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* From the Human Physiology Division (Drs. De Lorenzo, Maiolo, Mohamed, Andreoli, and Petrone-De Luca) and the Pulmonary Disease Division (Dr. Rossi), University of Rome "Tor Vergata."
Correspondence to: Antonino De Lorenzo, MD, Neuroscience Department, Faculty of Medicine and Surgery, Via di Tor Vergata, 135, 00133 Rome, Italy; e-mail: delorenzo{at}uniroma2.it
| Abstract |
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Design: Cross-sectional, observational.
Settings: Human Physiology Division, Faculty of Medicine and Surgery, "Tor Vergata" University, Rome, Italy.
Patients: Thirty obese adults (mean [± SD] baseline body mass index [BMI], 32.25 ± 3.99 kg/m2), without significant obstructive airway disease, were selected from among participants in a weight-loss program.
Measurements
and results: Anthropometric, body composition (BC), and
respiratory parameters of all participants were measured before and
after weight loss. Total and segmental lean body and FM were obtained
by dual-energy x-ray absorptiometry. Dynamic spirometric tests and
maximum voluntary ventilation (MVV) were performed. The BC parameters
(ie, body weight [BW], BMI, the sum skinfold
thicknesses, thoracic inhalation circumference, thoracic expiration
circumference, total FM, and trunk FM [FMtrunk]) were significantly
decreased (p
0.0001) after a hypocaloric diet. The mean vital
capacity, FEV1, FEF50, FEF2575,
expiratory reserve volume, and MVV significantly increased
(p
0.05) with weight loss. The correlation coefficient for
FEF2575 (r = 0.20) was numerically
higher than
FEF50 and
FEV1
(r = 0.14 and r = 0.08, respectively)
for the BW loss. Moreover, the correlation coefficient for
FEF2575 (r = 0.45) was significantly
higher (p
0.02) than those for
FEF50 and
FEV1 (r = 0.38 and
r = 0.15, respectively) for FMtrunk loss.
Conclusions: This study shows that a decrease in total and upper body fat obtained by restricted diet was not accompanied by a decrease in ventilatory muscle mass. FMtrunk loss was found to have improved airflow limitation, which can be correlated to peripheral airways function.
Key Words: dual-energy radiograph absorptiometry fat distribution forced expiratory flows pulmonary function weight loss
| Introduction |
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general, extensive research1 2 has shown that the location of body fat deposits is a more important determinant than the size of these deposits. It also has been shown that the presence of intra-abdominal visceral fat in the mesentery and omentum is a better predictor of coronary heart disease than the body mass index (BMI)3 and that neck and visceral fat accumulation is a risk factor for obstructive sleep apnea syndrome.4
Many studies also have demonstrated an association between excess weight or weight gain and pulmonary dysfunction.5 6 7 8 9 Specifically, weight gain tends to be accompanied by a decrease in vital capacity (VC) and FEV1 among adults, which is possibly attributable to the effect of obesity on chest-wall compliance or inactivity.10 Furthermore, expiratory reserve volume (ERV), which is related to abdominal and chest fat accumulation, is decreased in obese patients,11 and respiratory and airway resistance increases significantly with the level of obesity.12 13 14 15
Given that losses in body weight (BW) account for significant improvements in pulmonary function,16 17 18 19 dietary or surgical treatment of morbid obesity can be used to sufficiently improve lung-specific parameters and respiratory muscle function.16 17 18 In this context, many authors have investigated the relationship between body composition (BC) and respiratory functions. Specifically, lean body mass (LBM) has been found to be positively associated with respiratory functions, whereas fat mass (FM) in severely obese persons has a negative association.16 20 21
With regard to the effects of modifications in body fat distribution on pulmonary function, the studies20 21 conducted to date have shown conflicting results, thus the potential association remains unclear.8 It has been suggested22 that among severely obese persons, pulmonary function is impaired to a greater extent among those with upper body obesity, compared to persons with lower body obesity. It also has been suggested often that cardiopulmonary failure occurs only in overweight persons with predominately upper body obesity.
To study BC and fat distribution in humans, De Lorenzo et al16 proposed using dual-energy x-ray absorptiometry (DXA).23 Although DXA determines fat distribution indirectly, it produces the most accurate results, is the only technique capable of determining specific sites of fat deposition, and is preferred over anthropometric indexes for estimating fat distribution (eg, BMI, waist-hip ratio, and skinfold thickness). Furthermore, DXA produces accurate and detailed assessments of soft tissue (ie, FM and LBM) topographies by direct measurements of trunk, abdomen, thigh, and leg.24
The objective of the present study was to establish the relationship between loss of BW and pulmonary-function indexes, focusing on FEV1 and forced expiratory flows in the mid- and lower-half of VC (ie, forced expiratory flow at 50% of vital capacity [FEF50], forced expiratory flow at 75% of vital capacity, and forced expiratory flow at 25 to 75% of vital capacity [FEF2575]). Specifically, we evaluated the effect of the loss of total FM (FMtot) and segmental FM and of changes in LBM, after a restricted hypocaloric diet, on pulmonary functions in obese adults.
