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Review Neuromuscular efficiency during sit to stand movement in women with knee osteoarthritis Glykeria Patsika , Eleftherios Kellis, Ioannis G. Amiridis Laboratory of Neuromechanics, Department of Physical Education and Sport Sciences at Serres, Aristotle University of Thessaloniki, Greece article info Article history: Received 16 November 2010 Received in revised form 19 May 2011 Accepted 19 May 2011 Keywords: Arthritis Co-activation Hamstrings Quadriceps Sit-to-stand Strength testing abstract The purpose of this study was to investigate the neuromuscular efficiency of women with knee osteoar- thritis (OA) when performing a sit-to-stand movement and during maximum strength efforts. Twelve women with unilateral knee OA (age 60.33 ± 6.66 years, height 1.61 ± 0.05 m, mass 77.08 ± 9.2 kg) and 11 controls (age 56.54 ± 5.46 years, height 1.64 ± 0.05 m, mass 77.36 ± 13.34 kg) participated in this study. Subjects performed a sit-to-stand movement from a chair while position of center of pressure and knee angular speed were recorded. Furthermore, maximal isokinetic knee extension and flexion strength at 60°/s, 120°/s and 150°/s was measured. Surface, electromyography (EMG) from the biceps femoris (BF), vastus lateralis (VL) and vastus medialis (VM) was recorded during all tests. Analysis of var- iance (ANOVA) showed that during the sit-to-stand OA group demonstrated significantly lower knee angular speed (44.49 ± 9.61°/s vs. 71.68 ± 19.86°/s), a more posterior position of the center of pres- sure (39.20 ± 7.02% vs. 41.95 ± 2.49%) and a higher antagonist BF activation (57.13 ± 20.55% vs. 32.01 ± 19.5%) compared with controls (p < 0.05). Further, women with knee OA demonstrated a lower Moment-to-EMG ratio than controls in extension and eccentric flexion at 60°/s and 150°/s, while the opposite was found for concentric flexion at 60°/s (p < 0.05). Among other factors, the slower perfor- mance of the sit-to-stand movement in women with OA is due to a less efficient use of the knee extensor muscles (less force per unit of EMG) and, perhaps, a higher BF antagonist co-activation. This may lead subjects with OA to adopt a different movement strategy compared with controls. Ó 2011 Elsevier Ltd. All rights reserved. Contents 1. Introduction ......................................................................................................... 690 2. Method ............................................................................................................. 690 2.1. Subjects ....................................................................................................... 690 3. Instrumentation ...................................................................................................... 690 4. Procedure ........................................................................................................... 691 4.1. Electromyography preparation ..................................................................................... 691 4.2. STS protocol .................................................................................................... 691 4.3. Isokinetic protocol ............................................................................................... 691 5. Statistical analysis .................................................................................................... 691 6. Results.............................................................................................................. 691 6.1. STS task ....................................................................................................... 691 6.2. Isokinetics ..................................................................................................... 692 6.3. Moment-to-EMG ratio............................................................................................ 692 6.4. Antagonist muscle activation ...................................................................................... 692 7. Discussion ........................................................................................................... 692 Conflict of interest .................................................................................................... 693 References .......................................................................................................... 693 1050-6411/$ - see front matter Ó 2011 Elsevier Ltd. All rights reserved. doi:10.1016/j.jelekin.2011.05.006 Corresponding author. Address: Department of Physical Education and Sports Sciences of Serres, Aristotle University of Thessaloniki, Laboratory of Neurome- chanics, Ag. Ioannis, Serres 62122, Greece. E-mail address: [email protected] (G. Patsika). Journal of Electromyography and Kinesiology 21 (2011) 689–694 Contents lists available at ScienceDirect Journal of Electromyography and Kinesiology journal homepage: www.elsevier.com/locate/jelekin
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Page 1: Neuromuscular efficiency during sit to stand movement in women with knee osteoarthritis

Journal of Electromyography and Kinesiology 21 (2011) 689–694

Contents lists available at ScienceDirect

Journal of Electromyography and Kinesiology

journal homepage: www.elsevier .com/locate / je lek in

Review

Neuromuscular efficiency during sit to stand movement in womenwith knee osteoarthritis

Glykeria Patsika ⇑, Eleftherios Kellis, Ioannis G. AmiridisLaboratory of Neuromechanics, Department of Physical Education and Sport Sciences at Serres, Aristotle University of Thessaloniki, Greece

a r t i c l e i n f o a b s t r a c t

Article history:Received 16 November 2010Received in revised form 19 May 2011Accepted 19 May 2011

Keywords:ArthritisCo-activationHamstringsQuadricepsSit-to-standStrength testing

1050-6411/$ - see front matter � 2011 Elsevier Ltd. Adoi:10.1016/j.jelekin.2011.05.006

⇑ Corresponding author. Address: Department of PSciences of Serres, Aristotle University of Thessalonchanics, Ag. Ioannis, Serres 62122, Greece.

