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Weight Loss, Not Aerobic Exercise, Improves Pulmonary Function in Older Obese Men

^a Department of Medicine, Divisions of Gerontology, University of Maryland at Baltimore, Baltimore Veterans Administration Medical Center, Geriatric Research, Education, and Clinical Center
^b Department of Medicine, Divisions of Pulmonary Medicine, University of Maryland at Baltimore, Baltimore Veterans Administration Medical Center, Geriatric Research, Education, and Clinical Center
^c Department of Kinesiology, University of Maryland, College Park

Andrew P. Goldberg, Baltimore VA Medical Center, GRECC (18), 10 N. Greene Street, Baltimore, MD 21201-1524 E-mail: apgoldbe{at}umaryland.edu.

Decision Editor: William B. Ershler, MD

	Abstract

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Background. We evaluated the effect of weight loss (WL) or aerobic exercise (AEX) on pulmonary function in middle-aged and older (46–80 years) obese, sedentary men to determine the effect of reductions in body weight and increases in cardiorespiratory fitness on pulmonary function.

Methods. Subjects were randomly assigned to WL (), AEX (n ), or control (n ) groups. Maximal oxygen uptake (V.O₂max), body composition and anthropometrics, pulmonary function, and arterial blood gases were measured at baseline and after interventions.

Results. The 35 subjects who completed WL decreased weight by 11%, body fat percentage by 21% (p < .001), waist circumference by 8%, waist-hip ratio by 2%, and fat-free mass by 3% (p < .05). This resulted in a 3% increase in forced vital capacity (FVC) (4.08 ± 0.71 L vs 4.21 ± 0.76 L), a 5% increase in total lung capacity (6.62 ± 0.99 L vs 6.94 ± 0.99 L), an 18% increase in functional residual capacity (3.09 ± 0.58 L vs 3.66 ± 0.79 L), and an 8% increase in residual volume (2.20 ± 0.44 L vs 2.37 ± 0.52 L), with no change in forced expiratory volume in one second (FEV₁), FEV₁/FVC ratio, or carbon monoxide diffusing capacity. The change in FVC correlated with change in body weight (, p < .05). The 38 subjects who completed AEX increased V.O₂max by 14%, with no change in pulmonary function. There were no changes in 8 control subjects.

Conclusions. WL changes static lung volumes, not dynamic pulmonary function, in middle-aged and older, moderately obese, sedentary men. Some of the alterations in static lung function associated with aging may be due to the development of obesity and are modifiable by WL.

AGING is associated with declines in pulmonary function ⁽¹⁾⁽²⁾. Obesity is also associated with changes in static lung volumes. Obese subjects have lower expiratory reserve volume ⁽³⁾⁽⁴⁾, functional residual volumes ⁽³⁾⁽⁴⁾, total lung capacity (TLC) ⁽⁴⁾, and diffusion capacity for carbon monoxide (DLCO) ⁽⁴⁾ compared with age-matched normal subjects. In addition, abdominal fat distribution is independently related to reduced forced vital capacity (FVC) and forced expiratory volume in one second (FEV₁) in middle-aged men ⁽⁵⁾⁽⁶⁾. Therefore, the increase in body fat and decline in maximal oxygen uptake (V.O₂max) with age may account for some of the changes in respiratory function attributed to aging.

Increases in body fat percentage ⁽⁷⁾ and abdominal body fat ⁽⁸⁾⁽⁹⁾ and decreases in V.O₂max ^(10)(11) occur with increasing age. Regular aerobic exercise (AEX) improves V.O₂max in older subjects ^(12)(13), although it is not known whether this also affects pulmonary function. Weight loss (WL) produced by various surgical procedures improves pulmonary function ⁽⁴⁾. However, it is not known whether decreasing body weight by using hypocaloric nutritional intervention improves pulmonary function in older, moderately obese subjects. We hypothesized that some of the changes in pulmonary function with aging are due to declines in V.O₂max and/or increases in body fat rather than to biological aging processes alone. Thus, it is possible that AEX or WL may offset some of the age-related decline in pulmonary function in obese, sedentary, older men. The present study sought to determine the independent effects of WL and AEX on pulmonary function in moderately obese, healthy, nonsmoking, sedentary, middle-aged and older healthy men.