| Materials and Methods |
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The study comprised 30 mildly obese adults (7 men and 23 women; mean [± SD] age, 42 ± 12 years; mean height, 1.64 ± 0.11 m) who were randomly selected from among participants in a weight-loss program at the "Tor Vergata" University. In general, approximately 70 to 80% of program participants were women and 20 to 30% were men ("Tor Vergata" University internal departmental statistics). The program is based on a hypocaloric Mediterranean diet, which has proven to be effective in weight-loss programs.12 13 16 Diets were individualized based on resting energy expenditure, excess BW, height, age, gender, and level of engagement in sports activities (DietoSystem, version 1.25; Terapia Alimentare; Milan, Italy). Diet protein intake levels were calculated as 1 g/kg of BW, as described elsewhere.25 Both current and ex-smokers were included in the study. During the study period, no changes in lifestyle or smoking habits were observed.
Exclusion Criteria
Following routine clinical examinations, we excluded from this
analysis persons with respiratory symptoms and/or an
FEV1/FVC ratio < 76% of the predicted value.
We also excluded persons who, at the end of the weight-loss program,
showed stationary weight or weight gain; none of the persons excluded
for stationary weight or weight gain underwent follow-up tests for
respiratory function.
Measurements
All of the patients were examined at enrollment into the program
(baseline survey) and on its completion (follow-up survey) 6 months
later (ie, immediately after the acute phase of BW loss and
before the occurrence of any lean tissue repletion).
Anthropometric and BC parameters were measured for all participants. Specifically, BW (in kilograms; measured with participants clothed in underwear with bare feet) was measured to the nearest 0.01 kg using a digital scale (Body Master; Rowenta, Germany). Height was measured using a stadiometer. BMI was calculated as weight/height2 (in kg/m2 )
We measured skinfold thickness and circumference parameters, in accordance with standard methods,26 using Holtain calipers (Bryberian, UK). A sum of four skinfolds was calculated (ie, biceps, triceps, subscapular, and suprailiac skinfolds). Thoracic inhalation circumference (TorInh) was measured at total lung capacity, and thoracic expiration circumference (TorExp) was measured at residual volume using a standard tape measure. Total LBM (LBMtot), total FM (FMtot), trunk LBM (LBMtrunk), and trunk FM (FMtrunk) were measured using DXA total body scans of relatively low energy (Lunar DPX densitometer, version 3.6; Lunar Radiation Corp, Madison, WI).27 At both baseline and follow-up, patients were investigated under standard conditions. BW loss was determined by subtracting their weight at follow-up from that at baseline.
Dynamic spirometric tests were performed using a portable open circuit spirometer (KIT-Cosmed spirometer; Cosmed; Rome, Italy) in the standing position, in accordance with the guidelines of the American Thoracic Society.28 At both baseline and follow-up, forced expiratory blows were performed three times, and the best value obtained from the maximum expiratory flow-volume curve was considered in the analysis of FVC, VC, FEV1, FEF50, and FEF2575. Maximum voluntary ventilation (MVV) was determined by fast, deep breathing for 12 s.
To study changes in respiratory functions at different degrees of weight loss, participants were divided into three subgroups based on the extent of loss in BW and FMtrunk. The three levels were defined by visually inspecting scatter plots (Fig 1 ) of losses. For BW, the three subgroups were as follows: < 3.49 kg (n = 5); 3.50 to 6.49 kg (n = 10); and > 6.50 kg (n = 13). For FMtrunk, the three subgroups were as follows: < 1.49 kg (n = 5); 1.50 to 2.99 kg (n = 10); and > 3.00 kg (n = 13).
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0.05.
Simple regression analysis and analysis of variance were performed to
establish different correlation coefficients between spirometric
parameters and losses in BW and FMtrunk. | Results |
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0.0001) in
the mean values for BC parameters (ie, BW, BMI, sum of
skinfolds, TorInh, TorExp, FMtot, and FMtrunk), whereas no significant
differences were observed for LBMtot or LBMtrunk.
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With regard to respiratory parameters, the mean VC,
FEV1, FEF50,
FEF2575, ERV, and MVV significantly increased
(p
0.05) with weight loss (Table 2
), whereas no significant changes were found for FVC, peak expiratory
flow (PEF), FEV1/VC ratio,
FEV1/FVC ratio, or
FEF2575.