E-mail address: [email protected] (G. Patsi

The purpose of this study was to investigate the neuromuscular efficiency of women with knee osteoar-thritis (OA) when performing a sit-to-stand movement and during maximum strength efforts. Twelvewomen with unilateral knee OA (age 60.33 ± 6.66 years, height 1.61 ± 0.05 m, mass 77.08 ± 9.2 kg) and11 controls (age 56.54 ± 5.46 years, height 1.64 ± 0.05 m, mass 77.36 ± 13.34 kg) participated in thisstudy. Subjects performed a sit-to-stand movement from a chair while position of center of pressureand knee angular speed were recorded. Furthermore, maximal isokinetic knee extension and flexionstrength at 60�/s, 120�/s and 150�/s was measured. Surface, electromyography (EMG) from the bicepsfemoris (BF), vastus lateralis (VL) and vastus medialis (VM) was recorded during all tests. Analysis of var-iance (ANOVA) showed that during the sit-to-stand OA group demonstrated significantly lowerknee angular speed (44.49 ± 9.61�/s vs. 71.68 ± 19.86�/s), a more posterior position of the center of pres-sure (39.20 ± 7.02% vs. 41.95 ± 2.49%) and a higher antagonist BF activation (57.13 ± 20.55% vs.32.01 ± 19.5%) compared with controls (p < 0.05). Further, women with knee OA demonstrated a lowerMoment-to-EMG ratio than controls in extension and eccentric flexion at 60�/s and 150�/s, while theopposite was found for concentric flexion at 60�/s (p < 0.05). Among other factors, the slower perfor-mance of the sit-to-stand movement in women with OA is due to a less efficient use of the knee extensormuscles (less force per unit of EMG) and, perhaps, a higher BF antagonist co-activation. This may leadsubjects with OA to adopt a different movement strategy compared with controls.

� 2011 Elsevier Ltd. All rights reserved.

Contents

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6902. Method . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 690

2.1. Subjects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 690

3. Instrumentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6904. Procedure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 691

4.1. Electromyography preparation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6914.2. STS protocol . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6914.3. Isokinetic protocol. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 691

5. Statistical analysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6916. Results. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 691

6.1. STS task . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6916.2. Isokinetics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6926.3. Moment-to-EMG ratio. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6926.4. Antagonist muscle activation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 692

7. Discussion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 692Conflict of interest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 693References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 693

ll rights reserved.

hysical Education and Sportsiki, Laboratory of Neurome-

ka).

Page 2: Neuromuscular efficiency during sit to stand movement in women with knee osteoarthritis

Fig. 1. Illustration of the position of the center of pressure (CoP) in the medio-lateral (x) and antero-posterior (y) axis in women with knee osteoarthritis (OA) (a)and controls (b) (the graph is based on the mean group value, for each group).

690 G. Patsika et al. / Journal of Electromyography and Kinesiology 21 (2011) 689–694

1. Introduction

Knee osteoarthritis (OA) is associated with functional disability(Dekker et al., 1993; O’Reilly et al., 1998), pain (O’Reilly et al., 1998;Slemenda et al., 1997), quadriceps dysfunction (Maly et al., 2006),joint stiffness (Sharma et al., 2003) and instability (Dieppe, 1993;O’Reilly et al., 1998; Slemenda et al., 1997). People suffering fromknee OA have difficulties in performing daily activities (ADL), suchas walking, using stairs and standing up from a chair (Gur and Ca-kin, 2003; Hortobagyi et al., 2005; Pai et al., 1994). Because of allthese symptoms, individuals with knee OA tend to gradually re-duce their participation in physical activity (Dekker et al., 1993)and impairments in quality of life are observed (Hortobagyiet al., 2005; Pai et al., 1994; Zeni et al., 2010).

Sit-to-stand (STS) is a mechanically demanding task (Riley et al.,1991) which involves transferring the body from the sitting to thestanding position (Hodge et al., 1989). STS is an important dailymovement and it is considered a predictor of functional ability,especially in elderly people (Guralnik and Winograd, 1994). There-fore, the ability of people with knee OA to perform STS tasks is ofparticular interest (Gross et al., 1998; Lord et al., 2002; Pai et al.,1994).

People with knee OA rise from a chair much slower than con-trols (Pai et al., 1994). This is probably linked to power andstrength impairments (Lord et al., 2002; Yamada and Demura,2009) as STS performance involves force exertion by gross muscles,such as the hip and the knee extensors (Lord et al., 2002). Researchhas shown that individuals with knee OA show a lower strengthcapacity of the knee extensors (Hortobagyi et al., 2004; Slemendaet al., 1997), but possible impairments in hamstring musclestrength are not clear (Hou, 2007; Slemenda et al., 1997; Gur andCakin, 2003). Examination of multiple muscle strength deficits dis-played by people with knee OA is a necessary pre-requisite tounderstand the mechanisms underlying functional impairmentsdisplayed by these individuals.

