scholarly journals Relation between trunk fat volume and reduction of total lung capacity in obese men

2012 ◽  
Vol 112 (1) ◽  
pp. 118-126 ◽  
Author(s):  
R. A. Watson ◽  
N. B. Pride ◽  
E. Louise Thomas ◽  
P. W. Ind ◽  
J. D. Bell

Reduction in total lung capacity (TLC) in obese men is associated with restricted expansion of the thoracic cavity at full inflation. We hypothesized that thoracic expansion was reduced by the load imposed by increased total trunk fat volume or its distribution. Using MRI, we measured internal and subcutaneous trunk fat and total abdominal and thoracic volumes at full inflation in 14 obese men [mean age: 52.4 yr, body mass index (BMI): 38.8 (range: 36–44) kg/m2] and 7 control men [mean age: 50.1 yr, BMI: 25.0 (range: 22–27.5) kg/m2]. TLC was measured by multibreath helium dilution and was restricted (<80% of the predicted value) in six obese men (the OR subgroup). All measurements were made with subjects in the supine position. Mean total trunk fat volume was 16.65 (range: 12.6–21.8) liters in obese men and 6.98 (range: 3.0–10.8) liters in control men. Anthropometry and mean total trunk fat volumes were similar in OR men and obese men without restriction (the ON subgroup). Mean total intraabdominal volume was 9.41 liters in OR men and 11.15 liters in ON men. In obese men, reduced thoracic expansion at full inflation and restriction of TLC were not inversely related to a large volume of 1) intra-abdominal or total abdominal fat, 2) subcutaneous fat volume around the thorax, or 3) total trunk fat volume. In addition, trunk fat volumes in obese men were not inversely related to gas volume or estimated intrathoracic volume at supine functional residual capacity. In conclusion, this study failed to support the hypotheses that restriction of TLC or impaired expansion of the thorax at full inflation in middle-aged obese men was simply a consequence of a large abdominal volume or total trunk fat volume or its distribution.

1986 ◽  
Vol 60 (4) ◽  
pp. 1198-1202 ◽  
Author(s):  
F. D. McCool ◽  
B. M. Pichurko ◽  
A. S. Slutsky ◽  
M. Sarkarati ◽  
A. Rossier ◽  
...  

Previous studies suggest that abdominal binding may affect the interaction of the rib cage and the diaphragm over the tidal range of breathing in quadriplegia. To determine whether abdominal binding influences rib cage motion over the entire range of inspiratory capacity, we used spirometry and the helium-dilution technique to measure functional residual capacity (FRC), inspiratory capacity, and total lung capacity (TLC) in eight quadriplegic and five normal subjects in supine, tilted (37 degrees), and seated positions. Combined data in all three positions indicated that, with abdominal binding, FRC and TLC decreased in normal subjects [delta FRC = -0.33 + 0.151 (SD) P less than 0.01); delta TLC = -0.16 + 0.121, P less than 0.05]. In quadriplegia there was also a reduction in FRC with binding (delta FRC = -0.32 + 0.101, P less than 0.001). However, TLC increased in quadriplegia (delta TLC = 0.07 + 0.061, P less than 0.025). In an additional six quadriplegic and five normal subjects, we used magnetometers to define the influences of abdominal binding on rib cage dimensions and TLC. In quadriplegia, rib cage dimensions were increased at TLC with abdominal binding, whereas there was no change in normals. Our data suggest that this inspiratory effect of abdominal binding on augmenting rib cage volume in quadriplegia is greater than the effect of impeding diaphragm descent, and thus abdominal binding produces a net increase in TLC in quadriplegia.


1995 ◽  
Vol 79 (4) ◽  
pp. 1199-1205 ◽  
Author(s):  
J. C. Yap ◽  
R. A. Watson ◽  
S. Gilbey ◽  
N. B. Pride

