Kinematics and kinetics during walking in individuals with ...382087/UQ382087_OA.pdf · Kinematics...

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Kinematics and kinetics during walking in individuals with gluteal tendinopa- thy Kim Allison, Tim V. Wrigley, Bill Vicenzino, Kim L. Bennell, Alison Grimaldi, Paul W. Hodges PII: S0268-0033(16)00017-6 DOI: doi: 10.1016/j.clinbiomech.2016.01.003 Reference: JCLB 4107 To appear in: Clinical Biomechanics Received date: 17 September 2015 Accepted date: 7 January 2016 Please cite this article as: Allison, Kim, Wrigley, Tim V., Vicenzino, Bill, Ben- nell, Kim L., Grimaldi, Alison, Hodges, Paul W., Kinematics and kinetics during walking in individuals with gluteal tendinopathy, Clinical Biomechanics (2016), doi: 10.1016/j.clinbiomech.2016.01.003 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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Kinematics and kinetics during walking in individuals with gluteal tendinopa-thy

Kim Allison, Tim V. Wrigley, Bill Vicenzino, Kim L. Bennell, AlisonGrimaldi, Paul W. Hodges

PII: S0268-0033(16)00017-6DOI: doi: 10.1016/j.clinbiomech.2016.01.003Reference: JCLB 4107

To appear in: Clinical Biomechanics

Received date: 17 September 2015Accepted date: 7 January 2016

Please cite this article as: Allison, Kim, Wrigley, Tim V., Vicenzino, Bill, Ben-nell, Kim L., Grimaldi, Alison, Hodges, Paul W., Kinematics and kinetics duringwalking in individuals with gluteal tendinopathy, Clinical Biomechanics (2016), doi:10.1016/j.clinbiomech.2016.01.003

This is a PDF file of an unedited manuscript that has been accepted for publication.As a service to our customers we are providing this early version of the manuscript.The manuscript will undergo copyediting, typesetting, and review of the resulting proofbefore it is published in its final form. Please note that during the production processerrors may be discovered which could affect the content, and all legal disclaimers thatapply to the journal pertain.

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Title

Kinematics and Kinetics during walking in Individuals with Gluteal Tendinopathy

Authors & Affiliations:

Kim Allisona, Tim V Wrigley

a, Bill Vicenzino

b, Kim L Bennell

a, Alison Grimaldi

c and Paul W.

Hodgesb

a The University of Melbourne, Department of Physiotherapy, 161 Barry St, Parkville, VIC 3010

Australia

Email: [email protected] , [email protected], [email protected]

b The University of Queensland, School of Health & Rehabilitation Sciences, Brisbane, QLD

4072, Australia

Email: [email protected], [email protected]

c Physiotec Physiotherapy, 23 Weller Rd, Tarragindi, QLD, 4121, Australia

Email: [email protected]

Corresponding Author

Kim Allison

Department of Physiotherapy, University of Melbourne

161 Barry St Parkville, VIC 3010 Australia

Ph: +61 3 83444171 Fax: +61 3 8344 4188 Email: [email protected]

Word count abstract: 250

Word count main text: 4140 (proposed deletions tracked)

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Abstract

Background. Lateral hip pain during walking is a feature of gluteal tendinopathy but little is

known how walking biomechanics differ in individuals with gluteal tendinopathy. This study

aimed to compare walking kinematics and kinetics between individuals with and without gluteal

tendinopathy.

Methods. Three-dimensional walking-gait analysis was conducted on 40 individuals aged 35 to

70 years with unilateral gluteal tendinopathy and 40 pain-free controls. An analysis of covariance

was used to compare kinematic and kinetic variables between groups. Linear regression was

performed to investigate the relationship between kinematics and external hip adduction moment

in the gluteal tendinopathy group.

Findings. Individuals with gluteal tendinopathy demonstrated a greater hip adduction moment

throughout stance than controls (standardized mean difference ranging from 0.60 (first peak

moment) to 0.90 (second peak moment)). Contralateral trunk lean at the time of the first peak hip

adduction moment was 1.2 degrees greater (P=0.04), and pelvic drop at the second peak hip

adduction moment 1.4 degrees greater (P=0.04), in individuals with gluteal tendinopathy. Two

opposite trunk and pelvic strategies were also identified within the gluteal tendinopathy group.

Contralateral pelvic drop was significantly correlated with the first (R=0.35) and second peak

(R=0.57) hip adduction moment, and hip adduction angle with the second peak hip adduction

moment (R=-0.36) in those with gluteal tendinopathy.

Interpretation. Individuals with gluteal tendinopathy exhibit greater hip adduction moments and

alterations in trunk and pelvic kinematics during walking. Findings provide a basis to consider

frontal plane pelvic control in the management of gluteal tendinopathy.

