustment for confounders and other comments Adjusted for age, alcohol use, and smoking; bivariate adjustment for cholesterol, BMI, and blood pressure did not alter findings; follow-up to Yano, Reed, McGee (1984) Point estimate for low leisure-time physical activity was adjusted toward the null after consideration of other CHD risk factors Extensive control for confounding variables; ancillary analysis on postinfarction patients also yielded null association Adjusted for age, smoking, cholesterol, and blood pressure No adjustment for confounding; association only noted for vigorous physical activity Possible protective association among moderate activity group No clear linear trend Inverse association remained statistically significant after adjustment for confounding One of two studies to simultaneously evaluate activity and fitness in relation to CHD mortality Physical Activity and Health Table 4-2. Continued Study Population Definition of physical activity or cardiorespiratory fitness Shaper, Wannamethee, Walker (1994) Rodriguez et al. (1994) 5,694 British men aged 40-59 years; 9.5-year follow-up 7,074 Hawaiian men of Japanese ancestry aged 45-68 years, 23-year follow-up Cardiorespiratory fitness Peters et al. (1983) Lie, Mundal, Erikssen (1985) Erikssen (1986) Sobolski et al. (1987) Ekelund et al. (1988) Slattery et al. 2,779 male Los Angeles County public safety employees aged < 55 years; 4.8-year average follow-up 2,014 Norwegian employed men aged 40-59 years; 7-year follow-up 1,832 Norwegian men aged 40-59 years; 7-year average follow-up 2,109 Belgian men aged 40-55 years in 1976-1978; 5-year follow-up 3,106 North American men aged 30-69 years, 8.5-year average follow-up 2,431 US male railroad Self-report of physical activity at baseline; 6-point scale data analyzed by hypertensive status Self-report of 24-hour habitual physical activity in 1965-1968 Submaximal aerobic capacity estimated from cycle ergometer test; age-specific median split used to determine low/high fitness Near maximal cycle ergometer exercise test; total work in quartiles Near maximal cycle ergometer exercise test; total work in quartiles Submaximal aerobic capacity estimated from cycle ergometry test Submaximal aerobic capacity estimated from exercise test Submaximal exercise heart rate on Definition of coronary heart disease Fatal and nonfatal heart attack (n = 311; 165 normotensive, 146 hypertensive) Incident cases of fatal and nonfatal CHD (n = 340) Incident cases of fatal and nonfatal myocardial infarction (n = 36) Incident cases of fatal and nonfatal CHD Incident cases of fatal and nonfatal myocardial infarction and CHD death Incident cases of fatal and nonfatal myocardial infarction and sudden death (n = 36) Death due to CHD (ICD-8 41 0-414) Death due to CHD (1988) employees; 17- through standard (3 min) treadmill test (ICD-8 410-414) 20-year follow-up evaluation Hein, 4,999 Copenhagen Submaximal aerobic capacity Fatal myocardial infarction Suadicani, men aged 40-59 years; estimated from cycle ergometer (ICD-8 410-414) Gyntelberg 17-year follow-up exercise test (n = 266) (1992) from 1970/1971 100