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Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary (2007)

Chapter: 2 Physical Activity, Health Promotion, and Chronic Disease Prevention

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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Page 43
Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Page 45
Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Page 46
Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Page 47
Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Page 48
Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Page 49
Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Page 50
Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Page 51
Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Page 52
Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Page 53
Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Page 54
Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
×
Page 55
Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
×
Page 56
Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
×
Page 57
Suggested Citation:"2 Physical Activity, Health Promotion, and Chronic Disease Prevention." Institute of Medicine. 2007. Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary. Washington, DC: The National Academies Press. doi: 10.17226/11819.
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Page 58

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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

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.

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.

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).

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.

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.

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-

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.

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

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,

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

28 PHYSICAL ACTIVITY WORKSHOP All four of these factors respond favorably to exercise intervention. In one small study (Arciero et al., 1999), two groups of middle-aged or older individuals with either impaired glucose tolerance or mild type 2 diabetes were treated for 10 days, either with exercise (energy expendi- ture was about 420 kilocalories/day) or a dietary restriction of approxi- mately 1,100 kilocalories/day. After treatment, both groups disposed of more glucose at any insulin concentration—that is, their muscles were more insulin sensitive. The improvement by the exercise group, however, was significantly better than that of the dietary restriction group. Westerterp (2000) reviewed evidence that habitual activity level and exercise have little or no effect on the age-related decline in muscle mass but that habitual activity and exercise training clearly have positive ef- fects on muscle function. These effects include muscle fiber type, capil- lary density, aerobic capacity, and others. Still lacking is evidence of associations of muscle quality with chronic disease risk. Concluding Remarks Dr. Kohrt emphasized that there is moderate to strong evidence that physical activity plays an essential role in the maintenance of bone health, although information is lacking on the type and dose of activity required to optimize the benefits. Whether physical activity helps to pre- vent the development of OA is not known, but there is moderate to strong evidence that physical activity has beneficial effects on pain and disability in people with knee OA. Aerobic exercise has little effect on the preservation of muscle mass but has multiple favorable effects on muscle quality. Conversely, strength training helps to preserve muscle mass with aging. MENTAL AND NEUROLOGICAL HEALTH Presenter: Patrick J. O’Connor Many mental health and neurological concerns may have some association with physical activity. Dr. O’Connor discussed the evidence relating physical activity to the nine disorders that are identified in Figure 2-3.

29 HEALTH PROMOTION AND DISEASE PREVENTION 30 25 Lifetime prevalence per yea 20 Lifetime prevalence 15 10 5 0 Pa M Al An M Sl Su CF Ea S zh oo ee rk xie bs tin S ei d in p ta g ty m so di nc er n's so e 's rd ab er us s e Selected conditions or disorders FIGURE 2-3 Estimated lifetime prevalence of selected mental health and neu- rological disorders. NOTE: CFS = chronic fatigue syndrome; MS = multiple sclerosis. SOURCES: de Rijk et al. (1997); Herbert et al. (2001); Jason et al. (1999); Kessler et al. (2006); Morin et al. (2006); Slaughter et al. (2001). The disorders are shown in decreasing order of the lifetime prevalence of each and are addressed below in that order. Notably, Alzheimer’s disease and Parkinson’s disease will become more prevalent as the U.S. popula- tion ages. Anxiety Approximately 50 epidemiological studies address physical activity and anxiety. About 85 percent of these show less severe symptoms of anxiety among physically active adults and youth. For example, the Na- tional Comorbidity Study of U.S. adults ages 15–54 years indicates that, after adjusting for a number of variables, persons who are rarely or never physically active tend to report more anxiety disorders than do those who are regularly or occasionally active.

30 PHYSICAL ACTIVITY WORKSHOP Only one randomized controlled trial (Broocks et al., 1998) ad- dresses the relationship between physical activity and anxiety disorders. The results are shown in Figure 2-4. Notably, when compared with pla- cebo, either 10 weeks of aerobic exercise or treatment with a standard antianxiety medication resulted in significantly better scores on the anxi- ety scale used. Animal models provide plausible mechanisms for the benefit of physical activity in reducing anxiety. For example, Dishman (1997) and Fulk et al. (2004) demonstrated anxiety-related changes in behavior and brain biology in rats that had access to a running wheel. In short, there is a large body of evidence from epidemiological stud- ies of physical activity and anxiety. Physical activity is consistently asso- ciated with fewer symptoms of anxiety, the odds of symptoms are reduced by 25 to 50 percent, dose–response is plausible, and a small but increasing body of evidence suggests biologically plausible mechanisms by which physical activity could improve anxiety. 30 25 Score on the Hamilton Anxiety Scale 20 Aerobic exercise 15 Clomipramine Placebo 10 5 0 0 2 4 6 8 10 Treatment time (weeks) FIGURE 2-4 Comparison of the effects of aerobic exercise training, clomipramine treatments, and placebo on anxiety. Randomized controlled trial of 46 outpatients with panic disorder. SOURCE: Broocks et al. (1998). Reprinted with permission from the American Journal of Psychiatry, Copyright 1996. American Psychiatric Association.

