Physical Activity and Obesity: Their Interaction and Implications for Disease Risk and the Role of Physical Activity in Healthy Weight Management
Robert F. Zoeller Jr, PhD Am J Lifestyle Med. 2007;1(6):437-446. ©2007 Sage Publications, Inc.
Abstract and Introduction
The prevalence of overweight and obesity is increasing at an epidemic rate. Increased adiposity, especially central or visceral adiposity, is predictive of cardiovascular disease/coronary heart disease, metabolic syndrome, and type 2 diabetes mellitus. The increased risk for cardiovascular disease/coronary heart disease and metabolic abnormalities associated with abdominal obesity may be mediated, at least in part, by increased systemic inflammation. Greater physical activity and/or fitness may reduce inflammation associated with greater visceral adiposity. Increased adiposity and low levels of physical activity and/or fitness are risk factors for atherosclerotic disease and type 2 diabetes, as well as the increased mortality associated with them. Increased physical activity/fitness reduces disease and mortality risk regardless of body mass index but does not completely abrogate the risks associated with obesity. Both moderate to vigorous physical activity and weight loss independently reduce the risk for type 2 diabetes and improve glucose/insulin metabolism via different mechanisms. Physical activity on the order of 2500 to 2800 kcal/wk may be necessary to prevent weight gain or maintain weight loss. Strength training is recommended as an adjunct to regular aerobic exercise but not as the primary mode of exercise for weight loss. Individuals are strongly encouraged to engage in regular physical activity because of the known health benefits, regardless of whether that activity results in weight loss.
Based on the most recent data from the National Health and Nutrition Examination Survey, and using body mass index (BMI) as the criterion measure, the prevalence of overweight and obesity in the United States continues to rise and has increased significantly just from 1999 to 2004. In adults, overweight is defined as a BMI of 25 to 29.9. Obesity is defined as a BMI ≥ 30; extreme (formerly morbid) obesity is defined as a BMI ≥ 40. Among men, the prevalence of obesity increased from 27.5% in 1999-2000 to 31.1% in 20032004. In women, the prevalence of obesity was high but unchanged (33.4% in 1999-2000 to 33.2% in 2003-2004). The prevalence of extreme obesity in 20032004 was 2.8% for men and 6.9% in women. Finally, differences in the prevalence of obesity by race/ethnicity continued with 45% and 36.8% for non-Hispanic blacks and Mexican Americans, respectively. In children, overweight is conservatively defined as a BMI at or above the ninety-fifth percentile. In 1999-2000, 13.8% and 14.0% of female and male children/adolescents, respectively, were overweight. This increased to 16.0% and 18.2%, respectively, by 2003-2004.
The most recent National Health and Nutrition Examination Survey data also reflect the well-recognized associations between obesity and risk factors for cardiovascular disease (CVD), including type 2 diabetes mellitus (T2DM) and the metabolic syndrome. In those individuals with reported diabetes, hypertension, or dyslipidemia, the percentage of persons who were overweight or obese was 82%, 85%, and 84%, respectively. Over the past 2 decades, it has become apparent that abdominal adipose tissue has unique metabolic properties and may be more predictive of CVD, the metabolic syndrome, and T2DM than is BMI or measures of overall adiposity.[1-5] Abdominal or central obesity is most commonly assessed by measuring waist circumference or waist-to-hip ratio. From 1988-1994 to 1999-2000, mean waist circumference of adult Americans increased from 95.3 cm to 98.6 cm in men and from 88.7 cm to 92.2 cm in women.
Despite these rather alarming trends, a recent analysis revealed that only 40.3% of obese patients were advised to lose weight by their family physicians, down from 42.3% in 1994. An evaluation of an academic pediatric hospital found that only little more than half (53%) of the children who met the above described criteria for overweight were identified as such by their primary care physicians. Interestingly, although a majority (69%) of the children's charts contained an "adequate" dietary history, only 15% included information regarding physical activity and/or television watching.
