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Extremely short duration high intensity training substantially improves insulinaction in young sedentary males

BMC Endocrine Disorders 2009, 9:3 doi:10.1186/1472-6823-9-3

John A Babraj ([email protected])Niels BJ Vollaard ([email protected])

Cameron Keast ([email protected])Fergus M Guppy ([email protected])

Greg Cottrell ([email protected])James A Timmons ([email protected])

ISSN 1472-6823

Article type Research article

Submission date 10 September 2008

Acceptance date 28 January 2009

Publication date 28 January 2009

Article URL http://www.biomedcentral.com/1472-6823/9/3

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Extremelyshortdurationhighintensityintervaltrainingsubstantiallyimproves

insulinactioninyounghealthymales

1JohnABabraj*,1NielsBJVollaardNBJ*,1CameronKeast,1FergusM

Guppy,1GregCottrelland1,2JamesATimmons

1TranslationalBiomedicine,SchoolofEngineeringandPhysicalSciences,

Heriot-WattUniversityEdinburgh,Scotlandand2TheWenner-GrenInstitute,

ArrheniusLaboratories,StockholmUniversity,Sweden.

*Theseauthorscontributedequallytothiswork

E-mailaddresses

JAB [email protected]@hw.ac.ukCK [email protected] [email protected] [email protected] [email protected]:

ProfessorJamesATimmons

TranslationalBiomedicine,

Heriot-WattUniversityEdinburgh

RiccartonEH144AS

Scotland,UK


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Abstract

Background: Traditional high volume aerobic exercise training reduces

cardiovascular and metabolic disease risk but involves a substantial time

commitment.Extremely lowvolumehigh-intensity interval training(HIT) has

recentlybeendemonstratedtoproduceimprovementstoaerobicfunction,but

it is unknown whether HIT has the capacity to improve insulin action and

henceglycemiccontrol.

Methods:Sixteenyoungmen(age:212y;BMI:23.73.1kgm -2;VO2peak:

489mlkg-1min-1)performed2weeksofsupervisedHITcomprisingofatotal

of 15 min of exercise (6 sessions; 4-6 x 30-s cycle sprints per session).

Aerobic performance (250-kJ self-paced cycling time trial), and glucose,

insulin and NEFA responses to a 75-g oral glucose load (oral glucose

tolerancetest;OGTT)weredeterminedbeforeandaftertraining.

Results:Following2weeksofHIT,theareaundertheplasmaglucose,insulin

and NEFA concentration-time curves were all reduced (12%, 37%, 26%

respectively,allP


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middleagedsedentarypopulationswhootherwisewouldnotadheretotime

consumingtraditionalaerobicexerciseregimes.

Background

Theprevalenceoftype2diabetes(T2D)israpidlyincreasingworld-wideand,

forexample,intheUnitedStatesitreached17.5millionpeoplein2007[1].

Aside from the associated reduction in quality-of-life and the increase in

morbidityandmortalityfortheaffectedindividuals,theeconomicburdenwas

estimated at$116 billion inexcessmedical expenditures and $58 billion in

reducedproductivity[1].Similarly,theestimateddirectandindirecteconomic

costsofcardiovascular disease (CVD) in theUSfor 2008are estimatedat

$287billion[2].

The risk of developingCVD andT2D can be modified by regular physical

activity[3].However,thereisnoconsensusonthenatureofexercisetherapy

required toprovideadequatehealth benefits, particularly with regard to the

volume-intensity relationship. Furthermore, as we do not understand the

precise mechanisms which link physical activity and a reduced risk of

developing CVD or T2D, the scientific rationale for current health guides

needstobeimproved[4].Forexerciseguidelinestoyieldapositiveeconomic

benefit for society, as well as a health benefit for the individual, not only

should the regime reliablymodify key disease risk factors, itmust also be

plausibletoimplement.


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Metabolic adaptations associated with traditional aerobic exercise training

correlate with improved insulin action and glycemic control [5, 6]. These

effects appear to be independent of changes inbody composition [7], and

someevidencesuggeststhatgreaterimprovementsininsulinsensitivitymay

beachievedwithhigher trainingintensities[8-10].Current recommendations

for improving glycemic control involve performing moderate to vigorous

intensityaerobicandresistanceexerciseforseveralhoursperweek[11,12].

However, the generalpopulation fails to followsuch regimesdue to lackof

time,motivationandadherence[13].Thissuggeststhatthecurrentfocuson

time-consumingmoderateintensityphysicalactivity,aimedatincreasingtotal

energyexpenditure,may not beoptimal for reducing the riskofdeveloping

T2D.

