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Transcript
ExercisePhysiology:TheoryandApplicationtoFitnessandPerformance
ByScottPowers&EdwardHowley
Chapter4ExerciseMetabolism
SummaryCreatedbyDanHechler
ClassLectureExercisePhysiologyIDr.LaurieMilliken,UMassBoston,Fall2015
OxygenConsumption
-Pulmonaryoxygenuptake
-Oxygenmeasuredatlung,nottissues
-SteadyState
1.Oxygendemandismetbyoxygendelivery
2.Bloodlactatedoesn’taccumulate
3.Exercisecancontinueatthisrateuntillimitationsotherthanoxygenalterperformance
EnergyRequirementsatRest
-100%ofATPproducedbyaerobicmetabolism
-Bloodlactatelevelslow
-Resting02consumptionis.25L*min-1or3.5ml*kg-1*min-1
-Rest2/3fuelcontributedbyfats(betaoxidation)and1/3fuelcontributedbyCHO(aerobic
glycolysis)
OxygenDeficit
-TheperiodduringwhichlevelofoxygenconsumptionisbelownecessarytosupplyallATP
required.
-OxygendemandincreasesIMMEDIATELYandoxygenconsumptionlagsbehind.
-AnaerobicSystemsprimaryfuelsourceduringthisportion
-Trainedindividualshavealoweroxygendeficitduetotheirhigheraerobiccapacity(increased
cardiacoutput,largepercentageofblooddirectedtoactivemuscle,reachsteadystatemore
rapidlyakasmalleroxygendeficit,lessproductionoflacticacid.)
ReasonforLagofOxygen
-Inadequateoxygensupplytocontractingmuscles
-Delaybecausestimuliforoxidativephosphorylationrequiresometimetoreachtheirfinal
levelsandhaveafulleffect(ETCisstimulatedbyADPandPiandhasanincreasedeffectasPCis
brokendown)
OxygenDebtorEPOC
-Oxygenuptakeremainselevatedaboverestintorecovery
-“Repayment”forO2deficitatonsetofexercise
-EPOCreflectsthatonly20%elevatedO2consumptionusedto“repay”deficit
-Oxygendebt=VO2recovery-VO2pre-exerciseatrest(forsametimeperiod)
-QuantityofO2debt(litersofO2)dependsonintensityofexercisedone
2PortionsofOxygenDebt/EPOC
1.Rapidportionof02debt
-ReysnthesisofstoredPC
-ReplenishingmuscleandbloodO2stores
2.SlowportionofO2debt
-Elevatedheartrateandbreathing=increasedenergyneed
-Elevatedbodytemperature=increasedmetabolicrate
-Elevatedepinephrineandnorepinephrine=increasedmetabolicrate
-Conversionoflacticacidtoglucose(gluconeogenesis)
RemovalofLacticAcidFollowingExercise
-70%oflacticacidisoxidized(usedassubstratebyheartandskeletalmuscle)
-20%convertedtoglucose
-10%convertedtoaminoacids
Lacticacidisremovedmorerapidlywithlightexerciseinrecovery
-Optimalintensityis30-40%VO2Max
MetabolicResponsestoProlongedExercise
Hot/Humidenvironmentorathighintensity
-Upwarddriftinoxygenuptakeovertime
-Duetobodytemperatureandrisingepinephrineandnorepinephrine
MetabolicResponsestoIncrementalExercise
-Oxygenuptakeincreaseslinearlyuntilmaximaloxygenuptake(VO2Max)isreached
-VO2MaxphysiologicalceilingfordeliveryofO2tomusclewhichisaffectedbygeneticsand
training.
