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Quantifying Plantar Flexor Muscles Stiffness During Passive and Active Force
Generation Using Shear Wave Elastography in Individuals With Chronic
Stroke

Article in Ultrasound in Medicine & Biology · February 2024

DOI: 10.1016/j.ultrasmedbio.2024.01.072

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Contents lists available at ScienceDirect

Ultrasound in Medicine & Biology

journal homepage: www.elsevier.com/locate/ultrasmedbio

Original Contribution

Quantifying Plantar Flexor Muscles Stiffness During Passive and Active Force
Generation Using Shear Wave Elastography in Individuals With Chronic
Stroke
Kalthoum Belghith a,b, Mustapha Zidi a, Jean Michel Fedele b, Rayan Bou-Serhal b,
Wael Maktouf a,*
a
Bioengineering, Tissues and Neuroplasticity, UR 7377, University of Paris-Est Creteil, Faculty of Health/EPISEN, Creteil, France
b
CLINEA group, Clinique du Parc de Belleville, Paris, France

A R T I C L E I N F O Objectives: This study aims to investigate the mechanical properties of paretic and healthy plantar flexor muscles
and assesses the spatial distribution of stiffness between the gastrocnemius medialis (GM) and lateralis (GL) dur-
Keywords: ing active force generation.
Skeletal muscle Methods: Shear wave elastography measurements were conducted on a control group (CNT, n=14;
Paresis age=59.9±10.6 years; BMI=24.5±2.5 kg/m2) and a stroke survivor group (SSG, n=14; age=63.2±9.6 years;
Stiffness BMI=23.2±2.8 kg/m2). Shear modulus within the GM and GL was obtained during passive ankle mobilization at
Shear wave elastography
various angles of dorsiflexion (P0 =0°; P1=10°; P2=20°; P3=-20° and P4=-30°) and during different levels
Ankle joint
(30%, 50%, 70%, 100%) of maximal voluntary contraction (MVC). Muscle activations of GM, GL, soleus and tibia-
lis anterior were also evaluated.
Results: The results revealed a significant increase in passive stiffness within the paretic plantar flexor muscles
under high tension during passive mobilization (p<0.05). Yet, during submaximal and maximal MVC, the paretic
plantar flexors exhibited decreased active stiffness levels (p<0.05). A notable discrepancy was found between the
stiffness of the GM and GL, with the GM demonstrating greater stiffness from 0° of dorsiflexion in the SSG
(p<0.05), and from 10° of dorsiflexion in the CNT (p<0.05). No significant difference in stiffness was observed
between the GM and GL muscles during active condition.
Conclusion: Stroke affects the mechanical properties differently depending on the state of muscle activation. Nota-
bly, the distribution of stiffness among synergistic plantar flexor muscles varied in passive condition, while
remaining consistent in active condition.

Introduction impaired neural control hinders this sliding filament mechanism,

Spastic paresis, a commonly observed motor disorder that often
develops following a stroke [1], is characterized by increased muscle
tone and stiffness [2]. These symptoms are a result of various alterations
in the mechanical properties of the affected muscles [3]. Consequently,
after a stroke, these changes can significantly impact the muscles’ ability
to generate the necessary force for carrying out routine daily activities,
making rehabilitation and therapeutic interventions crucial for regain-
ing functionality [4].
The total force generation relies on both, the active force, from
contractile components and the passive force, from elastic compo-
nents, both playing significant roles in muscle function and mechan-
ical behavior [5]. The active force becomes affected due to the
disruption in neural stimulation. Actin and myosin normally interact
and slide past each other, resulting in the shortening of muscle
fibers and generating force for voluntary muscle contractions. The
leading to a decreased ability of the muscle to generate active force
and produce movement. Following a stroke, alterations also occur in
the passive force generated by the non-contractile elements of the
muscle [6]. These changes can be attributed to poststroke modifica-
tions in the structural composition and properties of elastic proteins,
which impact the magnitude of the passive force [7]. This magni-
tude depends on stiffness of both the muscle fibers and surrounding
connective tissue. As a result, modifications in passive force proper-
ties, such as resistance to stretching or deformation, significantly
influence the overall mechanical properties of the muscle [8]. Quan-
tifying the changes, in both active and passive forces, allows us to
gain a more profound insight into the mechanisms that drive muscle
adaptation when functional demands are altered after a stroke. This
understanding is crucial for the development of effective rehabilita-
tion strategies aimed at enhancing motor recovery and improving
the quality of life for stroke survivors.

