Muscularcompensationandlesionoftheanteriorcruciateligament:ContributionofthesoleusmuscleduringrecoveryfromaforwardfallP.Colnea,P.Thoumiea,b,c,*aINSERMUMRS731,33boulevarddePicpus,75012Paris,FrancebUniversite PierreetMarieCurie-Paris6,33boulevarddePicpus,75012Paris,FrancecServicedeRe e ducationNeuro-orthope dique,HopitalRothschildAPHP,33boulevarddePicpus,75012Paris,FranceReceived9November2005;accepted4April2006AbstractBackground. Knee stability following an anterior cruciate ligament lesion has been widely studied. Only recent studies focused on thecontributionofthesoleusmuscle.Ourpurposewastocharacterizethedynamicandmuscularactivityofbalancerecoveryinhealthysubjects and patients with an anterior cruciate ligament rupture. The role of the soleus was investigated in the ipsilateral compensationdevelopedtostabilizethekneeandinthecontralateralcompensationtorecoverbalance.Methods. Twelve anterior cruciate ligament decient patients, ten anterior cruciate ligament repaired patients and 14 control subjectswererecordedduringaforwardfallinvolvingsteppingtorecoverbalance.Findings.Thedynamicofthecentreofgravityremainednormalwhencomparedtothecontrolgroupregardlessofthetreatment,suggesting an adapted compensation to knee instability in this situation. A bilateral increase in soleus activity was related to an increasedduration in the balance recovery process in all patients. Patients used one of two strategies to recover balance regardless of the treatment:reducingthesteplength, involvinganearlyrecruitmentofthesoleusbeforeheel contact, oranticipatingbrakingwithasimilarsteplengthrequiringapredominantactivityofthehamstrings.Interpretations.Theseresultssuggestthatbilateralactivityofthesoleusisinvolvedtocompensateforinstabilityandhighlightthecontributionof thesoleustorehabilitationafterananteriorcruciateligament lesion, not onlyasacompensatorymuscleactingatthekneelevelbutalsoatahigherlevelinthebilateralcontrolofstance.2006ElsevierLtd.Allrightsreserved.Keywords: Anteriorcruciateligament;Neuromuscularcontrol;Soleusmuscle;Balancerecovery1.IntroductionThe control of postural balance depends on various sys-tems(nervoussystem, locomotorapparatus). Alesioninanyof thesecanleadtoaperturbationof postural reac-tions.Inclinicalpractice,pathologymayassociateseverallesionsthatperturbthecontrolofequilibrium.Thisisthecase followingalesionof the anterior cruciate ligament(ACL) when there persists a risk of knee instability (Noyeset al., 1983), linkednot only tothe suppressionof themechanical propertiesoftheligamentbutalsotothelossof theproprioceptivecontrol of thejoint exertedbythemechanoreceptors of the ACL (Adachi et al., 2002; Johans-sonetal.,1991).After an ACL injury, some people (called copers) areable to return to their daily and sporting activities, stabiliz-ingtheir kneewithout requiringsurgical repair, whereasothers (callednon-copers) cannot (Noyes et al., 1983;Rudolphet al., 2001). For thesepatients, surgical repair0268-0033/$-seefrontmatter 2006ElsevierLtd.Allrightsreserved.doi:10.1016/j.clinbiomech.2006.04.002*Correspondingauthor.E-mailaddress:philippe.thoumie@rth.aphp.fr(P.Thoumie).www.elsevier.com/locate/clinbiomechClinicalBiomechanics21(2006)849859of the ligament restores the mechanical stability of theknee. However, whether the proprioceptive aerences afteran ACL reconstruction can be regenerated remains contro-versial(Bonmetal.,2003;Iwasaetal.,2000).In all cases, an understanding of the muscular synergiesrequired to regain a stable knee after an ACL lesion is cru-cial indevisingappropriate rehabilitation. Manystudies(Berchucket al., 1990; Alkjaer et al., 2003; Beardet al.,1996; Boerboometal., 2001; Kvist, 2004; Rudolphetal.,2001; Torryetal., 2004)havesoughttodeterminewhichcompensationsareappliedwithanACLlesion(repairedor not) especiallyduringthestancephaseof gait. Thesestudies have shown various neuromuscular, kinematicand kinetic adaptations, but have not identied a commonknee stabilisation strategy in subjects who compensate wellandrecovernormalkneefunction.Thestudyofmuscularsynergies stabilizing the knee after an ACLlesion hasfocussedprimarilyonthehamstrings, thequadricepsandthegastrocnemiusmuscles(Solomonowetal., 1987; Bar-atta et al., 1988; Lass et al., 1991), which are directlyresponsible for mediating the motor function and the activestabilityoftheknee. FewstudieshaveinvestigatedsoleusmuscleactivityafteranACLlesion(Ciccotti etal., 1994;Rudolph and Snyder-Mackler, 2004; Rudolph et al., 2001).Tworecentstudies(Sherbondyetal.,2003;Eliasetal.,2003),however,suggestthatonefunctionofthesoleusinaclosedkineticchaincouldbetohelpprotect theACLby pulling back the proximal part of the tibia and prevent-ingits anterior displacement. However, theexperimentalprotocolof thesestudies did not correspond to a real situ-ation of loading on the knee. Because the soleus is involvedincontrollinguprightposture, thekinesiological studyofthesoleusmustbepairedwithaglobalevaluationofbal-ance; several authors have highlighted a bilateral perturba-tion of the unilateral stance after a ligament lesion(Lysholmetal.,1998).SincecompensationsofanACLlesionarefoundwhenthekneeis unstable(especiallyinaclosedkineticchainwhenthestressesarehigher),thestudyofsituationsotherthan normal gait have been proposed (Alkjaer et al., 2002;Rudolph and Snyder-Mackler, 2004) to analyze knee insta-bilityafteranACLlesion.Andso, thestudyofbalancerecoverycouldconstituteaninterestingparadigmtocharacterizetheadaptationofthemotorcommandwhenfacedwithasituationofinsta-bility. Preventing a fall when starting from an inclined posi-tion, anexperimental paradigminitiallydescribedbyDoetal.