31 HEALTH PROMOTION AND DISEASE PREVENTION Depression Nearly 100 studies, most of them quite recent, report on associations between physical activity and depression or symptoms of depression. Approximately 90 percent of the studies show less severe symptoms of depression among physically active adults and youth. The reduction in the odds of symptoms is 30 to 50 percent. In the Harvard Alumni Study, persons who engaged in more hours of sports or play per week (or who expended more kilocalories by physical activity per week), measured in the 1960s, had a reduced risk for depres- sion during a 23- to 27-year follow-up period (Paffenbarger et al., 1994). A meta-analysis of 14 randomized controlled trials showed that exer- cise training reduced symptoms of depression (Lawlor and Hopker, 2001). The standardized mean difference in effect size equaled -1.1, and the confidence interval did not overlap with zero. Many of the trials, however, had methodological limitations. More recently, Dunn and col- leagues (2005) conducted a large, rigorously controlled randomized trial that produced results consistent with those of the meta-analysis. Rodent data show that activity wheel running increases brain-derived neurotropic factor (BDNF) and BDNF mRNA (ribonucleic acid) in the hippocampus and ventral tegmental area (Russo-Neustadt et al., 2000; van Hoomissen et al., 2003). In addition, the running attenuates copula- tory deficits in an olfactory bulbectomy model of depression (Chambliss et al., 2004). In summary, the size of the literature is large, physical activity gen- erally is associated with reduced symptoms of depression, a dose– response is plausible (Dunn et al., 2001), randomized controlled trials (of variable quality) show antidepressant effects of exercise, and evidence suggests biologically plausible mechanisms for the preventive effects of physical activity on anxiety. Physical Activity and Sleep Many neurological disorders are associated with poor sleep, and poor sleep itself can have important health-related outcomes. There are ap- proximately 70 sleep disorders, the most studied of which are insomnia and obstructive sleep apnea. One prospective cohort study (Morgan, 2003) examined self-reported insomnia and self-reported physical activ- ity and found that those who reported more activity were less likely to

32 PHYSICAL ACTIVITY WORKSHOP develop insomnia. A cross-sectional study that examined obstructive sleep apnea using polysomnography shows a very large benefit—that less sleep apnea is associated with more reported physical activity (Peppard and Young, 2004). At least 13 cross-sectional studies show that the chances of having interrupted sleep are lower among persons who are engaged in more physical activity than among persons who have less physical activity or are sedentary (Akerstedt et al., 2002; Kawamoto et al., 2004; Kim et al., 2000; Kravitz et al., 2003; Liu et al., 2000; Morgan, 2003; Nasermoaddeli et al., 2005; Ohayon, 2004; Ohida et al., 2001; Phillips et al., 2000; Sherrill et al., 1998; Surkan et al., 2005; Tynjala et al., 1999). Only two of the 13 trials, Nasermoaddeli et al. (2005) and Surkan et al. (2005), had confidence intervals that overlapped with 1.0, suggesting that the benefit of physical activity is unlikely due to chance. All the randomized controlled trials show positive effects of exercise training on symptoms of poor sleep (Guilleminault et al., 1995; King et al., 1997, 2002; Littman et al., 2006; Singh et al., 1997, 2005; Tworoger et al., 2003). Little or no research has been conducted on the biological mecha- nisms by which exercise could plausibly affect sleep. Indirect evidence suggests that acute bouts of exercise can induce circadian phase shifts (Van Reeth et al., 1994), influence adenosine metabolism (Benington and Heller, 1995), and activate neurological circuits hypothesized to help people feel less anxious and depressed (Youngstedt, 2005). Poor sleep is strongly associated with depression. In summary, the size of the literature is modest, but it shows that physical activity is consistently associated with both fewer self-reported sleep problems in cross-sectional studies and improved sleep quality in randomized controlled trials. Limited indirect evidence suggests biologi- cally plausible mechanisms by which physical activity could improve sleep or prevent sleep disorders. Physical Activity and Substance Use or Abuse Dr. O’Connor was not able to find evidence of associations between physical activity and illicit drug use, and thus did not address this topic in his presentation. Although a large number of epidemiological studies have data on alcohol consumption, generally alcohol use is one of the exposure variables measured rather than an outcome.

