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EditorialOfficeNotes:
RES 11479.R1
INVITEDREVIEWSERIES:ObesityandRespiratorydisordersSeriesEditor:AmandaJPiperReceived:15August2011
Invitedtorevise:24August2011Revised:29August2011
Accepted:3September2011
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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
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
8/3/2019 Obesity and Respiratory Function
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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
8/3/2019 Obesity and Respiratory Function
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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.
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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