Obesity and Respiratory Function

8/3/2019 Obesity and Respiratory Function

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EditorialOfficeNotes:

RES 11479.R1

INVITEDREVIEWSERIES:ObesityandRespiratorydisordersSeriesEditor:AmandaJPiperReceived:15August2011

Invitedtorevise:24August2011Revised:29August2011

Accepted:3September2011


2/30

Theimpactofobesityonrespiratoryfunction*StephenW.Littleton,MD

Pulmonary, Critical Care, and Sleep Medicine, Cook County Hospital and Rush University

MedicalCenter;Chicago,USA

Correspondingauthor:

StephenW.Littleton,MD

Pulmonary,CriticalCare,andSleepMedicine

AttendingPhysician,CookCountyHospital

AssistantProfessorofMedicine,RushUniversityMedicalCenter

1900W.PolkSt.,Rm.1416

Chicago,IL60612

(312)8647380,fax(312)8647394

[email protected]

Authorsbiography:Dr.LittletonisanattendingphysicianinthedivisionofPulmonary,CriticalCare,andSleep

MedicineatCookCountyHospitalinChicago,andanAssistantProfessorofmedicineatRush

UniversityMedicalCenter.Hisresearchinterestsincludethepathophysiologyofrespiratory

failureandhypercapnia.

This is an Accepted Article that has been peer-reviewed and approved for

publication in the Respirology, but has yet to undergo copy-editing and proof

correction. Please cite this article as an "Accepted Article"; doi:

10.1111/j.1440-1843.2011.02096.x


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AbstractObesityhaslongbeenrecognizedashavingsignificanteffectsonrespiratoryfunction.

Thetopic

has

been

studied

for

at

least

the

last

half

century,

and

some

clear

patterns

have

emerged.Obesepatientstendtohavehigherrespiratoryratesandlowertidalvolumes.Total

respiratorysystemcomplianceisreducedforavarietyofreasons,whichwillbediscussed.Lung

volumestendtobedecreased,especiallyexpiratoryreservevolume(ERV).Spirometry,gas

exchange,andairwayresistancealltendtoberelativelywellpreservedwhenadjustedforlung

volumes.Patientsmaybemildlyhypoxaemic,possiblyduetoventilationperfusion

mismatchingatthebaseofthelungs,wheremicroatelectasisislikelytooccur.Weightloss

leadstoareversalofthesechanges.Forallofthesechanges,thedistributionoffat,i.e.,upper

versuslowerbody,maybemoreimportantthanbodymassindex.

Keywords: lungvolumes,obesity,pulmonaryfunctiontests,pulmonarygasexchange,respiratorymechanics.

Shorttitle: Impactofobesityonrespiratoryfunction


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IntroductionTheassociationbetweenobesityandrespiratorydysfunctionisalmostasoldas

recordedhistory.

Dionysius,

atyrant

of

Heraclea,

was

born

inapproximately

360

BC.

He

was

describedasbeingveryobese,andthroughdailygluttonyandintemperance,increasedtoan

extraordinarydegreeofCorpulencyandFatness,byreasonwhereofhehadmuchadoetotake

breath.Itwasalsowrittenofhimthathewaschokedbyhisownfat.1

DionysiuswasnotuniqueinancientGreektimes.Magas,theKingofCyrene,whodiedin

approximately258BC,wasweighteddownwithmonstrousmassesoffleshinhislastdays;in

facthechokedhimselftodeath.1

Therehavebeensimilardescriptionsofobesityinmorerecenttimesaswell.In1816,

WilliamWadd,whosetitlewasSurgeonExtraordinarytotheKing,publishedatreatisein

whichhenoted,accumulationoffat...cannotfailtoimpedethefreeexerciseoftheanimal

functions.Respirationisperformedimperfectly,orwithdifficulty.Intheappendix,he

mentionedthreepatientswhohadbeensuffocatedbyfat.1 But,specifically,whatarethe

imperfectionsintherespirationofobesepatients?