33 HEALTH PROMOTION AND DISEASE PREVENTION Alcohol A large cross-sectional study by Mukamal et al. (2006) indicates that, on average, those who abstained from alcohol were more sedentary than those who engaged in moderate drinking. Among male runners, the relationship between alcohol consumption and running distance was cur- vilinear: those who ran less than 16 kilometers per week or more than 64 kilometers per week consumed less alcohol per week. Cigarette Smoking Dr. O’Connor highlighted the 15 largest studies that provide data on some type of physical activity and smoking (Baumert et al., 1998; Blair et al., 1985; Boyle et al., 2000; Epstein et al., 1976; Haddock et al., 1998; Hickey et al., 1975; Holme et al., 1981; Pate et al., 1996; Reynolds et al., 2004; Simones et al., 1995; Steptoe et al., 1997; Tretli et al., 1985; Wagner et al., 2003; Ward et al., 2003). The studies ranged in size from nearly 6,000 to more than 128,000 subjects. In general, they showed a negative association between physical activity and smoking. Ten small to moderate-sized randomized controlled trials examined physical activity and smoking cessation (Ussher, 2005). In general, the effects favor exercise, but none of the studies provides strong evidence that physical activity enhances a smoking cessation program. Summary A large literature addresses physical activity related to alcohol con- sumption and smoking. Several cross-sectional studies suggest nonlinear relationships between physical activity and alcohol consumption. Physi- cal inactivity generally is associated with more smoking in cross- sectional studies. A modest number of randomized controlled trials failed to show that increased physical activity levels lead to significant im- provements in smoking cessation. Causal mechanisms have rarely been studied.

34 PHYSICAL ACTIVITY WORKSHOP Alzheimer’s Disease Ten prospective cohort studies report on the relationship between the level of physical activity and the odds of developing Alzheimer’s disease (Abbott et al., 2004; Larson et al., 2006; Lindsay et al., 2002; Podewils et al., 2005; Rovio et al., 2005; Scarmea et al., 2001; Verghese et al., 2003; Wilson et al., 2002a,b; Yoshitake et al., 1995). Although most of the studies show a positive effect, three of the 10 studies (Verghese et al., 2003; Wilson et al., 2002a,b) show a nonsignificant effect; and one of the three studies with nonsignificant findings (Wilson et al., 2002b) had the largest sample size of the 10 cohort studies. Three case–control studies (ranging in size from 60 to 193 cases) report a protective effect of physi- cal activity against Alzheimer’s disease (Broe, 1990; Friedland et al., 2001; Kondo et al., 1994). As reviewed by Heyn et al. (2004), 10 randomized controlled trials have been conducted in older adults with cognitive impairment to exam- ine the effect of exercise on cognitive performance. On average, the ef- fect size (improved cognitive performance) was moderate. Two studies provide plausible mechanisms for beneficial effects of physical activity in relation to Alzheimer’s disease. Transgenic mouse models of Alzheimer’s disease show that wheel running decreased ex- tracellular amyloid-β plaques in the frontal cortex and hippocampus (Adlard et al., 2005). A study with a different mouse model found posi- tive effects of physical activity related to up-regulation of hippocampal neurotrophin and brain-derived neurotrophic factor and to increased hippocampal neurogenesis (Wolf et al., 2006). Dr. O’Connor summarized the small to moderate amount of litera- ture relating physical activity to Alzheimer’s disease, emphasizing that physical activity consistently has beneficial effects both on disease de- velopment in the observational studies and on cognitive performance in the intervention studies in cognitively impaired older adults. Some evi- dence supports biologically plausible mechanisms by which physical activity can prevent or attenuate the development of Alzheimer’s disease. Physical Activity and Eating Disorders There is limited literature on the association between physical activ- ity and eating disorders, and the findings from available studies are con- troversial and difficult to interpret. There are no randomized controlled

