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79:1199-1205, 1995. ;J Appl PhysiolJ. C. Yap, R. A. Watson, S. Gilbey and N. B. PrideEffects of posture on respiratory mechanics in obesity

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Effects of posture on respiratory mechanics in obesityJ. C. H. YAP, R. A. WATSON, S. GILBEY, AND N. B. PRIDEDepartment of Medicine, Royal Postgraduate Medical School, Hammer-smith Hospital,London W12 ONN, United Kingdom

Yap, J. C. H., R. A. Watson, S. Gilbey, and N. B. Pride.Effect s of posture on respiratory mechanics in obesity. J .AppZ. PhysioZ. 79(4): 1199- 1205, 1995.-Increased abdomi-nal mass in obesity should enhance normal gravitational ef-fects on supine respiratory mechanics. We have examinedrespiratory impedance (forced oscillation over 4-26 Hz ap-plied at the mouth during tidal breathing), maximum inspira-tory and expiratory mouth pressures (MIP and MEP), andmaximum effort flow-volume curves seated and supine inseven obese subjects (0) (mean age 51 yr, body mass index43.6 kg/m2) and seven control subjects (C) (mean age 50 yr ,body mass index 21.8 kg/m2). Seated mean total lung capacitywas smaller in 0 than in C (82 vs . 100% of predicted); ratioof functional residual capaci ty (FRC) to total lung capaci tyaveraged 43% in 0 and 61% in C (P < 0.01). Total respiratoryresistance (Rrs) at 6 Hz seated was higher in 0 (4.6cmH20 l 1-l l s) than in C (2.2 cmH20 l 1-l l s; P < 0.001); totalrespiratory reactance (Xrs) at 6 Hz was lower in 0 than inC. In C, on changing to the supine posture, mean Rrs at6 Hz rose to 2.9 cmH20 l 1-l l s, FRC fell b y 0.68 liter, and Xrsat 6 Hz showed a small fall . In 0, despite no further fall inFRC, supine Rrs at 6 Hz increased to 7.3 cmH20 l 1-l l s, andmarked frequency dependency of Rrs and falls in Xrs devel-oped. Seated, MIP and MEP in C and 0 were similar; supinethere were small falls in MEP and maximum expiratory flowin 0. The site and mechanism of the increase in supine Rrsand reduction in supine Xrs and the mechanism maintainingsupine FRC in obesity all need further investigation.lung volumes; resistance; reactance

IN NORMAL SUBJECTS there is a reduction in functionalresidual capacity (FRC) and an increase in airway resis-tance on adopting the supine posture (16); most of thereduction is due to the gravitational effects of the ab-dominal contents, resulting in the relaxed diaphragmtaking up a more expiratory position. In obese subjectsthe mass load on the chest wall in the supine postureis increased. Because the obese subject already has areduced FRC and small expiratory reserve volume(ERV) in erect postures (4, 11, 29, 30, 33), any furtherfall might lead to considerable airway closure and arte-rial hypoxemia when awake, whereas such changeswould augment any tendency to develop severe hypox-emia in obese subjects with obstructive sleep apnea.A few studies have been made of postural changesin subdivisions of lung volume (4, 30) and pulmonaryand chest wall compliance (19) in obese subjects, but amajor problem in studying the effects of the supineposture on respiratory mechanics in obesity is the dif-ficulty in obtaining reliable esophageal pressure mea-surements (17). Such measurements are least reliableat small lung volumes in the supine posture and whenthere is a considerable mass load on the esophagus. Inthe present study we have used the forced oscillationtechnique applied at the mouth to estimate airflow re-sistance and reactance in sitting and supine postures

in obese and control subjects. In these subjects we havealso studied other changes in respiratory mechanics bymeasuring subdivisions of static lung volumes, maxi-mum expiratory flow-volume curves, and maximum ef-fort inspiratory and expiratory mouth pressures. Theresults have been compared with the effects of massloading of the abdomen in the supine posture in normalsubjects.MATERIALS AND METHODSSubjects

For the main study seven obese subjects without pulmo-nary disease or spirometric evidence of airway obstructionand with a mean body mass index (BMI) of 43.6 kg/m2 werecompared with seven age-matched control subjects with amean BMI of 21.8 kg/m2 (Table 1). Five of the obese subjectshad never smoked; the remaining two were ex-smokers whohad smoked for 9 and 1 pack-yr, respectively. One obese manhad mild obstructive sleep apnea. All had a normal chestradiograph. In an additional five normal subjects, the effect sof mass loading of the abdomen on subdivisions of lung vol-ume and on oscillation mechanics were studied in the supineposition. Written consent was obtained from all subjects, andthe protocol was approved by the Research Ethics Committeeof this medical school.Measurements