(1982),impliestheuseofanadaptedstrategywhichaimstopreventthefall ofthecentreofgravitybytakingseveralsteps.Severalauthorshavedescribedthecontribu-tion of the soleus in this process and their relationship withthe dynamics of the centre of gravity (Do et al., 1982, 1999;ThoumieandDo,1996).The aim of this work was to study the dynamics of bal-ancerecoveryandthemuscularactivitiesafteraforwardfall inpatientspresentinganACLlesion, andincontrolsubjects. Ourhypotheseswerethatchangesintheactiva-tionofthesoleuscouldbeassociatedwithadierentbal-ance recoverystrategyafter anACLlesion(repairedornot), andthat surgical restorationof thestabilityof theknee should be associated with a modication of the strat-egy used by the ACLDsubjects. Moreover, a bilateralstudyof the soleus wouldalsohelpdistinguishbetweenthe compensation directly linked to the lesion in ipsilateralmuscularactivityandthatof contralateral activitywhichaimstocontrolgeneralbalance.2.Methods2.1.PatientsThreegroupsofsubjectstookpartinthestudy:acon-trolgroupcomprising14healthysubjectswithnopathol-ogy of the knee, a group of 12 ACL decient knee patients(ACLD) having an unilateral lesion of the ACL conrmedclinically (Lachman test) and by magnetic resonance imag-ing, a group of 10 ACLknee surgically reconstructedpatients (ACLR) with an unilateral lesion of the ACL con-rmed during surgery. Knee joint pain, eusion and limita-tionofthefull kneejointrangeofmotionwereexclusioncriteria of the study.Two of the patients were regular participant in high levelsportactivitiesandsurgicallytreated2.5monthsafterthelesion. All others were recreational sport participants, onlyparticipating occasionally in sport activities like skiing andjoggingduringholidays.Theyweresurgicallytreatedonlyiftheyexperiencedinstabilityofthekneeduringdailylifesincetheirlesion. All reconstructedpatientsweretreatedby the technique of Kenneth Jones except one recon-structedbythetechniqueofMacIntosh.Most of thepatients havingarelativelypoor level offunctional activitiestheywereassessedbeforethetest bya questionnaire relevant totheir capacities for walking,goingupanddownstairsandjogging.Atthetimeofthetestallpatientsarmedtofeelnodiscomfortindailylifeactivities. Laxityof thekneejoint wasassessedclinicallyand qualitatively by the same evaluator manually perform-ingtheLachmantest. All ACLDpatientsshowedsigni-cant drawersigns bycomparisontoACLRsubjects andcontrol group. The force of the quadriceps assessedbythe maximal voluntary isometric contraction manuallyresisted (break test) and by squatting ability was consideredasnormal.Thebalancerecoverytestwasperformedatleastthreemonths after the initial lesion(0.253years) or surgicaltreatment (0.453.5 years). Acomparison of the timeelapsed between the test and the lesion or the surgery(respectively22(21) monthsinACLDand11(12)monthsinACLR) didnot showstatistical dierencewithregardtothe treatment (Wilcoxontest, P = 0.34). All patientsunderwent6weeksofrehabilitationprogramsfromvari-ousphysiotherapistsinprivatepracticesorrehabilitationcentres. Thethreegroups of subjects werehomogeneousin terms of height [1.73(0.1) min CTL, 1.7(0.09) min850 P.Colne ,P.Thoumie/ClinicalBiomechanics21(2006)849859ACLDand1.78(0.09) minACLR], age[29(11) years inCTL, 38(10) years inACLDand27(8) years inACLR],andweight [73(10) kginCTL, 74(11) kg inACLDand76(13) kginACLR].Allsubjectsrstgavetheirinformedconsent.2.2.MaterialWe usedthe experimental paradigmdescribedbyDoetal. (1982). Inthisparadigm(Fig. 1), thesubjectstandsonaforceplateinaforwardinclinedposture(15). Thebodyis straight, the arms hangalongside the bodyandthe eyes look straight ahead. The subject is held by arestrainingdevicecomposedof anabdominal belt andahorizontal steel cable connected to an electromagnetmountedonadynamometer.Thedeviceisreleased,with-out the subjects knowledge, causing the subject to fall for-ward. The subject is instructed to take a fewsteps torecoverbalance.A60 120 cmAMTI forceplate(AMTI, Watertown,MA, USA) recorded the ground reaction force. Data wererecorded with a sampling rate of 500 Hz. Recordingsstarted50 ms beforethereleaseof therestrainingdeviceandcontinuedfor850 msafterward. Eachtrial wasana-lyzed individually. Then, the values of each parameter wereaveragedforeachsubject, andthetotal meanvaluewascalculatedforallthesubjectsofthesamegroup.ThesurfaceEMGactivityofvemuscles:soleus,tibia-lis, hamstrings medial (semi tendinosus) and lateral (femo-ris biceps), rectus femoris (quadriceps) was recorded in themoving limb then in the stance limb for the control group.A special attentionwas paid to characterizethe activityofthe soleus. Electrodes were placed at the medial part of theshank near the tibial bone to avoid cross-talk withgastrocnemius.Forthepatientgroup,thesamemuscleswererecordedontheinjuredside. Whenbalancewasrecoveredbystep-ping with the injured side, the activity of the soleus and tib-ialis of the contralateral healthy stance side was alsorecorded, sincethesemuscleswerelikelytoparticipateincontrollingthefall(MichelandDo,2002).Muscular activity was recorded using a bipolar detectionmode. Theskinwas rst lightlyabradedandcleanedtoreduceimpedance.Then,thesurfaceelectrodes(diameter:1 cm) were axed to the skin over the relevant muscle bel-lies, spaced 2 cm centre to centre and aligned parallel to theunderlying muscle bre direction. The lead wires wereaxedtotheadjacentsegmentstopreventinterferenceoftheEMGsignal. Areferenceelectrodewasaxedtothesubjects wrist.TheEMGsignal wasampliedtwice: rstbyapreamplier(gain1000,dierentialamplierofgreatimpedance10 