35 HEALTH PROMOTION AND DISEASE PREVENTION trials that have examined the effects of physical activity on eating disor- ders. This is an area where further research is needed. Physical Activity and Parkinson’s Disease The size of the literature addressing physical activity and Parkinson’s disease is small. Observational studies show mixed evidence that physi- cal activity is associated with a reduced risk of Parkinson’s disease (Chen et al., 2005; Logroscino et al., 2006). Of the four case–control studies (Frigerio et al., 2005; Kuopio et al., 1999; Sasco et al., 1992; Tsai et al., 2002), all but Kuopio et al. (1999) show the odds of Parkinson’s disease in the active group being lower than those in the less active group. Three small randomized controlled trials (Miyai et al., 2002; Schenkman et al., 1998; Schmitz-Hubsch et al., 2006) all show positive effects of 4 to 10 weeks of exercise on spinal flexibility, movement speed, and disease symptoms when compared to usual care. Data from rodent models of Parkinson’s disease suggest biologically plausible mechanisms by which physical activity could prevent or attenuate Park- inson’s disease (Cohen et al., 2003; Fisher et al., 2004; Poulton and Muir, 2005; Tillerson et al., 2003). Notably, exercise has been shown to down-regulate the dopamine transporter (Fisher et al. 2004). Physical Activity and Chronic Fatigue Syndrome The literature on physical activity and chronic fatigue syndrome is small, and epidemiological studies of this condition rarely have included measures of physical activity. Five relatively small randomized con- trolled trials all show a positive effect of exercise training on symptoms of chronic fatigue syndrome (Fulcher and White, 1997; Moss-Morris et al., 2005; Powell et al., 2001; Wallman et al., 2004; Weardon et al., 1998). In a review of randomized controlled trials of groups of medical patients and other adults, 70 trials show that exercise training consis- tently reduces symptoms of fatigue (Puetz et al., 2006).

36 PHYSICAL ACTIVITY WORKSHOP Physical Activity and Multiple Sclerosis The literature on physical activity and multiple sclerosis is very small: one cross-sectional study (Stuifbergen et al., 2006), one 5-year prospective cohort study (Stuifbergen et al., 2006), no case-control stud- ies, eight randomized controlled trials (Mostert and Kesslering, 2002; Oken et al., 2004; Petajan et al., 1996; Romberg et al., 2004, 2005; Solari et al., 1999; van den Berg et al., 2006; Wiles et al., 2001), and no studies of causal mechanisms. Most of the studies have few subjects, and the effects observed, although consistently favorable, are small. Physical Activity and Suicide The few studies consistently find a small correlation in the direction of a protective effect of sports participation among youth on suicide idea- tion and attempt (Oler et al., 1994; Page et al., 1998; Tomori and Zalar, 2000; Unger, 1997), but the association is not consistent for physical ac- tivity and suicidal thoughts and behavior (Brosnahan et al., 2004; Brown and Blanton, 2002; Paffenbarger et al., 1994; Simon et al., 2004). Physical Activity and Other Mental and Neurological Conditions The literature addressing three additional conditions—schizophrenia, pain disorders, and self variables (e.g., self-concept, self-efficacy, self- esteem)—was not examined. The size of the literature is very small for schizophrenia and large for the other two conditions. Each of these con- ditions is an important topic that might merit further attention. In discus- sion, it was pointed out that the lifetime prevalence of low back pain is higher than 50 percent, that physical inactivity is a risk factor for low back pain (Vuori, 2001), and that a meta-analysis of 61 randomized con- trolled trials showed that exercise was more effective than usual care by the general practitioner and just as effective as conventional physical therapy for chronic low back pain (Hayden et al., 2005).