BreathingpatternsofobesepatientsPatientswhoaremorbidlyobese(BMI 40kg/m

2)haveincreasedrespiratoryratesas

comparedwithnormalsubjects.Infourstudies,themeanrespiratoryrateofobesesubjects

rangedfrom15.321breathsperminute,whilethatofnormalsubjectsrangedfrom1012

breathsperminute.25

Tidalvolumetendstobesignificantlylowerinobesesubjects,35

althoughthisfindingisnotuniversal.2Despitethedecreaseintidalvolume,theincreasein


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respiratoryrateissuchthatminuteventilationissignificantlyincreased,andwasshowntobe

11L/minorgreaterinmoststudies.2,4,5

Howdoes

the

obese

patient

achieve

this

higher

respiratory

rate?

Isthere

achange

in

breathtiming,oristheflowratehigher?Itseemsthatthereisachangeinbreathtiming,but

reportsonexactlywhatthosechangesarehavebeeninconsistent.Sampsonshowedthatthere

wasadecreaseininspiratorytime[TI],withoutasignificantdecreaseinexpiratorytime[TE],and

nochangeinmeaninspiratoryflow.3Incontrast,bothBurkiandBaker,andChlifetal.showed

thatTEdecreasedwithoutanychangeinTIorinspiratoryflowrates(aswellassimilarexpiratory

flowrates).2,5

Finally,PankowshowedthatTIandTEweredecreasedbutdidnotreportthe

statisticsonflowrates.4DecreasesinTImayarisefromincreasedactivityofchestwall

receptorsorfromchangesincentralbreathtiming,3whereasdecreasesinTEcouldbeduetoan

increasedexpiratoryflowrateasaresultofdecreasedtotalrespiratorycompliance,2or

persistentdiaphragmaticactivityextendingintoexhalation.3ItseemsthatbothTIandTEare

affectedbyobesity,althoughtheexactpatternofchangesmayvaryamongindividuals.

RespiratorymechanicsTotalrespiratorysystemcomplianceisundoubtedlyreducedinobesepatients.

610

However,theresultsarecontradictoryastowhetherthisreducedcomplianceisduetoreduced

chestwallcompliance,lungcompliance,orsomecombinationofthetwo.

In1960,NaimarkandCherniackshowedthatchestwallcompliancewasreducedin

obeseindividuals(andwasespeciallyreducedinthesupineposition),whereaslungcompliance

wasnormal.7Fouryearslater,Sharpetal.showednearlytheexactopposite:thatadecreasein


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lungcompliancewaslargelyresponsible.8Usinganoninvasivemethod,Surattetal.showed

thechestwallofobesepatientstobenormalwhiletheywereseated.11Oesophagealpressures,

andthereforecalculationsoflungandchestcompliance,changedbetweentheseatedand

supinepositions.7,12

Thesestudieswere performedonawakepatients,inwhomrespiratory

muscleactivitymayhaveinterferedwiththemeasurements.

WhenHedenstiernaandSantessonperformedsimilarstudiesonparalyzed,supine

subjects,chestwallcompliancewasfoundtobenormalandlungcompliancewasreduced.9

Pelosietal.studiednearlyequallyobesepatientsunderthesameconditions,andfoundthat

bothchestandlungcompliancewerereduced.10

Itislikelythatbothdecreasedlungcomplianceanddecreasedchestwallcompliance

contributetoalesscompliantrespiratorysysteminobesepatients.Decreasedlungcompliance

islikelytobetheresultofdecreasedlungvolumes,leadingtomicroatelectasis,whichshifts

normalrespirationsintothesinusoidalratherthanthelinearportionofthepressurevolume

curve.9,10

Chestwallcompliancemaybedependentonthepatternoffatdistributionina

particularpatient.Itisknownthatmassloadingofthelowerthoraxandupperabdomenof

supine,paralyzedsubjectsaffectschestwallcompliancemoresothanmassloadingofthe

upperthorax.13Therefore,chestwallcompliancemaybemorerelevantinpatientswithhigher

waisttohipratios.