Central Adiposity, Inflammation, and CVD
In the past decade, atherosclerosis has come to be understood as an inflammatory disease.[9-12] A growing body of evidence further demonstrates that greater adipose tissue mass, especially visceral adipose tissue, directly contributes to systemic inflammation.[13-15] The proinflammatory state associated with abdominal obesity has been proposed as a common underlying condition linking CVD, insulin resistance/ T2DM, and the metabolic syndrome.[16-18] Although a complete discussion of the complex physiology and mechanisms of adipose-related inflammation is beyond the scope of this review, it is increasingly evident that visceral adipose tissue secretes a veritable host of proinflammatory cytokines. Greater levels of central adiposity have been shown to be associated with higher circulating levels of these proinflammatory proteins such as interleukin-6 (IL-6), tumor necrosis factor–alpha (TNF-alpha), and C-reactive protein (CRP).[19-21]
Physical Activity and Fitness as Mediators of Systemic Inflammation
A 2005 literature review of lifestyle interventions and systemic inflammation observed that 9 of 12 studies reviewed demonstrated an inverse relationship between physical activity or fitness and markers of inflammation, after controlling for BMI or other measures of adiposity. Colbert et al demonstrated that a greater self-reported level of physical activity (≥180 min/wk) was associated with significantly lower levels of IL-6, TNF-alpha, and CRP in 3075 elderly men and women (aged 70-79 years). After controlling for total and visceral fat, the association with IL-6 remained significant. This was one of the few studies to examine the relationship between nonexercise physical activity (kilocalorie/kilogram/week) and inflammatory markers. Even after controlling for total and visceral fat, increasing levels of nonexercise physical activity were associated with lower levels of IL-6 and CRP.
King et al examined levels of inflammatory markers related to the type of physical activity. Specifically, they examined jogging, swimming, cycling, aerobic dancing, other dancing, calisthenics, gardening, and weight lifting. After controlling for covariates including BMI, only jogging or aerobic dance performed ≥12 times per month was associated with lower levels of CRP. Only aerobic dance was associated with lower fibrinogen levels and white cell count. Unfortunately, no data were collected on exercise intensity or duration, which may represent major confounds to these findings.
More recently, data from 3042 men and women (mean age, 46 years) involved in the ATTICA study demonstrated that both moderate and vigorous intensity physical activity (4-7 kcal/min and >7 kcal/min, respectively) was associated with lower levels of CRP, fibrinogen, IL-6, TNF-alpha, and amyloid-A, as well as a reduced white cell count. These associations remained significant after controlling for BMI and other covariates. More specifically, those engaging in regular vigorous physical activity had 29% lower levels of CRP, 22% lower levels of amyloid-A, 20% lower concentrations of TNF-alpha, 32% lower IL-6, 11% lower fibrinogen, and 19% lower white cell counts.
A cross-sectional analysis of 27 158 women (mean age, 54.7 years) participating in the Women's Health Study found that although BMI was more strongly related to inflammatory and other cardiovascular markers, physical activity was associated with more favorable biomarker levels within BMI categories. Data from the Aerobics Center Longitudinal Study demonstrated a strong negative relationship between measured physical fitness and CRP levels. The adjusted odds ratios for high CRP levels across fitness quintiles (from lowest to highest fitness) were 1.0 (reference), 0.43 (95% confidence interval [CI], 0.22-0.85), 0.33 (95% CI, 0.17-0.65), 0.23 (95% CI, 0.12-0.47), and 0.17 (95% CI, 0.08-0.37).