MX)containedinacase(550 g,8channels)and attached to the subjects belt. The preamplier (LPM-CNRS, Orsay, France) was connected to a second amplierbya4 m-longcable.Thegainofthesecondamplierwasadjustable from1000 to 50000. The bandwidth of theamplication chain was between 3 Hz and 2000 Hz, cover-ing the range of the EMG signal. The analogue signals werecollected then converted into digital signals by a CED 1042card controlled by a PC. The sampling rate was 1000 Hz.2.3.ProtocolanddataprocessingEach of the subjects (control and patient) performed 20trials(tenstartingwiththerightlowerlimbandtenwiththeleftone).Software calculated the coordinates of the centre of footpressure and the dynamics of the centre of gravity from theground reaction force. The vertical acceleration of the sub-jects centre of gravity (z00G) was calculated by dividing thedierencebetweenthevertical component of thegroundreactionforce andthe subjects weight by the subjectsmass (z00G = (RZ-P)/m). The vertical velocity (z0G) andposition (zG) of the CG were calculated by successive inte-gration. Thedisplacement of thecentreof foot pressurewasusedtocalculatethelengthoftherststeptakentorecoverbalance.EachoftheEMGsignalsrecordedwasprocessedindi-vidually. The latencies of beginning and end of the variousEMG bursts were markedfor each trial, in order to calcu-late their mean values as well as the mean duration of eachEMGburst(dierencebetweenthestartandendlatenciesforeachsubject).Themeanvalueforeachgroupwascal-culatedusingthemeanvaluesobtainedforeachsubject.MechanicalandEMGdataobtainedforeachgroupofsubjects were compared 2 to 2 using a non-parametricMannandWhitneytest (StatviewsoftwareforPC). ThethresholdofsignicancedierenceusedwasP < 0.01.3.Results3.1.MechanicalaspectResults were analysed separately in patients and controlgroups. Sincethelaxityof thekneewas dierent inthepatientgroupaccordingtotreatment, datawereanalysedFig.1. Experimentalsetup forstudying balance recovery after a forwardfall.P.Colne ,P.Thoumie/ClinicalBiomechanics21(2006)849859 851rst according to the treatment. However, since no statisti-cal dierence was found in the patient group with regard tothe treatment, the resultswere then comparedfor all com-binedpatients.3.1.1.ControlgroupThe control subjects showa reproductive behaviouridentical tothatpreviouslydescribedbyDoetal. (1982).Balancerecoveryincludesrstatwo-footstancereactionphasefromrelease(t0)totoe-o(TO)withadurationof263(SD: 24) ms. It isfollowedbyastepexecutionphasefrom toe-o to heel contact (HC) with a swing phase dura-tion of 211(32) ms, with the contralateral foot remaining instance.Thenthegroundacceptancephaseoftheswingingfootoccurs,precedingexecutionofthesecondstep.Vertical biomechanical eventsofbalancerecoveryrstshow(Fig. 2)anegativevalueofthevertical accelerationof the CG(z00G1), whichcorresponds tothe fall of theCGfollowingthereleaseof therestrainingdevice. Then,thereactionphaseoccurscorrespondingtothereverseofz00Greachingapositivevalue(z00G2) beforetoe-o. Thelatency of z00G2 is 187(15) ms and its amplitude is3.17(1.03) m s2. Step execution begins with toe-o, endingwithfootcontactoftheswinginglimb.Balance recovery ends whenthe rear foot leaves theground (executing the second step), at which time thelengthofthestep, whoseamplitudeis0.754(0.06) m, andthedurationofbalancerecoverywhichis592(43) ms, aremeasured. Thevertical velocityof theCG(z0G) showsanegative peak(z0Gmin) correspondingtothebrakingofbalance recovery (brake peak, BP). This appears after heelcontact. The amplitude of the vertical velocity of the CG atheelcontact(z0GHC)is 0.225(0.07) m s1.Theheightofthe CG (zG) measured at heel contact is slightly lower thanitsinitialvaluebeforethereleaseoftherestrainingdevicethedierencebeing0.008(0.021) m.3.1.2.ComparisonofdatainACLDandACLRsubjectsThe values of the patients data (ACLD and ACLR) aredisplayedinTable 1. Acomparisonof bothgroups ofpatients (ACLD, ACLR) does not showany dierencelinkedtothetreatment. Thisistrueforboththetempo-ral-spatial parameters of balance recovery and the subjectskinematicparameters. Theentirebalancerecoverydura-tion and the duration of its various phases are not statisti-callydierentineithergroupofpatients.Noristhereanystatistical dierence in the dynamic of the CG or the lengthoftherststepinthesetwogroups.Fig.2. RecordingsofbiomechanicalparametersandEMGactivitiesfromtherightandleftsoleusduringabalancerecoverystep(rightlimbmoving).Single trial for a control subject: z00G, z0G, zG are respectively the vertical acceleration, velocity and position of the centre of the gravity (U for upward)z0Gministhenegativepeakofthevertical velocityandcorrespondstothebraking ofthebalancerecovery (BPpeakofbrakingspeed),xP andyPtheantero-posterior and lateral displacement of the foot pressure (f for forward and s for stance,L for the length of the step), SOLm and SOLs, raw EMGactivityofthesoleusfromthemovingandthestancelimb.852 P.Colne ,P.Thoumie/ClinicalBiomechanics21(2006)8498593.1.3.ComparisonofdatainpatientandcontrolgroupsregardlessofthetreatmentData for the control group and the patient group are dis-played in Table 2. A comparison of the dynamics of the CGshowsthat boththelatencyof z00G2, comprisedbetween208(30) msand195(35) msinbothsubgroupsofpatients,and its amplitude, comprised between 3.20(1.13) m s2and 2.98(1.16) m s2in both subgroups of patients, are sim-ilar in the patient and control groups [latency 187(1.03) ms,amplitude 3.17(1.03) m s2]. The vertical velocity of thecentreofgravityatTOandHCaswell astheamplitudeof the peak of braking (z0Gmin) are identical in the patientand