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LungvolumesTheeffectsofobesityonlungvolumeshavebeenstudiedextensively.Figure1

summarizestheeffectsofobesityonlungvolumes.Oneofthemostconsistenteffectsof

obesityonlungvolumesisadecreaseinexpiratoryreservevolume(ERV).1421

ERVdecreasesas

BMIincreases.14,17,19,22,23

Onestudyofpulmonaryfunctiontestsin373patientswithawide

rangeofBMIshowedthatthosewithmildobesity(BMI3035kg/m2)hadanERVofonly42.4

29.3%ofpredicted.ThatstudyalsoshowedthatERVdecayedexponentiallywithincreasing

BMI(Fig.2).17Anotherstudyshowedthatsuperobeseindividuals(BMI 60kg/m

2,ora

height/weightratioof1)hadanERVofonly17.89.6%ofpredicted.19

AnequallyconsistentnegativecorrelationbetweenobesityandFRCcanbe

demonstrated,althoughthechangesarelessdramatic.14,17,23,24

IndividualswithaBMI>40

kg/m2haveanFRCof66.612.3%ofpredicted.Ifthereisanexponentialrelationshipbetween

BMIandERV,thenthesameshouldholdtrueofFRC,andthiswasshowntobethecase.Given

thatthereisasignificantbutverymodesteffectofBMIonRV,thenthereductioninFRCisdue

tothereductioninERV.17

IfobesityreducesERVandFRC,thenwemightexpectasimilareffectonTLC.Inreality,

TLCisnotaffectedunlesspatientsaremassivelyobese.Olderstudieswithlimitednumbersof

patientsshowedasignificantdifference,onlywhennormalsubjectswerecomparedtothose

withaheighttoweightratioof1.11.2(BMIof55kg/m2foraperson183cmtall,andgreaterif

thepersonisshorter),22orifthecohorthadameanbodyweightof23439.6%oftheideal

(BMIofapproximately46.6kg/m2).

2Asmallbutmorerecentstudydidnotfindasignificant


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differenceinTLCwhentwogroupswithmeanBMIsof25.5and38.8werecompared.25

However,whentheBMIoftheobesegroupwas47,whereasthatofthenormalgroup

remainedat25,asignificantdifferenceemerged.21Significantbutprobablyclinically

unimportantdifferencesdidemergewhenlargergroupsofpatientswerestudied.Onestudy

foundthattheTLCofagroupofsubjectswithameanBMIof34was15%belowpredicted

whencomparedwiththatofagroupwithameanBMIof27.20Inanotherstudy,therewasa

0.5%decreaseinpredictedTLCforeachunitincreaseinBMI,althoughmeanTLCinthegroup

withBMI 40wasonly12%belowpredicted,onaverage.17

Howdoesobesityhavetheseeffectsonlungvolumes?Oneproposedmechanismisthat

abdominalfatdisplacesthediaphragmintotheabdomen.26Thisissupportedbyonestudythat

showedlungvolumeswereaffectedmoreinpatientswithawaisttohipratio>0.95(upper

bodyfatdistribution).27Inaddition,chestwalladipositymaysimplycompressthethoraciccage,

leadingtolowerlungvolumes.26Thisissupportedbythesimilarpatternobservedwhenlung

volumesaremeasuredafterelasticstrappingofthechest,28althoughthereissomequestionas

towhetherobesityactsasamass(threshold)loadoranelasticload.13Itislikelythatbothplay

aroleindecreasinglungvolumes,anditwouldbedifficulttoisolateandstudyonecomponent

independently.

Recently,MRIhasbecomethepreferredmethodforlocalizingandquantifying

adiposity.29Nostudieshavebeendoneyetonwhetherabdominaladiposityasdeterminedby

MRIiscorrelatedwithreducedlungvolumes,butarecentpreliminarystudyexploredathird

possiblemechanismfortheeffectofobesityonlungvolumes:isthereanincreaseinthoracicor


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mediastinalfatinobesepatients?Normalweightsubjects(BMI25.0)werecomparedwith

obesesubjects(BMI38.8).Theobesesubjectswerethendividedintotwogroups:thosewitha

TLC80%ofpredicted(obese

normal).Althoughobesesubjectsdidhavemoremediastinalfatthannormalsubjects,there

wasnodifferenceinmediastinalfatbetweentheobeserestrictedandtheobesenormal

subjects.Infact,theonlydiscernibledifferencebetweenthetwoobesegroupswasthe

intrathoracicvolumeatfullbreathhold;124%ofpredictedTLCintheobesenormalgroup,and

105%ofpredictedTLCintheobeserestrictedgroup.Theauthorshypothesizedthatareduction

indiaphragmaticexcursionduetoabdominalfatwasresponsible.25

AnotherrecentstudyusedMRItocompareendexpiratorylungvolume(EELV)andfat

distributioninobesemenandwomen(BMIof354and372,respectively)withthatin

normalsubjects.Surprisingly,thatstudyshowedlittlevariationinthedistributionoffat

betweennormalsubjectsandobesesubjects,forbothmenandwomen.Thisunderscoresthe

difficultyofteasingouttherelativecontributionsofchestwallandabdominalfattoalterations