Keywords

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Gluteal tendinopathy; gait; kinetics; kinematics; external hip adduction moment; walking

Highlights

Hip adduction moment during walking is larger in those with gluteal

tendinopathy

Pelvic obliquity is associated with hip adduction moment in gluteal

tendinopathy

Two trunk and pelvic strategies are seen during walking in gluteal

tendinopathy

Addressing gait biomechanics may be relevant for gluteal tendinopathy

management

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1. Introduction

Gluteal Tendinopathy (GT) is a prevalent, recalcitrant cause of hip pain (18, 54) and disability

(19) most frequently affecting women aged 40-60 years (19). Individuals with GT frequently

report lateral hip pain during walking (7, 18), which can lead to a reduction in activity levels and

subsequent detrimental effect on health and well-being (18). Although it is postulated that GT

involves abnormal biomechanics during walking (7, 25, 28, 43), there has been little formal

investigation to confirm or characterize abnormalities. Identification of biomechanics associated

with GT may guide effective treatment of this chronic condition.

GT involves tendinopathic change of the gluteus medius and/or gluteus minimus tendons (8, 33,

39), two primary hip abductors (1, 41). Previous research has identified hip abductor weakness in

individuals with GT (2, 54), which may have relevance for walking. Force from the hip abductor

muscles is required to control the position of the pelvis in the frontal plane on the stance leg

during walking (1, 23, 55). This is particularly needed in order to balance the external hip

adduction moment caused primarily by the path of the external ground reaction vector medial to

the hip (53, 55). The medio-lateral position of the trunk, and to a lesser extent the pelvis, directly

influences the medio-lateral position of the centre of mass in the frontal plane and the magnitude

of the external hip adduction moment (Figure 1); thus trunk kinematics are an important variable

for investigation during walking in individuals with GT. Pelvic position during walking in GT

has been studied by visual observation in two studies with conflicting findings (8, 54). During the

stance phase of walking, hip abductor muscle weakness has been shown to be associated with

contralateral pelvic drop and lateral pelvic translation in the frontal plane (56), likely resulting in

a shift of the body‟s center of mass away from the stance limb and a greater external hip

adduction moment. The likely net effect of these biomechanical patterns is greater loads through

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the gluteal tendons on the weight-bearing limb, which may contribute to the development or

persistence of GT.

The primary aim of this study was to compare trunk, pelvis and hip kinematics and kinetics

during walking using three-dimensional motion analysis in individuals with GT and controls with

no history of GT, lumbar spine or lower limb pain. We hypothesized that individuals with GT

would demonstrate a greater external hip adduction moment, hip adduction angle, contralateral

pelvic drop and lateral pelvic translation than controls during the stance phase of walking.

2. Methods

2.1 Participants

Forty individuals aged 35-70 years with clinical and radiological diagnosed GT, and 40 age- and

sex-comparable controls were recruited via online and local newspaper advertising. The GT and

control groups were comparable in age, height and number of males and females; however the

GT group was significantly heavier, had greater BMI and inter-ASIS distances (i.e. greater pelvic

width) (all P<0.05) (Table 1), consistent with previous descriptive studies. The median

(Interquartile Range (IQR)) duration of lateral hip pain symptoms for GT participants was 28

(28) months. The median (IQR) values of average and worst pain experienced over the past week

reported on the NRS were 5 (1) and 7 (1), respectively.

Inclusion criteria for GT participants were a primary report of unilateral hip pain at the greater

trochanter (20, 43, 54) for ≥ 3 months with an average intensity of ≥4 on an 11-point numeric

pain rating scale (NRS) („0‟ no pain‟; „10‟ worst pain imaginable). Physical assessment was

performed by a qualified physiotherapist to confirm the clinical diagnosis of GT and exclude a

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clinical diagnosis of intra-articular hip pathology; the latter defined by reproduction of groin pain

during a passive hip quadrant test (38). Clinical diagnosis of GT was defined as reproduction of

lateral hip pain ≥4/10 on the NRS with palpation of the greater trochanter (20, 54) plus at least

one pain-provocative clinical test for GT (8, 20, 26, 35): (1) Hip FADER (14), (2) Hip FADER

static de-rotation test (35) , (3) Hip FABER (46), (4) Modified Ober‟s Test (31), (5) Static hip

abduction at end range Ober‟s Test position (46) or (6) 30-second single-leg-stance test (35).