Evidence from randomized controlled studies is limited in this area. However, there are a handful of studies suggesting that exercise training or increased physical activity is associated with lower levels of inflammatory markers. A 6 month interventional study compared a hypocaloric diet with or without exercise in their ability to reduce markers of systemic inflammation in 34 obese, postmenopausal women. The exercise intervention was treadmill walking 3 d/wk for 45 to 60 min/ session at 65% to 70% heart rate reserve. Only the diet-plus-exercise group demonstrated significant reductions in CRP, IL-6, soluble IL-6 receptors (sIL-6R), and soluble TNF receptor 1 (sTNFR1). The changes in IL-6, sIL-6R, and sTNFR1 were significantly different between groups. The changes in CRP and sIL6R were independent of changes in body weight, and changes in sTNFR1 and sIL-6R were inversely correlated with changes in maximal oxygen uptake (VO2max).
The HERITAGE Family Study examined the effects of 20 weeks of exercise training on CRP levels in 652 sedentary but healthy adults. The training program was performed on cycle ergometers 3 d/ wk, progressing to 50 minutes at 75% of baseline VO2max. This protocol resulted in a substantial (17.8%) increase in VO2max. However, reduction in CRP levels occurred only in the individuals with high baseline levels of CRP. The positive relationship between baseline CRP levels and exercise-induced changes has been observed elsewhere and may represent a potential confound.
In a 20-year follow-up of 4252 elderly men (aged 40-59 years at baseline), Wannamethee et al found that physical activity level was inversely associated with levels of CRP and other inflammatory markers, even after adjusting for BMI and other covariates. In those men who went from "at least lightly active" to inactive, the levels of these markers were similar to those men who had been inactive throughout the follow-up period. Those who were inactive at baseline but increased their levels of activity had levels similar to those men who had remained continuously active.
Nine months of endurance training in preparation for running a marathon significantly reduced CRP levels in 10 runners compared with nonexercising controls. The authors noted that the reduction in a marker of systemic inflammation was unexpected given that intense physical activity such as running is associated with an inflammatory response of muscles and tendons.
It is important to note that not all studies have found that an exercise intervention reduces levels of inflammatory markers.[33-38] The populations in these studies ranged from overweight and/or obese girls and teenagers[33,34] to high-risk adults.[35-37] Of particular interest was a 6-year interventional trial involving 140 middle-aged men that found CRP levels were not significantly improved in the exercise-intervention group compared with the control group. However, this study suffered from serious methodological issues in that there was never, at any point during the study, any attempt to control for or document physical activity levels in the control group. Especially because 25% of the control group significantly improved their aerobic fitness over the course of the study, it is very difficult to draw any meaningful conclusions from these data.
Abdominal/visceral adiposity is associated with a greater risk for CVD, T2DM, and other metabolic disorders. Increased systemic inflammation has been proposed as an important link between central adiposity and increased atherosclerotic disease risk. Greater physical activity and/or fitness may attenuate the inflammation associated with central adiposity.
The "Fitness Versus Fatness" Debate
Although it is well established that both increased body fat and low levels of physical activity and/or fitness are associated with increased mortality, T2DM, and CVD, it is not precisely clear as to their relative importance or how they interact. Several issues related to research in this area contribute to the lack of clarity in this matter. First, physical activity and physical fitness are not equivalent. More specifically, cardiorespiratory fitness, defined here as the ability to deliver and use oxygen during sustained activity and typically quantified as VO2max, has been shown to be only modestly correlated with physical activity, with correlations ranging from 0.09 to 0.60. Furthermore, assessment of physical activity usually relies on self-reported data, whereas physical or cardiovascular fitness is measured more objectively and, arguably, precisely. Studies assessing the impact of obesity on morbidity and mortality often control for covariates such as cholesterol levels, hypertension, and so forth. If one accepts the premise that obesity exerts its adverse effects via these and other risk factors, then it is possible that the association between adiposity and health and longevity may be obscured.