37 HEALTH PROMOTION AND DISEASE PREVENTION Concluding Remarks Dr. O’Connor provided a qualitative summary of the size and quality of the evidence about the mental and neurological conditions he covered. For anxiety, depression, alcohol use, and smoking, the size of the litera- ture is large and its quality is high to very high. A moderate amount of high-quality information is available about sleep, Alzheimer’s disease, and feelings of fatigue. For the other conditions, the size of the literature is small and the quality is low to moderate. PHYSICAL ACTIVITY AND DIABETES AND OTHER METABOLIC DISORDERS Presenter: Judith G. Regensteiner1 Dr. Regensteiner stated that a wealth of strong data is available to support the use of physical activity in the prevention and treatment of type 2 diabetes mellitus. This presentation began with background in- formation and then covered physiological studies, observational studies, randomized controlled trials, and meta-analyses related to physical activ- ity and type 2 diabetes mellitus. Background Diabetes is a public health problem in the United States: approxi- mately 21 million children and adults—7 percent of the population— have diabetes, but only about 14.6 million have been diagnosed (Sigal et al., 2006). A large majority of the people with diabetes have type 2 dia- betes. The estimated number of persons with prediabetes is 54 million. The prevalence of diabetes is lower among Caucasians than among per- sons of some other racial/ethnic groups. Among persons with type 2 dia- betes, two of three deaths are caused by CVD, myocardial infarction, or stroke. Figure 2-5 illustrates that men and women with diabetes have substantially higher mortality from heart disease than do persons without diabetes. 1 Dr. Regensteiner acknowledged assistance from Richard Hammon, M.D., Dr.P.H. and Steven N. Blair, P.E.D.

38 PHYSICAL ACTIVITY WORKSHOP 29.9 Diabetes 30 Mortality per 100-person-years* No diabetes 23.0 19.2 20 11.5 11.0 10 7.1 6.3 3.6 0 Men Women Men Women All heart disease Ischemic heart disease FIGURE 2-5 Mortality due to heart disease in men and women with or without diabetes. NOTE: *Age-adjusted. SOURCE: Adapted from Gu et al. (1998). Reprinted with permission from The American Diabetes Association. Copyright ©1998 American Diabetes Associa- tion. From Diabetes Care, Vol. 21, 1998; 1138–1145. Compared with people without diabetes, people with diabetes have a higher prevalence of a number of conditions such as • hypertension, • blood lipid abnormalities (Sigal et al., 2006), and • reduced exercise capacity (Regensteiner et al., 1998), including lower maximal oxygen consumption (VO2max) and submaximal measures of cardiorespiratory fitness. Impaired glucose metabolism, hyperinsulinemia, and increased insu- lin resistance are associated with sedentary behavior among those with diabetes and among those with prediabetes. Physical activity can attenuate adverse effects in the progression from normal glucose metabolism to clinical type 2 diabetes and various complications, as shown in Figure 2-6. In contrast, physical inactivity accelerates these unfavorable metabolic and cardiovascular events.

39 HEALTH PROMOTION AND DISEASE PREVENTION FIGURE 2-6 Relationship of physical activity with the progression from nor- mal glucose metabolism to clinical type 2 diabetes and increased risk of cardio- vascular diseases and other complications. NOTE: CHD = coronary heart disease. SOURCE: LaMonte et al. (2005a). Reprinted, with permission, from LaMonte MJ, Blair SN, and Church TS. Physical activity and diabetes preven- tion. J Appl Physiol 99:1205–1213, 2005. Biological mechanisms by which physical activity may enhance metabolic and cardiovascular health and thereby confer protection against the negative effects of diabetes include structural and biochemi- cal changes in skeletal muscle; improved maximal oxygen uptake and functional capacity, lipid factors, hepatic secretions, counterregulatory hormone concentrations or activity; and improvements in comorbid con- ditions (LaMonte et al. 2005a). Physiological Data A recent meta-analysis (Thomas et al., 2006) provides evidence that regular moderate intensity exercise benefits cardiorespiratory fitness in persons with diabetes and that higher intensity exercise would have an even greater effect. Even a single bout of moderate exercise has a pro- found effect on glucose metabolism that may last up to about 18 hours (Devlin et al., 1987). In addition, repeated bouts of exercise appear to