Forced osciZZation technique. The technique and equipmentas described by Landser et al. (14) were used. The subjectssupported the cheeks and floor of the mouth with the palmsof their hands to minimize dissipation of the applied flow inthe upper airway. The head and neck were kept in a neutralto slightly extended position. Oscillation mechanics weremeasured during tidal breathing via a large-bore mouthpieceand with a noseclip in place.The oscillation apparatus consisted o f a loudspeaker thatwas attached to a tube leading to a screen pneumotacho-graph. A complex signal of sinusoidal sound-wave oscillationcontaining all harmonics of 2 Hz up to 26 Hz was applied bythe loudspeaker. The signal was presented as prepro-grammed pseudorandom noise, the sequence being repeatedevery 0.5 s for a 16-s period. During oscillation, mouth pres-sure and airflow were recorded by two identical differentialtransducers (Validyne MP45) and fed into a Fourier analyzer,ensemble averaged over the measurement period of 16 s, andcalculated to give the values of impedance at ~-HZ intervalsfrom 2 Hz up to 26 Hz. The derived values were the mean ofboth inspiratory and expiratory impedance over the severalbreaths of the 16-s period. This impedance was further ana-lyzed as the in-phase component [resistance (Rrs)] and theout-of-phase component [reactance (Xrs)] of pressure andflow. The in-phase component of the signal, Rrs, is an indexof airflow resistance analogous to resistance derived by othermethods such as body plethysmography. The oscillatory fre-quency at which reactance is zero is resonant frequency (f,) .The reliability of the derived values was indicated by a coher-ence function for measurements at each frequency. Resultswere only accepted when coherence was >0.95; in some sub-

0161-7567/95 $3.00 Copyright 0 1995 the American Physiolo gical Society 1199

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1200 POSTURE AND RESPIRATORY MECHANICS IN OBESITYTABLE 1. Characteristics of subjects

Obese Control

Male/FemaleAge, YrHt, mw kgBody mass index, kg/m2Pulmonary function seated

314 21551.1+4.8 50.125.01.66t0.03 1.7320.03

119.9z8.4 65.923.943.622.5 21.850.7

TLC, %pred 82.122.7 99.623.7FE&, %pred 88.424.2 113.827.1FEVJFVC, % 89.32 1.0 81.623.6Raw, cmH,O l 1-l l s 4.92 1.0 2.020.4Values are mean t SE for 7 subje cts in each group. TLC, total

lung capacity; FE&, forced expiratory volume in 1 s; FVC, forcedvital capacity; Raw, airway resistance; %pred, % predicted.

jects, coherence at 2 Hz fell below this value, so we reportonly results at 4-26 Hz. Three consecutive sets of measure-ments over 16 s were made while the subject breathed quietlyand continuously via the mouthpiece.For measurements in the supine posture, the oscillationapparatus was supported by a gantry over the subject wholay supine on a couch. Care was taken to ensure that a similarslightly extended position of the head and neck was sustainedin this position. The two differential pressure transducerswere positioned in the perpendicular axis so that their orien-tation was not altered between sitting and supine postures.

We also monitored breathing pattern and changes in lungvolume during oscillation measurements by integrating themouth flow signal to obtain tidal volume. This was displayedon a strip-chart recorder. At the end of each oscillation mea-surement, a full inspiration was made to relate tidal volumeto total lung capacity (TLC), previously determined by con-stant-volume body plethysmography in the sitting position,and to calculate absolute midtidal lung volume (MTLV) andFRC. In estimating the eff ect s of posture on subdivisions oflung volume, it was assumed TLC was unchanged in boththe obese and control groups. Published evidence suggeststhat although there are small reductions in TLC in the supineposture, these are similar in obese and normal subjects (seeDISCUSSION). To allow fo r postural changes in MTLV andFRC, measurements of Rrs were expressed as specific totalRrs (SRrs) calculated as (Rrs l MTLV).