	Methods

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Subject Recruitment, Screening, and Selection
This study was approved by the University of Maryland and the Johns Hopkins, Bayview Medical Center Human Studies Institutional Review Boards. All subjects provided informed consent prior to participation. Healthy, nonsmoking, sedentary, obese (120%–160% of ideal body weight) male volunteers who were 46–80 years of age () were recruited for this research study as previously described ^(12)(13)(14). A total of 586 male subjects responded to recruitment strategies, including advertisements in local newspapers and presentations at regional social clubs. Medical history and other questionnaires were returned by 349 subjects. Exclusion criteria included a history of diabetes, hypertension, hyperlipidemia, congestive heart failure, and cardiac, pulmonary, renal, or liver disease. Subjects with a physical limitation to endurance exercise training were also excluded. An exercise treadmill test achieving more than 85% of the predicted maximal heart rate (220 beats per minute - age) was performed according to the Bruce protocol to exclude patients with previously undiagnosed exercise-induced myocardial ischemia by electrocardiogram. Because patients with significant pulmonary disease would have had a reduced ability to exercise train, subjects were excluded if their FEV₁/FVC ratio was less than 60% of predicted.

A total of 170 male subjects were randomized to: WL, AEX, or a weight maintenance control. An unequal randomization was performed in which 85% of the subjects were randomized to either WL () or AEX () interventions, and 15% to control (). In this article, we report results on the 81 patients who had baseline and postintervention pulmonary function testing and completed WL, AEX, or control phases. Of the 170 subjects who entered the study and were randomized, 48 out of 73 (66%) completed WL, but only 35, or 73%, completed pulmonary function testing; 52 out of 71 (73%) completed AEX, but only 38, or 73%, completed pulmonary function testing; and 18 out of 26 (69%) controls completed the final testing, with 8 (44%) completing the pulmonary function testing. The majority of subjects who failed to complete pulmonary function testing cited scheduling difficulties and hesitancy to undergo an arterial blood draw as reasons for not participating. We previously reported cross-sectional cardiopulmonary and metabolic data on 132 of these men ^(13)(14), and the effects of WL and AEX on glucose and lipid, metabolic, and blood pressure risk factors for coronary artery disease ^(12)(13). Baseline physical characteristics of the subjects who did not complete pulmonary function testing were not significantly different than those of the subjects who completed the study.

Study Protocol
Subjects had their weight, diet, and physical activity stabilized prior to baseline testing ⁽¹³⁾. After completion of baseline testing, the WL group was placed on a hypocaloric American Heart Association (AHA) Phase I diet calculated to achieve an average WL of approximately 10% of their baseline weight using the Harris-Benedict equation ⁽¹⁵⁾. On average, this required a reduction in baseline calories by 250–400 kcal/day. The men attended weekly group WL sessions with a goal of decreasing their body weight by >10% over a 9-month period. The AEX group entered a 9-month-long supervised AEX. Subjects trained predominantly (>90%) on treadmills and occasionally cycle ergometers for 30–45 minutes three times per week. The initial intensity of the exercise was set at 50%–60% of the subject's heart rate reserve (maximal heart rate - resting heart rate) ⁽¹⁶⁾. Exercise intensity was gradually increased to 70%–80% of heart rate reserve for 30–45 minutes per session. The goal was for the men to increase their absolute V.O₂max by 10% while maintaining their body weight and continuing to consume an AHA Phase I diet. This allowed us to evaluate the effects of AEX independent of weight loss changes that may have occurred as a result of the AEX program. After 9 months of the AEX or WL intervention, each subject's body weight and V.O₂max were stabilized for 1 month prior to reevaluation by calculating calories for weight maintenance and adjusting diets to maintain body weight during exercise training. Subjects were stabilized at a V.O₂max by calculating the intensity required to maintain V.O₂max. In general, this required exercising at approximately 70% of heart rate reserve. The control subjects continued to consume an isocaloric AHA Phase I diet for the entire study period. They were instructed not to lose weight or change their diets or level of physical activity. The controls attended 1-hour dietary counseling meetings on a weekly basis to assure compliance to the protocol. Adherence to the protocol was set at an attendance of greater than 75% in each program for inclusion of data in the analyses. The dropouts occurred early on in the protocol due to time constraints that resulted in failure to meet the attendance requirments. All subjects who completed the protocol attended more than 75% of the sessions.