LactateThresholdorAnaerobicThreshold
-Pointwhichbloodlacticacidrisessystematicallyduringincrementalexercise
-Appearsat50-60%inuntrainedsubjects
-Appearsathigherworkratesfortrainedsubjects(65-80%)VO2Max
-Bestpredictorofenduranceperformance
-Bloodlactatelevelsreach4mmol/L
ExplanationsforLactateThreshold
-Lowmuscleoxygen(hypoxia)
-Acceleratedglycolysis(NADHproducedfasterthanitisshuttledintomitochondriaandexcess
NADHincytoplasmconvertstopyruvicacidtolacticacid
-Recruitmentoffast-twitchmusclefibers(LDH(LactateDehydrogenase)isozymeinfastfibers
promoteslacticacidformation)
-Reducedrateoflactateremovalfromblood
MechanismstoExplaintheLactateThreshold
PracticalUsesofLactateThreshold
-Predictionofperformance(CombinedwithVO2Max)
-Planningtrainingprograms
MarkeroftrainingintensitybychoosingtrainingHRbasedonLT
Lactatetheculpritofmusclesoreness?
• Lactateisoftentimesincorrectlyblamedforthemusclesorenessindividualsexperience
-DelayedonsetmusclesorenessorDOMS
-Experienced24to48hoursafterexercises
• PhysiologicalevidencerefutinglactateequallyDOMS
-Lactateremovalisrapid(within60minutes)postexercisesession
• TruecauseofDOMS?
-Microscopicinjuriestomusclefiberswhichleadstoinflammation
EstimationofFuelUtilization
Respiratoryexchangeratio(RERorR)
R=VCO2/VO2
ExerciseDurationandFuelSelection
Prolongedlowintensityexercise
-ShiftfromCHOmetabolismtowardfatmetabolism
-Duetoincreasedrateoflipolysiswhichisthebreakdownoftriglyerides->glycerol+FFAthrough
theenzymeHSL
-Stimulatedbyrisingbloodlevelsofepinephrine
InteractionofFatandCHOMetabolismDuringExercise
-“Fatsburnintheflameofcarbohydrates”
-Glycogenisdepletedduringprolongedhigh-intensityexercise
1.Reducedrateofglycolysisandproductionofpyruvate
2.ReducedKrebscycleintermediates(Oxaloacetate
3.Reducedfatoxidation(fatsaremetabolizedbyKrebscycle)
SourcesofCHODuringExercise
1.Muscleglycogen,primarysourceofCHOduringhighintensityexerciseandsuppliesmuchof
CHOinfirsthourofexercise
2.Bloodglucose
-Fromliverglycogenolysis
-PrimarysourceofCHOduringlow-intensityexercise
-Importantduringlong-durationexercise(asmuscleglycogenlevelsdecline)
SourcesofFatDuringExercise
1.Intramusculartriglycerides
-Primarysourceoffatduringhighintensityexercise
2.PlasmaFFA
-Fromadiposetissuelipolysis(Triglyerides->glycerol+FFA
-FFAconvertedtoAcetyl-CoAandentersKrebscycle
-Becomesmoreimportantasmuscletriglyceridelevelsdeclineinlong-durationexercise
CHOFeedingviaSportsDrinks
-DepletionofmuscleandbloodCHOstorescontributestofatigue
-IngestionofCHOcanimprovesenduranceperformance
-Duringsubmaximal(<70%VO2max),longduration(>90minutes)exercise
-30-60gramsofCHOperhourarerequired
-Mayalsoimproveperformanceinshorter,higherintensityevents
SourcesofProteinDuringExercise
1.Proteinsbrokendownintoaminoacids
-Musclecandirectlymetabolizebranchchainaminoacidsandalanine
-Livercanconvertalaninetoglucose
2.Contributes(approx.2%)tototalenergyproductionduringexercise
-Mayincrease5-10%lateinprolonged-durationexercise
LactateasFuelSourceDuringExercise
1.Canbeusedasfuelsourcebyskeletalmuscleandheart
-ConvertedtoAcetyl-CoAandentersKrebscycle
2.Canbeconvertedtoglucoseintheliver
-CoriCycle
3.Lactateshuttle
-Lactateproducedinonetissueandtransportedtoanother
TheCoriCycle
•
•
•
Lactatecreatedbyskeletalmuscleistransportedtotheliver
Liverthenconvertsthelactatetoglucosethroughgluconeogenesis
Newglucoseistransportedbacktomuscleandisutilizedasfuel