40 PHYSICAL ACTIVITY WORKSHOP have a cumulative beneficial effect on glucose metabolism. Exercise training in persons with diabetes also has a very significant effect in terms of improving VO2max, measures of submaximal exercise perform- ance, and other measures of fitness (Brandenburg et al., 1999). Observational Studies of Diabetes Prevention Large observational studies that assessed physical activity using questionnaires all suggest a benefit of increasing levels of physical activ- ity for preventing diabetes (Helmrich et al., 1991; Hsia et al., 2005; Manson et al., 1991). Data from the British Regional Heart Study (Wannamethee et al., 2000), Iowa Women’s Health Study (Folsom et al., 2000), and Study of Eastern Finns (Hu et al., 2003) provide additional supportive evidence. Similarly, observational studies that assessed physi- cal activity with objective measures of cardiopulmonary fitness reported that better fitness reduced the risk of developing diabetes (Lynch et al., 1996; Wei et al., 1999). Randomized Controlled Trials of Type 2 Diabetes Prevention One of the earliest trials (Cederholm, 1985) demonstrated that diet plus exercise reduced the risk of developing diabetes. A trial in China (Pan et al., 1997) included an exercise treatment arm and found that even modest changes in exercise without change in diet reduced the risk of developing diabetes. The Diabetes Prevention Study in Finland (Eriksson et al., 1999; Tuomilehto et al., 2001) and the Diabetes Prevention Pro- gram in the United States (Knowler et al., 2002) provide strong evidence that intensive lifestyle modifications, including diet and exercise inter- ventions, reduce the risk of developing diabetes. In the Diabetes Preven- tion Program study, weight loss was the dominant predictor of a reduced incidence of diabetes. However, both diet and physical activity predicted weight loss, and physical activity had a strong independent effect. Sub- sequently, studies in India (Ramachandran et al., 2006) and in Japan (Kosaka et al., 2005) provide similar results, including the independent effect of physical activity (Hamman et al., 2006).

41 HEALTH PROMOTION AND DISEASE PREVENTION Dose–Response Data According to the Nurses Health Study (Hu et al., 1999), the Iowa Women’s Health Study (Folsom et al., 2000), and the Study of Eastern Finns (Hu et al., 2003), approximately 30 minutes of moderate intensity exercise at least 5 days per week provides a substantial (25 percent to 36 percent) reduction in the risk of type 2 diabetes mellitus. Studies of Cardiovascular Event Prevention Among Persons with Type 2 Diabetes Among persons with diabetes, observational studies have shown that those who exercise or are more fit have a reduced risk of cardiovascular morbidity and mortality than do less active or less fit individuals (Blair et al., 1989; Gregg et al., 2003; Hu et al., 2001, 2004; Tanasescu et al., 2003). Data from the Diabetes Prevention Study in Finland show that all types of physical activity (e.g., recreational and occupational) are benefi- cial in reducing cardiovascular events and mortality (Hu et al., 2004). Physical Activity and Other Metabolic Disorders In a recent review, Bassuk and Manson (2005) report that body weight maintenance, insulin sensitivity and glycemic control, blood pres- sure, dyslipidemia, and inflammation and endothelial function all are impacted by the level of physical activity. In the Diabetes Prevention Program, the risk of developing the metabolic syndrome was lower for the lifestyle (diet and exercise) group than for the metformin (drug treatment) group or the placebo group (Orchard et al., 2005). Very few studies have addressed physical activity and type 1 diabe- tes mellitus, a condition that is much less prevalent than type 2 diabetes. Cross-sectional studies report correlations between glycemic control and aerobic fitness or physical activity, and the few prospective trials provide equivocal data with regard to glycemic control (Riddell and Iscoe, 2006)—in part because of the danger of hypoglycemia.

42 PHYSICAL ACTIVITY WORKSHOP Concluding Remarks Dr. Regensteiner emphasized the strong evidence indicating that physical activity and moderate intensity exercise have a major role in the prevention of type 2 diabetes and in the prevention of CVD events and death among people with type 2 diabetes. In addition, physical activity and regular exercise are very important in the treatment of type 2 diabe- tes. Areas requiring additional study include both the causes and treat- ments of exercise impairments (that is, reduced ability to exercise) associated with type 1 and type 2 diabetes, and exercise and type 2 diabe- tes in children and adolescents. DISCUSSION Mechanisms of Action of Exercise in Diabetes Discussant: Laurie J. Goodyear An understanding of how exercise results in health benefits can be helpful in developing prescriptions for exercise. Dr. Goodyear provided an example relating to diabetes. Exercise works to promote the uptake of glucose by the muscle by a mechanism that is completely different from that of insulin. In particular, exercise appears to work through a protein called AMP-activated protein kinase (AMPK). Metformin, the leading diabetes drug, seems to work in the same way. A major question from people with diabetes and from medical students is, “How much exercise is needed to gain a physiological effect that promotes glucose up- take into the muscle and thereby reduce the need for medication?” Physical Activity and Cognition Discussant: Bradley Hatfield (Presented by Rodney K. Dishman) Physical activity and cognition is an emerging area of study that shows much promise. The measurement of mental function is challeng- ing. Hendrie et al. (2006) defined elements of the cognitive domain, which range from intelligence to the executive functions of problem