Maximum effort flow-volume curves and spirometry.Forced expiratory volume in 1 s (FE&), forced vital capacity(FVC), and maximum effo rt expiratory and inspiratory flow-volume curves were recorded by using a lo-liter dry rolling-seal spirometer (model 842, Ohio Instruments). The flow-volume curves were displayed on an X-Y storage oscilloscope(model 613, Tektronix, Beaverton, OR), and permanent cop-ies were obtained on a hard-copy thermal Tektronix 4610printer for later analysis of peak expiratory flow (PEF) andmaximum expiratory flow rate at 50 and 25% of the re-maining vital capacity (VC) of the firs t sitting position. Tocompare sitting with supine values we assumed TLC hadfallen by 100 ml in both control and obese subjects in thesupine position.Maximum respiratory muscle pressures. Mouth pressuresduring maximum efforts against a closed airway were re-corded with a Validyne pressure transducer. Maximum expi-ratory pressure (MEP) was recorded during ef forts at TLC,and maximum inspiratory pressure (MIP) at was recordedFRC; the best pressures sustained over 1 s were recorded.

Oxygen saturation (Sao,). Sao, was measured with anOhmeda Biox 3740 pulse oximeter.VisuaZ analog scale (VAS) for dyspnea. The subjects were

asked to indicate how breathless they fe lt on a line that ex-tended from 0 to 10. They were not allowed to refer to previ-ous scoring during each assesssment of VAS when theychanged position.

Body plethysmography. At the start of the study airwayresistance (Raw) (9) and thoracic gas volume and TLC (8)were measured by using a constant-volume body plethysmo-graph*

Mass-loading of anterior chest waZZ. Bags containing leadshot to a total of 25 kg were placed across the lower rib cageand epigastrium of the supine subjects. Measurements ofsubdivisions of lung volumes and oscillation mechanics weremade after the subjects had been breathing quietly for -2min with the load applied.Protocol

The subjects were first familiarized with all the techniquesof measurements. TLC and Raw were then measured in thebody plethysmograph. Measurements of oscillation mechan-ics, maximum inspiratory and expiratory flow-volume curves,MIP and MEP, and VAS for dyspnea were recorded. Sao, wasmonitored continuously.

The subject then lay down, and after 5 min a further set ofmeasurements of oscillation mechanics, flow-volume curves,MIP and MEP, and VAS was made. The subject then returnedto the sitting posture, and after 5 min a third set of thesemeasurements were obtained.For each of the three sets of measurements, the mean o fthree successive reproducible measurements were made.Comparisons with predicted values were made by using stan-dard European reference values (22).Statistical Analysis

Mean values were compared by using paired and unpairedt-tests as appropriate.RESULTS

There were no systematic differences in the two setsof sitting measurements made before and after lyingsupine; the results presented and used for statisticalanalysis are those seated before adoption of the supineposition.Static Lung Volumes

Even after correction for the slightly smaller heightin the obese subjects, values of TLC and its subdivi-sions in the sitting position were smaller in the obesesubjects than in the control subjects. In addition tothese absolute changes, FRCITLC was considerablysmaller in the obese than in the control subjects (P

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POSTURE AND RESPIRATORY MECHANICS IN OBESITY 1201

sitting supineObese

sitting supineControl

TLC

FRCRV

FIG. 1. Mean va lues for subd ivisions of total lung capacity (TLC)in obese and control subje cts in sitting and supine postures. FRC,functional residual capacity; RV, residual volume; ERV, expiratoryreserve volume. TLC is assume d not to change significantly on adop-tion of supine posture (see text).

not significant. Reactance was considerably lower in theobese than in the normal subjects (P < 0.04).CHANGES BETWEEN SUPINE AND SITTING POSTURES.The absolute and proportional increase in sitting Rrsat 6 Hz was considerably greater in the obese (P 85%. On adoption of thesupine posture, there were small reductions (NS) inFVC and FE& in both groups, but falls in peak expi-ratory flow were larger in the obese subjects (P < 0.01).Maximum Respiratory Pressures (Table 4)

7.8kO.4210.050.79

Values are means + SE of 7 subje cts in each group. Rrs, totalrespiratory resistance; SRrs, spe cific total respiratory resistance ;Xrs, total respiratory reactance.

MIP and MEP were similar in the two groups seated,but there was a small fall in MEP in obese subjects inthe supine position (mean sitting, 99 cmH20; supine,87 cmH,O; paired t-test, P = 0.09).