* Corresponding author. Bioengineering, Tissues and Neuroplasticity, UR 7377, University of Paris-Est Cr
eteil, Faculty of Health, Cr
eteil, France.
E-mail address: wael.maktouf@u-pec.fr (W. Maktouf).

https://doi.org/10.1016/j.ultrasmedbio.2024.01.072
Received 13 October 2023; Revised 24 January 2024; Accepted 30 January 2024

0301-5629/© 2024 World Federation for Ultrasound in Medicine & Biology. All rights reserved.
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Shear wave ultrasound elastography is a technique applied for quan- Materials

tifying material proprieties of healthy and pathological muscles, such as
paretic muscles [9]. Several studies have investigated passive muscle
stiffness using shear wave ultrasound [10−12] and reported high stiff-
ness in the paretic muscle 13−15. However, the effect of stroke on mus-
cle stiffness under active conditions is still limited as highlighted by
Huang et al. [15]. Recently, we demonstrated that ankle muscle stiffness
is differently affected by stroke depending on active and passive states
of ankle muscles during dorsiflexion, as seen when comparing stiffness
during passive mobilization and while standing [16]. To date, only two
studies [3,17] have extensively explored the active state, but their find-
ings have been contradictory. Saadat et al. [17] assessed isometric con-
tractions in the biceps and observed higher stiffness on the nonparetic
side compared to the paretic side. In contrast, Lee et al. [3] found no sig-
nificant difference in SWV between paretic and control muscles during
various levels of maximal voluntary contraction. It is crucial to empha-
size that these studies exclusively focused on the upper limbs and not
the lower limbs, that are commonly affected by spastic paresis [18].
Both disuse and compensatory gait patterns resulting from lower
limb stroke impairment, such as limited range of motion and muscle
weakness in dorsiflexion [19], could potentially lead to non-uniform
muscle mechanical changes. These changes may contribute to the
observed variations in modulus values within specific joint angle ranges
[[13,15]]. Moreover, emerging evidence indicates that stroke-related
alterations, in synergistic lower limb muscles exhibit variations, with
increased stiffness, predominantly observed in the medial gastrocnemius
(GM) compared to the gastrocnemius lateralis (GL) [14]. However, little
is known about the spatial distribution of stiffness across synergistic
muscles during the generation of active force following a stroke.
The objectives of this study were: (i) to examine the mechanical
properties of the paretic and healthy plantar flexor muscles, during the
generation of passive and active forces from SWE protocol; and (ii) to
assess the spatial distribution of stiffness between the GM and GL
muscles during the generation of active force.
Materials and methods
An Aixplorer® ultrasound scanner (Supersonic Imagine, version 6.1,
Aix-en-Provence, France) was used in Shear Wave mode (musculoskele-
tal preset, penetration mode) to quantify muscle stiffness in GM and GL
using an ultrasound probe positioned parallel to the fibers (4 − 15 MHz,
SL15-4; SuperSonic Imagine, Aix-en-Provence, France). Acoustic gel was
used as an interface between the skin and the probe. The shear waves
generation and propagation through the adjacent tissues were calculated
using a speckle-tracking algorithm. Tissue displacement maps were used
to calculate shear-wave velocity (SWV, m/s) in each pixel of the map.
Then, the shear modulus (μ) was calculated as follows μ ˆ ρ : SWV 2 ,
where ρ is the muscle mass density (1000 kg/m3)
The medial regions were identified for the GM and GL using B-mode
elastography. To ensure consistent assessment of the same region under
different testing conditions, we marked the probe locations for each
region on the skin with waterproof ink. Subsequently, the ultrasound
images were exported from Aixplorer’s software for further processing
and analysis.
An isokinetic dynamometer (Biodex 4 Medical Systems, Inc, Shirley,
NY, USA) was used during the assessments. The participants were placed
in the prone position with the knee fully extended, the hip positioned at
0° and the ankle joint carefully aligned with the rotation center of the
ergometer. The ankle joint was positioned in a state where the ankle
muscles were completely relaxed. This specific position to each subject
was designated as the 0° position within the isokinetic system.
Electromyographic (EMG) data were recorded using Trigno Wirless
EMG system (Delsys, Inc., Boston, USA). Four sensors were placed on
GM, GL, Soleus (SOL) and Tibialis anterior (TA). Before attaching the
electrodes, the skin was carefully shaved and cleaned using an abrasive
cleaner and alcohol swab to reduce impedance. EMG sensors were
placed, on the belly of each muscle, in parallel to muscle fibers con-
formed to SENIAM recommendations [20]. EMG placement was care-
fully checked using ultrasound to ensure that the electrodes were
positioned longitudinally to the muscle fascicle alignment and away
from neighbouring muscles [21].