control groups. In the same way, the height of the CG atheel contact of the swinging foot is not statistically dierentfrom that of the control [mean values of the fall of the CGcomprised between 0.004(0.020) m and 0.001(0.016) m inthepatientgroupversus 0.008 m(0.021)inthecontrol].For all patients, the braking time with respect to heel con-tact (db = tz0Gmin-tHC) shows twodierent behaviourswhen the balance recovery step is performed with theinjuredside(Fig.3).Somesubjectsbrakebeforeheelcon-tact [db < 0: meanvalue 16(18) ms] while others brakeafter heel contact [db > 0: mean value 20(17) ms versus26(20) ms in control]. Ten subjects (6 ACLD and 4 ACLR)brakebefore(B,braking)and12subjects(6ACLDand6ACLR) brake after (NB, non-braking). The distributionof subjects inbothgroupsshowsnolinkwitheitherthetreatment (rehabilitation alone or surgery) or with the timeelapsed sincethe injury or surgery [respectively19(16) and13(11) months inthe BandNBgroups, WilcoxontestP = 0.71, NS].The length of the step performed by the patients (Fig. 3)followsthesametwo-groupdistributionregardlessoftheswing limb. The length of the step is not statistically dierentfrom that of the control group for the group which brakesbefore [uninjured side 0.686(0.135) mand injured sideTable2Mean values of the temporo-spatial components of the balance recovery step and the biomechanical parameters of the dynamic of the centre of gravityafteraforwardfall,pergroup,withrespecttothetimeofbrakingParameters Control Brakingpatients Non-brakingpatientsSwinginglimb Normal Uninjuredside Injuredside Uninjuredside InjuredsideBalancerecoveryduration(ms) 592(43) 667(41)**668(44)**654(67)**660(82)**Toe-olatency(ms) 263(24) 290(43) 294(41) 289(34) 282(47)Heel-olatency(ms) 474(46) 536(40)*536(57)*522(44)*519(58)*Swingphaseduration(ms) 211(32) 247(20)*242(26)*233(26)*236(30)*db(ms) 26(20) 9(10) 16(17)**,11(17) 20(17)Z00G1latency(ms) 57(9) 51(8) 52(10) 54(9) 54(11)Z00G1amplitude(m s2) 1.21(0.27) 0.94(0.35) 0.87(0.29) 0.99(0.28) 1.02(0.24)Z00G2latency(ms) 187(15) 209(32) 208(30) 202(34) 195(35)Z00G2amplitude(m s2) 3.17(1.03) 3.08(0.89) 3.20(1.13) 2.87(0.89) 2.98(1.16)Z0GamplitudeatHC(m s1) 0.225(0.07) 0.241(0.057) 0.212(0.09) 0.199(0.093) 0.221(0.091)DZGatHC(m) 0.008(0.021) 0(0.018) 0.001(0.016) 0.004(0.018) 0.004(0.02)Steplength(m) 0.754(0.068) 0.686(0.135) 0.664(0.147) 0.555(0.18)**,0.539(0.16)**,Vs(m s1) 3.6(0.5) 2.8(0.7)**2.8(0.6)**2.4(0.7)**2.3(0.6)**dbisthebrakingtime(=tz0Gmin-tHC).Vsisthevelocityofthestep(=ratioofthelengthofthesteptotheswingphaseduration).Pvalues:*P < 0.05,**P < 0.01,signicantlydierentfromcontrol; P < 0.05, P < 0.01,signicantlybetweensubgroups.Table1Mean values of the temporo-spatial components of the balance recovery step after a forward fall and the biomechanical parameters of the dynamic of thecentreofgravitypergroupwithrespecttothetreatment(ACLD,ACLR)andrespectivePvaluesParameters ACLD ACLR PvalueSwinginglimb Uninjuredside Injuredside Uninjuredside InjuredsideBalancerecoveryduration(ms) 665(50) 657(53) 654(64) 672(81) NSToe-olatency(ms) 291(45) 301(92) 285(39) 296(45) NSSwingphaseduration(ms) 234(24) 234(25) 245(24) 245(31) NSZ00G1latency(ms) 55(9) 54(10) 49(8) 53(12) NSZ00G1amplitude(m s2) 0.99(0.33) 0.98(0.25) 0.93(0.29) 0.92(0.30) NSZ00G2latency(ms) 208(18) 199(28) 201(38) 204(39) NSZ00G2amplitude(m s2) 3.27(0.88) 3.46(1.05) 2.60(0.75) 2.62(1.09) NSZ0GamplitudeatHC(m s1) 0.246(0.08) 0.253(0.077) 0.185(0.069) 0.175(0.086) NSDZGatHC(m) 0.004(0.018) 0.003(0.014) 0.001(0.016) 0.000(0.023) NSSteplength(m) 0.616(0.169) 0.596(0.169) 0.613(0.180) 0.596(0.166) NSZ00G1:negativepeakoftheverticalaccelerationofthecentreofgravity(CG)beforetoe-ooftheswinglimb.Z00G2:positivepeakoftheverticalaccelerationofthereactionphase(beforetoe-o).Z0GatHC:verticalvelocityoftheCGatheelcontact(endoftheswingphase).DZGatHC,variationoftheheightoftheCGatheelcontact.P.Colne ,P.Thoumie/ClinicalBiomechanics21(2006)849859 8530.664(0.147) mversus0.754(0.068) mincontrol]whileitissignicantly shorter in the group which brakes after[uninjured side 0.555(0.178) m; injured side: 0.539(0.161) mversus 0.754(0.068) m in control, P < 0.01].Thebalancerecoverydurationmeasuredattheendofthe rst step is always greater in the patient group with meanvalues comprised between 660(67) ms and 668(44) ms versus592(43) ms in control. The dierence is signicant (P < 0.01)regardless of the moving limb or time of braking (Table 2).If we consider the duration of the various phases of balancerecovery, the swing phase, comprised between TO and HC,is the onlyone whose durationis signicantlyincreased[respectively294(41) msand282(47) msintheBandNBgroups versus 263(24) ms in control, the level of signicanceis lower P < 0.05].The meanvelocityof stepexecution(Vs, ratioof thelengthof the steptothe swingphase duration) appearstobeslower intheentireACLgroupwithmeanvaluescomprised between 2.3(0.6) m s1and 2.8(0.6) m s1versus3.6(0.5) m s1incontrol. Thedierenceis signicant fortheBandNBgroups(P < 0.01).3.2.EMGaspectResults were analysed separately in patients and controlgroups. Although the mechanical pattern of balance recov-erydoesnotshowanydierencebetweentheACLRandACLD subjects, EMG data were rst analysed with respecttothetreatment,thenfortheentiregroup.3.2.1.ControlgroupOnthemovinglimb, eachmuscleshowstwoburstsofEMG(Figs. 3and4). The soleus is the rst muscle tobecome active. Its activity starts 65(11) ms after the releaseof the restraining device and ceases 189(31) ms after [dura-tion 124(31) ms]. This burst occurs before the positive peakofvertical accelerationoftheCGandendsashortwhileafterwards. This