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1202 POSTURE AND RESPIRATORY MECHANICS IN OBESITYA 3

2

-- sittinga supine

0 4 8 12 16 20 24 28Frequency (Hz)6 3-

2- n=7F l-T -o O; -I-,o -2-s!!x -3:-4-

-5 , , , , , , . , I , 9 , 10 4 8 12 16 20 24 28

Frequency (Hz)FIG. 3. Total respiratory reactance (Xrs) at different oscilla tion

frequencies in control subje cts (A) and obese subje cts (B). Resu ltsobtained during tidal breathing in sitting a nd supine pos itions arecompared. Resonant frequency is frequency at which Xrs is zero,indicated by position at which Xrs frequency curve crosse s horizontaldotted line. AI1 values are mean + SE for 7 subje cts in each group.

Oxygen Saturation (Table 4)In the sitting position mean Sao, was slightly lowerin the obese subjects than in the control subjects. Inthe control subjects there was no change on adopting

TABLE 3. FVC maneuvers in sitting and supinepositionsObese Control

FE&, litersSittingSupine

FVC, litersSittingSupine

FEVJFVC, %SittingSupine

PEF, I/sSittingSupine

MEF 50% vc, l/SSittingSupine

MEF 25% vc , l/SSittingSupine

2.3920.14 3.58t0.182.1750.13 3.4250.192.6920.17 4.3120.222.50+0.15 4.11kO.2489.321.04 81.623.5986.820.91 81.623.948.7220.95 8.9OkO.626.9720.68 8.6420.613.28t0.38 3.8520.422.7120.39 3.6050.391.2050.16 1.4350.250.8650.15 1.19+0.18

Values are means + SE of 7 subje cts in each group. PEF, peakexpiratory flow; MEFSO% vc and MEF25% vc, maximu m expiratory flowwhen 50 and 25% of vital capacity remains to be expired, respectively.

TABLE 4. Oxygen saturation and maximum effortmouth pressures in sitting and supine positionsObese Control P Value

Oxygen satura tion, %SittingSupine

Maximum inspiratory96.3kO.42 97.320.57 0.1894.720.92 97.320.64 0.04

pressure, cmH20SittingSupine

Maximum expiratory94217 95510 NS90218 94217 NS

pressure, cmH20Sitting 99+15 93+13 NSSupine 87~16 95216 NSValues are mean + SE of 7 subje cts in each group. NS, not signifi-

cant.

the supine posture, but there was a small fall from 96.3to 94.7% in the obese subjects (paired t-test, sitting vs.supine, P = 0.052). In the supine posture mean Sao2was lower in the obese than in the control subjects(unpaired t-test, P = 0.04).Mass Loading in Normal Subjects

In the five additional normal subjects there was asmall fall in VC on adopting the supine posture (mean5.0-4.7 liters), and ERV fell from a mean of 2.3 litersto 0.9 liter. Changes in oscillation mechanics betweensitting and supine positions were similar to those inthe main control group, with Rrs rising and Xrs fallingat all frequencies in the supine position (Fig. 4). MeanRrs at 6 Hz was 1.75 cmHzO? l s sitting and 2.70cmHzO 01-l l s supine; mean Xrs at 6 Hz was -0.07cmH20 l 1-l l s sitting and -0.58 cmH20 l 1-l l s supine;and mean fR was 6.1 Hz sitting and 9.7 Hz supine (P

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POSTURE AND RESPIRATORY MECHANICS IN OBESITY 1203

n=5 -- sittingsupineh loaded

0 4 8 12 16 20 24 28Frequency (Hz)B 3,

1 , I , I , I , I f 1 1 *

0 4 8 12 16 20 24 28Frequency (Hz)FIG. 4. Mean values of Rrs (A) and Xrs (B) at different oscillatio n

frequencies during tid .a1 breathing in 5 normal subje cts studied sit-ting, supine unloaded, and supine with an added anterior chest wall

Technical FactorsWe did not measure FRC in the supine posture inthese studies but derived change in FRC and residualvolume (RV) by measuring VC and its subdivisions inthe supine posture and assuming changes in TLC weresmall and similar in normal and obese subjects. Mea-sured reductions in VC and FVC in the supine positionaveraged 200 ml in both control and obese subjectsin the present study. Two previous studies of TLC onchanging posture have shown mean falls of 140 ml innormal and of 200 ml in obese subjects (30) and of137 ml in normal and of 115 ml in obese subjects (4),respectively. Changes in RV with posture are agreed