Recently an extremely low volume high-intensity interval training paradigm

(HIT),consistingofnomorethan7.5minutesofexerciseperweek,hasbeen

proposed as a novel, time-efficient exercise regime for improving aerobic

fitness [4, 14]. We speculated that it should be possible to substantially

improve insulin action using HIT despite a negligible contribution to total

energyexpenditureasthistrainingmodelwouldsubstantially reducemuscle

glycogen stores. Compared to traditional strategies for reduction of risk

factorsofCVDandT2D,theextremelylowvolumeofexerciserequiredwith

HIT may promote adherence and thus represent a genuinely preventative

publichealthstrategy.

Methods


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Subjects

Twenty-five young healthy sedentary or recreationally active men were

recruited to participate in this study, with none engaged in a structured

endurancetrainingprogram.Subjectswererandomlyallocatedtooneoftwo

partsofthestudy.Sixteensubjects(meanSD:212y;8217kg;1.830.08

m;BMI:23.73.1kgm-2;VO2max:489mlkg-1min-1)wereallocated tothe

mainpartofthestudy,andcompletedthefullexperimentalprocedures.The

remainingninesubjects(meanSD:238y;739kg;1.780.09m;23.01.4

kgm-2;VO2max: 4711mlkg-1min-1) tookpart ina separateexperiment to

determine intra-individual variation in response toanoralglucose tolerance

test,anddidnotperformHIT.Therewerenosignificantdifferencesintheage,

height,weight,BMIorVO 2maxbetweenthetwogroupsofsubjects.Subjects

wereinformedoftheexperimentalprotocolbothverballyandinwritingbefore

givinginformedconsent.Furthermore,allsubjectswereinformedabouthow

potential life-style changes could affect the results of the study, and were

requested tomaintaintheir normaldietandlevelsofphysicalactivity (apart

from the training program) throughout the durationof the study. The study

protocolwasapprovedbytheinstitutionalEthicsCommitteeandconductedin

accordancewiththeHelsinkiDeclaration.

Experimentalprocedures

Baselineaerobicperformanceandhealthparametersweredeterminedovera

2-weekperiodpriortocommencementofthetrainingprogram.


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Oralglucosetolerancetest(OGTT)

Subjectsrefrainedfromperforminganystrenuousphysicalactivityfor2days

prior to the OGTT, and attended the laboratory having fasted overnight.

Venous bloodsampleswere collected byvenepuncture before, and 60, 90

and120minafteringestionof75gglucose(FisherScientific,Loughborough,

UK)dissolvedin100mlofwater.Plasmawasseparatedbycentrifugation(10

minat1600g)andstoredat-20Cuntilanalysisofglucose,insulinandNEFA

concentrations. Plasma glucose concentrations were measured using an

automaticanalyzer(YSIStat2300,YellowSpringInstruments,YellowSpring,

OH) and plasma insulin concentrations were determined by ELISA

(Invitrogen,UK).Plasmainsulinwasmeasuredonlyforsamplestakenat0,

60, and 90 min. Plasma NEFA concentrations were determined by a

colorimetric assay (Wako Chemicals, Germany) using a modified protocol.

Briefly,3.75lofplasmasamplesandstandardsofknownconcentrationwere

pipettedintoa96-wellplate.75lofcolourreagentAwasaddedtoeachwell

andincubatedat37Cfor10min.150lofcolourreagentBwasaddedand

incubatedfora further10minat37C.Theplatewasthenremovedfromthe

incubator and allowed tocool to roomtemperature prior to theabsorbance

being read at 550 nm. Coefficients of variation (CV) for duplicate samples

were3%forglucose,5%forinsulin,and8%forNEFAs.

VO2peaktest

On a separate occasion, subjects performed an exhaustive incremental

cyclingtest(LodeExcaliburSport,Groningen,theNetherlands)todetermine

maximal power output (Wmax) and maximal oxygen uptake capacity


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(VO2peak)usinganonlinegasanalysissystem(SensorMedics,Bilthoven,the

Netherlands).Aftercyclingat30Wfor1min,poweroutputwasincreasedby

30Wmin-1untilvolitionalexhaustion.VO2peakwasdeterminedasthehighest

valueachievedovera20-speriod.

Timetrials

Endurance performance was determined to provide an integrated

physiological readout to facilitate comparison of the present study with

previous studies which provided data from muscle biopsy samples [15].