inlungvolumes.Thestudydidshowasignificantrelationshipbetweenvisceralfat,i.e.,fat

surroundingtheabdominalorgans,anteriorsubcutaneousfat(bothabdominalandchestwall),

andEELV(expressedas%TLC).30Thestudyalsohighlightedthefactthatbothchestwalland

abdominalfatlikelyplayaroleinderangementoflungvolume.

FurtherresearchonquantificationofabdominalfatbyMRIislikelytobeforthcoming,

andwillbeveryhelpfulinelucidatingtheexactmechanismsthatareatwork.


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SpirometryObesitygenerallydoesnotdepressFEV1orFVCunlesspatientsaremassivelyobese.The

FEV1/FVCratio

ispreserved.

2,17,1921,24,25,27,3133Figure

1shows

the

typical

spirogram

of

an

obese

patient.Onelargestudyshowedastatisticallysignificanttrendinmenandanearlysignificant

correlationinwomen,betweenFEV1,FVC,andBMI,althoughFEV1inmenwithameanBMIof

33.6wasclosetonormalat93%ofpredicted.32Eveninmassivelyobeseindividuals,theeffects

aremodest.OnestudyshowedthatthemeanFEV1in18patientswithweighttoheightratios

>1was68.75.9%ofpredicted.19TheseeffectsdisappearedwhenFEV1andFVCwereadjusted

forthesmallreductioninlungvolumes.

Again,itseemsthatthepatternofobesityismoresignificantthanBMIalone.

AbdominalobesityisgenerallycorrelatedwithreductionsinFEV1andFVC,withsome

exceptionsbeingnotedforwomenandcertainagegroups,dependingonthestudy.27,31,32,34

Thelargeststudyinvolvedalmost20,000subjectsandshowedaninverselinearcorrelation

betweenwaisttohipratioandFEV1andFVC.34 Othermeasurementsofabdominalobesitythat

haveshownassociationswithspirometricparametersarebiceps27andsubscapularskinfold

thickness,31waistcircumference,

35andabdominalheight.

32

AirwayresistanceAirwayresistanceisusuallyincreasedinobeseindividuals,andthisisatleastpartly

relatedtothelowerlungvolumesatwhichobesepatientsnormallybreathe,leadingtoclosure

ofthesmallerairways.20,21,24

Onecasecontrolledstudyof190subjectsshowedthattheairway

resistanceofobesemen(meanBMI47)wasalmosttwicethatofnormalcontrolsubjects.


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Interestingly,althoughthedifferencesinairwayresistancebetweennormalweightandobese

womenweresignificant,theyweremuchlessprofound.However,whenairwayresistancewas

adjustedforlungvolumes,therewasnodifferencebetweenthenormalsubjectsandtheobese

subjects.21Anotherstudyshowedaverystrongcorrelationbetween%predictedFRCand

airwayconductance(theinverseofairwayresistance),butnotbetweenconductanceandBMI.

DirectmeasurementsconfirmedthatairwaycalibreandBMIwerecorrelatedinmen,butonly

weaklycorrelatedinwomen.However,thesamestudyshowedthatthedecreaseinlung

volumesonlyaccountedforaportionoftheincreaseinairwayresistance.36Similarly,another

studyshowedthatthedecreaseinmidtidallungvolumedidnotaccountfortheincreasein

totalrespiratoryresistancemeasuredatthemouth.24

Thereasonsfortheinconsistencyinthesefindings,especiallythedifferencesbetween

thegenders,areunclear.Airwayremodellingsecondarytoinflammatoryadipokines,oreven

directlipiddepositionintheairwaysaretwopossibleexplanations.37Giventhedifferences

betweenthegenders,somehormonalinterplaymayalsobeinvolved.

Oxygenation,ventilation,perfusionandgasexchangeObesepatientsmayhaveanormal,

8,3840,orslightlyreducedPaO2.

