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2 Physical Activity, Health Promotion, and Chronic Disease Prevention The scope of effects of physical activity in health promotion and chronic disease prevention is broad, and the workshop devoted two ses- sions to the topic as it relates to the general population. This chapter ad- dresses four major topics: • Cardiovascular disease (CVD), all-cause mortality, and cancer • Bone, joint, and muscle health and performance • Mental and neurological health • Diabetes and other metabolic disorders Brief coverage of mechanisms of action in diabetes and of physical activ- ity and cognition appears under the discussion section, followed by points raised by participants during the group discussion. CARDIOVASCULAR DISEASE, ALL-CAUSE MORTALITY, AND CANCER Presenter: Steven N. Blair Dr. Blair’s presentation began with a historical overview of the topic and the identification of exposure assessment issues, followed by a dis- cussion of physical activity and the relationships among CVD, all-cause mortality, and cancer. As the volume of evidence is very large and time was limited, Dr. Blair selected data pertaining to different populations to illustrate these relationships. 17

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18 PHYSICAL ACTIVITY WORKSHOP Background Historical Overview Although Hippocrates and Galen recognized the benefits of physical activity, the beginning of exercise science occurred in the twentieth cen- tury. In the early 1920s, August Krogh and A.V. Hill won separate Nobel Prizes in physiology and medicine for work related to physical activity. A study of London transport workers (Morris et al., 1953) showed much lower rates of coronary occlusion and of death from heart attack among the physically active conductors than among the sedentary drivers. Based on these results, Morris and colleagues formulated the hypothesis that vigorous physical activity helps protect against coronary heart disease (CHD). A study of the relationship of physical activity at work to CHD deaths among longshoremen (Paffenbarger and Hale, 1975) provided further strong evidence of the benefits of physical activity. Exposure Assessment Issues Self-reported questionnaires have provided valuable evidence of re- lationships between physical activity and disease outcomes. Nonetheless, some of them have led to a large amount of misclassification. Misclassi- fication, in turn, has led to an underestimation of the observed effect. The objective assessment of physical activity levels, such as the use of accel- erometers or specific fitness tests, is expected to provide stronger evi- dence of the effects of physical activity or inactivity on various health outcomes. Physical Activity, Fitness, and Cardiovascular Disease Figure 2-1 illustrates the results obtained from a study of CVD death rates for women and men by fitness category (obtained using an objec- tive test of fitness). Steep inverse gradients occur across the fitness cate- gories. Especially notable is the very large difference in CVD death rates between the low fit and the moderately fit group. That is, one need only achieve the moderately fit category to derive considerable benefit.

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19 HEALTH PROMOTION AND DISEASE PREVENTION 16 14 Deaths/10,000 person years 12 Fitness Group 10 Low 8 Mod High 6 4 2 0 Women Men FIGURE 2-1 Cardiovascular death rates by fitness groups and sex. Death rates are adjusted for age, examination year, and other risk factors. The Aerobic Cen- ter Longitudinal Study (ACLS) objective test of fitness was used to classify fit- ness groups. SOURCE: Blair et al. (1996). Reprinted, with permission, from JAMA 276(3):205–210. Copyright ©1996 American Medical Association. The measurement of inactivity or sedentary behavior may be another useful approach to examining the relationship of physical activity to CVD. For example, Manson and colleagues (2002) showed an increase in the multivariate-adjusted relative risk of CVD with an increase in the number of hours per day spent sitting. Work by Hambrecht and colleagues (2004) shows that, among indi- viduals with documented coronary artery disease, the group randomly assigned to exercise (20 minutes per day on a cycle ergometer and a 60- minute group aerobic exercise class once per week) had greater event- free survival and exercise capacity than the group assigned to standard treatment and angioplasty. Unpublished data from the Aerobics Center Longitudinal Study (LaMonte et al., 2005b) show that for both men and women, a greater fitness level is associated with decreasing rates of CVD deaths, CHD events, or CHD deaths. Fitness was assessed by a maximal exercise test on a treadmill and was categorized by the highest level of metabolic equivalent (MET) expenditure. In a multivariate analysis, the reduction of risk per MET was approximately 10 to 15 percent for the various end points in both women and men.