Subjects performed two self-paced cycling time trials in which they were

instructedtocomplete250 kJ ofworkas fastaspossible.The linear factor

waschosentoproduceapoweroutputcorrespondingto75%ofWmaxata

pedal rate of 90 rpm. No encouragement was given, and subjects were

blinded from information on time, power output and pedal frequency. The

amountofwork(kJ)completedwascalledoutevery25kJ.Timetrialswere

spacedatleasttwodaysapart.Althoughthefirstofthetwopre-trainingtrials

wasmainlyusedasafamiliarisationtrial,thefastesttimeachievedinthetwo

trialswasconsideredtobestrepresentthepre-trainingperformanceleveland

usedintheanalysis(19outof25subjectsperformedbetterinthesecondtrial

thaninthefamiliarisationtrial).

Sprintintervaltraining

The sprint training protocol was similar to that used previously by

Burgomasteretal.[4,14].Sixsessionsofsprintintervalexercisewerespread

over14days,with1or2daysofrestbetweeneachsession.Each training


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session consisted of 4-6 repeated 30-s all-out cycling efforts against a

resistanceequivalent to7.5%ofbodyweight (Wingate tests),with4minof

recoverybetweensprints.Duringrecovery,subjectsremainedonthebikeand

either rested orcycledata lowcadencewithout resistance.Thenumberof

sprints increased from4during the first twosessions, to5 in the thirdand

fourthsessions,and6inthelasttwosessions.Totaltimecommitmentwas

17-26minpersession,involvingonly2-3minutessprintexercise.

Post-trainingassessment

AsecondOGTTwasperformedaftercompletionofthetrainingprogram.In

order to determine whether potential changes were due to acute effects

attributabletothelasttrainingsession,subjectsweretestedeithertwo(n=10),

orthree(n=6)daysafterthelastboutofexercise.Onedayafterthesecond

OGTT subjects performed a third cycling time trial in order to determine

changesinaerobicperformance.

Intra-individualvariabilityintimetrialperformanceandOGTT-response

Inordertoassessnormalintra-individualvariationinresponsetoanOGTT

overaperiodof severalweeksas used inthepresentstudy,ninesubjects

performedan identical protocol to thetraininggroupbutwithoutperforming

the six training sessions. Coefficients of variation (CV) for repeated

measurements within individual subjects were determined for baseline

glucose and NEFA levels, for glucose and NEFA area under the plasma

curve,andfortimetrialperformance.


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Calculationsandstatisticalanalysis

Areaunder the plasmacurve(AUC)was calculated using the conventional

trapezoid rule. The Cederholm index, which represents peripheral insulin

sensitivity[16],wascalculatedusingtheformula:

ISICederholm=75000+(G0-G120)1.151800.19BW/120Gmeanlog

(Imean)

WhereBWisbodyweight,G0andG120areplasmaglucoseconcentrationat0

and120min(mmoll-1),andImeanandGmeanarethemeaninsulin(mUl-1)and

glucose(mmoll-1)concentrationsduringtheOGTT.

AlldataarepresentedasmeansSEM.Plasmaglucose,insulin,andNEFA

responsestothepre-trainingandpost-trainingOGTTswereanalyzedusing

two-way repeatedmeasuresANOVAwith post hoc StudentNewman-Keuls

tests. Differences between pre-training and post-training data for time trial

performance,AUCsforplasmaglucose,insulin,andNEFAlevels,andinsulin

sensitivityasmeasuredbytheCederholmindexwereanalyzedusingpaired

samplet-tests.Pearsonscorrelationcoefficientwasusedtoassessbivariate

correlations between baseline values of, and changes in the variables

performance, AUCs of glucose, insulin, and NEFAs, and the Cederholm

Index.SignificancewasacceptedatP


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Fastingplasmaglucoseconcentrationswereunalteredafter2weeksofHIT.

Inthepre-trainingOGTT,plasmaglucoseconcentrationwaselevated60min

afterthe75gglucosebolus(Figure1A;0min:5.00.1v60min:6.50.4

mmoll-1;P


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There was a trend towards a decrease in baseline plasma NEFA

concentrationsfollowingHIT(Figure1C;pre:35036moll-1vpost:290

39moll-1,P=0.058).Inthepre-trainingOGTT,plasmaNEFAconcentration

wasdecreased60minafterthe75gglucosebolus(Figure1C;0min:350

36moll-1v60min:25548moll-1;P


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Improvementsinglucose,insulin,andNEFAresponsesweresimilarwhether

assessed two or three days following the final training session (mean

reductioninglucoseAUC:2dpost1210%,3dpost194%;insulinAUC:2

dpost349%,3dpost389%;NEFAAUC,2dpost2321%,3dpost27

9%).