Body Composition
Body mass index (BMI) was calculated as a person's weight in kilograms divided by the squared height in meters. The waist circumference and the waist-hip ratio (WHR), measured as the ratio of the minimal abdominal circumference divided by the circumference at the maximal gluteal protuberance, were used as indices of body fat distribution. Body density was determined by hydrostatic weighing at baseline and after intervention. Body fat percentage was calculated after corrections for the residual lung volume ⁽¹⁷⁾ and fat mass ⁽¹⁸⁾ were calculated. Fat-free mass (FFM) was calculated as body weight minus fat mass.

Measurement of V.O₂max
V.O₂max was measured in all subjects by using a modified Balke protocol as previously described ⁽¹⁹⁾. The grade was increased every 2 minutes until volitional exhaustion. All V.O₂max tests fulfilled at least two of the following three criteria: (i) heart rate at maximal exercise was more than 95% of the age-adjusted maximal heart rate (220 - age); (ii) respiratory exchange ratio was >1.10; and (iii) a plateau in oxygen uptake was achieved on the basis of a change in V.O₂ of <0.2 L/min during the final two V.O₂ collections. If two of these three criteria were not met, the test was repeated. At baseline, all subjects required at least two tests to meet two of the three criteria. About 10%, or 8 to 10 of the 81 subjects, required a third max test. During postintervention testing, very few subjects (<5%) required a third test.

Pulmonary Function Testing
Triplicate forced expirations were performed on a Stead-Wells spirometer (Warren E. Collins, Braintree, MA) to FEV₁ and FVC. TLC, vital capacity, functional residual capacity (FRC), and volume (RV) were measured both by helium dilution and body plethysmography (Warren E. Collins, Braintree, MA). Single-breath DLCO was performed on a Collins modular lung analyzer (Warren E. Collins, Braintree, MA) using standard techniques. At least two reproducible flow-volume curves were obtained from each patient in a sitting position. Arterial blood samples were collected in the sitting position for blood gas analysis (Blood Gas Analyzer, model IL513; Instrumentation Laboratory, Inc., Edison, NJ). Pulmonary function was measured at least 48 hours but not more than 72 hours after the last exercise session in the AEX group.

Statistical Methods
Major predefined primary outcomes measures included body weight, waist circumference, WHR, body fat percentage, V.O₂max, FEV₁, FVC, FEV₁/FVC ratio, TLC, FRC, RV, DLCO, and partial pressures of oxygen (PO₂) and carbon dioxide (PCO₂) in arterial blood. Repeated measures analysis of variance was used to compare variables within and between the three groups. Post-hoc means comparisons between groups at baseline and between the changes (postintervention value - preintervention value) in variables were analyzed statistically using a Tukey-Kramer Honestly Significant Difference test. Comparison of means within a group (pre to post) was performed using a paired t test with a Bonferroni correction factor. Relationships between the baseline variables were assessed using linear regression. Pearson product moment correlation coefficients were calculated between the following: (i) changes in body composition, body fat distribution, and V.O₂max and the changes in pulmonary function tests in both the WL and AEX groups for those variables that significantly changed as a result of the intervention; and (ii) changes in all measured variables and age. All data are expressed as mean ± SD. Statistical significance was set at p < .05 for all analyses.