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20 PHYSICAL ACTIVITY WORKSHOP A very recent report from the Nurse’s Health Study (Whang et al., 2006), using self-reported data, shows a substantial decrease in the age- adjusted hazard ratio for sudden cardiac death among women who spend more than 3.9 hours per week in moderate to vigorous physical activity. This is one of the first reports to show a relationship between physical activity and a lower risk of sudden cardiac death in women. Evidence is accumulating that coronary artery calcium is an indicator of subclinical CHD among men and women (LaMonte et al., 2005c). A study of 710 asymptomatic men with a coronary artery calcium score of greater than 100 found a very large reduction in the relative risk of CHD events for those having an exercise tolerance of 10 or more METS (Lamonte et al., 2006). Barlow and colleagues (2006) reported on the risk of incident hyper- tension among healthy women by fitness group. After adjusting for age and other relevant factors, the risk of developing hypertension was mark- edly decreased for women in the moderate fitness group and even further decreased for women in the high fitness group. Earlier work had demon- strated this relationship among men. All-Cause Mortality Physical activity has been associated with a decreased risk of death in various population groups. A prospective study of 17,265 men and 13,375 women ages 20–93 years in Copenhagen found a substantial de- crease in the risk of death among those who spent 3 hours per week commuting to work by bicycle compared to those who did not commute by bicycle (Andersen et al., 2000). Among the men and women ages 60 years and older, the multivariate-adjusted relative risk for all-cause mor- tality decreased substantially by fitness level. Among men, the death rate for those ages 80 years or older in the high fitness group was lower than that for the least fit men ages 60 to 69 years (Blair and Wei, 2000). Among men, the relative risk for all-cause and CVD mortality is consistently lower for the fit when compared to the unfit across body fat categories (Lee et al., 1999). In other words, being moderately fit is asso- ciated with a substantially greater chance of survival even among those with 25 percent of their body weight as fat. Similarly, among men with metabolic syndrome, those in the moderate and high cardiorespiratory fitness groups have increasingly lower all-cause mortality than do the less fit men (Katzmarzyk et al., 2004).

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21 HEALTH PROMOTION AND DISEASE PREVENTION The length of time required to complete a 400-meter walk—a differ- ent kind of objective fitness test—is a predictor of mortality, CVD, and mobility disability among women and men ages 70 to 79 years at base- line (Newman et al., 2006). Differences in energy expenditure measured with doubly labeled water methods produce similar results (Manini et al., 2006). Measuring physical activity level by accelerometer, Garg and col- leagues (2006) found than men and women with peripheral artery disease had decreasing multivariate-adjusted rates of all-cause mortality with increasing levels of physical activity. Findings in a paper by Erikssen and colleagues (1998) are consistent with those of a number of other papers reporting decreasing multivariate- adjusted relative risk of mortality with improvements in cardiorespiratory fitness. Changing one’s fitness level affects mortality risk. These obser- vations strengthen the causal inference for the effect of physical activity in lowering the risk of death. Physical Activity, Fitness, and Cancer The body of literature on physical activity and cancer is smaller than that discussed above, but it is growing. Three examples of relevant study results follow: • Women diagnosed with breast cancer had a lower multivariate- adjusted relative risk of death and of recurrence if they obtained at least 3 MET-hours of activity per week than if they had a lower exercise level (Holmes et al., 2005). • In a study of men with gastric cancer in Japan, the least fit one- fourth of the group (tested by cycle odometer) were much more likely to die of gastric cancer than was the more fit group (Sa- wada et. al., 2003). • Farrell and colleagues (2006) report that the inverse association of cardiorespiratory fitness with cancer mortality remains after adjustment for the percentage of body fat.