Radiological inclusion criterion was a primary MRI diagnosis of GT defined as per Blakenbaker

et al. (10). Exclusion criteria included radiological evidence of hip osteoarthritis (Kellegren

Lawrence Grade≥2 on plain X-ray (30)), BMI > 36 kg/m2 (due to difficulties with skin marker

placement for 3D gait analysis), previous lower limb surgery, any neurological or systemic

diseases affecting the musculoskeletal system. Control participants underwent phone screening

to ensure they met the following inclusion criteria: aged 35–70 years, BMI ≤ 36kg/m2, absence of

any musculoskeletal injury, lower limb surgery, neurological or systemic diseases affecting the

musculoskeletal system. Ethics approval was obtained from the institutional Human Research

Ethics Committee and all participants provided written informed consent.

2.2 GT related lateral hip pain history

In the GT group, lateral hip pain severity was measured using the NRS and reported as average

and worst pain experienced over the past week.

2.3 Walking Analysis

Participants underwent three-dimensional gait analysis while walking barefoot along a ten-metre

walkway (such that each consecutive trial was in the opposite direction along the walkway), at

their self-selected comfortable walking speed rating any pain experienced on the NRS.

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Twenty seven spherical retro-reflective markers were placed on the trunk (C7, T1, T12), pelvis

(ASIS, PSIS), and lower limb (3-marker triad over the lateral thigh, 3-marker triad over the

lateral tibial shank, lateral femoral condyles, lateral malleoli, calcaneus, second and fifth

metatarsal bases, first and fifth metatarsal heads) in accordance with Besier et al (6). Kinematic

data were recorded at 120 Hz using a twelve-camera (MX F20/F40) Vicon motion capture system

(Vicon, Oxford, UK). Ground reaction force data were collected at 1200 Hz using two force

plates (Advanced Mechanical Technology Inc., Watertown, MA) embedded in the movement

laboratory floor. Walking speed was derived from photoelectric timing gates 4 meters apart. Each

participant performed 6-15 walking trials in order to collect six trials (three in each direction)

with single full contact foot strikes on the force plate (20N threshold) for the study limb. Knee

joint center locations were derived from mean helical axes calculated from five consecutive

squats to 45 degrees knee flexion (6). Hip joint centres were determined using regression

equations by Harrington et al (27).

Marker trajectory data and ground reaction force data were low-pass filtered at 6 Hz with a dual-

pass 2nd

order Butterworth filter. Hip joint, pelvis and trunk angles were calculated from the

walking trials using Vicon BodyBuilder software (6). Pelvic angles were extracted using a

rotation-obliquity-tilt Cardan angle sequence (4). Lateral pelvic translation in the frontal plane

was represented by the distance of the calcaneal marker relative to the floor-projected midline,

defined by a vertical line from the midpoint between the ASIS markers. This value was

normalized to half the distance between the ASIS markers (to account for the likely wider base of

support with greater pelvic width (53)) and expressed as a percentage, to provide simple relative

quantification of the position of the calcaneus to the midline of the participant (0% representing

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a position of the calcaneus directly under the midline and 100% under the ASIS). Lateral trunk

lean was expressed by the frontal plane angle of the trunk segment (defined by the sternum, C7

and T10 markers) in relation to the laboratory coordinate system. Maximum values of hip

adduction, contralateral pelvic drop (obliquity), contralateral trunk lean, and lateral pelvic

translation, were determined at the time of the first hip adduction moment peak, minimum

moment in mid-stance, and second moment peak for each of the six walking trials and averaged.

Joint moments were calculated from the walking trials using inverse dynamics in Vicon Body

Builder software (UWA model (6)) and normalized to body weight times height (Nm/BW.Ht%)

to account for body size. The maximum external hip adduction moments for each trial were

determined during 0-50% and 50-100% of stance, representing the first and second hip adduction

moment peaks respectively, and the minimum value between the two peaks to represent the mid-

stance moment. The values of the six trials were then averaged.

2.4 Data analysis

For control participants, a “test hip” was designated in a random manner using a coin toss. Data

analyses were performed using Statistical Package for the Social Sciences (SPSS), version 22

(IBM, New York, USA). Data were explored for normality and homogeneity of variance prior to

analysis. Independent t-tests were used to compare descriptive data and spatiotemporal variables

of walking between groups when normally distributed, and Mann-Whitney U tests for non-

normal data. Given the potential effect of speed on walking biomechanics, an analysis of co-

variance (ANCOVA) with walking speed (velocity, m/s) as a covariate, was used to compare

kinematic and kinetic variables between the two groups. Linear regression was performed to

investigate the relationship between kinematics and the magnitude of the hip adduction moment

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in the GT group. Alpha was set at 0.05 for all analyses. The standardized mean difference (SMD)

was calculated to estimate the effect sizes for statistically significant outcomes (13).