Participants Methods

28 individuals divided into two distinct groups were recruited Participants were placed in a prone position on the isokinetic
(Table 1). The control group (CNT) consisted of 14 healthy individuals machine and instructed to relax completely. From the neutral position
with no history of neurological or muscular disorders. The stroke survi- (Figure 1), the ankle joint was passively mobilized from a plantar flexion
vor group (SSG) consisted of 14 stroke survivors with spastic hemipare- to a dorsal flexion at a slow angular velocity (2°/s) to evaluate the range
sis. The study received Institutional Ethics Committee approval of motion (ROM). Participants had to remain as relaxed as possible and
(CPP2022-038=000117). The procedures were conducted according to to stop the ankle rotation when they felt a maximum stretch that they
the principles expressed in the Declaration of Helsinki. were able to tolerate [22]. From the neutral position (P0 = 0°), 4 posi-
tions were identified (P1 = 10°; P2 = 20°; P3 = -20° and P4 = -30°).
For P1 and P2 positions, the ankle was in dorsal flexion. For P3 and P4,
Table 1 the ankle was in plantar flexion. For each position, the SWE measure-
Subject characteristics ment was performed twice in each previously determined region in a
randomized order separated by a 1-min rest period. Then, participants
Characteristics CNT (n = 14) SSG (n = 14)
were asked to perform three maximal voluntary contraction (MVC) to
Sex (male: female) 9: 5 10: 4 normalize EMG data recorded during different positions [23].
Age (y) 59.9 ± 10.6 63.2 ± 9.6 Maximal and submaximal contractions were performed using the
Height (m) 1.6 ± 0.2 1.7 ± 0.1
isokinetic dynamometer (BIODEX). Participants were positioned in a
Weight (kg) 66.5 ± 11.7 77.3 ± 12.9
BMI (kg.m−²) 24.5 ± 2.5 23.2 ± 2.8 prone position with the ankle fixed in the isokinetic dynamometer’s
Time post-stroke (months) NA 6.9 ± 1.5 neutral position (P0). For Maximal contractions (100% MVC), sub-
Affected side (L: R) NA 6: 8 jects were asked to perform a sustained isometric contraction at a
Spasticity (yes:no) NA 13: 1
maximum effort. For submaximal contractions (30%, 50%, 70% of
Maximal Ankle dorsiflexion ROM 27.9 ± 5.6 22.1 ± 2.6
Maximal Isometric plantar flexors contraction 83.8 ± 9.4 32.5 ± 10.4 MVC), the participants received immediate visual feedback on their
(N/m) %MVC torque to achieve the experimenter’s target %MVC torque.
Maximal Isometric dorsiflexion contraction (N/ 40.3 ± 4.9 24.4 ± 8.9 Once the desired torque level was reached, an ultrasound image was
m) taken. For each MVC torque level, the SWE measurement was per-
Maximal activation of GM (µv) 542.4 ± 3.6 394 ± 9.8
formed twice in each muscle in a randomized order. Each trial had
Maximal activation of GL (µv) 417.7 ± 2.8 254.1 ± 5.4
a maximum duration of five seconds, and subjects were allowed rest