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22 PHYSICAL ACTIVITY WORKSHOP Concluding Remarks We have and are accumulating a very large amount of evidence on the effects of physical activity and fitness on a variety of health out- comes. For nearly every health outcome examined and in nearly every subgroup of the population, physical activity provides benefits. Dr. Blair expressed the view that there is a sufficient evidence base for under- standing the benefits of physical activity and chronic disease prevention, and he suggested that the U.S. Department of Health and Human Ser- vices move forward with a process for developing physical activity guidelines for Americans. BONE, JOINT, AND MUSCLE HEALTH AND PERFORMANCE Presenter: Wendy M. Kohrt In addressing the role of physical activity in bone, joint, and muscle health and performance, Dr. Kohrt focused on bone mineral content (BMC)—the amount of mineral at a particular skeletal site, such as the femoral neck, lumbar spine, or total body; bone mineral density (BMD)—the value determined by dividing the bone mineral content by the area of a scanned region; osteoporotic fracture risk, osteoarthritis, and muscle mass and function (quality). Performance related to mobility and functional abilities was covered by Dr. Fielding. (See Chapter 6, Physical Activity and Special Considerations for Older Adults.) Bone Health Many studies show positive effects of either a physically active life- style or exercise interventions on intermediate markers of bone health, such as BMC and BMD. The evidence regarding the effects of physical activity on the risk of osteoporosis comes from randomized controlled trials of exercise intervention, meta-analyses of those trials, trials of the effects of immobilization and unloading, observational studies, and oth- ers. The intensity of the exercise appears to be a key determinant of the osteogenic response.

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23 HEALTH PROMOTION AND DISEASE PREVENTION Intervention Studies A meta-analysis from the Cochrane database involved 18 exercise in- tervention trials involving more than 1,400 postmenopausal women (Bonaiuti et al., 2002). Results were reported as mean differences be- tween the exercise and the control groups and the change in BMD in per- centile units. Any type of exercise showed a benefit (approximately a 1.8 percent increase on lumbar spine BMD, and walking benefited both spine and hip BMD). A slightly larger meta-analysis by Wallace and Cumming (2000) found that impact exercise had significant benefits among postmeno- pausal women on both lumbar spine and femoral neck BMD. Nonimpact exercise (primarily weight lifting) benefited lumbar spine BMD in post- menopausal women. Essentially the same results were found in studies involving premenopausal women. Randomized controlled trials of exer- cise interventions in men and children generally have shown benefits on BMD, but they have not yet been included in meta-analyses. Observational Studies Physical activity and risk of fracture The question remains about whether an increase in BMD—along with balance, mobility, and muscle strength—decreases the risk of fractures. No randomized controlled trials are available, but some prospective observational studies provide useful data about physical activity and hip fracture risk. The report by Feskanich et al. (2002) from the Nurses’ Health Study of more than 60,000 women serves as a good example. The physical activity data are self-reported. The incidence of hip fracture was collected for a 12-year period. The women with the highest level of activity measured in MET- hours per week had about a 50 percent relative risk reduction in hip frac- ture. Similarly, as walking time increased, hip fracture risk decreased; those who walked more briskly appeared to gain more benefit. The women who became less active over a 6-year period had a statistically significant increase in risk for hip fracture. Effects of unloading or reduced loading Extreme conditions of physical inactivity or reduced mechanical loading (such as limb immobi- lization, bed rest, microgravity) cause rapid and profound bone loss. The likelihood for full recovery of mineral is low. A meta-analysis of the ef-

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24 PHYSICAL ACTIVITY WORKSHOP fects of bed rest (Law et al., 1991) suggests that 3 weeks of bed rest dou- bles the risk for hip fractures during the subsequent 10 years. A study by van der Poest et al. (1999) compared the BMD of a person’s fractured tibia to that of the healthy tibia for 5 years after the fracture. The 8-week period of unloading subsequent to the fracture resulted in a substantially lower BMD in the injured limb even 5 years after the fracture. Data Limitations Little evidence is available on dose–response with respect to how the type, frequency, duration, and/or intensity of exercise affects bone. Be- cause the duration of follow-up in intervention studies has been quite short, little is known about the extent to which the benefits of the inter- ventions are retained. Bone strength (e.g., resistance to fracture) cannot be measured directly in humans, and there is a paucity of information on the relationship between BMD and bone strength. Therefore, the effects of physical activity on BMD may not accurately reflect the effects on resistance to fracture. Animal Studies On the other hand, a study conducted in rats showed that loading causes small changes in BMC and BMD that resulted in very large in- creases in bone strength (Turner and Robling, 2003), as illustrated in Figure 2-2. Thus evidence in animals suggests that physical activity or mechanical loading probably affects the skeleton in a way that translates into large gains in bone strength.