Increased abdominal mass in obesity should enhance normal gravitational effects on supine respiratory mechanics. We have examined respiratory impedance (forced oscillation over 4–26 Hz applied at the mouth during tidal breathing), maximum inspiratory and expiratory mouth pressures (MIP and MEP), and maximum effort flow-volume curves seated and supine in seven obese subjects (O) (mean age 51 yr, body mass index 43.6 kg/m2) and seven control subjects (C) (mean age 50 yr, body mass index 21.8 kg/m2). Seated mean total lung capacity was smaller in O than in C (82 vs. 100% of predicted); ratio of functional residual capacity (FRC) to total lung capacity averaged 43% in O and 61% in C (P < 0.01). Total respiratory resistance (Rrs) at 6 Hz seated was higher in O (4.6 cmH2O.l-1.s) than in C (2.2 cmH2O.l-1.s; P < 0.001); total respiratory reactance (Xrs) at 6 Hz was lower in O than in C. In C, on changing to the supine posture, mean Rrs at 6 Hz rose to 2.9 cmH2O.l-1.s, FRC fell by 0.68 liter, and Xrs at 6 Hz showed a small fall. In O, despite no further fall in FRC, supine Rrs at 6 Hz increased to 7.3 cmH2O.l-1.s, and marked frequency dependency of Rrs and falls in Xrs developed. Seated, MIP and MEP in C and O were similar; supine there were small falls in MEP and maximum expiratory flow in O. The site and mechanism of the increase in supine Rrs and reduction in supine Xrs and the mechanism maintaining supine FRC in obesity all need further investigation.


1981 ◽  
Vol 50 (2) ◽  
pp. 292-298 ◽  
Author(s):  
S. M. Fortney ◽  
E. R. Nadel ◽  
C. B. Wenger ◽  
J. R. Bove

We produced left lower lobe (LLL) pneumococcal pneumonia in seven dogs and measured lung volumes and pulmonary mechanics before (day 1) and 48 h after (day 3) development of the infection. Compared with seven control dogs, total lung capacity (TLC) and functional residual capacity (FRC) decreased 550 and 140 ml, respectively, representing a 15% reduction from the initial value in both cases. Compliance measured during tidal breathing decreased by 30%, and even when corrected for the smaller FRC on day 3, specific compliance (CLsp) was reduced. At autopsy, the infected LLL had an excess weight of 89 g, and its 50% reduction in gas volume accounted for the decrease in TLC from day 1 to day 3. Compared with control dogs, there were no changes in the deflation pressure-volume curves of the noninfected lung of the pneumonia dogs. These results indicate that the reduction in TLC in bacterial lobar pneumonia was small and resulted from the reduced gas volume of the infected lobe. Assuming that the increased weight gain in the LLL represented 89 ml of exudate that filled alveoli, we propose that bacterial pneumonia reduced gas volume at FRC by filling alveoli with inflammatory exudate and further decreased TLC by preventing these alveoli from inflating. The reduced CLsp suggested nonventilation of air spaces in addition to those that were liquid filled and was consistent with nonventilation of the entire LLL.


1962 ◽  
Vol 17 (6) ◽  
pp. 871-873 ◽  
Author(s):  
Donald F. Tierney ◽  
Jay A. Nadel

We made concurrent measurements of the functional residual capacity (FRC) with the body plethysmograph (thoracic gas volume) and by 7-min and prolonged open-circuit nitrogen dilution methods (communicating gas volume). The mean difference between the 7-min communicating gas volume and the thoracic gas volume in 13 healthy subjects was only 0.13 liters. The thoracic gas volume averaged 0.99 liters larger than the communicating gas volume after 7 min of O2 breathing in 13 patients with emphysema. The communicating gas volume at 12–18 min was the same as the thoracic gas volume in 11 of 13 patients but was smaller in the other 2. When the thoracic gas volume was used to measure FRC, the total lung capacity averaged 142% of predicted normal in 13 patients with emphysema. Submitted on January 4, 1962


1981 ◽  
Vol 50 (2) ◽  
pp. 283-291 ◽  
Author(s):  
S. N. Mink ◽  
R. B. Light ◽  
L. D. Wood

We produced left lower lobe (LLL) pneumococcal pneumonia in seven dogs and measured lung volumes and pulmonary mechanics before (day 1) and 48 h after (day 3) development of the infection. Compared with seven control dogs, total lung capacity (TLC) and functional residual capacity (FRC) decreased 550 and 140 ml, respectively, representing a 15% reduction from the initial value in both cases. Compliance measured during tidal breathing decreased by 30%, and even when corrected for the smaller FRC on day 3, specific compliance (CLsp) was reduced. At autopsy, the infected LLL had an excess weight of 89 g, and its 50% reduction in gas volume accounted for the decrease in TLC from day 1 to day 3. Compared with control dogs, there were no changes in the deflation pressure-volume curves of the noninfected lung of the pneumonia dogs. These results indicate that the reduction in TLC in bacterial lobar pneumonia was small and resulted from the reduced gas volume of the infected lobe. Assuming that the increased weight gain in the LLL represented 89 ml of exudate that filled alveoli, we propose that bacterial pneumonia reduced gas volume at FRC by filling alveoli with inflammatory exudate and further decreased TLC by preventing these alveoli from inflating. The reduced CLsp suggested nonventilation of air spaces in addition to those that were liquid filled and was consistent with nonventilation of the entire LLL.