	Results

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The baseline relationships between age, V.O₂max, and body composition are shown in Table 1 . At baseline, age correlated inversely with FVC, TLC, FEV₁ (p < .01), and FEV₁/FVC ratio ( p < .05). V.O₂max correlated significantly with FVC, FEV₁, and FEV₁/FVC ratio (p < .01). FFM correlated with all of the pulmonary function variables except FEV₁/FVC ratio, whereas body fat percentage only correlated with FRC (p < .01). Age did not correlate with the percentage change of any pulmonary function variable. Furthermore, a post-hoc t test between the absolute and relative change in the pulmonary function variables showed no significant difference ( p > .05) between the middle-aged (45–60 years) and older (>60 years) subjects.

	Discussion

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In both younger and older subjects, obesity impairs pulmonary function. Results of this study and our previous report ⁽¹⁴⁾ confirm that FRC is reduced in mild to moderately obese middle-aged and older men. The impact of various methods of weight loss on pulmonary function was examined in several previous studies. In morbidly obese patients, gastroplasty improved RV, TLC, FRC, FEV₁, and FVC ⁽⁴⁾. Conversely, weight gain results in a decline in FEV₁ and FVC ⁽²⁰⁾. Our inability to detect differences in FEV₁ may be due to a lower magnitude of weight loss compared with the average 34.2 kg loss after gastroplasty reported by Thomas and colleagues ⁽⁴⁾. Furthermore, the decline in FEV₁ after weight gain reported by Wise and colleagues ⁽²⁰⁾ was seen in smokers participating in a smoking cessation program, as compared with the nonsmoking group evaluated in the present study. Therefore, differences in both population and magnitude of weight loss may account for the lack of change in dynamic pulmonary function in the present study.

The findings in this study indicate that WL, but not an increase in V.O₂max, improves static lung volumes but not dynamic lung function in these moderately obese men. This suggests that the prevention of obesity modifies changes in pulmonary function that are associated with an increase in body fat percentage. Because aging is often associated with a sedentary lifestyle and obesity, some of the age-related changes in respiratory function may be caused by changes in body composition. Thus, some of the purported age-related decline in pulmonary function may be modifiable by WL and thus is not due solely to primary aging processes.

This is the first study to examine the independent effects of WL and AEX on pulmonary function in healthy, middle-aged and older, moderately obese, sedentary men. Subjects selected were free of significant cardiovascular and pulmonary disease, did not smoke, and were not receiving medications for these conditions. This permitted us to evaluate the effects of weight loss and exercise on pulmonary function independent of cardiopulmonary disease, cigarette smoking, and other comorbidities. Furthermore, the subjects' exercise habits and weight were stabilized for one month prior to and after the study period to ensure that changes in pulmonary function were the result of the respective interventions. Although keeping the subjects in the AEX group weight-stable served to evaluate the independent effects of exercise, participation in an exercise program can result in greater weight loss than we report in the AEX group and therefore can potentially impact static lung volumes in obese individuals. Exercise-induced weight loss may be even greater for exercise prescriptions involving more frequent participation, possibly eliciting a more pronounced change in static lung volumes.

This study as well as our previous findings ⁽¹⁴⁾ show an association between pulmonary function and both age and V.O₂max (Table 1 ). Results from Alfaro and co-workers ⁽²¹⁾ suggest that improvements in FVC and FEV₁ in chronic obstructive pulmonary disease (COPD) patients occur after an exercise rehabilitation program. Because aging is associated with decreases in both pulmonary function ^(1)(2)(14) and V.O₂max ^(10)(11), we hypothesized that the patients in the AEX group would improve pulmonary function in parallel with the change in V.O₂max. However, pulmonary function did not improve in the AEX group, suggesting that increasing aerobic fitness does not increase pulmonary function in healthy, middle-aged and older, moderately obese men who do not smoke or have a history of COPD.