Intra-individualvariationintimetrialperformanceandresponsetoanOGTT

In subjects not performing the HIT program, no significant differences

between the first and second OGTTs were observed for plasma glucose

(AUC:67147v65940mmolminl-1)andNEFAs(AUC:240351611v

22599 2544 molminl-1), nor for time trial performance (1477214 v

1491245s).Coefficientsof variationfor the repeatedmeasurementswere

2.1% for the time trial, 4.9% and 7.0% for fasting glucose and NEFA

concentrations,and8.1%and8.2%forglucoseandNEFAAUCsrespectively.

Discussion

Whileregularexercisetrainingrepresentsoneofthemostpowerfulstrategies

toreducethedevelopmentofmetabolicdiseaseinhealthyadults[17],most

adults failtomeet currentguidelinesforparticipation [18].Theseguidelines

largely focus on the time spent carrying out moderately intense activity (or

totalenergyexpenditure),typicallyrequiremanyhoursofexerciseeachweek

and can fail to modify risk factors relevant for disease prevention [19]. In

addition, as time commitment is perceived as a major barrier, driving or

contributing to low compliance, then these guidelinesmaynot be themost

logical approach for improving public health. In the present study we


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demonstrateforthefirsttimethatonlyafewminutesofhighintensityinterval

exerciseperformedovertwoweeksisrequiredtosubstantially improveboth

insulin action and glucose homeostasis in sedentary youngmales. This is

both a physiologically important observation and potentially useful as it

highlightsapreventativeinterventionthatcouldlogicallybeimplementedas

an early strategy to prevent age related development of cardiovascular

disease.

Interestingly,despiteemployinglong-termtraininginterventions(2-16months)

the majority of studies investigating classic aerobic [10, 20-25] or strength

training programs [26-28] have observed only a reduction in insulin area

under the curve (AUC) in response to a glucose load following training,

without a concomitant reduction in glucose AUC, indicating only a partial

improvementininsulinaction.Furthermore,walkingbasedinterventionsmay

not reduce risk factors in the target populationwhereprevention is the key

objective[19].Somelongitudinalexercisestudieshaveshownreductionsin

glucose AUC [29-31], but post-training OGTTs were performed within 24

hoursofthelastexerciseboutandthereforereflectthecombinedimpactof

acute and chronic exercise [32]. In contrast, Hughes et al demonstrated

reduced glucose AUC in elderly subjectswithout a concomitant change in

insulinAUC[33].

Thelowvolume,highintensitytrainingutilizedinthecurrentstudysignificantly

reducedbothglucoseAUC(-12%)and insulinAUC(-37%),withasustained

improvedinsulinactionuntilatleastdaythreeafterthelastexercisesession.


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Thiswasachievedwithoutchangesinbodyweight,andwithaweeklyenergy-

cost of training of ~225 kcal during the first trainingweek and ~275 kcal

during the second training week. This very modest increase in calorie

consumption is in stark contrast to the ~2000-3000 kcalweek-1 consumed

duringatypicalaerobictrainingprogram[25,34].Thisimplies,butdoesnot

prove,thatthemechanismunderpinningthebenefitsweobservedwithHIT,

maybedistinctfromthoseresponsibleforthemoremodestimprovementsin

insulinactionwithclassictime-consumingaerobictraining.Whilemuchfocus

isbeinggiventoincreasingcalorieconsumptiontowardoffweightgain,itis

clear that improving metabolic fitnessmay be just as important as limiting

gainsbodymassindex.

Failure for insulin to adequately control blood glucose following a meal is

knownasinsulinresistance.Skeletalmuscle isconsideredthemajortissue

responsiblefortheuptakeofglucosefollowingameal,oraglucoseorinsulin

challenge [35] such that it is entirely reasonable to assume that the

improvement in glucose and insulin AUC observed in the present study

reflected improved muscle glucose uptake. The limiting step in glucose

disposal is considered to be its transport into the skeletal muscle [6] and

GLUT4 is the most abundant glucose transporter in skeletal muscle.