16,19 Thereasonsfor

thedifferencesintheresultsofthesestudiesareunclear,butmayberelatedtoobesity

hypoventilationsyndrome,sinceonestudyshowedameanPaCO2of46.72.5mmHg.19One

studyof37massivelyobesepatients(BMIofapproximately50)showedarelativelynormal

meanPaO2of83.22.5mmHg,38whereasanotherstudyof25patientswithameanBMIof


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49.0showedanearlyidenticalmeanPaO2of887mmHg.40Itisnotclearwhethersimple

obesity,inandofitself,issufficienttocausearterialhypoxaemia.

Itdoes

seem,

however,

that

obesity

causes

amild

widening

of

the

AaO2

gradient.

Inthe

twopreviouslymentionedstudies,thesubjectswithBMIsof4950werefreeofpulmonary

diseaseandhadAaO2gradientsof22.62.838and199mmHg,

40respectively.Therefore,

althoughobesitycancauseamildwideningoftheAaO2gradient,thisisnotsufficienttocause

frankhypoxaemia.

ThewideningoftheAaO2gradientislikelycausedbyventilationperfusionmismatch.

Thelungbasesarerelativelyoverperfusedandunderventilatedwhenobesepatientsare

studiedinthesittingposition,41andwhentheyarerecumbent.

42Thisisduetotheclosureof

smallairwaysindependentlungzones.43Thiswouldcausethepatterndiscussedearlier;i.e.,a

reductioninERVwitharelativelyunchangedRV.

Furthermore,thereisalsoacorrelationbetweenERVandbothhypoxaemiaandAaO2

gradient.Inonestudy,V/QwasmuchmorecloselymatchedinfourobesesubjectswithanERV

of49%ofpredictedthaninfoursubjectswithanERVof21%ofpredicted.Theselattersubjects

hadidenticalperfusiontothelowerlungzones,butamuchhigherproportionofventilationto

theupperlungzones.41AnotherstudyshowedalinearrelationshipbetweenPaO2andabsolute

ERV,andmanyofthesepatientshadaclosingvolumeinexcessofERV.

39

Onceagain,weseea

significantrelationshipbetweenthepatternofobesityandpulmonaryfunction.Recentwork

hasshownasignificantlinearrelationshipbetweenwaisttohipratioandPaO2,PaCO2,andA

aO2gradient.40


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Gasexchange(DLCO)seemstoberelativelywellpreservedinsubjectswithsimple

obesity.8,19,22,44,45

Whencorrectedforlungvolume(DLCO/VA),valuesmaybeelevatedin

extremelyobese(height/weightratio>1.10)comparedtonormalweightindividuals,22although

thisfindinghasnotbeenconsistentlyreported.19Onestudyinwhichfactorsthatwere

correlatedwithanincreasedDLCO/VAwereexaminedretrospectively,showedthatareduction

inVCwasacommonfinding,andthatobesitywasacommoncauseofthisreduction.46

DLCO/VAmaybeincreasedinobesepatientsduetoanincreaseinpulmonarybloodvolume8,46

ExerciseSinceobeseindividualshaveahigherbasalmetabolicrate(VO2)thanleansubjects,itis

notsurprisingthattheyhaveahigheroxygenconsumptionduringexerciseforanygivenwork

rate.44,47,48,45

TheslopesoftheVO2toworkratelinesarethesameasinnormalweight

individuals,implyingthatitistheincreaseinbasalratethatisresponsiblefortheincreasein

VO2atagivenworkrate,althoughthismayalsoresultfromtheextraenergyneededtomove

heavierlegsduringcyclingexerciseprotocols.49 Obesepatientsalsotendtohavealower

anabolicthreshold.50TheAaO2gradient,andPaO2ifitisabnormal,actuallyimproveduring

exercise.49Augmentedtidalvolumeshelptoopentheclosed,dependentlungunits,whichare

thoughttobetheprimarycauseoftheincreasedAaO2gradient.51

InadditiontohavingalowerAaO2gradient,obesepatientsaugmenttheiroxygen

intakebyincreasingtheirtidalvolumesandrespiratoryratesduringexercise,similartonormal

weightsubjects.However,astheyburnmoreoxygen,theyneedtoaugmenttheirminute

ventilationtoanevengreaterextentthannormalweightsubjects.Thisisachievedmainly


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throughahigherrespiratoryrate,astheirtidalvolumesarenotgenerallygreater.44,48,50

The

reasonwhyisunclear.Itmaybesimplyduetocentralbreathtiming,butagain,weseesome

evidencethatitcouldberelatedtobodyfatdistributionleadingtoimpaireddiaphragmatic

excursion,andthereforeaninabilitytoaugmentexercisetidalvolumesanyfurther.