Performance of any task depends not only on maximum forcegeneration capacity, but also on the magnitude of muscle activa-tion. In fact, Hortobagyi et al. (2004) have shown that people withknee OA are less efficient than healthy people in utilizing the kneeextensor muscles. The neuromuscular efficiency is translated intothe ability of an individual to generate force (or moment of force)for the same level of muscle activation (Tesch et al., 1990). Evi-dence in non-symptomatic elderly people suggests that lowermuscle strength might increase quadriceps activation (Wheeleret al., 1985) and vertical momentum during STS movement (Paiand Rogers, 1990) which is indicative of a lower neuromuscularefficiency. To our knowledge, neuromuscular efficiency during sin-gle-joint and multi-joint tasks in people with knee OA is not clear.If knee OA affects neuromuscular efficiency of the quadriceps mus-cles but not the hamstrings, then general strengthening programsshould be designed accordingly. Furthermore, if knee OA altersmuscle activation strategies during the STS task, then changes injoint co-ordination strategies may be observed. Such informationmay be useful for the design of more effective exercise programsfor these individuals.

Neuromuscular performance is associated not only with theability to effectively utilize the agonist muscles during a givenmovement, but also on antagonist activation (Kellis, 1998). Co-activation is defined as the concurrent activity of agonist andantagonist muscles surrounding the knee joint (Kellis and Baltzo-poulos, 1998). During single-joint maximum strength tests, theprimary role of co-activity is to increase joint stiffness and, per-haps, to stabilise the knee joint (Baratta et al., 1988; De Luca andMambrito, 1987). Antagonist activation during maximum strengthtests is higher in the elderly (Izquierdo et al., 1999) but evidence

suggests that it does not differ between women with knee OAand controls (Heiden et al., 2009). During multi-articular move-ments, however, co-activation of quadriceps and hamstring mus-cles, may serve to achieve a better control of force transfer fromthe hip to the knee via the bi-articular components of these musclegroups (Roebroeck et al., 1994). Whether such co-activity is mod-ified in people with OA during maximum strength tests and STSis not clear.

The purpose of this study was to investigate the differences inactivation during an isokinetic and STS test between women withknee OA and typical individuals. We hypothesized that the lowstrength capacity together with high co-activity might indicatethat individuals with knee OA are less efficient in performing STSmovement.

2. Method

2.1. Subjects

A total of 23 females, 12 with knee OA (age 60.33 ± 6.66 yr,height 1.61 ± 0.05 m, mass 77.08 ± 9.2 kg) and 11 controls (age56.54 ± 5.46 yr, height 1.64 ± 0.05 m, mass 77.36 ± 13.34 kg) vol-unteered to participate in this study. All women with knee OAhad grade II or III unilateral OA, as evidenced by radiographicassessment based on the (Kellgren and Lawrence (1957)) criteria.Healthy women had no pain or any injury of the knee or hip joint.All participants signed a written informed consent form, approvedby the Aristotle University Ethics Committee.

3. Instrumentation

Maximum isokinetic tests were performed on a Cybex (CYBEXDivision of Lumex, Ronkonkoma, New York) isokinetic dynamom-eter. The electromyographic (EMG) measurements were taken bya Biopac System (Biopac Systems Inc., Goleta, CA, USA) and the datawas analyzed using AcqKnowledge (Version 3.9.1., Biopac SystemsInc., Goleta, CA, USA). A twin-axis goniometer (Model TSD 130B,Biopac Systems, Inc., Goleta, CA, USA) was used to record the angu-

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G. Patsika et al. / Journal of Electromyography and Kinesiology 21 (2011) 689–694 691

lar position of the knee. A Biopac MP100 Acquisition Unit (BiopacSystems Inc., Goleta, CA, USA) was used to collect angular position,moment and the EMG signals during the test.

Table 1Mean angular speed and center of pressure location in anteroposterior (A/P) andmediolateral (M/L) axis during sit-to-stand movement in individuals with osteoar-thritis (OA) and controls.

Group n Ang. speed (�/s) Center of pressure location

A/P (%) M/L (%)Mean/SD Mean/SD Mean/SD

OA 12 44.49 ± 9.61 39.20 ± 7.02 56.24 ± 3.49Controls 11 71.68 ± 19.86* 41.95 ± 2.49* 58.76 ± 3.56

* Significantly different compared with the OA group, p < 0.05.

Fig. 2. The antagonist RMS–EMG activity of biceps femoris (BF) and the agonistvastus lateralis (VL) and vastus medialis (VM) during sit-to-stand movement inwomen with knee osteoarthritis (OA) and controls. ⁄Significantly different com-pared with the OA group, p < 0.05.