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Figure 1. Experimental set-up. (a) Position of the ankle joint at the relaxation position on the isokinetic system. (b) Identification of muscle regions. (c) Probe position
to determine muscle stiffness. (d) Illustration of different ankle positions.
as required. Alongside these trials, muscle activations were recorded
using EMG.
Data analysis
Data were processed using Matlab software (Matlab R2021b, Math-
Works, Natick, USA). Ultrasound images were exported from Aixplorer’s
software. Image processing converted each pixel of the color map into a
shear modulus based on the recorded color scale. Mean shear modulus
values were calculated in a 15 mm × 15 mm region of interest in differ-
ent regions of each muscle fascicular area.
The raw EMG signals recorded from the different assessments were
processed through a second-order Butterworth digital filter with a band-
pass range of 15−500 Hz to remove noise or movement interference
[24]. Then, data were smoothed using root mean square analysis (RMS)
with a 20-ms window [23]. For the MVC assessments, a moving window
with a width of 20 ms was used to find the maximum RMS EMG activity
resulting from the MVC. Finally, all RMS EMG data from the different
tests were normalized to RMS EMG during MVC [25].
Statistical analyses
The sample size was calculated using the Freeware G*Power (version
3.1.9.4) [26]. The current sample size was determined based on the
study of Lee et al. [27], which examined shear wave speeds in the bilat-
eral biceps brachii muscles of individuals with stroke using SSI24, they
reported an effect size, Cohen’s d = 1.52 when comparing the paretic
and control sides. Assuming similar effect size Cohen’ d = 1.5, control
of type I error (alpha = 0.05) and Type II error (beta = 0.90), our sam-
ple size calculations indicated that a minimum of 12 participants per
group would be required [20].
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GM, gastrocnemius medialis; GL, gastrocnemius lateralis.
Statistical analyses were performed using the Prism 7.0 software
package (GraphPad Software, Inc., San Diego, USA). The Kolmogorov-
Smirnov test was employed to verify the normality of data distribution,
while the Levene test was used to ascertain the homogeneity of variance.
When data met parametric assumptions, we applied a two-factor
ANOVA analysis (Angle × Group) for GM and GL in the passive condi-
tion. Similarly, a two-factor ANOVA analysis (% MVC × Group) was
used for the GM and GL in the active condition. To differentiate between
the GM and GL, a one-way ANOVA analysis was conducted for the shear
modulus at each angle and each MVC level. Post hoc tests were carried
out using the Bonferroni procedure following each ANOVA. The
reported values are the means ± standard deviation, with statistical sig-
nificance set at the 5% level (p < 0.05).
Results
The measurements of shear modulus in the GM and GL for each
group during passive mobilization of the ankle joint were illustrated in
Figure 2. We observed a significant main effect of Angle on both GM
(F = 27.6; p < 0.001) and GL (F = 20.8; p < 0.01). The shear modulus
increased substantially when the angle was moved from 0° to 20° of dor-
siflexion in CNT and SSG (p < 0.05) (Fig. 3). In terms of Group, there
was a significant main effect observed for both GM (F = 45.3; p <
0.001) and GL (F = 37.6; p < 0.001). The SSG showed a notably higher
shear modulus than the CNT at 20° of dorsiflexion (p < 0.05).
The shear modulus measurements taken in GM and GL for each
group during maximal and submaximal voluntary contractions were
illustrated in Figure 4. We observed a pronounced main effect of %MVC
on both GM (F = 243.6; p < 0.001) and GL (F = 199.8; p < 0.001). The
shear modulus notably escalated when %MVC increased from 30% to
100% in both the CNT and SSG (p < 0.05) (Fig. 5). Regarding the Group
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Figure 2. Shear modulus−angle relationship of gastrocnemius medialis (a) and gastrocnemius lateralis (b) of control group (CNT) and stroke survivors’ group (SSG)
during the passive mobilization of the ankle joint. *: significant difference between ankle angles (0° and 10° or 0° and 20°), p < 0.05. +: significant difference between
ankle angles (10° and 20°), p < 0.05. #: significant difference between groups, p < 0.05.