2010 ◽  
Vol 108 (6) ◽  
pp. 1605-1612 ◽  
Author(s):  
R. A. Watson ◽  
N. B. Pride ◽  
E. Louise Thomas ◽  
J. Fitzpatrick ◽  
G. Durighel ◽  
...  

Restriction of total lung capacity (TLC) is found in some obese subjects, but the mechanism is unclear. Two hypotheses are as follows: 1) increased abdominal volume prevents full descent of the diaphragm; and 2) increased intrathoracic fat reduces space for full lung expansion. We have measured total intrathoracic volume at full inflation using magnetic resonance imaging (MRI) in 14 asymptomatic obese men [mean age 52 yr, body mass index (BMI) 35–45 kg/m2] and 7 control men (mean age 50 yr, BMI 22–27 kg/m2). MRI volumes were compared with gas volumes at TLC. All measurements were made with subjects supine. Obese men had smaller functional residual capacity (FRC) and FRC-to-TLC ratio than control men. There was a 12% predicted difference in mean TLC between obese (84% predicted) and control men (96% predicted). In contrast, differences in total intrathoracic volume (MRI) at full inflation were only 4% predicted TLC (obese 116% predicted TLC, control 120% predicted TLC), because mediastinal volume was larger in obese than in control [heart and major vessels (obese 1.10 liter, control 0.87 liter, P = 0.016) and intrathoracic fat (obese 0.68 liter, control 0.23 liter, P < 0.0001)]. As a consequence of increased mediastinal volume, intrathoracic volume at FRC in obese men was considerably larger than indicated by the gas volume at FRC. The difference in gas volume at TLC between the six obese men with restriction, TLC < 80% predicted (OR), and the eight obese men with TLC > 80% predicted (ON) was 26% predicted TLC. Mediastinal volume was similar in OR (1.84 liter) and ON (1.73 liter), but total intrathoracic volume was 19% predicted TLC smaller in OR than in ON. We conclude that the major factor restricting TLC in some obese men was reduced thoracic expansion at full inflation.


PEDIATRICS ◽  
1959 ◽  
Vol 24 (2) ◽  
pp. 181-193
Author(s):  
C. D. Cook ◽  
P. J. Helliesen ◽  
L. Kulczycki ◽  
H. Barrie ◽  
L. Friedlander ◽  
...  

Tidal volume, respiratory rate and lung volumes have been measured in 64 patients with cystic fibrosis of the pancreas while lung compliance and resistance were measured in 42 of these. Serial studies of lung volumes were done in 43. Tidal volume was reduced and the respiratory rate increased only in the most severely ill patients. Excluding the three patients with lobectomies, residual volume and functional residual capacity were found to be significantly increased in 46 and 21%, respectively. These changes correlated well with the roentgenographic evaluation of emphysema. Vital capacity was significantly reduced in 34% while total lung capacity was, on the average, relatively unchanged. Seventy per cent of the 61 patients had a signficantly elevated RV/TLC ratio. Lung compliance was significantly reduced in only the most severely ill patients but resistance was significantly increased in 35% of the patients studied. The serial studies of lung volumes showed no consistent trends among the groups of patients in the period between studies. However, 10% of the surviving patients showed evidence of significant improvement while 15% deteriorated. [See Fig. 8. in Source Pdf.] Although there were individual discrepancies, there was a definite correlation between the clinical evaluation and tests of respiratory function, especially the changes in residual volume, the vital capacity, RV/ TLC ratio and the lung compliance and resistance.