4. Procedure

4.1. Electromyography preparation

EMG signal was collected using bipolar Ag–Ag/Cl surface elec-trodes (center-to-center distance 2 cm). The skin was shaved withalcohol wipes to remove any dead cells. The electrodes were placedaccording to S.E.N.I.A.M. recommendations (Hermens et al., 2000).For the hamstrings, electrodes were placed on the long head of thebiceps femoris (BF), half way on the line between the ischial tuber-osity and the head of the fibula. The exact position for the vastusmedialis (VM) was half-way between the lateral femoral epicon-dyle and grater trochanter and for the vastus lateralis (VL) overthe distal position of the muscle, 10 cm above and medially fromthe superior border of patella. A common ground electrode wasplaced on the bony surface on the lateral epicondyle.

The EMG signal was amplified (gain 1000, input impedance10 MX, CMRR 130 dB), filtered using a band-pass filter (15–450 Hz), full-wave rectified and the root mean square (RMS) wascalculated with a step of 10 samples.

4.2. STS protocol

Participants were seated on a chair with the knee and hip angleat 90� of knee flexion (full extension: 0�). The feet were placedparallel to each other on the floor so that one limb contacted ona pressure platform (Comex S.A., Loran Engineering, Bologna, Italy).For the OA group, subjects had their affected leg on the platform,while the control group used their dominant leg. From this posi-tion, subjects rose from a chair with their hands placed on theirhips. After five practice trials, the participants performed three tri-als at normal speed (Gross et al., 1998).

The angular knee speed was estimated by numerical differenti-ation of the angular position data. The average center of pressure(CoP) position was expressed in an orthogonal system attachedto the foot data (Fig. 1) and it was normalized as percentage of footlength (A/P axis) and width (M/L), to reduce inter-subjectvariations.

In a pilot study, we found that the average angular knee jointspeed during the STS movement was approximately 55–65�/s. Forthis reason, the agonist VM and VL EMG signals during the STS move-ment were normalized as percentages of EMGs obtained duringmaximum concentric knee extensor tests at 60�/s. In turn, sincethe hamstrings work eccentrically during the STS movement, theantagonist BF EMG was normalized as a percentage of the corre-sponding EMG during maximal isokinetic eccentric effort at 60�/s.

4.3. Isokinetic protocol

Participants were secured with straps on the chair with hip flex-ion at an angle of 115�. The axis of rotation was aligned with thelateral femoral condyle. The range of motion was from 0� (fullextension) to 90�. A warm-up of three maximal efforts at protocolspeeds was performed. The main protocol consisted of five maxi-mal concentric and eccentric efforts of the knee extensors and kneeflexors at 60�/s, 120�/s and 150�/s with a rest interval of 20 s be-tween sets. Participants also performed three maximal isometriccontractions (MVC) of the knee extensors and flexors at 65� and35�, respectively.

The repetition displaying the maximum moment was furtheranalyzed. The average moment and RMS signals from 10� to 80�

of knee flexion were calculated (window selected to avoid inertialeffects). Subsequently, all agonist EMGs were normalized as a per-centage of MVC values. In addition, two types of variables wereanalyzed. First, as an index of neuromuscular efficiency, we calcu-lated the Moment-to-EMG ratio (Kellis, 1999; Tesch et al., 1990)separately for extension and flexion. For the extension, an averageEMG of VM and VL muscles was used. Second, the antagonist RMSEMG was normalized as a percentage of the RMS of the same mus-cle when acting as agonist at the same angular velocity.

5. Statistical analysis

For the STS test, group differences in muscle activation, angularspeed and CoP were examined using independent t-tests.

For isokinetic tests, a three-way analysis of variance (2 � 2 � 3)was applied to examine group differences in moment of force andEMGs for each type of muscle action (eccentric, concentric) andangular velocity (60�/s, 120�/s, 150�/s). Significant F values were fol-lowed by Tukey’s post hoc tests to determine significance betweenindividual means. The level of significance was set at p < 0.05.

6. Results

6.1. STS task

The t-tests showed that OA group demonstrated statisticallysignificant lower angular speed (t21 = 4.24, p < 0.05) and a moreposterior CoP position (t21 = 1.23, p < 0.05) than controls (Table 1).

The group EMG values during the STS test are presented inFig. 2. No statistically significant group differences in VM and VLwere found (p > 0.05). The BF activity in OA group was significantly

Page 4: Neuromuscular efficiency during sit to stand movement in women with knee osteoarthritis

Table 2Mean (±SD) moment-to-RMS EMG ratios at different testing conditions for womenwith osteoarthritis (OA) and healthy women.

n �/s Moment-to-RMS ratio

Knee extension Knee flexion

Concentric Eccentric Concentric EccentricMean/SD Mean/SD Mean/SD Mean/SD

OA 12 60 0.61 ± 0.71 1.01 ± 0.18 0.61 ± 0.11 0.37 ± 0.07Controls 11 1.20 ± 0.22* 3.07 ± 1.57* 0.36 ± 0.14 0.54 ± 0.14**