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25 HEALTH PROMOTION AND DISEASE PREVENTION Nonloaded 2,000 80 Loaded 5% 94% 1,500 60 7% 64% BMC and BD Fu and U 1,000 40 500 20 0 0 BMC BMD FU U 2 (mg) (mJ) (mg/cm ) (N) FIGURE 2-2 Effects of mechanical loading on bone mineral content, bone min- eral density, ultimate force (the maximum amount of force supported before failure), and energy to fail (the amount of energy absorbed by the bone before failure). NOTE: BMC = bone mineral content, BMD = bone mineral density, FU = ulti- mate force, N = newtons, U = energy to fail, and mJ = millijoules. SOURCE: Adapted from Turner and Robling (2003). Reprinted with permission from Exerc Sport Sci Rev. Possible Mechanisms by Which Physical Activity Reduces Risk for Osteoporotic Fracture Four mechanisms may explain the beneficial effects of physical ac- tivity in reducing the risk of osteoporotic fracture. Physical activity 1. Increases bone mineral accrual during maturation 2. Attenuates the rate of bone mineral loss during aging 3. Enhances bone strength 4. Reduces the risk of falls by improving muscle strength, flexibil- ity, coordination, and balance

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26 PHYSICAL ACTIVITY WORKSHOP Summary of Effects of Physical Activity on Bone Moderate to strong evidence indicates that physical activity plays an important role in optimizing bone health during the developmental years; but the long-term effects of benefit are not well known, and dose– response information is lacking. In adulthood, moderate to strong evi- dence from observational studies suggests that physical activity helps prevent fractures, and randomized controlled trials indicate benefits of physical activity on such useful biomarkers as BMD. The effects of ex- treme disuse are very deleterious. Dose–response data are lacking. Joint Health Very little information is available about the pathogenesis of os- teoarthritis (OA) and about a role for physical activity in the primary prevention of the disease. Scant evidence is available for a direct relation of physical activity (especially vigorous activity) and articular volume in children (Jones et al., 2003). Systematic reviews, however, indicate that exercise has benefits in the management of OA. Roddy et al. (2005) ex- amined the evidence base for the role of exercise in the management of hip and knee OA and differentiated research-based evidence from expert opinion. Their literature base included 57 intervention trials of exercise for knee OA, 9 intervention trials of exercise for hip OA, and 3 system- atic reviews of exercise for knee or hip OA. When they summarized the evidence, they rated it to be very high for the exercise benefits for people with knee OA. In particular, after pooling all the trials and minimizing the variability, the effect sizes range from 0.3 to 0.5 for the effect of ex- ercise on pain. In contrast, they found very little evidence to support a benefit for individuals with hip OA. The amount of evidence also was very low for the type of exercise to recommend, contraindications for exercise, the relationship of exercise to the progression of the OA, and several other propositions. As with bone health, dose–response data are lacking. Muscle Health In contrast with bone health and joint health, muscle health is not di- rectly linked with a chronic disease. A few chronic diseases, however,