1991 ◽  
Vol 70 (6) ◽  
pp. 2611-2618 ◽  
Author(s):  
T. Mutoh ◽  
W. J. Lamm ◽  
L. J. Embree ◽  
J. Hildebrandt ◽  
R. K. Albert

Abdominal distension (AD) occurs in pregnancy and is also commonly seen in patients with ascites from various causes. Because the abdomen forms part of the "chest wall," the purpose of this study was to clarify the effects of AD on ventilatory mechanics. Airway pressure, four (vertical) regional pleural pressures, and abdominal pressure were measured in five anesthetized, paralyzed, and ventilated upright pigs. The effects of AD on the lung and chest wall were studied by inflating a liquid-filled balloon placed in the abdominal cavity. Respiratory system, chest wall, and lung pressure-volume (PV) relationships were measured on deflation from total lung capacity to residual volume, as well as in the tidal breathing range, before and 15 min after abdominal pressure was raised. Increasing abdominal pressure from 3 to 15 cmH2O decreased total lung capacity and functional residual capacity by approximately 40% and shifted the respiratory system and chest wall PV curves downward and to the right. Much smaller downward shifts in lung deflation curves were seen, with no change in the transdiaphragmatic PV relationship. All regional pleural pressures increased (became less negative) and, in the dependent region, approached 0 cmH2O at functional residual capacity. Tidal compliances of the respiratory system, chest wall, and lung were decreased 43, 42, and 48%, respectively. AD markedly alters respiratory system mechanics primarily by "stiffening" the diaphragm/abdomen part of the chest wall and secondarily by restricting lung expansion, thus shifting the lung PV curve as seen after chest strapping. The less negative pleural pressures in the dependent lung regions suggest that nonuniformities of ventilation could also be accentuated and gas exchange impaired by AD.


1988 ◽  
Vol 64 (6) ◽  
pp. 2482-2489 ◽  
Author(s):  
P. Leblanc ◽  
E. Summers ◽  
M. D. Inman ◽  
N. L. Jones ◽  
E. J. Campbell ◽  
...  

The capacity of inspiratory muscles to generate esophageal pressure at several lung volumes from functional residual capacity (FRC) to total lung capacity (TLC) and several flow rates from zero to maximal flow was measured in five normal subjects. Static capacity was 126 +/- 14.6 cmH2O at FRC, remained unchanged between 30 and 55% TLC, and decreased to 40 +/- 6.8 cmH2O at TLC. Dynamic capacity declined by a further 5.0 +/- 0.35% from the static pressure at any given lung volume for every liter per second increase in inspiratory flow. The subjects underwent progressive incremental exercise to maximum power and achieved 1,800 +/- 45 kpm/min and maximum O2 uptake of 3,518 +/- 222 ml/min. During exercise peak esophageal pressure increased from 9.4 +/- 1.81 to 38.2 +/- 5.70 cmH2O and end-inspiratory esophageal pressure increased from 7.8 +/- 0.52 to 22.5 +/- 2.03 cmH2O from rest to maximum exercise. Because the estimated capacity available to meet these demands is critically dependent on end-inspiratory lung volume, the changes in lung volume during exercise were measured in three of the subjects using He dilution. End-expiratory volume was 52.3 +/- 2.42% TLC at rest and 38.5 +/- 0.79% TLC at maximum exercise.


2008 ◽  
Vol 105 (6) ◽  
pp. 1864-1872 ◽  
Author(s):  
Z. Hantos ◽  
Á. Adamicza ◽  
T. Z. Jánosi ◽  
M. V. Szabari ◽  
J. Tolnai ◽  
...  

Absolute lung volumes such as functional residual capacity, residual volume (RV), and total lung capacity (TLC) are used to characterize emphysema in patients, whereas in animal models of emphysema, the mechanical parameters are invariably obtained as a function of transrespiratory pressure (Prs). The aim of the present study was to establish a link between the mechanical parameters including tissue elastance (H) and airway resistance (Raw), and thoracic gas volume (TGV) in addition to Prs in a mouse model of emphysema. Using low-frequency forced oscillations during slow deep inflation, we tracked H and Raw as functions of TGV and Prs in normal mice and mice treated with porcine pancreatic elastase. The presence of emphysema was confirmed by morphometric analysis of histological slices. The treatment resulted in an increase in TGV by 51 and 44% and a decrease in H by 57 and 27%, respectively, at 0 and 20 cmH2O of Prs. The Raw did not differ between the groups at any value of Prs, but it was significantly higher in the treated mice at comparable TGV values. In further groups of mice, tracheal sounds were recorded during inflations from RV to TLC. All lung volumes but RV were significantly elevated in the treated mice, whereas the numbers and size distributions of inspiratory crackles were not different, suggesting that the airways were not affected by the elastase treatment. These findings emphasize the importance of absolute lung volumes and indicate that tissue destruction was not associated with airway dysfunction in this mouse model of emphysema.


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