OA 12 120 0.71 ± 0.17 0.69 ± 0.20 0.41 ± 0.16 0.46 ± 0.13Controls 11 1.03 ± 0.23* 2.23 ± 0.71* 0.31 ± 0.09 0.51 ± 0.09

OA 12 150 0.30 ± 0.07 0.60 ± 0.17 0.33 ± 0.09 0.36 ± 0.09Controls 11 0.85 ± 0.21* 2.37 ± 0.86* 0.27 ± 0.05 0.55 ± 0.11**

* Significant main effect for group, values collapsed for speed and muscle action arehigher compared with OA, p < 0.05.** Significantly different compared with OA based on post-hoc analysis, p < 0.05.

692 G. Patsika et al. / Journal of Electromyography and Kinesiology 21 (2011) 689–694

(t21 = 5.08, p < 0.05) higher compared to the value observed for typ-ical individuals.

6.2. Isokinetics

As the effects of muscle action and angular velocity on isokinet-ic moment and EMG are known (Kellis and Baltzopoulos, 1998),only the interaction effects involving ‘‘group’’ differences as wellas the main effects for ‘‘group’’ will be presented.

6.3. Moment-to-EMG ratio

The Moment-to-EMG values are presented in Table 2. TheANOVA showed a non significant three-way interaction effect onextension Moment-to-EMG ratio (F2,21 = 0.21, p > 0.05). However,there was a significant main effect for group (F1,21 = 114.58,p < 0.05), as the OA group showed a lower ratio (collapsed for mus-cle action and speed conditions) than controls. For the knee flexors,there a significant three-way interaction effect on Moment-to-EMG ratio (F2,21 = 3.73, p < 0.05). Post-hoc Tukey tests indicatedthat the OA group demonstrated a lower ratio at eccentric 60�/sand 150�/s while the opposite was found for the concentric testat 60�/s (p < 0.05).

6.4. Antagonist muscle activation

The antagonist EMG values are presented in Table 3. For the BF,there was no statistically significant three-way interaction(p > 0.05). There was, however, a significant main effect for group

Table 3Antagonist muscle activation at different concentric and eccentric angular velocities betw

n �/s Antagonist muscle activation

VL VM

Concentric Eccentric CoMean/SD Mean/SD M

OA 12 60 14.08 ± 3.31 16.90 ± 7.68 13Controls 11 19.44 ± 13.16 15.02 ± 7.67 20

OA 12 120 18.19 ± 5.56 29.32 ± 13.47 25Controls 11 16.89 ± 7.76 20.99 ± 8.74 20

OA 12 150 21.61 ± 8.06 28.30 ± 9.74 26Controls 11 22.16 ± 10.74 21.83 ± 6.89 21

* Significant main effect for group, values collapsed for speed and muscle, p < 0.05.** Significantly different compared with osteoarthritis (OA) based on post-hoc analysis,

(F1,21 = 10.07, p < 0.05), as the OA group showed a greater BF antag-onist EMG compared with controls. For the antagonist VL activity,no statistically significant interaction or main effects wereobserved (p > 0.05). In contrast, there was a significant three-wayinteraction effect (F2,21 = 6.45, p < 0.05) on antagonist VM EMG.Post-hoc Tukey tests showed a higher VM EMG at eccentric 60�/sin the OA group than controls. In addition, the OA group demon-strated a significantly higher (F1,21 = 7.00, p < 0.05) VM activation(collapsed across testing conditions) than the control group.

7. Discussion

The OA women were not able to rise from a chair as easily as thecontrol group, as they displayed less knee angular speed, a moreposterior position of the CoP and higher antagonist BF activation.This was accompanied by a lower isokinetic knee extension Mo-ment-to-EMG ratio in the OA group compared with controls.

Maintaining postural balance during the STS movement isachieved when the ground reaction force vector passes in frontof the hip and the ankle, but far behind the knee (Roebroecket al., 1994; Kelley et al., 1976). Consequently, the posterior shiftof the CoP vector seen in the OA group (Table 1) indicates an alter-ation of postural balance compared with typical individuals. Thishas two implications: first, it signifies a higher leverage relativeto each joint and a higher joint loading, especially around the kneeand, second, it means that women with knee OA were at an in-creased risk to fall back to the seat.

The posterior shift of the CoP in women with knee OA is the re-sult of various changes or impairments that occur as a result of thiscondition. First, in this study the OA group displayed a much lowerknee angular speed compared with controls (Table 1). This clearlyindicates a lower strength capacity, especially of the knee exten-sors and it is in agreement with previous studies (Pai et al.,1994). This strength impairment would ultimately cause womento utilize other strategies to perform the given task. These includechanges in magnitude or timing of activation of relevant muscula-ture, an increase of activation of the weaker muscles and changesin the kinematics of the involved segments.