Given that individuals can use different trunk and pelvic strategies to compensate for hip

abductor muscle dysfunction, we performed additional exploratory analysis to elucidate

subgroups within the GT group. We tested the hypothesis that different strategies were

represented in the GT group (high contralateral trunk lean and high pelvic tilt; high ipsilateral

trunk lean and reduced pelvic tilt (as recognized in hip osteoarthritis (50, 52, 56))) by

identification of participants with largest and smallest trunk lean (greater or less than one SD

from the mean) at the three moment time points and investigated the relationship between trunk

and pelvic position with linear regression for these individuals.

3. Results

Significant between-group differences were identified in all spatiotemporal variables of walking.

Participants with GT had a shorter step length (mean difference –0.04 metres; 95% CI -0.08, -

0.01, P=0.01, SMD=0.67) and walked at a slower velocity (mean difference -0.1 m/sec; 95% CI -

0.2, -0.05, P=0.001, SMD=0.75) than controls. Median (IQR) pain intensity reported during

walking in the GT group was 2 (1) on the NRS.

During the stance phase of walking, significant between-group differences were evident in both

kinetic (Table 2 and Figure 2) and kinematic variables (Table 2 and Figure 2), with between

group differences consistent if sexes were analysed separately. Individuals with GT demonstrated

a greater first peak (0-50% stance) hip adduction moment (mean difference 0.56 Nm/BW.Ht%;

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95%CI 0.1, 1.1, P=0.02, SMD=0.60), mid-stance (minimum between peaks) hip adduction

moment (mean difference 1.3 Nm/BW.Ht%; 95% CI 0.4, 1.7, P=0.002, SMD=0.69) and second

peak (50-100% stance) hip adduction moment (mean difference 1.8 Nm/BW.Ht%; 95% CI 0.8,

2.7, P<0.001, SMD=0.90).

With respect to walking kinematics (Table 2 and Figure 2), individuals with GT demonstrated

greater contralateral trunk lean at the time of the first peak hip adduction moment (mean

difference 1.2 degrees; 95% CI 0.04, 2.4, P=0.04, SMD=0.49) and greater contralateral pelvic

drop at the time of the second peak hip adduction moment (mean difference 1.4 degrees; 95%CI

0.04, 2.8, P=0.04, SMD=0.47). No significant between-group differences were identified with

respect to hip adduction angle, internal rotation angle, or lateral translation of the pelvis.

Relationships between the magnitude of the external hip adduction moment and kinematic and

spatiotemporal variables in the GT group are presented in Table 3. There was a small but

significant positive correlation between the first peak hip adduction moment and both pelvic drop

(R=0.354, R2=0.126, P=0.03) and step length (R=0.362, R

2=0.063, P=0.03). Although no

kinematic variables were significantly correlated with the magnitude of the mid-stance moment,

velocity (R=0.145, R2

=0.104, P=0.04) and step length (R=0.250, R2=0.063, P=0.03) explained

10.4% and 6.3% of the variation, respectively. Contralateral pelvic drop was positively

correlated, and hip adduction negatively correlated, with the magnitude of the second peak hip

adduction moment; pelvic obliquity explained 32.8% (R=0.573, R2=0.328, P=0.000) and hip

adduction explained 13.1% (R=0.362, R2=0.131, P=0.02) of the variation.

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As it was expected that individuals may present with several different strategies of interaction

between pelvic and trunk motion, data were also considered with respect to possible subgroups

planned a priori. Individuals with contralateral and ipsilateral trunk lean greater than 1 SD from

the mean were identified in the GT group (Figure 3). Descriptive characteristics of these

individuals and ratio of males to females were comparable in both subgroups and to the group as

a whole (Supplementary material Table 1.). Consistent with our hypothesis, when the

relationship between trunk lean and pelvic obliquity was evaluated for these “outlier” individuals,

trunk position was negatively correlated with pelvic position during stance (higher ipsilateral

trunk lean corresponded to lower pelvic obliquity, and higher contralateral lean corresponded to

higher pelvic obliquity). The correlation was significant at the time of first peak hip adduction

moment (R=-0.619, R2=0.383, P=0.03) which corresponds to the period of weight acceptance.

4. Discussion

This is the first study to evaluate walking biomechanics using 3-dimensional gait analyses in

individuals with GT and to contrast these data with observations for pain-free controls. The

principal finding of the present study is that individuals with GT demonstrated a greater external

hip adduction moment throughout the stance phase of walking than healthy controls. There were

also small, but significant, between-group differences in trunk lean during early stance and

contralateral pelvic drop during late stance. The small size of these differences was not surprising

considering our observation that there are subgroups within the GT group (comparable in age and

gender to each other and to the group (Supplementary Table 1.)) with opposite patterns of trunk

and pelvic motion during walking, presumably an indicator of poor control by the hip abductor

muscles. Of potential clinical importance for interpretation of the kinetic findings, contralateral

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pelvic drop explained a significant amount of the variability in the peak hip adduction moments,

and more than any other kinematic or spatiotemporal variable.

