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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
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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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Fig. 2
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Fig. 3