Second, the changes in STS task may be due to a redistributionof the moments exerted around the lower limb joints (Roebroecket al., 1994). In this study, both groups showed similar vastiiEMG (Fig. 2). It has been shown that mono-articular muscles(VM and VL) are activated during the STS movement, by exertingknee extension moment (Roebroeck et al., 1994). In this respect,one might suggest that vastii contribution to resultant knee exten-sion moment remained unaffected by OA (Fig. 2). This probably hasled to a slower STS performance, given the lower maximumstrength capacity of these individuals. However, an unaltered VM

een two groups.

BF

ncentric Eccentric Concentric Eccentricean/SD Mean/SD Mean/SD Mean/SD

.84 ± 3.78 27.09 ± 15.27 27.53 ± 9.91 21.77 ± 16.16

.09 ± 13.59* 11.27 ± 5.65*,** 23.44 ± 19.97* 17.05 ± 8.91*

.12 ± 10.29 27.28 ± 9.85 24.87 ± 4.16 26.56 ± 9.96

.08 ± 7.23* 19.90 ± 8.64* 23.85 ± 7.50* 20.84 ± 8.85*

.22 ± 9.64 33.85 ± 8.87 36.00 ± 13.07 42.42 ± 18.04

.30 ± 5.83* 31.34 ± 11.87* 16.51 ± 6.97* 29.91 ± 17.36*

p < 0.05.

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and VL activity may have served to maintain muscle stiffness(Sharma et al., 2003) and to reduce joint pain (Fisher and Pender-gast, 1997).

Roebroeck et al. (1994) proposed that due to its bi-articularfunction, the BF muscle exerts force which acts around the hip, partof which is transferred through the rectus femoris to the knee joint.If this is the case, then the OA group performed the STS movementby using the BF muscles dominantly as hip extensors so that theupper body is transferred to full extension (Lindemann et al.,2003). This seems to be in line with previous observations thatpeople with knee OA perform daily activities by utilizing theirhip muscles more than the knee muscles (Hortobagyi et al.,2004; Zeni et al., 2010). In this way, load is transferred from the af-fected (knee) to the relatively unaffected hip joint (Pai et al., 1994).However, the OA group showed a slower STS movement than typ-ical individuals. Therefore, it may be suggested that the higher BFforce (as a result of higher activation) was probably not transferredto the knee via the rectus femoris, as expected.

An alternative explanation might be that part of a higher BFactivity observed by women with knee OA is related to the needfor a better knee joint stability and stiffness due to pain and dis-comfort. This seems to be consistent with previous findings duringdaily activities (Hortobagyi et al., 2004; Zeni et al., 2010). From amechanical point of view, if the OA group performs the STS move-ment by displaying a smaller resultant knee joint moment, a sim-ilar agonist (VM and VL) and higher antagonist (BF) activation,movement performance can be considered as inefficient. This pro-vides support to previous suggestions that a higher level of muscleco-activation predominantly explains the high energetic cost ofperforming daily activities, especially in older people (Hortobagyiand DeVita, 2000).

The issue of neuromuscular efficiency in OA group is betterillustrated when examining isokinetic testing. This is becausethe amount of co-activation is expected to be lower during a sin-gle-joint (isokinetic) than a multi-joint (STS) movement (Kellis,1998). Two aspects are worth noticing: first, it appears thatthe OA group showed a lower maximum extension Moment-to-EMG ratio than typical women (Table 2). This provides sup-port to the aforementioned reduced strength capacity per unitof activation during the STS task in individuals with OA. In addi-tion, the present results indicate that knee OA mainly affectsquadriceps activation, but not the hamstrings (Slemenda et al.,1997). This may, partly, explain why the OA group tends to relyon their hamstring muscles when performing the STS movement.In fact, the unaffected neuromuscular efficiency of the hamstringmuscles during lengthening (eccentric) contractions is of partic-ular importance for people with OA, as eccentric hamstring func-tion is critical for performing various daily activities (Millingtonet al., 1992). Second, the higher antagonist activation (Table 3)observed in the OA group probably serves to stabilize the knee(Kellis, 1998) and to reduce joint pain when a subject performsa maximum isokinetic effort.

The above results collectively emphasize the inability of OAgroup to perform a typical daily activity as well as a maximum dy-namic effort. Future studies could examine whether altered muscleactivation in people with knee OA is accompanied by differentmovement strategies when performing daily movements. Moreimportantly, it should be determined how these changes in neuro-muscular performance are associated with pain, joint stability andprogression of the disease. Nevertheless, it is clear that exerciseprograms aiming to improve maximal concentric and eccentricstrength of the quadriceps, a lower knee muscle co-activationand better joint co-ordination may be more beneficial in improvingfunctional ability in OA patients.