Given the cross-sectional study design, we are unable to establish whether the higher hip

adduction moments and kinematic differences between groups are a consequence and/or cause of

GT. The external hip adduction moment, as measured during laboratory gait analysis in this

study, must be balanced by an internal hip abduction moment. Thus a greater external adduction

moment requires a greater internal hip abduction moment which involves greater active and

passive loading of the hip abductors (12, 55); most obviously the primary hip abductor muscles

gluteus medius and minimus (1, 23), the overlying tensor fascia lata (TFL) and upper gluteus

maximus (UGM) muscles, and the iliotibial band (ITB) that arises from these two latter muscles

(1, 41). In addition, greater contralateral pelvic drop observed in late stance, and in a subgroup of

GT participants (4 females, 1 male) throughout stance, might increase gluteal tendon tensile load

as the muscle-tendon units lengthen to the point where their length-tension relationship relies

more on passive tensile loading (including tendon) than active cross-bridge overlap; and/or result

in compression of the gluteal tendons against the greater trochanter. Further longitudinal studies

are required to determine whether the greater external hip adduction moments and kinematic

patterns identified here in individuals with GT might precede the development of GT, resulting in

cumulative overload of the gluteal tendons and thus contributing to the development and/or

perpetuation of GT.

In the presence of greater external hip adduction moments during walking, it is likely that

individuals with GT require greater activation of the hip abductor muscles, in order to control the

position of the pelvis in the frontal plane. The gluteus medius and minimus muscles are the

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primary hip abductors (1, 23) and contribute an estimated 70% of the hip abductor force required

to maintain level alignment of the pelvis in single leg stance, with the remaining 30% from the

TFL and UGM muscles via their insertion into the ITB (34). As walking requires only

submaximal activation of the hip abductor muscles (42, 44, 45), it is not surprising that maximal

isometric strength has not been shown to be directly related to the external hip adduction moment

in disease-free controls (42). This relationship is likely to be altered in the presence of hip

abductor weakness or pathology. We have recently shown maximal hip abductor strength deficits

of 32% on the affected hip in those with GT when compared to controls (2). Interestingly, in the

present study, individuals with GT exhibited: (1) 33% greater mid-stance hip adduction moments,

representing the period of single leg support; (2) 25% greater hip adduction moments during late

stance; and (3) 9% greater moments during early stance. Taken together these data imply that

individuals with GT have a greater requirement for hip abductor moment development (to

balance the larger external adduction moment) but lower hip abductor strength reserve to achieve

it (2). Consequently there would be greater tensile demand on active and passive structures of the

hip abductor muscles during walking in GT, with several implications.

Tensile loading, within safe limits, is thought to provide an anabolic stimulus for tendon integrity

in healthy tendon (15, 37), whereas the cumulative effects of excessive (32, 36) or reduced (49)

tensile load are detrimental to tendon health. The gluteus medius and minimus muscles are the

primary hip abductors (1), hence if increased external load pre-dated tendon pathology, they

would theoretically be the first muscles recruited for abductor force generation with potential for

tensile tendon overload. However, radiological studies have identified atrophic changes of the

gluteus minimus and medius muscles in those with GT (40, 47, 54) from which it is tempting to

speculate that these muscles (and tendons) are experiencing a reduction, rather than an increase

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in, contractile load. Although the present study design does not permit interpretation of the

relative contribution of each of the hip abductor muscles during walking, it is plausible that

greater demand for hip abductor force would drive supplementary recruitment of the TFL and

UGM muscles that exert their abductor force through the ITB (41, 51). This would lead to tension

in the ITB, known to increase compressive forces against the greater trochanter into which the

gluteal tendons insert (9). Given the relationship between activation of these muscles and ITB

tension and compression forces at the greater trochanter, further electromyographic investigation

of the hip abductor muscles during walking in individuals with GT is justified.

Compressive forces are known to alter tenocyte cell structure, collagen type production and

expression of large proteoglycans resulting in pathological tendon changes [see (16) for review].

Compression of the gluteal tendons against the greater trochanter as a result of ITB tension and/or

increased hip adduction is thought to be a primary aetiological factor in the development of GT

(11, 17, 25). ITB stiffness in standing, as measured by shear wave elastography, increases in

parallel with external hip adduction moments in healthy individuals (48). Tateuchi et al. showed a

27% increase in the magnitude of the external hip adduction moment, manipulated by pelvic drop

and contralateral trunk lean, resulted in a 25% increase in the shear elastic modulus of the ITB in

a group of 14 healthy individuals. The present study showed 33% greater external hip adduction

moments during mid-stance and 25% greater moments during late stance in individuals with GT

than healthy controls. Taken together with the data from Tateuchi et al, this could increase

stiffness of the ITB, with a potential to induce greater compressive forces against the gluteal

tendons at their insertion into the greater trochanter, and it is plausible that this might contribute

to development of GT.

