Andersons pediatric cardiology 591
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exercise.Thiscanhaveimplicationswhentryingtointerpretstudiesperformed
semisupineorsupine(e.g.,usedinsomelabstofacilitateforstress
echocardiography).Thiscanbeanimportantconsiderationindiagnoseswhere
venouspooling,autonomicfunction,orlimitedstrokevolumeaugmentationare
particularlyrelevant,suchasposturalorthostatictachycardiasyndromeorinthe
Fontancirculation.
Anincreaseinheartrateistheprimarymechanismfortheincreasedcardiac
outputathigherworkrates.Thisisreflectedintheessentiallylinearrelationship
betweenheartrateandconsumptionofoxygenasworkratesincrease(seeFig.
23.4).Thereforetheabilitytoincreaseheartratenormallyduringexerciseis
essentialtoachievinganormalaerobiccapacity.Thedifferenceincontentof
oxygenbetweenthearterialandmixedvenousbloodgraduallywidenswith
increasingworkrateandconsumptionofoxygen,asaresultofincreased
extractionofoxygenbytheexercisingmuscles.Theby-productsofmyocytic
metabolism,includinghydrogen,carbondioxide,andlactate,alllowerthepH,
therebyshiftingtheoxygen-hemoglobindissociationcurvedownandrightward,
favoringincreasedunloadingofoxygenattheleveloftheexercisingmuscle.
Suchunloadingismorepronouncedathigherintensitiesofexercise,whenthe
concentrationofmetabolicby-productsisgreater.Thiswillbediscussedinmore
detaillater,intherelationshipbetweenconsumptionofoxygenandcardiac
output.
DistributionofBloodFlow
Forconsumptionofoxygentoincreaseduringexercise,itisessentialthat
cardiacoutputnotonlyincreasebutthatbloodflowispreferentiallyshuntedto
theexercisingmuscles(Fig.23.5).Atpeakexercise,bloodflowtoexercising
musclemaybe80%ormoreofthetotalcardiacoutput.Theredistributionof
bloodflowisachievedbyacombinationofautonomicandmetabolic
vasoregulatorymechanisms.18Exerciseisessentiallyastateofincreased
sympatheticnervoussystemtone,whichisregionallyoverriddenbymetabolic
vasodilation.Theincreaseinsympathetictoneassociatedwithexerciseresultsin
ageneralizedconstrictionoftheprecapillaryresistancearterioles.
Simultaneously,thesympathetictoneincreasesheartrateandcardiac
contractility,resultinginincreasedcardiacoutput.18–20Vasodilationoccursatthe
leveloftheexercisingmuscleasaresultoflocalmetabolicchanges.Aerobic
andanaerobicmetabolism,excitation-contractioncoupling,andbreakdownof
adenosinetriphosphateallresultinthereleaseofpotentvasodilatorsintothe
interstitialspaces.Thesevasodilatorsincludefreepotassiumandhydrogenions,
carbondioxide,lactate,adenosinediphosphate,andinorganicphosphate.The
resultisaprofoundvasodilationofthevascularbedintheexercisingmuscles.
FIG.23.5 Parallelcircuitsofflowthroughthevarioussystemsoforgans,
bothatrestandduringpeakexercise.Notethatthecardiacoutput
increasesbyapproximatelyfivefoldfromresttostrenuousexercise.In
contrast,therelativedistributionofflowtothevarioussystemsis
significantlydifferentfromresttopeakexercise.Inbothstates,thered
squaresareproportionaltothepercentageofcardiacoutputreceivedby
theparticularsystem.Notethattheflowofbloodtothemuscleincreases
frombetweenapproximately15%to20%ofcardiacoutputatrestto80%
to85%ofthecardiacoutputatpeakexercise.(FromAstrandP,RodahlK.
TheMuscleandItsContraction.TextbookofWorkPhysiology,
PhysiologicalBasesofExercise.3rded.McGraw-Hill;1986:12–53.)
Vasoconstrictionofthesplanchnicvascularbedresultsineithernochangeor
adecreaseinflowofbloodtothegutandkidneys.Theeffectontheoverall
peripheralvascularresistancedependsonthesizeoftheexercisingmuscle
groups.Duringdynamicexercise,suchasrunning,whichuseslargemuscle
groups,thenetresultisasignificantdropinsystemicvascularresistance,despite