Inonelarge,relativelyrecentstudy,164morbidlyobesefemales(BMI44.81.3kg/m2)

weredividedintotwogroups:thosewithanupperbodydistributionoffat(waisthip

circumferenceratio 0.80)andthosewithalowerbodydistributionoffat. Allsubjectswere

exercisedtothepointofmaximumeffort.Thosewithanupperbodydistributionoffathada

significantlyloweranaerobicthreshold,andasignificantlyhigherVO2max.Inaddition,the

groupwithupperbodyfathadasignificantlyhigherrespiratoryrateandminuteventilationat

bothanaerobicthresholdandmaximalexercise,whereastidalvolumedidnotdiffer

significantly.Maximalexerciseworkloadwasequivalentinthetwogroups.50Theresultsfrom

thisstudyimplythatthegroupwithupperbodyfatwassimplyunabletoaugmenttheirtidal

volumeasmuchasthegroupwithlowerbodyfat,andtheincreaseinminuteventilationwas

insufficienttomeetmetabolicneeds.Thehigheroxygenconsumptioninthegroupwithupper

bodyfatmayhavebeenduetoahigheroxygencostofworkofbreathing(seebelow).Further

studiesusingMRIquantificationanddeterminationoffatdistributionarenecessarytoconfirm

theseinterestingfindings.

DyspnoeaObesityhaslongbeenthoughttobeacauseofdyspnoea,especiallyonexertion,but

datasupportingthishasbeenscarce.Arelativelyrecent,largestudyinvolving16,171


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participantsshowedthatobesitywasariskfactorforselfreporteddyspnoea.Individualsinthe

highestquintileofBMI(>31.0kg/m2)hadanoddsratioof2.66(95%CI2.353.00,P=0.001)for

reportingdyspnoeawhenwalkingupahill,ascomparedwiththoseinthecontrolquintile(BMI

22.124.8kg/m2).IndividualsinthehighestquintileofBMIwerealsomorelikelytoselfreport

asthmaortohaveusedabronchodilatorinthelastmonth,butweretheleastlikelytoactually

haveairflowobstruction(8.7%,comparedwith12.8%ofthoseinthecontrolquintile,P=

0.001).52Thishighlightsthefrequencyofmisdiagnosisamongthesepatients.

Whataretheoriginsofobesityrelateddyspnoea?Thedatainthisregardare

inconclusive,andgiventhecomplexmechanismsunderlyingdyspnoea,53thecauseislikelyto

bemultifactorial. Manypotentialcauseshavebeeninvestigated.Inonestudy,28obese

patientsweredividedintotwogroups:thosewithmildtomoderatedyspnoeaandthosewith

severedyspnoea.AlthoughBMIdidnotdiffersignificantlybetweenthegroups(47.57and

48.76kg/m2,respectively)thegroupwithseveredyspnoeahadsignificantlylowerTLC,FRC

andERVvalues,andtendedtohaveahigherrespiratorydrive.54 Otherstudieshaveshownthat

dyspnoeainobesesubjectsisrelatedtorespiratorymuscleperformance23,55

orribcagemuscle

activity,56afferentfeedbackfromwhichisknowntocontributetothesensationofdyspnoea.

53

Furthersupportingtheideathatincreasedrespiratorymuscleworkleadstodyspnoeainthese

patientsistheobservationthattheyalsohaveanincreasedoxygencostofbreathing.