In conclusion, this study showed that OA group rose from achair much slower and with a backward CoP shift than the con-

trols. These performance impairments might be associated with aless efficient utilization of the knee extensor muscles (less forceper unit of EMG) and, perhaps, a higher BF antagonist co-activa-tion. This leads women with OA not only to perform worse butthey may adopt alternative movement strategies to complete a gi-ven task.

Future studies could examine whether low moments producedat the hip and the knee are related to velocity dependent torquesby applying forward modeling techniques. This will allow an in-depth explanation of the changes in ground reaction forces andthe motion of the CoP during the sit-to-stand movement in womenwith knee OA.

Conflict of interest

There are no conflicts of interests.

References

Baratta R, Solomonow M, Zhou BH, Letson D, Chuinard R, D’Ambrosia R. Muscularcoactivation. The role of the antagonist musculature in maintaining kneestability. Am J Sports Med 1988;16(2):113–22.

De Luca CJ, Mambrito B. Voluntary control of motor units in human antagonistmuscles: coactivation and reciprocal activation. J Neurophysiol 1987;58(3):525–42.

Dekker J, Tola P, Aufdemkampe G, Winckers M. Negative affect, pain and disabilityin osteoarthritis patients: the mediating role of muscle weakness. Behav ResTher 1993;31(2):203–6.

Dieppe P. Management of osteoarthritis of the hip and knee joints. Curr OpinRheumatol 1993;5(4):487–93.

Fisher NM, Pendergast DR. Reduced muscle function in patients with osteoarthritis.Scand J Rehabil Med 1997;29(4):213–21.

Gross MM, Stevenson PJ, Charette SL, Pyka G, Marcus R. Effect of muscle strengthand movement speed on the biomechanics of rising from a chair in healthyelderly and young women. Gait Posture 1998;8(3):175–85.

Gur H, Cakin N. Muscle mass, isokinetic torque, and functional capacity in womenwith osteoarthritis of the knee. Arch Phys Med Rehabil 2003;84(10):1534–41.

Guralnik JM, Winograd CH. Physical performance measures in the assessment ofolder persons. Aging (Milano) 1994;6(5):303–5.

Heiden TL, Lloyd DG, Ackland TR. Knee extension and flexion weakness in peoplewith knee osteoarthritis: is antagonist cocontraction a factor? J Orthop SportsPhys Ther 2009;39(11):807–15.

Hermens HJ, Freriks B, Disselhorst-Klug C, Rau G. Development of recommendationsfor SEMG sensors and sensor placement procedures. J Electromyogr Kinesiol2000;10(5):361–74.

Hodge E, Banowsky L, Novick A, Lewis R, Streem S, Steinmuller D, et al. Alternativeimmunosuppressive strategies in the management of recipients of living relatedrenal transplants. Transplant Proc 1989;21(1 Pt 2):1609–14.

Hortobagyi T, DeVita P. Muscle pre- and coactivity during downward stepping areassociated with leg stiffness in aging. J Electromyogr Kinesiol 2000;10(2):117–26.

Hortobagyi T, Garry J, Holbert D, DeVita P. Aberrations in the control of quadricepsmuscle force in patients with knee osteoarthritis. Arthritis Rheum 2004;51(4):562–9.

Hortobagyi T, Westerkamp L, Beam S, Moody J, Garry J, Holbert D, et al. Alteredhamstring-quadriceps muscle balance in patients with knee osteoarthritis. ClinBiomech (Bristol, Avon) 2005;20(1):97–104.

Hou L, Song J, Xue Y. A study on isokinetic test for muscle strength of patients withunilateral knee osteoarthritis before total knee replacement. Chin J Rehabil Med2007;22(6):527–9.

Izquierdo M, Ibanez J, Gorostiaga E, Garrues M, Zuniga A, Anton A, et al. Maximalstrength and power characteristics in isometric and dynamic actions of theupper and lower extremities in middle-aged and older men. Acta Physiol Scand1999;167(1):57–68.

Kelley DL, Dainis A, Wood GK. In: Komi PV, editor. Mechanics and musculardynamics of rising from a seated position. Biomethanics V-B. Baltimore: University Park Press; 1976. p. 127–34.

Kellgren JH, Lawrence JS. Radiological assessment of osteo-arthrosis. Ann RheumDis 1957;16(4):494–502.

Kellis E. Quantification of quadriceps and hamstring antagonist activity. Sports Med1998;25(1):37–62.

Kellis E. The effects of fatigue on the resultant joint moment, agonist and antagonistelectromyographic activity at different angles during dynamic knee extensionefforts. J Electromyogr Kinesiol 1999;9(3):191–9.

Kellis E, Baltzopoulos V. Muscle activation differences between eccentric andconcentric isokinetic exercise. Med Sci Sports Exerc 1998;30(11):1616–23.

Lindemann U, Claus H, Stuber M, Augat P, Muche R, Nikolaus T, et al. Measuringpower during the sit-to-stand transfer. Eur J Appl Physiol 2003;89(5):466–70.