Aging appears to have a direct effect on pulmonary function independent of moderate obesity. The declines in pulmonary function with age are attributed to a decrease in respiratory muscle strength ⁽²²⁾, increased rib stiffness ⁽²²⁾, and decreased elasticity in the lungs ⁽²³⁾. Of the pulmonary function variables measured, only FRC and RV were lower at baseline compared with age-predicted levels (Table 3 ). Dynamic pulmonary function was normal. In a previous study, we showed a similar percentage reduction in age-predicted FRC for this population and a significant correlation between FRC and body fat percentage but not age ⁽¹⁴⁾. In this study, WL significantly increased FRC to almost 100% of age-predicted values, without any change in dynamic pulmonary function. This suggests that in obese older men, WL offsets changes in functional residual capacity, a static measurement of respiratory function that does not appear to be influenced by aging.

As obesity develops, alveoli and airways become restricted, resulting in a reduced ventilation/perfusion ratio and a subsequent decrease in arterial PO₂ ⁽²³⁾. Obesity is also associated with obesity-hypoventilation syndrome, which increases PCO₂ and lowers PO₂, potentially contributing to right-side heart failure ⁽²³⁾. The increase in FRC that occurred with WL suggests that constriction of small airways in dependent lung units occurs even with the moderate degree of obesity observed in these patients prior to the WL intervention. Although PO₂ did not change, our finding that FRC increases with WL may be important for individuals with moderate and severe obesity. When FRC is reduced, there is a collapse of peripheral airways (lung units) leading to vascular shunting, CO₂ retention, and decreased arterial PO₂ ⁽²³⁾. Thus, increasing static lung volumes, as in the present study, may have potential clinical benefits in cardiopulmonary disease associated with obesity and aging. However, results from the present study cannot be extrapolated to either patients with chronic lung disease or obese women, because healthy obese men only were studied in the present investigation.

In summary, these findings show that static lung volumes improve with weight loss but not with aerobic exercise in middle-aged and older, moderately obese, sedentary males. This suggests that weight loss has a positive impact on respiratory function but not on measures of dynamic pulmonary function in older obese males. Thus, these findings indicate that some of the alterations in pulmonary function attributed to aging are due to obesity and are potentially modifiable in obese men.

	Acknowledgments

 
Christopher J. Womack is supported by an NIA National Research Service Award (F32-AG05799). This research was supported by the Johns Hopkins Academic Nursing Home Award (PO1 AG-04402-05) (1K07 AG00608), a General Clinical Research Center Grant (M01 RR02719), and the Department of Veterans Affairs.

	Footnotes

 
The current address for Christopher J. Womack is Michigan State University, 3 IM Circle, Department of Kinesiology, East Lansing, MI 48824-1034.

Received July 13, 1999

Accepted November 30, 1999

	References

Top Abstract Methods Results Discussion References

 