activity corresponds tothe reactiontothe fall occurring just after release (Thoumie and Do,1996). The secondburst of the soleus appears after TO[433(63) msaftertherelease] andoccurs63(43) msbeforeheel contact, preparing to stabilize the swinging limb duringthegroundacceptancephase, withthekneeandankleinexion at the time of heel contact. The activity of the soleuscontinues during the unilateral stance which follows.The rst burst of the tibialis occurs 195(35) ms afterreleaseandends333(42) msafterwardswitha138(39) msmean duration, starting before TOand ending shortlyafterwards.Itallowsliftingthefootfromthegroundandswinging. The second burst of the tibialis starts435(47) ms after thereleaseandoccurs 64(29) ms beforeHC.Itpreparestostabilizetheankleatheelcontact.Fig. 3. Recordings of some of the biomechanical parameters of the balance recovery step and some of the EMG activities for a control subject (CTL), anACL subject who brakes before heel contact (B) and an ACL subject who brakes after heel contact (NB). Single trial for each subject. The swinging limbwas the left leg for the CTL and the injured leg for the ACL. Vertical solid line shows the time of release (t0) and the dotted lines correspond to the time oftoe o (TO, start of the step execution phase) and heel contact (HC, end of the swing phase). z00G and z0G are the vertical acceleration and velocity (U,upward), L on xP graph is the length of the rst step executed to recover balance (F, forward and L, step length, BP peak of braking speed). SOLm andHAMmarerespectivelythesoleusandhamstringsmuscleactivitiesofthemovinglimb.854 P.Colne ,P.Thoumie/ClinicalBiomechanics21(2006)849859The rst burst of the hamstrings medial (HamM) and lat-eral (HamL), respectively, lasts 114(51) ms and 127(40) ms.It occurs respectively 70(12) ms and78(25) ms after therelease andends afterward [respectively 183(55) ms and206(58) ms]. Thesebursts occur beforethepositivepeakof the vertical acceleration and end shortly afterwards. Theyact again as a posterior muscular activity reacting to the for-ward fall. The second burst of these muscles occurs378(63) ms and411(69) ms, respectively, after thereleaseduring the swing phase. These bursts start before HC[116(39) ms for HamM and 89(41) ms for HamL] to controlthe extension of the knee during the swing phase, and thentostabilizethelowerlimbduringthegroundacceptancephasewhilethehipandkneeareinexionatthetimeofheel contact. These muscular activities occur during the uni-lateral stance which follows.Quadriceps shows a rst burst occurring 178(47) msafter release andending 336(37) ms afterward[duration159(51) ms].ThisburstoccursaroundTO,startingalittlebeforeandendingafterward.Thisburstmakesitpossibletoextendthe knee duringthe swingphase. The secondburst of this muscle occurs 449(37) ms after the releaseand is located before HC 50(26) ms. It contributes to stabi-lize the knee at the time of heel contact then during the uni-lateralstance.On the stance limb, all muscles recorded show only oneburst of EMG. Activity of the soleus occurs 73(17) ms afterthe release and ends 486(55) ms afterward [duration413(55) ms]. This activity is located before the positivepeakof thevertical accelerationandceases at about thetime of heel contact of the swinginglimb. This activitycomprises an initial part corresponding to the bilateralstance reaction to the fall which is followed by a later partin unilateral stance to stabilize the stance limb and to con-troltheforwardbodyprogression(MichelandDo,2002).The tibialis shows varying degrees of activity dependingon the subject. It starts 97(10) ms after the release and ends470(51) ms after [duration 373(51) ms]. The bursts ofthe hamstring medial and lateral, respectively, last202(67) msand203(83) ms.Theybecomeactive70(10) ms-1000100200300400500600700800CTL NB CTL NBSols contra Tas contra ms******-1000100200300400500600700800CTL B NB CTL B NBHCms Solm ipsi Tam ipsi***NS***-1000100200300400500600700800CTL B NB CTL B NB CTL B NBQuam ipsi HamMm ipsi HamLm ipsi msHC***** ***NSB BFig. 4. MeanvaluesandstandarddeviationsofEMGactivitiesduringbalancerecoveryafteraforwardfall incontrol andpatientsregardlessofthetreatment. EMG burst of the moving limb (injured side for the patient). From bottom to top: rst EMG burst duration, onset of the second EMG burstandtimeofheelcontact(HC).Fromlefttorightonthediagrams:control(CTL),braking(B)andnon-braking(NB)groups.Rightsideofthegurecorrespondsto themean values of the moving limb,left sidecorresponds to that of the stance limb. HC isthe time of heel contact, Solm, Tam, Quam,HamM and HamL are respectively the Soleus, Tibialis, Quadriceps, Hamstrings medial and lateral muscle of the moving limb, IPSI correspond to the limbipsilateral to the lesion. Sols and Tas are the Soleus and Tibialis muscle of the stance limb, CONTRA corresponds to the limb contralateral to the lesion.