to be small (4, 30), so these previous studies of TLCagree closely with our observed changes in VC. In afurther study in our laboratory of 12 obese subjectsin whom FRC was measured by multibreath heliumdilution in both postures, mean values were 2.36 litersseated and 2.29 liters supine, confirming the impliedlack of fall in FRC found in the present study.Previous studies of mass loading of thorax and/orabdominal wall have produced large changes in thepressure-volume characteristics of the relaxed respira-tory system in both conscious and anesthetized normalsubjects (26). Nevertheless, mass loading in normalsubjects does not simulate the load of obesity fully be-cause it is applied acutely, is entirely external to theabdominal wall and is associated with a normal scaph-oid contour of the ventral abdominal wall, whereas in

obesity much of the mass load is intra-abdominal andthe supine contour of the abdominal wall is protuber-ant. Although the applied mass load was built up overa few minutes in our normal subjects, contraction ofabdominal muscles was obviously induced. The rele-vance of this experiment in untrained alert subjects tolong-term mass loading, as present in obesity, is there-fore uncertain.Changes in TLC and Subdivisions

Reductions in FRC and ERV in normal subjects mov-ing from the sitting to the supine posture were similarto those previously described in this (32) and other lab-oratories (16, 20) and presumably reflect changes inrelaxation volume of the respiratory system (Vr) dueto alteration of the pressure-volume characteristics ofthe chest wall and increases in intrathoracic blood vol-ume with posture (1).The reductions in TLC, VC, FRC, and ERV found inseated obese subjects were also similar to those foundby previous authors (4, 19, 26, 30, 33). The reductionin FRC and ERV, which is a function of increasingweight (23), has been assumed to be due to a reductionin Vr caused by a shift to smaller volumes of the pres-sure-volume curve of the relaxed chest wall. In con-trast, RV is not reduced, at least in middle-aged obesesubjects (4, 29, 30), probably because in such subjectsRV is limited by airway closure rather than the chestwall (15). The mechanism of the reduction in TLC isuncertain but presumably reflects a change in extra-pulmonary structures; conceivably, inspiratory descentof the diaphragm is impeded by restriction of anteriormovement of the abdominal wall. The strength of theinspiratory muscles in our obese subjects was normalat FRC, but we are not aware of studies of pleural andabdominal pressure at full inflation that would help toanalyze the cause of the reduction in TLC.Because of the increased mass of the abdomen inobese subjects, gravitational forces in the supine posi-tion would be expected to enhance the cranial move-ment of the diaphragm; the striking feature of our re-sults is our failure to find any further fall in FRC inobese subjects when they adopt the supine posture.Two previous studies (4,30) have shown that the meanfall in ERV in obese subjects adopting the supine posi-tion was -0.5 liter less than the fall in control subjectsof normal weight. RV presents an absolute lower limitto end-tidal volume, and published data imply that Vrcould fall below RV in obese subjects (19,26). Very lowvalues of ERV (

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1204 POSTURE AND RESPIRATORY MECHANICS IN OBESITYent obese subjects Sa o2 was only slightly lower in thesupine posture), and a larger lung O2 store should ob-structive apnea develop.

The failure of anterior chest wall mass loading tofurther reduce FRC and ERV in supine normal subjectsalso implies alterat ion in respiratory muscle activity.Abdominal muscle contraction was obviously inducedas the load was increased, attenuating the increasein abdominal pressure. Conceivably, tonic diaphragmactivity was also induced, opposing the deflat ionary ef-fect of the increase in abdominal pressure.Changes in Respiratory Mechanics With Posture

The changes found in normal subjects with recum-bency (increase in Rrs, fall in MTLV and FRC, reduc-tion in Xrs, and increase in fR) were al l of similar direc-tion and magnitude to those found in previous studies(16, 20, 32). Most of th e increase in Rrs can be ac-counted for by the reduction in MTLV as shown byearlier detailed studies of airway resistance vs. lungvolume (16) and as indicated by the small change inSRrs with change in posture in the present studies.