Page 6: Neuromuscular efficiency during sit to stand movement in women with knee osteoarthritis

694 G. Patsika et al. / Journal of Electromyography and Kinesiology 21 (2011) 689–694

Lord SR, Murray SM, Chapman K, Munro B, Tiedemann A. Sit-to-stand performancedepends on sensation, speed, balance, and psychological status in addition tostrength in older people. J Gerontol A Biol Sci Med Sci 2002;57(8):M539–43.

Maly MR, Costigan PA, Olney SJ. Determinants of self-report outcome measures inpeople with knee osteoarthritis. Arch Phys Med Rehabil 2006;87(1):96–104.

Millington PJ, Myklebust BM, Shambes GM. Biomechanical analysis of the sit-to-stand motion in elderly persons. Arch Phys Med Rehabil 1992;73(7):609–17.

O’Reilly SC, Jones A, Muir KR, Doherty M. Quadriceps weakness in kneeosteoarthritis: the effect on pain and disability. Ann Rheum Dis 1998;57(10):588–94.

Pai YC, Chang HJ, Chang RW, Sinacore JM, Lewis JL. Alteration in multijointdynamics in patients with bilateral knee osteoarthritis. Arthritis Rheum1994;37(9):1297–304.

Pai YC, Rogers MW. Control of body mass transfer as a function of speed of ascent insit-to-stand. Med Sci Sports Exerc 1990;22(3):378–84.

Riley PO, Schenkman ML, Mann RW, Hodge WA. Mechanics of a constrained chair-rise. J Biomech 1991;24(1):77–85.

Roebroeck ME, Doorenbosch CAM, Harlaar J, Jacobs R, Lankhorst GJ. Biomechanicsand muscular-activity during sit-to-stand transfer. Clin Biomech 1994;9(4):235–44.

Sharma L, Dunlop DD, Cahue S, Song J, Hayes KW. Quadriceps strength andosteoarthritis progression in malaligned and lax knees. Ann Intern Med2003;138(8):613–9.

Slemenda C, Brandt KD, Heilman DK, Mazzuca S, Braunstein EM, Katz BP, et al.Quadriceps weakness and osteoarthritis of the knee. Ann Intern Med 1997;127(2):97–104.

Tesch PA, Dudley GA, Duvoisin MR, Hather BM, Harris RT. Force and EMG signalpatterns during repeated bouts of concentric or eccentric muscle actions. ActaPhysiol Scand 1990;138(3):263–71.

Wheeler J, Woodward C, Ucovich RL, Perry J, Walker JM. Rising from a chair.Influence of age and chair design. Phys Ther 1985;65(1):22–6.

Yamada T, Demura S. Relationships between ground reaction force parametersduring a sit-to-stand movement and physical activity and falling risk of theelderly and a comparison of the movement characteristics between the youngand the elderly. Arch Gerontol Geriatr 2009;48(1):73–7.

Zeni JA, Rudolph K, Higginson JS. Alterations in quadriceps and hamstringscoordination in persons with medial compartment knee osteoarthritis. JElectromyogr Kinesiol 2010;20(1):148–54.

Glykeria Patsika completed her B.Ed. in Physical Edu-cation and Sport Sciences in Aristotle University ofThessaloniki and received her Master degree in Kinesi-ology (2009) from the same Department at Serres,Greece. She is currently a Doctoral student in Kinesiol-ogy at the Aristotle University of Thessaloniki and hermain research interests include muscle activation andmechanics of knee joint in people with knee osteoar-thritis.

Eleftherios Kellis is an associate professor in SportKinesiology at the Department of Physical Educationand Sports Sciences at Serres, Aristotle University ofThessaloniki, Greece. He obtained his B.Ed. in PhysicalEducation and Sport Sciences, at the Aristotle Universityof Thessaloniki, Greece (1993) and his Ph.D. at theDepartment of Movement Sciences and Physical Edu-cation, University of Liverpool, United Kingdom (1996).He has many research publications while he authored abook entitled ‘‘Neuromechanical principles of humanmuscle strength assessment’’ in 2008. He is a co-foun-der of the Laboratory of Neuromechanics at Serres,Greece and his main research interests include ham-

string muscle modeling and function, joint mechanics and clinical electromyogra-phy applications.

Ioannis G. Amiridis is an associate professor at theDepartment of Physical Education and Sports Sciencesat Serres, Aristotle University of Thessaloniki, Greece.He obtained his B.Ed. at the Department of PhysicalEducation and Sport Sciences in Aristotle University ofThessaloniki in 1987, his DEA in ‘‘Physiologie desAdaptations’’ at the Hopital Cochin – Paris V (1989) andhis PhD at the UFR-STAPS de Dijon – France (1995). Heis a co-founder of the Laboratory of Neuromechanics atSerres, Greece and his main research interests includeneuromuscular electrical stimulation, posture, aging,force variability and electromyography applications.