***P < 0.001,**P < 0.01.P.Colne ,P.Thoumie/ClinicalBiomechanics21(2006)849859 855and 75(13) ms after release and end shortly after TO,respectively273(67) msand278(79) msafterrelease. Thisactivityisshorterthanthatofsoleusandoccursprimarilyinreactiontothefall.Thequadricepsisactive151(56) msafter the release, a little later than the hamstrings, and ends443(58) ms afterwards. It serves primarilytosupport theunilateralstance.3.2.2.ComparisonofdatainACLDandACLRsubjectsWhenbalance recoveryis performedwiththeinjuredlimb moving, the respective durationof the rst EMGburstisnotdierentinthetwogroupsofpatients. Somedierencesareobservedincertainparametersof latency,buttheydonotaectthedurationoftheEMGactivitiesanddonotcharacterizeanyparticularbehaviourbetweentheACLDandACLRgroups.Only the second burst of the soleus and hamstrings med-ial occurs earlier in the ACLD group [respectively408(55) ms in the ACLDgroup and 431(56) ms in theACLR for soleus and 360(59) ms in ACLD and382(52) ms in ACLR for hamstrings]. The dierence is sig-nicant (P < 0.02 for the soleus and P < 0.01 for theHamM) but it does not aect the fact that the time betweenthe beginning of the second burst of EMG and the time ofHC[respectively94(33) msforthesoleusand106(62) msfor the hamstrings medial in the ACLD group and67(28) ms for soleus and77(45) ms for hamstringmedialinthe ACLRgroup] increases statisticallyfor these twomuscles as for the others in both groups of patients in com-parisonwiththecontrol.Intheuninjuredcontralateralstancelimb,thedurationofsoleusactivity[448(13) msinACLDand480(81) msinACLR] does not dier between the two groups of patients,butissignicantlyincreasedinthesegroupscomparedtothecontrol.Althoughthedurationofthetibialisislongerin the ACLR group, it is longer in both groups of patientswithrespecttothecontrol.In conclusion, respective latencies of the second burst ofthesoleusandhamstringsmedialaretheonlyparameterswhich dierentiate muscular activity in ACLDand ACLRpatientswhentheinjuredlimbisthemovingone.Whenbalance recoveryis performedwiththeinjuredstance limb, the duration of EMG activities does not dierbetweenthetwogroups of patients except for theham-stringslateralintheACLDgroup,wheretheEMGdura-tionis longer becauseof later termination. Theincreaseindurationis signicant inall muscles recordedinbothgroupsofpatientsincomparisonwiththecontrol, exceptforthequadriceps.3.2.3.ComparisonofdatainpatientandcontrolgroupsregardlessofthetreatmentIn both groups of patients, weobserveearlycompensa-tions with respect to the release of the restraining device, aswell as compensations preceding heel contact of the swing-inglimb, characterizingauniquepatternforeachof thetwogroups:BandNB(Fig.4).Whenbalance recoveryis performedwiththeinjuredlimbmoving, therst burstof thesoleusof injuredlimbshows the same duration in both groups of patients [respec-tively125(35) msand144(4) msfortheBandNBgroups]and control [124(32) ms]. Thesecond burstof the soleus isearlier inthe NBgroupwithrespect torelease [respec-tively 399(56) ms inthe NBgroupversus 450(43) ms inthe B group, and 433(63) ms in control, P < 0.001 for bothgroups] andalsoearlier withrespect toHC[respectively115(48) ms in the NBgroup versus 82(52) ms in the Bgroup and 63(43) ms in control, P < 0.001 for both groups].NotethatthereisthesamenumberofACLDandACLRsubjects in the NB group and that the respective latency ofthe second burst of the soleus in these two sub-groups doesnot dier withrespect torelease[respectively396(60) msand401(53) ms].Theactivityof thetibialisdoesnot dierbetweenthethree groups. The rst burst of the hamstrings (HamMandHamL)showsthesamedurationinall threegroups.The time elapsed between the beginning of the second burstof the hamstrings andHCis signicantly longer inthepatients thaninthecontrol [respectively160(31) ms and144(33) ms for HamMandHamLin the Bgroup and142(45) msand128(37) msforHamMandHamLintheBgroupversus116(39) msforHamMand89(41) msforHamLin thecontrol,P < 0.001forallmuscles].ThistimeisevenhigherforHamMintheBgroupthanintheNBgroup(P < 0.01).Therstburstofthequadricepsdoesnotdierinthethreegroups. ThetimeelapsedbetweenthesecondburstofthismuscleandHCishigherinbothACLgroupswithnostatisticaldierence.On the contralateral uninjured stance limb, the durationoftheburstsofthesoleus[466(40) msintheBgroupand466(81) msintheNBgroup] doesnot dierbetweenthetwogroups of patients. Thesameis truefor thetibialis[duration435(92) ms inthe Bgroupand424(74) ms intheNBgroup]. This durationis higher (P < 0.001) thanin the control for both muscles [respective duration incontrol 413(55) ms for thesoleus and373(51) ms for thetibialis].Whenbalance recoveryis performedwiththeinjuredstance limb, the duration of the bursts of all recorded mus-cles in the injured stance limb is higher in both ACL groupscomparedtothecontrol.ThedierenceissignicantwithrespecttothecontrolforallmusclesofbothgroupsACL(P < 0.001)exceptforthequadricepsintheNBgroup.4.DiscussionTheaimofthestudywastocharacterizethemuscularactivitiesanddynamicsofbalancerecoveryafteranACLlesion, andinparticular, toidentifytheroleofthesoleusbasedontreatment(rehabilitationaloneorsurgery). Ourresults show that while the activity of the soleus is dierentafter an ACLlesion, it corresponds more to a common strat-egyinthesubgroupsofpatientsandcannotbeexplained856 P.Colne ,P.Thoumie/ClinicalBiomechanics21(2006)849859solely by the passive mechanical instability of the kneerelatedtothelesionoftheligamentcorrectedbysurgery.The following discussion considers the modicationsobserved in the mechanical pattern of the balance recoverymotor program, the related modications of EMG and thedynamic stabilization of the knee after an ACL lesion.4.1.ModicationstothemechanicalbalancerecoverypatternafteranACLlesionOur results show that patients who have an ACL injuryareabletorecover balancewithout anydiscomfort thatwas suggested by the absence of modication in the dynam-ics of the centre of gravity: the position and falling velocityof the centre of gravity are similar at the end of the balancerecoveryprocessinallthegroupsandsubgroups.The strategy shared by both groups is characterized by asignicant increase in the balance recovery duration regard-less of the treatment or the moving limb, and regardless ofthetimesinceinjuryorsurgery. Thischangeisrelevant