Seated Rrs was considerably higher in the obese thanthe normal subjects, but as shown by the smaller differ-ences in SRrs (Table 2), a large part of the increase inRrs was due to the smaller lung volume at which themeasurement was made. Differences between Raw(measured at slightly smaller lung volume) and Rrswere small, confirming that the increased Rrs was notdue to increased resistance of the chest wall. Theseresults are similar to those of another recent study (33).The supine rise in Rrs in the obese subjects cannotbe attributed to a further reduction in midtidal lungvolume. The serial site of the supine increase in Rrscould be the intra- or extrathoracic airways or a changein chest wall properties. Mass load ing of the suprala-ryngeal airway by fat in the supine posture could in-crease its resistance (2, 13). In obesity there is an en-hanced increase in intrapulmonary blood volume whensupine (24), and this conceivably could lead to intrapul-monary airway narrowing, either directly or by stimu-lating reflex bronchoconstriction, as postulated in theorthopnea of heart failure. The shape of maximum ex-piratory flow-volume curves in our supine obese sub-jects favored an extrathoracic airway narrowing be-cause they showed a disproportionate fall in PEF withonly small changes in the later part of the curve, whichmight be expected if the rise in Rrs was due to intrapul-monary changes. Unfortunately, interpretation is com-plicated by the accompanying fall in MEP, which alsomight account for the disproportionate reduction inPEF. The enhanced frequency dependence of Rrs isequally inconclusive; whereas it might be due to in-creased inequalities of intrapulmonary time constantsand airway closure at small lung volume, it may simplyreflect an effect of upper airway shunt that developswhenever Rrs is increased and is not completely re-moved by the external support of the cheeks and floorof the mouth used in this study (21,31). Clearly, furtherstudies are needed to establish the serial site of theincrease in supine Rrs.

Xrs depends on the balance between effective respi-ratory system compliance (Crs) and inertance (Irs).Various models have been used to derive Crs and Irsfrom forced oscillation data (18, 20); it has been esti-mated that the larger part of the postural change innormal subjects was caused by a fall in Crs (20), whichmight be explained by stiffening of the lung (16,20) andpossibly the chest wall (16, 19), related to breath ing ata smaller lung volume. However, values of effectiveCrs estimated from impedance measurements (20) aremuch lower than static measurements of Crs obtainedwith the weighted spirometer technique. Furthermore,by using the latter technique, total Crs has not changedbetween sitting and supine positions in normal subjects(6, 10, 19>, although there are changes in its compo-nents with reductions in compliance of the rib cage andincreases in compliance of the diaphragm-abdomencompartment in supine subjects (10).

Obese subjects had lower sitting values of Xrs andhigher fR than d id control subjects and showed furtherstriking reductions in Xrs and increase in fR in thesupine position. There are few studies of Crs in obesesubjects. Naimark and Cherniack (19) found a reducedCrs in seated obese subjects and a small further fallwhen supine. The major component appeared to bestiffening of the chest wall. The differences in ventralabdominal wall contours between the seated and su-pine position, which are thought to account for the in-crease in supine abdominal compliance in normal sub-jects (27), clearly might not apply in grossly obese sub-jects. Other authors have failed to find any abnormalityin Crs (28), whereas increases in the tissue componentof Irs have also been described (25). Alternatively, thedecrease in total reactance might be due to an in-creased contribution from the low compliance of theupper airway, a further effect of an increased upperairway shunt. Precise interpretation of the changes inXrs will require more invasive investigations combin-ing direct measurements of pleural and gastric pres-sures with movements of the abdominal wall.

In contrast to the large falls in supine Xrs in obesity,mass loading of the anterior thorax and abdominal wallonly produced a small fal l in Xrs in supine normal sub-jects. This fall was presumably due to a reduction inanterior abdominal wall compliance induced by musclecontraction in response to the load; compliance of therib cage and lateral abdominal wall may not have beenaffected, thereby reducing the effect on total Crs (5).Mouth pressures on maximum inspiratory and expi-ratory efforts were similar in control and obese subjectswhen seated, as described before (3, 12). The only sig-nificant change when supine was a small fall in MEP inobese subjects that may reflect less effective abdominalmuscle contraction.

In summary, despite the increased gravitational loadin the supine position in obese subjects, FRC did not fallbelow seated values. This lack of further gravitationaleffect on FRC aids tidal expiratory flow and avoids ex-cessive airway closure and further hypoxemia. Despitethe lack of fal l in FRC, Rrs increased and Xrs decreased.The mechanical load on the inspiratory muscles, there-fore, was increased in the supine posture because of

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POSTURE AND RESPIRATORY MECHANICS IN OBESITY 1205both worsening of respiratory mechanics and the im-plied need to sustain end-tidal volume above Vr. 15 .

This work was supported by a Commonw ealth fellowship and bya grant from the British Lung Foundation.

Present address of J. C. H. Yap: Dept. of Medicine III, Tan TackSeng Hospital, Singapore.

Address for reprint requests: N. B. Pride, Dept. of Medicine, RoyalPostgraduate Medical Schoo l, Hammersm ith Hospital, London W12ONN, UK.

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18 .Received 27 January 1995; accepted in final form 27 April 1995.

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