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27 HEALTH PROMOTION AND DISEASE PREVENTION are associated with low muscle mass or impaired muscle function. These include osteoporosis, in which there is a direct association between mus- cle mass and bone mass; type 2 diabetes mellitus, in which the muscle is resistant to insulin-mediated glucose uptake; and congestive heart failure (CHF), in which there is skeletal muscle mitochondrial dysfunction. The abnormal muscle in CHF may be a result rather than a cause of the dis- ease, whereas low muscle mass and insulin resistance in muscle may be contributing factors to the etiology of osteoporosis and type 2 diabetes mellitus, respectively. Physical Activity and Muscle Mass A wealth of evidence indicates that high-intensity resistance exercise induces muscle hypertrophy and that this adaptive response is retained into very old age. Aerobic exercise has little or no anabolic effect on muscle, although disuse causes muscle atrophy. Aerobic fitness does not appear to have any impact on fat-free mass, whereas strength training enhances muscle mass and strength. Using fat-free mass as a surrogate for muscle mass, Holloszy and Kohrt (1995) showed that fat-free mass is preserved until approximately the age of 50 years. Thereafter, a decline occurs, which becomes steeper with advancing age. Combining those data with data from Hawkins et al. (2001) shows the following: (1) men and women who maintain very vigorous levels of endurance or aerobic activity have fat-free mass levels that are comparable to those of seden- tary individuals, and (2) the trajectory of change in fat-free mass over time appears to be quite similar in athletes and sedentary individuals. Similarly, Kyle et al. (2004) showed that fat-free mass, estimated with bioelectrical impedance, is essentially the same in sedentary and physi- cally active men and women. Physical Activity and Muscle Quality Dr. Kohrt identified the following characteristics of muscle quality: • Specific torque (Newton-meters per square centimeter) • Fatigue resistance • Metabolic function (e.g., insulin resistance) • Inflammatory state

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49 HEALTH PROMOTION AND DISEASE PREVENTION Holme I, Helgeland A, Hjermann I, Leren P, Lund-Larsen PG. 1981. Physical activity at work and at leisure in relation to coronary risk factors and social class. A 4-year mortality follow-up. The Oslo study. Acta Med Scand 209(4):277–283. Holmes MD, Chen WY, Feskanich D, Kroenke CH, Colditz GA. 2005. Physical activity and survival after breast cancer diagnosis. J Am Med Assoc 293(20):2479–2486. Hsia J, Wu L, Allen C, Oberman A, Lawson WE, Torrens J, Safford M, Limacher MC, Howard BV. 2005. Physical activity and diabetes risk in post- menopausal women. Am J Prev Med 28(1):19–25. Hu FB, Sigal RJ, Rich-Edwards JW, Colditz GA, Solomon CG, Willett WC, Speizer FE, and Manson JE. 1999. Walking compared with vigorous physical activity and risk of type 2 diabetes in women: A prospective study. J Am Med Assoc 282(15):1433–1439. Hu FB, Stampfer MJ, Solomon C, Liu S, Colditz GA, Speizer FE, Willett WC, Manson JE. 2001. Physical activity and risk for cardiovascular events in dia- betic women. Ann Intern Med 134(2):96–105. Hu G, Qiao Q, Silventoinen K, Eriksson JG, Jousilahti P, Lindstrom J, Valle TT, Nissinen A, Tuomilehto J. 2003. Occupational, commuting, and leisure-time physical activity in relation to risk for type 2 diabetes in middle-aged Finnish men and women. Diabetologia 46:322–329. Hu G, Eriksson J, Barengo NC, Lakka TA, Valle TT, Nissinen A, Jousilahti P, Tuomilehto J. 2004. Occupational, commuting, and leisure-time physical ac- tivity in relation to total and cardiovascular mortality among Finnish subjects with type 2 diabetes. Circulation 110(6):666–673. Jason LA, Richman JA, Rademaker AW, Jordan KM, Plioplys AV, Taylor RR, McCready W, Huang CF, Plioplys S. 1999. A community-based study of chronic fatigue syndrome. Arch Intern Med 159(18):2129–2137. Jones G, Bennell K, Cicuttini FM. 2003. Effect of physical activity on cartilage development in healthy kids. Br J Sports Med 37(5):382–383. Katzmarzyk PT, Church TS, Blair SN. 2004. Cardiorespiratory fitness attenuates the effects of the metabolic syndrome on all-cause and cardiovascular disease mortality in men. Arch Intern Med 164(10):1092–1097. Kawamoto R, Yoshida O, Oka Y, Takagi Y. 2004. Risk factors for insomnia in community-dwelling older persons. Geriat Gerontol Internat 4(3):163–168. Kessler RC, Coccaro EF, Fava M, Jaeger S, Jin R, Walters 2006. The prevalence and correlates of DSM-IV intermittent explosive disorder in the National Co- morbidity Survey Replication. Arch Gen Psychiatry 63(6):669–678. Kim K, Uchiyama M, Okawa M, Liu X, Ogihara R. 2000. An epidemiological study of insomnia among the Japanese general population. Sleep 23(1):1–7. King AC, Oman RF, Brassington GS, Bliwise DL, Haskell WL. 1997. Moder- ate-intensity exercise and self-rated quality of sleep in older adults. A random- ized controlled trial. J Am Med Assoc 277(1):32–37.