Physical Activity/Fitness, Adiposity, and Risk for CVD
An extensive review of the literature addressing the fitness versus fatness debate as it pertains to coronary heart disease (CHD) and/or CVD was published recently. The authors concluded, "Physically active lifestyle and/or a moderately high fitness level (ie, not in the bottom 20% of the population) reduces the risk of CVD/ CHD in overweight or obese persons." Although they suggested that overweight or obese individuals who are physically fit or active have levels of risk that approach those associated with those of lean, unfit persons, they also conceded that their risk is still greater than those who are fit/active and of normal weight. The authors further observed that the risk reduction associated with increased fitness or activity is greater in those who are overweight or obese compared with those of normal weight. Finally, they recommended that physical activity should be encouraged regardless of whether that activity induces weight loss. This recommendation is supported by the majority of the studies reviewed that found physical activity/fitness to be independent risk factors for CHD/CVD. These findings are supported by at least 2 more recent investigations.[41,42]
Obesity, Physical Activity/ Fitness, and All-Cause and CVD Mortality
Lee et al measured time to exhaustion during a maximal treadmill test and percentage body fat in 21 925 men (aged 30-83 years). All-cause and CVD mortality was then tracked during an 8-year follow-up. Unfit, lean men had a higher risk for cardiovascular and all-cause mortality than did fit, obese men after controlling for age, examination year, cigarette smoking, alcohol intake, and family history. Unfit men were found to have a higher risk of cardiovascular and all-cause mortality than did fit men in all body fat categories (lean, normal, obese).
A study of 9925 women (mean age, 42.9 years) also measured time to exhaustion on a maximal treadmill test but used BMI as the measure of adiposity. All-cause mortality was tracked over a mean of 11.4 years. The data revealed a strong negative relationship between cardiorespiratory fitness and BMI. Furthermore, in a multivariate analysis using BMI, cardiorespiratory fitness, age, baseline health status, and smoking status as variables, and in which each variable was adjusted for the other variables in the model, only cardiorespiratory fitness was predictive of all-cause mortality.
The Lipid Research Clinics Study tracked all-cause and CVD mortality in 2506 women and 2860 men originally tested in 1972 to 1976 until 1998, a +20-year follow-up. Cardiorespiratory fitness was quantified as time to reach age-predicted maximal heart rate during a Bruce treadmill protocol. Adiposity was assessed by BMI. For women, BMI was not associated with all-cause or CVD mortality, before or after controlling for fitness level. Compared to women in the highest quintile of cardiorespiratory fitness (reference group; hazard ratio, 1.0), the hazard ratios for all-cause mortality were significantly greater for the women in the 2 lowest quintiles of fitness (1.92 and 1.81 for the first and second quintiles, respectively). This increased risk remained significant after controlling for BMI (1.84 and 1.75, respectively). Women in the lowest quintile of fitness were also at increased risk for CVD mortality (hazard ratio, 3.05), which also remained significant after controlling for BMI (hazard ratio, 2.89).
In men, those in the 2 highest quintiles for BMI (26.8-28.6 and 28.7-39.4) were at increased risk for CVD mortality with hazard ratios of 1.58 and 1.66, respectively. After controlling for fitness, only those in the highest BMI quintile remained at significantly increased risk (hazard ratio, 1.56). Men in the two lowest fitness quintiles were also at increased risk for all-cause mortality that remained significant after controlling for BMI (hazard ratios, 1.63 and 1.59, respectively).
Crespo et al examined the relationship between physical activity, BMI, and all-cause mortality in 9824 men from the Puerto Rico Heart Health Study over a 12-year follow-up period. In men with a BMI between 18.5 and 29.9, all levels of physical activity were associated with a reduced mortality compared with sedentary men. The reduction in risk ranged from 26% to 51%, and the trend (lowest to highest activity) was significant. For men who were classified as obese (BMI ≥ 30), only men in the most active quartile demonstrated a reduced risk of mortality compared to obese, sedentary men.
