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.
Reduced functional residual capacity (FRC) is consistently found in obese subjects. In 10 obese subjects (mean +/- SE age 49.0 +/- 6 yr, weight 128.4 +/- 8 kg, body mass index 44 +/- 3 kg/m2) without respiratory disease, we examined 1) supine changes in total lung capacity (TLC) and subdivisions, 2) whether values of total respiratory resistance (Rrs) are appropriate for mid-tidal lung volume (MTLV), and 3) estimated resistance of the nasopharyngeal airway (Rnp) in both sitting and supine postures. The results were compared with those of 13 control subjects with body mass indexes of <27 kg/m2. Rrs at 6 Hz was measured by applying forced oscillation at the mouth (Rrs,mo) or the nose (Rrs,na); Rnp was estimated from the difference between sequential measurements of Rrs,mo and Rrs,na. All measurements were made when subjects were seated and when supine. Obese subjects when seated had a restrictive defect with low TLC and FRC-to-TLC ratio; when supine, TLC fell 80 ml and FRC fell only 70 ml compared with a mean supine fall of FRC of 730 ml in control subjects. Values of Rrs,mo and Rrs,na at resting MTLV in obese subjects were about twice those in control subjects in both postures. Relating total respiratory conductance (1/Rrs) to MTLV, the increase in Rrs,mo in obese subjects was only partly explained by their reduced MTLV. Rnp was increased in some obese subjects in both postures. Despite the increased extrapulmonary mass load in obese subjects, further falls in TLC and FRC when supine were negligible. Rrs,mo at isovolume was increased. Further studies are needed to examine the causes of reduced TLC and increases in Rrs,mo and sometimes in Rnp in obese subjects.
Ind PW, Bell JD. Reduction of total lung capacity in obese men: comparison of total intrathoracic and gas volumes. J Appl Physiol 108: 1605-1612, 2010. First published March 18, 2010 doi:10.1152/japplphysiol.01267.2009.-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/m 2 ] and 7 control men (mean age 50 yr, BMI 22-27 kg/m 2 ). 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 ϭ 0.016) and intrathoracic fat (obese 0.68 liter, control 0.23 liter, P Ͻ 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 Ͻ 80% predicted (OR), and the eight obese men with TLC Ͼ 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. magnetic resonance imaging; restricted total lung capacity; mediastinal volume ABOUT 50 YEARS AGO, IT WAS established that functional residual capacity (FRC) and expiratory reserve volume (ERV) are reduced in most seated obese subjects (14, 32). More recently, reduction in total lung capacity (TLC), formerly thought only to occur in massively obese subjects (28), has been found in some subjects with less severe obesity (17). Consistent with the development of a restrictive pattern of lung function in some obese subjects, prospective studies have shown that weight gain is associated with loss of vital capacity (VC) (6,7,34), while weight loss is associated with increase in VC (22,28,29,31).The mechanical factors reducing VC and TLC in obesity are uncertain, but it has been speculated that increased abdominal volume in some way reduces inspiratory descent of the diaphragm and consequent expansion of the thorax. Recent studies of induced ascites in dogs have shown that, at FRC, the lung-expanding action of the diaphragm was r...
Four methods for assessing airflow resistance were compared in seven normal adults at baseline and after inducing airway narrowing with inhaled methacholine. Airway resistance (Raw) was measured during panting at 1-2 Hz within a body plethysmograph; total lung resistance was measured by using an esophageal balloon during quiet breathing (RLq) and with doubling of frequency while maintaining the original tidal volume; total respiratory resistance (Rrs) was measured at 6 Hz during forced oscillation applied at the airway opening, and interruption resistance (Rint) was measured at midtidal expiratory flow. Three methods of obtaining Rint after airflow interruption were compared [smooth curve fit of mouth pressure (Pm) back extrapolated to valve closure; two-point linear fit of Pm back extrapolated to 15 ms after closure; and Pm at 100 ms after valve closure]. We found similar basal median values (cmH2O.l-1.s) of Raw (1.3), RLq (1.4), RL of double resting frequency (1.9), Rrs (1.7), and smooth curve fit of Pm back extrapolated to valve closure (1.5); basal values of two-point linear fit of Pm back extrapolated to 15 ms after closure (2.4) and Pm at 100 ms after valve closure (4.4) were considerably larger. After induced airway narrowing, all methods of measuring resistance showed significant increases; these were largest with RLq (median %change of 265) and smallest with the three Rint methods (median %change of 62-72). Rint and Rrs methods had poorer sensitivity for detecting bronchoconstriction than lung resistance of Raw. Of the Rint methods, end interruption pressure was the most sensitive.(ABSTRACT TRUNCATED AT 250 WORDS)
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