totheprevalent increaseintheswingphasedurationwhichconstitutes the essential parameter permitting the regulationof balance recovery (Do et al., 1999). Our study describes anew clinical situation where we observed an increase in theswing phase duration to control the moving velocity of thewhole body and to protect the injured knee during contactwith the ground after swinging. This result should be com-paredtotheobservations madebyAlkjaer et al. (2002)whodescribedalengtheningofthedurationofaforwardlungemovementin ACLDsubjects.Theinitialpartof themovement,correspondingtothegroundacceptancephaseof the foot as the knee was exing, was increased in non-cop-ers and copers, suggesting to the author that the lengtheningof the motor program could allow ACLD subjects to reactin case of instability of the knee.Besides this common increase in the duration of balancerecovery in all ACL subjects, a modication of the time ofbraking and of the length of the step could be seen allowingpatients to control the impact of the ground acceptance ofthe foot using one of these two strategies: one group of sub-jects brakes before ground contact of the foot when swing-ingwiththeinjuredlimb, withoutreducingthelengthofthestep. Anothergroupbrakes aftergroundcontact ofthe foot, like the control, bilaterallyshorteningthe stepto recover balance. A similar shortening strategy was foundin subjectshaving sustained a unilateral chronicdeaeren-tation (abolition of the Achilleous reex), whereas anexperimental blockingofthisreexresultedintheexecu-tionofanormal steplengthattheexpenseofaloweringof thecentreof gravity(ThoumieandDo, 1996). Theseauthors suggestedthat the strategyusedbythe subjectswith chronic deaerentation could result froma motorrelearning acquiredover time. Inour study, the resultsdonotseemtodependonamotorrelearningduringthetime elapsed since the initial lesion or surgical repair, sinceboth ACL groups (B and NB) are comparable with respecttothisparameter.Inthe same way, althoughwe didnot quantitativelyevaluatetheforceof thequadriceps andsoleus muscles,modications of balance recovery do not seem to be relatedtoamotordecitsincepatientsandcontrol donotshowanydierenceinthepositivepeakofverticalacceleration,showing evidence of the bilateral stance motor response. Insimilar situations, other authors (Rudolph and Snyder-Mackler, 2004; Lewek et al., 2003) showed that a dierencebetween ACLDcopers and non-copers was not simplyrelatedtoadecit inquadriceps strengthbut rather tothechronologyof muscularactivities. Furthermore, Wil-liamset al. (2004) recentlydemonstratedtheexistenceofa quadriceps motor control decit after a lesionof theACL.In our study, the mechanical pattern of ACLDandACLRpatients does not dier, suggesting that passivemechanical stabilityrestorationof thekneeaftersurgerydoesnot inuencetheparameterswehavestudied. Thenthedierencesobservedintheentirepatientgroupcannotbe interpreted in terms of passive mechanical stabilityalone. Snyder-Mackler et al. (1997) has shown that anteriorlaxity of the knee in ACLD subjects was poorly correlatedto the measurements of their functional capacities. Adecrease of the proprioceptive sensitivity of the knee isknownafteralesiontotheACL(Corriganet al., 1992),and the loss of the aerences resulting from the ACL injuryis a common decit in our ACLD and ACLR patients, thiswould be responsible for the modications of balancerecovery although the absence of a proprioceptive sensitiv-ity evaluation of the knee in our study does not allow us toarm it. Regardless of their nature, the two strategies usedbypatients are equallyeective inmaintainingposturalbalancesincetheypreventthefallofthecentreofgravitythat was observed after experimental blocking of muscularaerences(ThoumieandDo,1996).4.2.ModicationsofEMGactivityafterACLlesionOurresultsshowthesamegeneral patternofmuscularactivitiesinpatientsandincontrol duringbalancerecov-ery. The main dierences between the control and patientsconcern the latencies and durations of ipsilateral ham-strings and bilateral soleus muscle activation when theinjuredlimb is movingandall ipsilateralmuscles recordedwhen the injured limb is in stance. Two kinds of modica-tion are observed after an ACL lesion: a global increase indurations related to an increase in the duration of the bal-ance recoveryprocess andanearlier activationof somemuscles with respect to the release of the restraining deviceandrelativetothetimeofheelcontact,showingevidenceofanticipation.The increase in muscular activity duration when theinjuredlimbisthestanceoneislinkedtoanincreaseinthe balance recovery duration and probably to an increasein lower limb stiness and in knee stability, especially dur-ingtheunilateral stance. Hortobagyi andDeVita(2000)haveshownanincreaseinmuscularactivityandinlowerP.Colne ,P.Thoumie/ClinicalBiomechanics21(2006)849859 857limbstinesswhenelderlysubjectsstepdown. Theycon-clude that this is a strategy to compensate for their reducedmotorcontrolcapacities.We observedanincrease inthe contralateral activitydurationofbothrecordedmusclesintheuninjuredlimb.This suggests that muscular activity of the stance limbhelps protect the injured knee during the weight acceptancephaseofthefall afterswingingwiththeinjuredlimb, byslowing down the forward progression of the body, therebyreducing the impact of ground acceptance. This hypothesisissupportedbytheresultsof otherauthors(Michel andDo, 2002) whoconcludedthat thefunctionof thesoleusis to control the forward body progression in balancerecoveryandgaitinitiation.Inall ACLgroups, preparationforthegroundaccep-tance