A cohort of 116 564 women from the Nurses' Health Study were followed for 24 years to assess adiposity and physical activity as predictors of cardiovascular and all-cause mortality in women. The women were divided into tertiles of moderate to vigorous physical activity: <1 h/wk, 1 to 3.4 h/wk, and ≥3.5 h/wk. The latter group was designated as "active." Body mass index was also divided into tertiles: <25, 25-29.9 (overweight), and ≥30 (obese). Although greater physical activity was associated with reduced cardiovascular and all-cause mortality, even after controlling for BMI, it did not completely abrogate the increased risk associated with greater body weight. For example, active obese women still had nearly twice the overall risk of death compared to lean, active women. The authors concluded that excess body weight (BMI ≥ 25) and physical inactivity (<3.5 h/wk moderate to vigorous activity) together may account for 31% of premature deaths from any cause, 59% of deaths from CVD, and 21% of cancer deaths in nonsmoking women.
Hu et al examined the effects of physical activity and BMI on cardiovascular and all-cause mortality in 47 212 middle-aged men and women over a mean of 17.7 years. This study was one of the few to include both leisure time and occupational physical activity. Low physical activity was defined as being inactive in both categories. Moderate physical activity was defined as having reported 4 h/wk or more of some type of activity (walking, cycling, light gardening) or 3 h/wk of vigorous activity (running, swimming, competitive sports) for either leisure or occupational physical activity. High physical activity was defined as having reported 4 h/ wk of some kind of activity or 3 h/wk of vigorous activity for both leisure and occupational physical activity. Physical activity, moderate or high, was associated with a significant reduction in total and cardiovascular mortality independent of BMI in both men and women. Body mass index was associated with a significantly increased risk for total mortality even after controlling for physical activity level, age, study year, education, and smoking status. However, obesity (BMI, ≥30) but not overweight (BMI, 2529.9) was associated with an increased CVD mortality. The authors concluded that physical activity is independently associated with reduced total and cardiovascular mortality and reduces the risks associated with increased BMI.
Greater physical activity or fitness appears to reduce the risk of cardiovascular or all-cause mortality associated with being overweight or obese. However, even being very physically active or fit does not completely abrogate the increased risk of mortality associated with being obese. Individuals are encouraged both to maintain a normal/healthy body weight and to be regularly physically active.
The Interaction Between Obesity, Physical Activity/Fitness, and Risk for T2DM
A 2003 survey of 23 283 adults, of whom 1825 (7.8%) reported being diagnosed with diabetes, compared the prevalence of physical activity in diabetics and nondiabetics. Being physically active was defined as ≥30 minutes of moderate or vigorous activity, 3 times per week. Only 39% of diabetics were physically active compared to 58% of nondiabetics, a difference that was statistically significant. Using an even larger survey (n = 68 500, 6.3% with diabetes) and the same criterion for being considered physically active, this same group of investigators assessed the interaction of physical activity and BMI. Being physically active was associated with a lower prevalence of diabetes at any BMI. However, being overweight (BMI, 25-29.9), obese (BMI, 30-39.9), or extremely obese (BMI, ≥40) was associated with an increasingly greater prevalence of diabetes regardless of physical activity level.
Surprisingly few studies have examined the interaction between physical fitness and obesity and their association with T2DM. Wei et al examined the association between cardiorespiratory fitness and the incidence of impaired fasting glucose and T2DM over 6 years in 8633 nondiabetic men (30-79 years of age at baseline). Fitness level was sorted into tertiles (low, moderate, and high) by VO2max (metabolic equivalents [METs]). The mean MET levels for the low, moderate, and high fit groups were 9.3, 11.3, and 13.7, respectively. After controlling for high BMI (≥27) and other covariates, there was a strong, significant (P < .001) inverse relationship between fitness level and incidence of both impaired fasting glucose and T2DM. However, the incidence of T2DM did not differ between moderate and high fitness levels (P = .11).
Another study looked at both physical activity and fitness as predictors of the development of T2DM in 897 middle-aged men. After controlling for BMI, baseline glucose and triglyceride levels, age, parental history of diabetes, and alcohol consumption, both moderately intense physical activity (≥5.5 METs, 40 min/wk) and high cardiorespiratory fitness were associated with a reduced risk of T2DM (odds ratios of 0.44 and 0.26, respectively). Activities less than 5.5 METs in intensity, regardless of duration, were not protective of T2DM.