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FEV1,
FEF50, and
FEF2575)
and losses in BW and FMtrunk. Changes were calculated as the difference
between follow-up and baseline values. When considering BW loss, the
correlation coefficient was higher for
FEF2575 (r = 0.20) compared to
FEV1 (r = 0.08) and
FEF50 (r = 0.14). Similar results
were obtained when considering FMtrunk loss
(
FEF2575, r = 0.45,
p
0.02;
FEV1, r = 0.15; and
FEF50, r = 0.38; p
0.05).
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FEV1 and
VC progressively decreased with increasing BW loss, whereas the
coefficient for
FEF2575 showed an initial
increase by BW loss (from < 3.49 kg to 3.50 to 6.49 kg), followed by
a decrease (from 3.50 to 6.49 kg to > 6.50 kg).
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FEV1 and
VC initially decreased with
increasing loss (from < 1.49 kg to 1.50 to 2.99 kg); they then
increased (from 1.50 to 2.99 kg to > 3.00 kg). The correlation
coefficient for
FEF2575 progressively
increased with increasing loss (loss of > 3.00 kg,
r = 0.68 and p
0.02; loss of 1.5 to 2.99 kg,
r = 0.36; and < 1.49 kg,
r = 0.25).
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| Discussion |
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0.0001) with no
significant changes in LBMtot, and it was associated with improved
pulmonary function (ie, significant improvements in VC, ERV,
FEV1, FEF50, and
FEF2575). This finding is consistent with
reports of an association between improvements in VC and PEF and
unchanged LBMtot in weight-loss programs.11 We measured total and segmental FM and LBM using DXA. FMtrunk has been shown to be indicative of truncal obesity, which is associated with poor respiratory function.20 The association between forced expiratory flow rates over low- and mid-volume ranges and small airways function is known.29 These rates have been shown to be reduced in some obese individuals who had no evidence of obstructive airway disease.13 14 By contrast, the mechanisms underlying the decreased peripheral airway caliber in obese persons are not well known. It is believed that pulmonary blood volume is increased in obese patients, possibly leading to congestion of bronchial vessels in the airway submucosa, thickening of the airway wall, and decrease in airway size.30 Altered lipid metabolism of obese patients may amplify these effects; the presence of very low-density lipoproteins has been found to be related to the release of histamine, which is an effective mediator of vascular permeability and smooth muscle contraction in the airway.31 Furthermore, airway resistance, depending on the elastic recoil pressure of the lung, tends to increase the airway size at high pulmonary volumes and to reduce it at low pulmonary volumes when this pressure diminishes.12
In our study, the correlation coefficient for
FEF2575 was higher than that for
FEV1, for both BW loss and FMtrunk loss. This
may be due to
FEF2575 being more sensitive
to decreases in airflow limitation induced by BW and FMtrunk losses.
FMtrunk loss was found to improve airflow limitation, which might
result from improved peripheral airway function. Although smoking may
decrease small airways function, this was not evident from our results,
in that the number of smokers (ie, < 3) was not sufficient
for reaching statistical significance. We chose to analyze ERV because
it is a marker of pulmonary function that is sensitive to changes in
BW. However, the correlation coefficient (r = 0.26)
between changes in ERV and changes in FMtrunk did not reach statistical
significance.
We observed an association between improvements in the respiratory
parameters VC and FEV1 and the initial BW loss,
however, the extent of improvement decreased for greater BW loss.
Previous studies have shown that dietary treatment and gastroplasty for
morbid obesity are sufficient for inducing improvements in lung volume
and respiratory muscle performance.18
32
By contrast,
decreases in FVC and FEV1 are associated with
gains in BW,5
6
7
8
which is apparently consistent with our
finding of improved VC and FEV1 with greater BW
loss. The finding that this improvement was less evident for the
highest level of BW loss (ie, > 6.50 kg) could be
explained by the absence of changes, after moderate weight loss, in
LBMtot and upper LBM, in addition to decreased muscle work. In
addition, after weight loss, MVV showed a highly significant
(p
0.0001) improvement, which also is related to
respiratory muscle function. The finding that the correlation
coefficient for
FEF2575 tended to be higher
for a BW loss of 3.50 to 6.49 kg, with respect to the other two
subgroups, remains unclear.
Regarding FMtrunk loss, the finding that among patients with the
greatest loss (ie, > 3.00 kg), the correlation coefficient
for
FEF2575 was significantly higher
(p
0.02) than that among those with less extensive loss
(ie, < 1.49 kg and 1.50 to 2.99 kg) suggests that losses
in upper body fat may be responsible for improving the respiratory
parameters of small airways. Although we cannot explain the finding
that the
FEV1 and
VC correlation
coefficients initially decreased with increased FMtrunk loss (ie,
losses of < 1.49 kg and 1.50 to 2.99 kg), the increase coefficients
for the highest loss (> 3.00 kg) is fairly logical.
| Conclusion |
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| Acknowledgements |
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| Footnotes |
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Received for publication June 6, 2000. Accepted for publication December 18, 2000.
| References |
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