Itisalreadyknownthatobesepatientshaveahigheroxygencostofbreathing,evenat

rest.57Inarecentstudy,twogroupsofobesewomen,eightwithexertionaldyspnoea(BMI37

4kg/m2)andeightwithout(BMI365kg/m

2),wereinvestigated.Theywereexercisedata


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constantworkrateandalsounderwentaeucapnicvoluntaryhyperpnoeamanoeuvre.Their

perceptionsofbreathlessness,aswellastheoxygencostofbreathingweremeasuredduring

bothexperiments.Therewerenodifferencesbetweenthegroupswithrespecttopulmonary

functiontestsorrespiratorymechanics.Therewasastrong,statisticallysignificantrelationship

betweenoxygencostofbreathingandperceivedbreathlessness(Fig.4).Veryinterestingly,

therewerenodifferencesinpeakcardiovascularexercisecapacityorfatdistributionas

determinedbyMRI,betweenthegroups.58Itremainsunclearwhycertainobeseindividuals

haveahigheroxygencostofbreathingcomparedwithothers.

EffectsofweightlossonpulmonaryfunctionPerhapsoneofthebestwaysofstudyingtheeffectsofobesityonpulmonaryfunctionis

tostudythesamegroupofpatientsbeforeandafterweightloss.Itseemsthatmostofthe

changesassociatedwithobesityarereversedaftersignificantweightloss,andaretherefore

likelytobecausedbyobesityitself.ERV,thepulmonaryparameterthatismostconsistently

alteredinobesity,improvesafterweightloss.16,18,33,38,39,54,59,60

Onestudyshowedatriplingof

absoluteERVinpatientswhosemeanBMIdecreasedfrom45to39kg/m2afteraverylow

caloriediet.60Evenmodestweightloss(reductionofBMIfrom35to33kg/m

2)leadstomodest

butsignificantimprovementsinERV.33FRCandTLCalsoimprovetovaryingdegrees.

16,18,38,59,60

TheAaO2gradientalsotendstoimproveifBMIis>20kg/m2afterjejunoilealbypass.The A

aO2gradientislinearlycorrelatedwith BMI.39ThissupportsthehypothesisthatawidenedA

aO2gradientinobesityiscausedbyclosureofsomelungunitsfromaclosingvolumethatis

aboveERV,withresultantV/Qmismatch.Respiratorymuscleendurancealsoimproves,59

althoughmaximumvoluntaryventilationdoesnot.54AreductioninBMIfrom47.37.2to31.8


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5.1asaresultofgastricbypassledtoadecreaseinrespiratorydriveanddecreaseddyspnoea

in10patients.54Furtherstudyofthistopiccouldhelpexplainwhysomeobesepatients

experiencedyspnoea,whereasothersdonot.

Conclusion

Obesityhasmyriadeffectsonpulmonaryfunction.Respiratoryrateisusuallyincreased

inordertocompensateforthenormallydepressedtidalvolumes.Totalrespiratorysystem

complianceisdecreased;however,partitioningthisintochestwallandlungcomponentshas

shownconflictingresults.Lungvolumes,andespeciallyERV,arethemostconsistentlyaffected

respiratoryparameters. Oxygenationmaybeaffected,probablyasaconsequenceof

microatelectasisatthelungbases.Inindividualpatients,thedistributionoffatmaybemore

importantthanBMI.Notableomissionsfromthisreviewaretheeffectsofobesityon

respiratorymusclefunction,respiratorydrive,andupperairwaycollapsibility;thesetopicswill

beaddressedinotherreviewsinthisseries.Furtherresearchonthedistributionoffatandits

effectsmayhelptoelucidatethestillelusiveconceptsofdyspnoea,centralbreathtiming,and

chestwallmechanicsinobeseindividuals.


18/30

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Legendsforfigures:Figure1Summaryoftheeffectofobesityonlungvolumes.Expiratoryreservevolume(ERV)isdecreasedinobesity.Functionalresidualcapacity(thesumofERVandresidualvolume)is

usuallydecreasedaswell,buttoalesserextent,sinceRVisusuallyrelativelywellpreserved.

Tidalvolumeisusuallyreduced,butnottotheextentthatitisapparentinthisschematic.Total

lungcapacitycanbeslightlyreducedornormal.From:SoodA.Alteredrestingandexercise

respiratoryphysiologyinobesity.Clin.ChestMed.2009;30:445454.

Figure2Exponentialrelationshipbetweenexpiratoryreservevolume(ERV)andBMI.NotethatERVfallsbelowtherangeofnormal(


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Figure1


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Figure2


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Figure3


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Figure4

Obesity and Respiratory Function

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