Since 2004, at least 3 studies, with a total n of 111 154, have explored the interrelationship between physical activity and BMI in predicting the development of T2DM. Weinstein et al and Rana et al examined these relationships in women (n = 37 878, 6.9-year follow-up and n = 68 907, 16-year follow-up, respectively), whereas Hu et al followed 2017 men and 2352 women for a mean of 9.4 years. All of these studies concluded that although greater physical activity reduced the risk of developing T2DM associated with increasing BMI, the risk associated with overweight/ obesity was not completely abrogated.
Adiposity, Physical Activity/ Fitness, and Glucose and Insulin Metabolism
A recent cross-sectional study of 1514 men and 1528 women without CVD explored the relationship between physical activity level, measures of adiposity, insulin sensitivity, as well as fasting blood glucose and insulin. Both physical activity and adiposity were found to be independent predictors of insulin sensitivity. A sedentary lifestyle was associated with a significantly higher glucose and insulin as well as lower insulin sensitivity. Overweight or obese individuals in the most physically active group had fasting glucose levels and insulin sensitivity similar to those of subjects who were lean but inactive.
An interventional trial involving 47 older, sedentary, nondiabetic men compared diet-induced weight loss alone (WL), aerobic exercise alone (AEX), and weight loss plus aerobic exercise (WL + AEX) and their effects on glucose homeostasis. The interventions lasted 10 months and were also compared with a control group (CON). The AEX and WL + AEX groups produced similar weight loss that was significantly greater than that of the CON. Insulin response to an oral glucose tolerance test was significantly reduced in all of the interventional groups, but the reduction was significantly greater in the WL + AEX group compared with all other groups. Glucose tolerance improved significantly in the WL and WL + AEX groups but not in the AEX or CON groups. Based on these data, the authors concluded that aerobic exercise and weight loss improve glucose metabolism by differing mechanisms and recommended both to improve glucose tolerance and insulin resistance in this population.
A 12-week aerobic exercise program improved insulin sensitivity in 19 overweight and obese girls (mean age, 13.1 years) without any significant change in body weight or body fat. Lower limb fat-free mass (presumably muscle mass) increased by 6.2% and was shown to be significantly correlated with the improvement in insulin sensitivity.
Increased cardiorespiratory fitness has also been shown to be correlated with increased insulin sensitivity. After almost 10 weeks of moderate-intensity exercise training, insulin sensitivity was significantly improved in a cohort of 18 nondiabetic, sedentary, and overweight or obese men (mean age, 37.4 years). Mean aerobic capacity increased by 11% and was more strongly correlated with the improvement in insulin sensitivity than the reduction in visceral fat (r = 0.726, P = .001, and r = –0.544, P = .02, respectively).
Another important adaptation to regular physical activity is enhanced fat oxidation in skeletal muscle. Goodpaster et al put 25 volunteers (9 men, 16 women; mean age, 39.0 years) on a moderate-intensity exercise program and calorie-restrictive diet for 16 weeks. Fat mass was reduced, whereas aerobic power, rate of fat oxidation, and insulin sensitivity increased, all significantly. The improvement in fat oxidation was the strongest predictor of the increase in insulin sensitivity, accounting for 52% of the variance.
Greater adiposity and a sedentary lifestyle are independent risk factors for the development of T2DM. Regular physical activity (especially moderate to vigorous activity) has been shown to reduce the risk of developing T2DM, independent of BMI. However, greater physical activity/fitness does not completely abrogate the risk associated with obesity. Increased physical activity and weight loss may affect glucose and insulin metabolism by different mechanisms.