effect, we observed a significant main effect for both GM (F = 57.3; p <
0.001) and GL (F = 47.6; p < 0.001). The SSG exhibited a significantly
lower shear modulus than the CNT at 70% MVC and 100% MVC for GM,
and solely at 100% MVC for GL (p < 0.05).
The differential observations between the GM and GL muscles under
passive and active conditions were showed in Figure 6. For the passive
conditions, the one-way ANOVA analysis highlighted a marked muscle
main effect within both the CNT (F = 43.6; p < 0.001) and SSG
(F = 123.6; p < 0.001). In the CNT, the GM demonstrated a significantly
greater shear modulus in comparison to the GL at 10° (p < 0.05) and 20°
(p < 0.05) dorsiflexion angles. For the SSG, the GM’s shear modulus sur-
passed that of the GL at dorsiflexion angles of 0° (p < 0.05), 10° (p <
0.05), and 20° (p < 0.05). In the active conditions, the ANOVA analysis
revealed no significant disparity in the shear modulus between GM and
GL across the spectrum of MVC levels within both the CNT and SSG.
Discussion
The findings of the current study reveal that when subjected to high
tension during passive mobilization, the paretic plantar flexor muscles
showed an increase in passive stiffness. However, during submaximal
and maximal MVC, a contrasting observation was made, as the paretic
plantar flexors displayed reduced levels of active stiffness. Additionally,
the distribution of stiffness among the synergistic plantar flexor muscles
(GM and GL) varied in passive conditions but not in active conditions.
During passive mobilization of the ankle joint, results showed that
from 20° of dorsiflexion (Fig. 5), the paretic muscle exhibited higher
stiffness compared to the healthy muscle [10,21]. This alteration in
mechanical property within the paretic muscle could potentially be
attributed to an increase in collagen content in structures responsible for
regulating muscle elasticity, such as the perimysium, myofibrils [7], and
titin [28]. In contrast to the passive condition, during submaximal and
maximal MVC, it was observed that the healthy muscle displayed higher
stiffness than the paretic muscle (Fig. 6). These findings partially align
with the results of Saadat et al. [17], that evaluated isometric contrac-
tions in the biceps brachii and reported greater stiffness on the non-
paretic side compared to the paretic side. Conversely, Lee et al. [3]
found no significant difference in muscle stiffness between paretic and
healthy muscles during different levels of MVC. In our study, we focused
on the gastrocnemius muscles, while Lee et al. [3] examined the biceps
brachii. This could be explained by architectural and morphological dif-
ferences between the specific muscle types evaluated (biceps brachii vs.

Figure 3. Shear modulus (μ† maps in longitudinal plane of representative paretic and healthy gastrocnemii medialis during the passive mobilization of the ankle. CNT,
control groups; SSG, stroke survivors’ group.