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Contrary to our hypothesis, the only kinematic variables that differed systematically between

groups during walking were contralateral trunk lean during early stance and contralateral pelvic

drop during late stance. One consideration with respect to our findings was that differences were

in the range of a few degrees and might not be detectable clinically. However, our analysis shows

that within the GT group there are individuals with a degree of pelvic obliquity and trunk lean

that would be clinically detectable above that of the control average. Consistent with our

prediction, individuals in the GT group with the greatest contralateral lean typically exhibited

greater pelvic drop than those with the greatest ipsilateral trunk lean (Figure 3). Similar patterns

have been shown to represent time dependent adaptations to the presence of hip abductor

weakness or pain in hip OA (50, 52). In early stage of hip osteoarthritis there is increased

contralateral pelvic drop in the frontal plane during walking (52), whereas over time patients

often develop an ipsilateral trunk lean to reduce the demand on the hip abductors to control the

position of the pelvis in the frontal plane (50). Although we found similar kinematic patterns and

subgroups, post hoc analysis showed that contralateral trunk lean at the three moment time points

was not related to GT-symptom duration (R=0.74, R2=0.01, P=0.66; R = 0.21, R

2=0.00, P =0.90;

R=0.13, R2=0.02, P =0.45). Identification of GT subgroups in the present study may explain the

conflicting findings of the previous studies evaluating pelvic position during walking (8, 54) and

support evaluation of trunk and pelvic position during clinical observation of gait in order to

identify specific maladaptive gait patterns in those with GT.

With respect to interpretation of the kinematic data, the significant positive relationship between

contralateral pelvic drop and the magnitude of the peak hip adduction moments has potential

clinical relevance. Contralateral pelvic drop explained more variation in the magnitude of the

peak hip adduction moments (R2=12.6% and R

2=32.8% respectively) than any spatiotemporal or

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kinematic variable, contrasting the strong relationship between walking velocity and peak hip

adduction moment in healthy controls (42).Trunk angles did not correlate well with the hip

adduction moment, likely due to the spectrum of kinematic patterns seen in the GT group (as

highlighted by subgroup analysis), and/or the trunk segment used in the present study not

representing the primary contributor to the centre of mass. Increased central adiposity has been

identified in those with GT (21) and the GT group in the present study had a larger BMI and

pelvic width than those in the control group. Taken together, this data might suggest that the

pelvic segment represents a greater contribution to the position of the centre of mass in

individuals with GT when compared to controls. Although causality cannot be confirmed it is

reasonable to speculate that greater contralateral pelvic drop contributes to greater peak hip

adduction moments during walking in individuals with GT, potentially due to the associated

increased distance of the centre of mass from the hip joint centre in the medio-lateral direction

(Figure 1).

In contrast, hip adduction was negatively correlated with the magnitude of the second hip

adduction moment explaining 13.1% of the variation. Although lower moments (associated with

increasing hip adduction) likely represent a reduction in hip abductor muscle (and tendon)

loading, hip adduction may also be associated with greater compressive force of the gluteal

tendons against the greater trochanter; both factors mechanistic for tendon injury (3). The

relationship between both hip adduction and pelvic obliquity and the magnitude of the external

hip adduction moment supports the contemporary clinical notion that frontal plane hip and pelvic

control has relevance for development and persistence of GT (5, 24).

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This study has several key strengths. First, strict inclusion and exclusion criteria ensured that

participants within the GT group had a primary clinical and radiological diagnosis of GT in the

absence of intra-articular disease. This is unlike previous studies that relied on physical

characteristics of those with GT diagnosed by retrospective radiographs and/or radiological

diagnosis without clinical assessment to define GT pathology. Second, post hoc analysis of

kinematic variables underpinning the magnitude of the external hip adduction moment aids

clinically-helpful interpretation of the kinetics recorded in participants with GT. Consistent with

previous studies, this study consisted of predominantly females and groups were matched for

numbers of females and males. A limitation is that we did not investigate the controls with MRI

to exclude tendinopathy, although they were free of any complaints of hip or lower limb pain.

Second, differences between groups in pelvic width might have influenced the magnitude of the

external hip adduction moment (by influencing the distance of the centre of mass from the hip

joint centre), but we did not find a relationship between our measure of pelvic width (inter-ASIS

distance) and the hip adduction moment. Third, individuals in the GT group were heavier and had

a BMI that fell within the pre-obese range which infers higher levels of adipose, a risk factor for

tendinopathy (22). Although individuals in the GT group were heavier, we normalized moments

to body weight and height to account for body size.