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50 PHYSICAL ACTIVITY WORKSHOP King AC, Baumann K, O'Sullivan P, Wilcox S, Castro C. 2002. Effects of moderate-intensity exercise on physiological, behavioral, and emotional re- sponses to family caregiving: A randomized controlled trial. J Gerontology A Biol Sci Med Sci 57(1):M26–M36. Knowler WC, Barrett-Connor E, Fowler SE, Hamman RF, Lachin JM, Walker EA, Nathan DM, Diabetes Prevention Program Research Group. 2002. Reduc- tion in the incidence of type 2 diabetes with lifestyle intervention or met- formin. N Engl J Med 346(6):393–403. Kondo K, Niino M, Shido K. 1994. A case-control study of Alzheimer’s disease in Japan—significance of lifestyles. Dementia 5(6):314–326. Kosaka K, Noda M, Kuzuya T. 2005. Prevention of type 2 diabetes by lifestyle intervention: A Japanese trial in IGT males. Diabetes Res Clin Pract 67(2):152–162. Kravitz HM, Ganz PA, Bromberger J, Powell LH, Sutton-Tyrrell K, Meyer PM. 2003. Sleep difficulty in women at midlife: A community survey of sleep and the menopausal transition. Menopause 10(1):19–28. Kuopio AM, Marttila RJ, Helenius H, Rinne UK. 1999. Environmental risk fac- tors in Parkinson’s disease. Movement Disord 14(6):928–939. Kyle UG, Genton L, Gremion G, Slosman DO, Pichard C. 2004. Aging, physi- cal activity and height-normalized body composition parameters. Clin Nutr 23(1):79–88. LaMonte MJ, Blair SN, Church TS. 2005a. Physical activity and diabetes pre- vention. J Appl Physiol 99(3):1205–1213. LaMonte MJ, Jurca R, Kampert JB, Gibbons LW, Church TS, FitzGerald SJ, Barlow CE, Nichaman MZ, Blair SN, Radford NB. 2005b. Exercise tolerance adds prognostic value to the Framingham Risk Score in asymptomatic women and men. Circulation 112(17):SII–829. LaMonte MJ, FitzGerald SJ, Church TS, Barlow CE, Radford NB, Levine BD, Pippin JJ, Gibbons LW, Blair SN, Nichaman MZ. 2005c. Coronary artery cal- cium score and coronary heart disease events in a large cohort of asympto- matic men and women. Am J Epidemiol162(5):421–429. LaMonte MJ, FitzGerald SJ, Levine BD, Church TS, Kampert JB, Nichaman MZ, Gibbons LW, Blair SN. 2006. Coronary artery calcium, exercise toler- ance, and CHD events in asymptomatic men. Atherosclerosis 189(1):157–162. Larson EB, Wang L, Bowen JD, McCormick WC, Teri L, Crane P, Kukull W. 2006. Exercise is associated with reduced risk for incident dementia among persons 65 years of age and older. Ann Intern Med 144(2):73–81. Law MR, Wald NJ, Meade TW. 1991. Strategies for prevention of osteoporosis and hip fracture. BMJ 303(6800):453–459. Lawlor DA, Hopker SW. 2001. The effectiveness of exercise as an intervention in the management of depression: Systematic review and meta-regression analysis of randomised controlled trials. BMJ 322(7289):763–767.

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