43 HEALTH PROMOTION AND DISEASE PREVENTION solving and planning. The National Institutes of Health’s Cognitive and Emotional Health Project has the goal of identifying factors that can help people maintain or enhance their cognitive and emotional health as they grow older. Evidence is accruing that physical activity is linked to cognitive abil- ity and decline, but it is not yet sufficient for definitive conclusions. Not all areas of the brain age at the same rate, and executive processes are at special risk. In a summary of 18 randomized exercise intervention studies on cognitive function in persons age 55 and older, Colcombe and Kramer (2003) reported an overall effect size of 0.48, but the effect size varied for different functions. Thus, the type of task needs careful attention. Genetic factors also need to be considered to account for variations in central nervous system adaptations to exercise. A preliminary study (Schuit et al., 2001) suggests that physical activity decreases the risk of cognitive decline among those with a specific genetic predisposition for cognitive decline. Measurement specificity is another issue. One may be unable to see effects at the behavioral level because of strategic compen- sation by the central nervous system. Neuroimaging and genetics studies may be helpful in identifying “invisible” brain ailments and their rela- tionship to physical activity. Group Discussion Moderator: James R. Morrow During the group discussion, points raised by participants included the following: • Randomized controlled trials address effects of exercise on risk factors for CVD, such as blood pressure, and on mechanisms such as fibrinolytic activity and flow-mediated dilation. • Evidence regarding the acute benefits of single bouts of exercise merits consideration. Single bouts of exercise elicit most of the benefits in terms of glucose homeostasis. Persons with diabe- tes may need to be conditioned to be able to complete an acute bout of exercise that is long enough to have an impact on glucose metabolism.

44 PHYSICAL ACTIVITY WORKSHOP • Studies by Castaneda et al. (2002) and by Dunstan et al., (2002) address resistance training and type 2 diabetes, reduced blood pressure, improved muscle mass, reduced visceral fat, and im- proved glucose control. • Consideration needs to be given to dose–response data. The dose includes the frequency and quantity of exercise, how it is inte- grated into one’s lifestyle, and weekend or leisure-time exercise habits, among other factors. Dr. Andrea Dunn’s randomized controlled trial related to depression used five different exercise doses. William Krause’s work with the Studies of Targeted Risk Reduction Interventions through Defined Exercise may be useful. • At least two prospective studies, including research from the Framingham Study by Chaisson et al. (1999), address the relationship between muscle weakness and the risk of developing osteoarthritis. • A guidelines process could have many positive effects. The process needs to consider understandability, ease of use, rela- tionships with the built environment, and the target audience. Guidelines could focus on health promotion and disease preven- tion, but probably there is sufficient evidence to focus on guid- ance for people with currently active disease as well. Moreover, there is literature on interventions to help people increase their physical activity. Emphasis was placed on presenting the infor- mation in a way that leads to the adoption and maintenance of physically active lifestyles. REFERENCES Abbott R, White LR, Ross GW, Masaki GH, Curb JD, Petrovitch H. 2004. Walking and dementia in physically capable elderly men. J Am Med Assoc 292(12):1447–1453. Adlard PA, Perreau VM, Pop V, Cotman CW. 2005. Voluntary exercise de- creases amyloid load in a transgenic model of Alzheimer’s disease. J Neurosci 25(17):4217–4221. Akerstedt T, Knutsson A, Westerholm P, Theorell T, Alfredsson L, Kecklund G. 2002. Sleep disturbances, work stress and work hours: A cross-sectional study. J Psychosom Res 53(3):741–748.

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Adequacy of Evidence for Physical Activity Guidelines Development: Workshop Summary Get This Book
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Is there a sufficient evidence base for the U.S. Department of Health and Human Services (HHS) to develop a comprehensive set of physical activity guidelines for Americans? To address this question, the Institute of Medicine (IOM) held a workshop titled "Adequacy of Evidence for Physical Activity Guidelines Development" in Washington, DC on October 23-24, 2006, sponsored by HHS.

The workshop summary includes the presentations and discussions of more than 30 experts who were asked to consider the available evidence related to physical activity and the general population, as well as special population subgroups including children and adolescents, pregnant and postpartum women, older adults, and persons with disabilities. The summary provides an overview of the specific issues of relevance in assessing the quality and breadth of the available evidence.

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