The cross-sectional design means we are unable to establish a cause and effect relationship

between GT pathology and the kinematic and kinetic differences between groups, but provides a

strong foundation for future longitudinal studies. Specifically, randomized clinical trials are

required to establish whether modification of these biomechanical issues reduce symptoms and

improve function in individuals with GT. Furthermore, EMG studies are necessary to evaluate the

neuromuscular control of the hip abductor muscles during walking.

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5. Conclusion

This study showed that individuals with GT had higher external hip adduction moments and

alterations in trunk and pelvic kinematics during walking. Although present study design cannot

inform whether these patterns are a cause or effect of GT, our data provide evidence to suggest

that consideration of walking biomechanics may be relevant for the management of GT.

6. Acknowledgements

The study was supported by the National Health Research and Medical Research Council of

Australia (Program Grant: ID631717; Research Fellowships to KB: APP1058440 PH:

APP1002190) and the Physiotherapy Research Fund (PRF Seeding Grant to KA: S14-012). The

authors would like to acknowledge the work of Ms Pippa Nicholson in recruiting case

participants for the present study.

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Table 1. Participant characteristics (mean (SD) unless otherwise stated)

Gluteal

Tendinopathy

(n=40)

Control

(n=40)

Mean

Difference

(95% CI)

P value

Age, years‡ 54 (9) 54 (9) -0.3

(-4.3, 3.8)

0.97

Height, m 1.67 (0.09) 1.66 (0.09) 0.00

(-0.04, 0.04)

0.83

Mass, kg 74 (14) 67 (12) 6.4

(0.6, 12.3)

0.03*

Body mass index, kg/m2

26.3 (4.2) 24.0 (2.6) 2.3

(0.7, 3.8)

0.01*

Inter ASIS width, mm

263 (25) 230 (21) 33

(22, 44)

<0.001*

Sex, n (%)

Female 31 (78%) 31 (78%) - -

Male 9 (22%) 9 (22%)

- -

Symptomatic (test) hip* Left = 26,

Right = 14

Left = 17,

Right = 23

- -

Symptom duration,

months‡, median (IQR)

28 (28)

0 (0)

- -

Lateral hip pain severity,

(0-10), median (IQR)

- -

Average over past

week‡

5 (1) - - -

Worst over past week‡ 7 (1) - - -

During normal

paced walking‡

3 (3.5) - - -

During fast paced

walking‡

4 (4) - - -

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‡ Data not normally distributed, * Test hip for controls designated using a coin toss

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Table 2. Group biomechanical data (mean (SD))

Gluteal

Tendinopathy

(n=40)

Controls

(n=40)

Mean Difference

(95% CI)

P value

Spatiotemporal variables

Velocity (m/sec) 1.3 (0.16) 1.4 (0.16) -0.12 (-0.19, -0.05) 0.001*

Step length (m) 0.66 (0.08) 0.71 (0.07) -0.04 (-0.07, -0.01) 0.01*

External Hip Adduction Moment (Nm/BW.Ht (%))