1. Dockery DW, Ware JH, Ferris BG, et al. 1985. Distribution of forced expiratory volume in one second and forced vital capacity in healthy, white, adult never-smokers in six U.S. cities. Am Rev Respir Dis 131:511-520. [Medline]
2. Leblanc P, Ruff F, Milic-Emili J, 1970. Effects of age and body position on "airway closure" in man. J Appl Physiol 28:448-451. [Free Full Text]
3. Jenkins SC, Moxham J, 1991. The effects of mild obesity on lung function. Respir Med 85:309-311. [Medline]
4. Thomas PS, Cowen ERT, Hulands G, Milledge JS, 1989. Respiratory function in the morbidly obese before and after weight loss. Thorax. 44:382-386. [Abstract/Free Full Text]
5. Collins LC, Hoberty PD, Walker JF, Fletcher EC, Peiris AN, 1995. The effect of body fat distribution on pulmonary function tests. Chest. 107:1298-1302. [Abstract/Free Full Text]
6. Lazarus R, Sparrow D, Weiss ST, 1997. Effects of obesity and fat distribution on ventilatory function. Chest. 111:891-898. [Abstract/Free Full Text]
7. Chien S, Peng MT, Chen KP, Huang TF, Chang C, Fang HS, 1975. Longitudinal studies on adipose tissue and its distribution in human subjects. J Appl Physiol 39:825-830. [Abstract/Free Full Text]
8. Borkan GA, Hults DE, Gerzof SG, Robbins AH, Silbert CK, 1983. Age changes in body composition revealed by computed tomography. J Gerontol 38:673-677.
9. Enzi G, Gasparo M, Raimondo Biondetti P, Fiore D, Semisa M, Zurlo F, 1986. Subcutaneous and visceral fat distribution according to sex, age, and overweight, evaluated by computed tomography. Am J Clin Nutr 44:739-746. [Abstract/Free Full Text]
10. Dehn MM, Bruce RA, 1972. Longitudinal variations in maximal oxygen intake with age and activity. J Appl Physiol 33:805-807. [Free Full Text]
11. Jackson AS, Beard EF, Wier LT, Ross RM, Stuteville JE, Blair SN, 1995. Changes in aerobic power of men, ages 25–70 yr. Med Sci Sports Exerc 27:113-120. [Medline]
12. Coon PJ, Bleecker ER, Drinkwater DT, Meyers DA, Goldberg AP, 1989. Effects of body composition and exercise capacity on glucose tolerance, insulin and lipoprotein lipids in healthy older men: a cross-sectional and longitudinal intervention study. Metabolism. 38:1201-1209. [Medline]
13. Katzel LI, Bleecker ER, Colman EG, Rogus EM, Sorkin JD, Goldberg AP, 1995. Effects of weight loss vs aerobic exercise training on risk factors for coronary disease in healthy, obese, middle-aged and older men. JAMA 274:1915-1921. [Abstract/Free Full Text]
14. Meyers DA, Goldberg AP, Bleecker ML, Coon PJ, Drinkwater DT, Bleecker ER, 1991. Relationship of obesity and physical fitness to cardiopulmonary and metabolic function in healthy older men. J Gerontol Med Sci 46:M57-M65.
15. Harris J, Benedict F, 1919. A Biometric Study of Basal Metabolism in Man Carnegie Institute of Washington;, Washington, DC.
16. Kenney WL, , ed.American College of Sports Medicine's Guidelines for Exercise Testing and Prescription 5th ed. 1995:160Williams and Wilkins;, Baltimore, MD.
17. Behnke AR, Wilmore JH, 1974. Evaluation and Regulation of Body Build and Composition Prentice Hall;, Englewood Cliffs, NJ.
18. Siri WE, 1956. The gross composition of the body. Advances in Biological and Medical Physics. Vol. 4 239-280. Academic Press, New York.
19. Bruce RA, Horsten TR, 1969. Exercise testing in the evaluation of patients with ischemic heart disease. Prog Card Dis 11:371-390. [Medline]
20. Wise RA, Enright PL, Connett JE, et al. 1998. Effect of weight gain on pulmonary function after smoking cessation in the Lung Health Study. Am J Respir Crit Care Med 157:866-872. [Abstract/Free Full Text]
21. Alfaro V, Torras R, Prats T, Palacios L, Ibanez J, 1996. Improvement in exercise tolerance and spirometric values in stable chronic obstructive pulmonary disease patients after an individualized outpatient rehabilitation programme. J Sports Med Phys Fitness. 36:195-203. [Medline]
22. Turner JM, Mead J, Wohl ME, 1968. Elasticity of human lungs in relation to age. J Appl Physiol 25:664-671. [Free Full Text]
23. Bates DV, 198996–102. Respiratory Function in Disease 3rd ed. W.B. Saunders;, Philadelphia. 96–102.

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