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Figure 4. Shear modulus of gastrocnemius medialis (a) and gastrocnemius lateralis (b) during maximal and sub-maximal voluntary contractions. CNT, control groups;
SSG, stroke survivors’ group; MVC, Maximal voluntary contractions #: significant difference between groups, p < 0.05. *: significant difference between 100% vs.
70%, 50%, and 30% MVC. +: significant difference between 70% vs. 50% and 30% MVC.

gastrocnemius). In fact, various factors, such as differences in pennation
angle, fascicle length, and the presence of stiffer aponeuroses, can lead
to muscle-specific variations in the stress-strain relationship during
active contractions [29]. For example, Koo et al. [30] have shown corre-
lations between stiffness and architectural parameters, including cross-
sectional area and muscle mass. Additionally, Bernabei et al. [31] dem-
onstrated variability in stiffness among muscles with different architec-
tural characteristics, specifically the pennation angle, in muscles such as
the biceps brachii (parallel fibers), and gastrocnemius (highly pennate).
It is also worth considering the potential impact of tendon stiffness on
our results, as tendon compliance can play a significant role in the length
changes of muscle-tendon units under tension [32]. In the case of the
swine brachialis muscle [3], which has negligible tendon at both the ori-
gin and insertion, we can reasonably assume minimal tendon strain
[33], unlike the gastrocnemius muscle with the Achilles tendon, which
could contribute to passive stiffness. The lower active stiffness observed
in paretic plantar flexor muscles during MVC could be explained by
structural and architectural changes related to spastic paresis [34]. The
active stiffness is related to the actin-myosin cross-bridge attachment,
and it has been demonstrated that the paretic muscle undergoes several
changes in intrinsic properties, including extracellular matrix, contrac-
tile tissue, and intracellular proteins [28]. These changes could reduce
the number of attached cross-bridges [35] and could be responsible for
alterations in the actin and myosin filaments, thus causing a decrease in
the active stiffness of the paretic muscle [36]. There is evidence suggest-
ing that titin filaments play a role in muscle stiffness [37]. Titin is known
to contribute to muscle stiffness, particularly during activation, as it
undergoes changes in its material properties and adjusts its free spring
length [35]. Additionally, the interaction between titin, actin, and myo-
sin can impact the material properties of the muscle [37,38]. Any modi-
fications in the properties of titin and its interaction with other
components of the muscle, resulting from a stroke, may have an influ-
ence on the overall stiffness of the muscle.
The reason for the decrease in active stiffness in the paretic muscle,
despite higher passive stiffness, remains unclear. If we assume that
when muscles are in the active state, the stiffness measured corresponds
to the total stiffness [5], involves both elastic and contractile compo-
nents of the muscle. it is possible that the contribution of active compo-
nents to total stiffness is much greater than the contribution from
passive components, particularly at higher levels of activation [3]. The

Figure 5. Shear modulus (μ† maps in longitudinal plane of representative paretic and healthy gastrocnemii medialis during maximal and submaximal voluntary con-
traction. CNT, control groups; SSG, stroke survivors’ group; MVC, Maximal voluntary contraction.