phase of the injured moving limb is characterized byanincreaseinthetimeelapsedbetweentheburstofham-strings and heel contact. These results resemble the changesin the hamstrings activity of ACL subjects (facilitation, tim-ing of activation, duration, time of beginning and peak) pre-viouslyreportedinnormal orascent gait (Kalundet al.,1990;Lassetal.,1991;Beardetal.,1994;KvistandGill-quist,2001;Rudolphetal.,2001;Boerboometal.,2001).In the patients (B and NB), the early activation of the ham-strings compared to HC would signicantly reduce the stepexecution velocity in order to stabilize the knee at heel con-tact of the ground and thus to protect it. Early activation ofthe hamstrings with respect to heel contact also suggests ananticipation in the control of the forward translation of thetibia attributed to these muscles when the knee is extended inan open kinetic chain (Solomonowet al., 1987; Baratta et al.,1988). The early activation of the hamstrings medial is char-acteristic of the strategy of the B group compared to the NBgroup. SincepatientsoftheBgrouparetheonlyonestobrake before heel contact, the hamstrings medial could playa prevalent role in anticipating the stabilization of the kneeat heel contact for this group. This hypothesis can be relatedto that of Alkjaer et al. (2002) who showed that activity ofthe hamstrings medial (semi tendinosus) was greater as thekneeextendsinaforwardlungeinACLDcopersubjectscompared with non-copers and with the control.Theearlyactivation ofthe second burstof thesoleusischaracteristic primarily of the behaviour of the ACLD andNB groups. It does not seem to be related solely to the pas-sive mechanical instabilityof the knee since there is thesame number of ACLDandACLRsubjects inthe NBgroupandthat the respective time of activationof thesoleus does not dier in these two subgroups. Variousauthors (Sutherland et al., 1980; Ciccotti et al., 1994) havehighlightedthe role of the soleus instabilizingthe kneeduring the unilateral stance phase of gait and Ciccottiet al. (1994) reports that the activity of the soleus isincreasedatthisphaseinACLDsubjects.Recent studies (Elias et al., 2003; Sherbondy et al., 2003)reportedthatthesoleus(solicitedinamockclosedkineticchain situation) could act as an agonist of the ACL by pull-ing backwards the proximal part of the tibia. This action ofthe soleus is not inuenced by the position of the knee butisincreasedbyankleexion(Sherbondyet al., 2003). Inourstudy, themovinglimbisinexionat thekneeandanklewhenit contactstheground. Loweractivityof thesoleusinACLDnon-copers isoneoftheresultsdescribedby Rudolph and Snyder-Mackler (2004) during the injuredlimbgroundacceptancephaseafterstepping,whereasitisnot incopers compared tothe control. Rudolphet al.(2001) has also described in non-copers a signicant higheractivationofthesoleusduringweightacceptanceofgait,thatisconicting.Withoutanyrealtestpermittingtoclassifythesubjectsincopersornon-copers, it isdicult toconcludeinourstudyifthesubjectswerecopersornot. Indeed,itcanbenotedthat ACLpatients inthe studyof Rudolphwereall participantsinhighlevel sport activities, whichisnotthe case for our patients. At the time of the test our patientshaveall returnedtonormal dailylifeactivities(includingrecreational joggingforsome)withoutexperiencinginsta-bility of the knee, which suggests they developed anadapted strategy to stabilize the knee. In our study, the sec-ond burst of the soleus activity was signicantly earlier forboththeACLDandNBgroupswhatsuggeststhatthesegroups developed a strategy to stabilize the knee in a closedkineticchain.Apreviousstudy(Chmielewskietal.,2002)supports the hypothesis that training to control the unilat-eral stanceoftheinjuredlimbmodiesthetimingofthemuscularactivities stabilizingthekneeandimproves thefunctional capacities of ACLDnon-copers, highlightingthe modulation of quadriceps activity by soleus and bicepsfemoris. In the same way other authors (Torry et al., 2004)demonstratedtheexistenceoftwodierentcompensatorystrategies in walking in ACLD subjects who have all recov-eredagoodlevel ofsportsactivities(potentiallyqualiedascopersbytheauthor)andstressedthatstabilizationofthe knee can depend on dierent strategies in the same cat-egory of patients, which also seems to be in our study. Ourresults are in line with these previous studies and highlighttheroleofsoleusaccordingdierentstrategiestostabilizethekneewhateverthetreatment proposedafteranACLlesion.5.ConclusionThis study shows that a lesion of the ACL always resultsinachangetothebalancerecoverymotorprogram. Thelackof atrulycharacteristic patternafter rehabilitationorsurgerysuggeststhatthechangescouldbetheexpres-sion of a motor program resulting from the loss of the pro-prioceptive aerencesfromthe ACL.Ourresults highlightthe role of the soleus in compensating for the injured kneeand its bilateral activation in recovering balance regardlessof thestrategyused. Theyalsosuggest that thegoals ofrehabilitationcannot belimitedtotheinjuredkneeafteran ACLlesion (surgically repaired or not) but shouldinclude strengthening of the soleus and improving itsactivation.858 P.Colne ,P.Thoumie/ClinicalBiomechanics21(2006)849859AcknowledgmentWethankMsK.DeHaanforreviewingtheEnglishinthisarticle.ReferencesAdachi, N., Ochi, M., Uchio, Y., Iwasa, J., Ryoke, K., Kuriwaka, M.,2002. Mechanoreceptors in the anterior cruciate ligament contribute tothejointpositionsense.ActaOrthop.Scand.73,330334.Alkjaer, T., Simonsen, E.B., Peter Magnusson, S.P., Aagaard, H.,Dyhre-Poulsen, P., 2002. 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