1st peak 6.2 (1.0) 5.6 (1.0) 0.56 (0.1, 1.1) 0.02*

Mid-stance dip 4.0 (1.6) 2.9 (1.6) 1.3 (0.4, 1.7) 0.002*

2nd

peak 7.1 (2.0) 5.3 (2.1) 1.8 (0.8, 2.7) <0.001*

Hip Adduction Angle, degrees

At 1st peak HAM 7.9 (4.0) 7.4 (4.2) 0.5 (-1.4, 2.5) 0.60

At Mid-stance

HAM

9.0 (3.8) 8.3 (3.8) 0.7 (-1.1, 2.4) 0.46

At 2nd

peak HAM 6.0 (3.8) 6.4 (4.0) -0.4 (-1.9, 1.5) 0.64

Hip Internal Rotation Angle, degrees

At 1st peak HAM -1.3 (8.6) -1.2 (8.6) 0.06 (-3.9, 4.3) 0.97

At Mid-stance

HAM

-2.0 (8.4) -2.5 (8.7) 0.5 (-3.3, 4.4) 0.78

At 2nd

peak HAM 4.7 (9.1) 4.1 (9.0) 0.6 (-3.3, 4.5) 0.78

Contralateral Pelvic Drop (pelvic obliquity) Angle a, degrees

At 1st peak HAM 4.0 (2.3) 4.2 (2.3) -0.3 (-1.3, 0.8) 0.59

At Mid-stance

HAM

3.5 (2.5) 3.7 (2.5) -0.2 (-1.3, 0.9) 0.71

At 2nd

peak HAM 4.2 (3.0) 2.8 (3.0) 1.4 (0.04, 2.8) 0.04*

Lateral Translation of Pelvis (%Inter ASIS distance/2) b

At 1st peak HAM 21.7 (7.2) 21.6 (7.6) 0.04 (-3.4, 3.3) 0.98

At Mid-stance

HAM

15.6 (8.0) 13.5 (8.5) 2.1 (-1.6, 5.9) 0.26

At 2nd

peak HAM 16.6 (8.6) 14.2 (9.1) 2.3 (-1.7, 6.4) 0.25

Trunk Angle c, degrees

At 1st peak HAM 0.50 (2.4) 1.7 (2.5) -1.2 (-2.4, -0.04) 0.04*

At Mid-stance

HAM

0.83 (2.5) 1.8 (2.4) -0.90 (-2.0, -0.24) 0.12

At 2nd

peak HAM -1.0 (2.7) 0.16 (2.6) -1.3 (-2.4, -0.2) 0.06

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Kinematic values denote angles at the time of the external hip adduction moment

(HAM) first peak, mid-stance minimum and second peak.

a Positive pelvic obliquity indicates the contralateral pelvis is dropped relative to the

stance limb

b 0% = position of the calcaneus directly under the midline, 100% = position of the

calcaneus directly under the ASIS

c Ipsilateral trunk lean is positive,

* significant between group difference.

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Table 3. Linear regression of frontal plane kinematic and spatiotemporal variables

and external hip adduction moment (HAM) during stance in individuals with gluteal

tendinopathy

1st Peak

(Nm/BW. Ht(%))

Mid-stance

(Nm/BW. Ht(%))

2nd

Peak

(Nm/BW.

Ht(%))

Hip adduction angle, degrees

At 1st

peak HAM R=0.062

R2=0.004

P=0.71

- -

At mid-stance HAM

- R=0.125

R2=0.016

P=0.44

At 2nd

peak HAM

- - R=-0.362

R2=0.131

P=0.02*

Pelvic Obliquity, degrees

At 1st

peak HAM R=0.354

R2=0.126

P=0.03*

- -

At mid-stance HAM

- R=0.067

R2=0.067

P =0.68

-

At 2nd

peak HAM

- - R=0.573

R2=0.328

P=0.000*

Lateral Translation of Pelvis, Minimum Foot Placement: ½ Inter ASIS (%)

At 1st

peak HAM R=0.277

R2 =0.077

P=0.08

-

At mid-stance HAM

- R=0.016

R2=0.000

P=0.92

-

At 2nd

peak HAM

- - R=0.105

R2 =0.011

P=0.520

Trunk Lean, degrees

At 1st

peak HAM R=0.223

R2 = 0.050

P=0.18

- -

At mid-stance HAM

- R=0.023

R2 = 0.001

P=0.89

-

At 2nd

peak HAM - - R=0.064

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R2 = 0.004

P=0.71

Spatiotemporal variables

Velocity R=0.145

R2=0.021

P=0.20

R=0.322

R2=0.104

P=0.004*

R=0.123

R2=0.015

P=0.28

Step length R=0.250

R2=0.063

P=0.03*

R=0.285

R2=0.08

P=0.01*

R=0.073

R2=0.005

P=0.52

* P<0.05

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Figure captions.

Figure 1. The external hip adduction moment represented as the resultant force

derived from the distance (D) of the centre of mass from the hip joint centre and the

ground reaction force vector. Increasing pelvic obliquity is associated with an

increased distance of the centre of mass from the hip joint centre, which can be

compensated by ipsilateral trunk lean (compensated Trendelenburg). Contralateral

trunk lean should be accompanied by greater pelvic obliquity (uncompensated

Trendelenburg)

Figure 2. Group ensemble averages for kinematic and kinetic variables. Data are

shown for GT (red) and control (black) participants as mean (solid line) and standard

deviation (dashed line).

Figure 2 caption (below figure)

FP:1/2 inter-ASIS(%) indicates the position relative position of foot placement

(calcaneus marker) to the midline of the participant (where 0% represented a position

of the calcaneus directly under the midline and 100% directly under the ASIS)

Figure 3. Evaluation of relationship between trunk lean and pelvic angle. Data are

plotted for the three hip adduction moment time-points (peaks and intervening

minimum). GT participants with trunk lean > 1 SD (as above or below the dashed

lines on the y axis corresponding with the GT group mean + 1 SD and – 1SD

respectively) are plotted against pelvic obliquity in the lower panels. Outliers in the

GT group with ipsilateral trunk lean have less pelvic obliquity, and those with

contralateral trunk lean have greater pelvic obliquity as demonstrated by the stick

figure.

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Fig. 1

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