The Role of Physical Activity in Preventing Unhealthy Weight Gain
Most but not all epidemiological studies have found that greater physical activity is protective of weight gain over time. Littman et al examined the association between physical activity and weight gain after the age of 45 in more than 15 000 men and women over a 10-year follow-up. Increasing MET hours and sessions per week, regardless of intensity, were inversely related to weight gain. Obese men and women who performed 75 to 100 minutes per week of fast walking gained 5 to 9 lb less than did nonwalkers. More vigorous activities, such as jogging, attenuated weight gain in most subgroups, but slow walking, swimming, and weight lifting did not.
Data from the Aerobics Center Longitudinal Study were used to determine the relation between mean daily physical activity level and weight change over a mean of 5 years in 2501 healthy men aged 20 to 55 years at baseline. Physical activity level was quantified as total daily energy expenditure relative to resting metabolic rate. Weight gain was greatest in the men who decreased their physical activity. For those men in the low physical activity level group at baseline, an increase to moderate or high physical activity level was associated with weight loss over time.
Haapanen et al followed 2695 women and 2564 men from 1980 to 1990. Those individuals who were inactive for the entire decade or those who decreased physical activity gained weight. Specifically, these individuals had significantly greater odds of gaining 5 kg or more over the study period compared to those who were continuously active or increased their physical activity.
Schmitz et al also studied weight change over a 10-year period in the Coronary Artery Risk Development in Young Adults Study. The participants were 5115 men and women, aged 18 to 30 years at baseline. Change in physical activity was found to be inversely related to change in body weight for all race (black and white) and gender subgroups.
An 11-year follow-up of 9357 women (aged 20—49 years at baseline) and 21 685 men (aged 20—69 years at baseline) who were all normal weight at baseline showed that although leisure time physical activity had a moderate effect on changes in BMI over the follow-up period, even high levels of physical activity did not prevent weight gain. Bak et al conducted a longitudinal study of 1143 obese juvenile men and 1278 juvenile men of normal weight who were military draftees in 1943 to 1977 (median age, 19 years). Follow-up examinations were performed in 1982 to 1984 and 1991 to 1993. There were no significant effects of either leisure time or occupational physical activity and development of obesity in the normal weight group or maintenance of obesity in the obese group. However, greater body weight at baseline was associated with an increased risk of leisure time physical activity at follow-up.
There are very few prospective, randomized controlled trials examining the effect of physical activity in preventing weight gain. Donnelly et al randomized 131 overweight college students to a supervised exercise program or control group for 16 months. Seventy-four participants completed the study including all laboratory testing. At the end of the trial, exercise energy expenditure was 3340 kcal/wk for men and 2195 kcal/ wk for women. Men who completed the exercise program lost a mean of 5 kg compared to no change for those in the control group. Women in the control group gained approximately 3 kg, whereas those completing the exercise intervention maintained their baseline weight.
Although not a randomized control trail, the Pound of Prevention Study examined the effects of a 3-year community-based weight loss program on 826 female and 218 male volunteers. The program included a dietary intervention targeted at reducing fat intake and increasing physical activity. For both men and women, the most consistent findings were positive associations between self-reported fat intake and weight gain and a negative association between self-reported frequency of physical activity and weight gain. Frequency of high-intensity physical activity demonstrated an even stronger negative association regardless of gender.
In 2003, the International Association for the Study of Obesity released the following statement regarding physical activity and prevention of unhealthy weight gain:
The current physical activity guideline for adults of 30 minutes of moderate intensity activity daily, preferably all days of the week, is of importance for limiting health risks for a number of chronic diseases including coronary heart disease and diabetes. However for preventing weight gain or regain this guideline is likely to be insufficient for many individuals in the current environment. There is compelling evidence that prevention of weight regain in formerly obese individuals requires 60-90 minutes of moderate intensity activity or lesser amounts of vigorous intensity activity. . . . For children, even more activity time is recommended. A good approach for many individuals to obtain the recommended level of physical activity is to reduce sedentary behaviour by incorporating more incidental and leisure-time activity into the daily routine.