IncreasedGLUT4concentrationwithendurancetraininghasbeensuggested

tobeanimportantfactorregulatinginsulinsensitivity[6,33].Burgomasteret

al. reportedthatskeletalmuscleGLUT4 levels increaseby ~20%afterone

weekofHIT,andremarkablyremainedelevatedover6weeksoftrainingand

asubsequent6-weekperiodofdetraining[14].Giventhesimilaritybetween


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ourstudyandtheaerobicperformanceimprovement,protocolsandsubjects

in the Burgomasteret al studies, these studies shouldbecomparable and

thus an increase in GLUT4 may partly explain our findings. However,

increasedGLUT4concentrationdoesnotalwaysfullyexplaintraining-induced

improvementsininsulinsensitivityandkeyregulatoryproteinsdown-streamin

the insulin signalling pathway are more activated in response to insulin

following aerobic training [36]. HIT produces similar changes in skeletal

musclemarkersofcarbohydrateandlipidmetabolismtoaerobictraining[37],

soitshouldbeinvestigatedwhetherHITalsoproducessimilaradaptationsof

the insulin signalling pathway as seen following traditional aerobic training

[36].

Improvedwholebodyglucosedisposalfollowingtraininghasbeenassociated

withanincreaseininsulinstimulatedglycogensynthesis[38].HIThasatleast

twonovelfeatures,firstlyunlikewalkingormoderateintensityaerobictraining,

it involves the activation of a large muscle mass and secondly this is

associatedwithaveryhighglycogenbreakdown-turnover.Thecombinationof

thesetwofactorsmeansthatagreaterproportionofmusclefibreswillneedto

replenish their carbohydrate stores, compared with what would be

encounteredfollowingmoderateintensityaerobictraining.Musclecontraction

underconditionsofmetabolicstress(suchasincurredduringHIT)resultsin

veryrapidglycogendegradation[39]andthiswouldalmostcertainlyalterthe

bindingofavarietyofglycogenassociatedproteins[40,41].Thuswesuspect

that remodelling of the glycogen pool, altering the molecules branching

architecture[38],maywellbeimportantinregulatingskeletalmuscleinsulin


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sensitivity following HIT. Currently, high intensity muscle contraction is the

only feasiblestrategy for remodellingof the entiremuscle glycogenpool in

humans.

Insulin sensitivity may also be regulated by plasma NEFA concentration.

Pharmacological lowering of plasma NEFA levels has been shown to

positively regulate insulin sensitivity during anOGTT [39], whereas raising

plasmaNEFA concentration, through lipid infusion, lowers glucose infusion

rateduringperipheralinsulinemia-euglycemiainyoungmen[40].Incontrast,

exercisetraininghasbeenshowntohavelittleornoeffectonfastingplasma

NEFA concentration, insulin mediated lipolysis or NEFA release during

exercise [41-44]. In the present study, HIT was associated with a 17%

decrease in fasting plasma NEFA concentration without a concomitant

changeinfastinginsulin.Furthermore,therewasa26%reductioninNEFA

AUC during OGTT following HIT despite a 37% reduction in the plasma

insulinAUC.Thissuggeststhatinsulinwasabletoinhibitlipolysistoagreater

extent followingHIT andwhile these changesaremoremodest than those

observedwith lipidpoweringdrugs, the long termsbenefitsmay still beof

significance.

Conclusion

We demonstrate for the first time that low volume, high intensity interval

exerciseinvolvingonly~250kcalofwork,issufficienttoachievesignificant

improvements in glycemic control in sedentary young adults. This study is

limitedtothemeasurementofwholebodyinsulinsensitivitywhichmakesthe


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interpretation of our data incomplete. Analysis of tissue specific responses

through biopsy studies would enhance the present study by allowing

determinationofthemechanisms involvedin theimprovementsobservedat

thewholebodylevel.Nevertheless,ourdataandthefindingsbytheGibala

lab[4,37,45-49]suggestthatcurrentguidelines,withregardstooptimizing

exerciseprescription toyield thebest healthoutcomes,maynotbeoptimal

andcertainly requirefurtherdiscussion.Ourfindingswarrant furtherstudies

investigatingtheeffectivenessofHITinimprovingglycemiccontrolinhealthy

middleagedindividualsatriskofdevelopingT2DandinpatientswithT2D.

CompetingInterests

Noauthorsreportanycompetinginterests

Authorscontribution

JBandNBJVparticipatedinthestudydesign,analysis,writingandeditingof

themanuscript,CK,FMGandGCparticipatedindatagenerationandstudy

analysis.JATconceivedthestudyideaandparticipatedinthestudydesign,

writingandeditingofthemanuscript.

Acknowledgements

WewouldliketothanksMartinJGibalaforhisinsightfulcommentsduringthe

preparationofthisstudyandmanuscript.

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Figure1 Responsetoanoralglucoseloadpre-andpost-HIT.PlasmaconcentrationsandAUCforA:glucose,B:insulinandC:NEFAs.(*:P


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