Physical Activity and Sustained Weight Loss
Unfortunately, most studies do not support increasing physical activity, either alone or in combination with a calorie-restrictive diet, to be an effective means to produce weight loss.[70-72] However, physical activity appears to play a major role in long-term maintenance of weight loss.[70-73] In 1999, Wing reviewed the outcomes of 10 randomized controlled trials comparing weight loss with aerobic exercise alone to a control group. Six of the studies demonstrated a significantly greater weight loss with aerobic exercise compared to the control group. Regardless, whether significant or not, the differences in the amount of weight lost were less than 5 lb.
Wing also reviewed 13 studies comparing diet only with diet plus aerobic exercise. Four of these studies also had an additional diet plus resistance training group. Only 2 of the studies that added aerobic exercise to a dietary intervention produced an additional weight loss that was significantly greater from that achieved with diet alone. Adding resistance exercise to diet did not produce additional weight loss in any of the studies.
Finally, 6 follow-up studies, ranging from 48 weeks to 2 years, were reviewed to evaluate the long-term effect of adding regular exercise to a dietary intervention. Only 2 of the studies demonstrated a significant enhancement of long-term weight loss (18 months and 2 years after intervention) with the addition of exercise to diet. The absolute differences were 8.0 kg (18 months after intervention) and 4.1 kg (2 years after intervention).
Before drawing any conclusions from these trials, there are at least 2 important points to consider. In virtually all of these studies, the caloric expenditure reported for the exercise interventions was less than that currently recommended for long-term weight loss, and as such, it should not be surprising that the exercise-induced weight loss was not significant. Second, the number of subjects in each study was relatively small, with the vast majority having fewer than 50 participants. A more recent review of the role of exercise in promoting weight loss also incorporated a meta-analysis that increased the statistical power of the analyses. The randomized controlled trials in this review and meta-analysis only included studies that incorporated a follow-up of at least 12 months' duration to assess long-term maintenance of weight loss. A summary of the meta-analyses follows:
These data suggest that regular physical activity is advantageous for sustained weight loss.
How Much Physical Activity Is Required for Sustained Weight Loss?
There is a general consensus that 2500 to 2800 kcal/wk (60-90 min/d of moderate-intensity physical activity) is required for long-term weight loss as reflected in the recommendations and consensus statements of the US Department of Health, American College of Sports Medicine, and International Association for the Study of Obesity.
These recommendations are supported by data from the National Weight Control Registry, a database of approximately 5000 individuals who have minimally lost 30 lb for at least 1 year (mean weight loss is about 30 kg for a mean of 5.5 years). Data collected on these "successful losers" indicate that more than 90% of participants expend approximately 2800 kcal/wk in physical activity.
Resistance Training and Weight Loss
Despite claims in the popular literature, strength training is not recommended as the primary mode of exercise for weight loss. Although strength/ resistance training has been shown to preserve fat-free mass when coupled with a calorie-restrictive diet, it has not been shown to enhance weight loss either alone or in combination with a dietary intervention.[70,72,73,75] Despite the apparent ability of resistance training to maintain muscle mass in the presence of calorie deficit, it does not appear to be able to prevent the decrease in resting energy expenditure associated with weight loss. In the absence of a dietary intervention, some studies have shown that high-intensity resistance training can significantly increase resting energy expenditure for 16 hours or more.[77-81] However, these findings are based on a very small number of subjects and are not supported by the results of other investigations.[82-84] As such, resistance training is not recommended as the primary form of exercise to promote or enhance weight loss. However, weight training may provide an advantage in maintaining fat-free mass with a weight loss intervention.
Address for correspondence: Robert F. Zoeller Jr, PhD, Department of Exercise Science & Health Promotion, Florida Atlantic University, 2912 College Ave, Davie, FL 33314; e-mail: email@example.com .
Robert F. Zoeller Jr, PhD, from the Department of Exercise Science & Health Promotion, Florida Atlantic University, Davie, Florida.