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Figure 6. Comparison between the gastrocnemius medialis and lateralis during the passive (a) and active (b) conditions. *: significant difference between muscles, p <
0.05
increase in passive stiffness observed in the paretic muscle becomes
inconsequential when the muscle is activated, as any contribution of
passive stiffness to total stiffness becomes negligible. This phenomenon
could be attributed to the relative mass of contractile versus noncontrac-
tile tissue in a large muscle, such as the gastrocnemius. It is important to
highlight that the assessment of active stiffness in our study was con-
ducted during isometric contractions at a neutral position of 0°. Interest-
ingly, no significant difference in passive stiffness was observed
between the paretic and healthy groups at this position, with values
being consistently low. These findings provide further support for the
hypothesis that the overall stiffness is primarily influenced by the active
component, which is significantly impacted by the stroke. This suggests
that the alterations in active stiffness resulting from the stroke play a
critical role in the observed changes in total stiffness. To confirm this
hypothesis, future studies should explore active stiffness in various con-
traction angles or modalities.
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Results demonstrated significant variations in passive stiffness
between the GM and GL muscles [39−41], which may be attributed to
the structural characteristics of the human triceps surae and Achilles ten-
don [42]. While the GM and GL muscles merge via their aponeuroses
into a common Achilles tendon to insert on the calcaneus, the GM mus-
cle has a more distal muscle-tendon junction [43], potentially influenc-
ing the distribution of passive stiffness. Furthermore, the Achilles
tendon is built up of fascicles, which originate from the parts of the tri-
ceps surae [44,45]. Namely, the fascicles formed by the tendon fibers of
the Achilles tendon can be torn separately, suggesting that they work
independently [46], potentially contributing to the observed differences
in passive stiffness between the GM and GL muscles.
When examining active stiffness, our results yielded no significant
divergence between the GL and GM muscles under different levels of
MVC, irrespective of whether the muscles were in a paretic or healthy
state. The uniformity of stiffness distribution exhibited in both GM and
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K. Belghith et al.
GL muscles, despite their distinct anatomical characteristics, under-
scores the multifaceted interplay of muscle properties and their
responses to various physiological conditions. Typically, the GL is associ-
ated with longer fascicle lengths in contrast to the GM [47], while the
GM is characterized by its shorter fascicle lengths and more pronounced
fascicle angles [48]. Yet, these architectural variances, contrary to what
might be anticipated, do not seem to substantively affect the distribution
of stiffness between the GM and GL. This is true for paretic and healthy
states, suggesting that the interrelationship between muscle stiffness
and architecture may not be as straightforward as once thought. This
observation finds resonance with the study of Cui et al. [49], demon-
strating that the stiffness of muscles in felines exhibited a linear relation-
ship with force, and this relationship held steady across different muscle
architectures. This consistent behavior might imply a level of universal-
ity in the muscle’s mechanical response to force irrespective of its archi-
tectural makeup. This leads us to suggest that the SWV, an indicator of
tissue stiffness, may remain invariant across muscles when activation
and sarcomere lengths are kept constant. This implies that variations in
the actively generated forces would proportionally influence the SWV
[31,33]. Given these findings, it is apparent that muscle force and archi-
tectural characteristics are interconnected in complex ways that require
more comprehensive investigations. This is crucial as it will not only
deepen our understanding of muscle biomechanics but may also pave
the way for more targeted therapeutic approaches in conditions such as
poststroke muscle alterations.
Limitations and perspectives
A limitation of this study was the measurement of the SWV in penni-
form muscles. It has been suggested that measurement of SWV with
small deviations from the fiber direction, as described by the probe-fas-
cicle angle, may be potentially inaccurate [27]. Thus, the muscular
architecture in terms of pennation can influence SWV [50]. However, it
should be noted that previous studies on the gastrocnemius muscle have
shown relative reproducibility of stiffness measurements [51]. In addi-
tion, we utilized the shear modulus as an indicator of stiffness, assuming
a density of 1000 kg/m³. However, pathological conditions such as spas-
tic myopathy can alter density. Thus, further studies could verify this
hypothesis and enhance our understanding of these potential variations.
Based on clinical classification of stroke, stroke survivors in this study
were in the chronic phase, which corresponds to a limit in the temporal
study. As a result, it would be interesting to investigate mechanical prop-
erties change of the paretic muscle when stroke survivors are in the
acute or subacute phases.
Conclusion
From SWE, this study aimed to investigate the mechanical properties
of paretic plantar flexor muscles during passive and active force. Our
findings revealed a significant increase in passive stiffness within the
paretic plantar flexor muscles under high tension during passive mobili-
zation. However, during submaximal and maximal MVC, a contrasting
observation was made, as the paretic plantar flexors displayed reduced
levels of active stiffness. Notably, the distribution of stiffness among syn-
ergistic plantar flexor muscles varied in passive condition, while remain-
ing consistent in active condition. These observations underscore the
importance of considering the contractile component when quantifying
muscle stiffness. By gaining a deeper understanding of how mechanical
properties are modified in response to passive and active muscle behav-
iors, these results hold significant clinical implications.
Data availability
The raw data supporting the conclusion of this article will be made
available by the authors, without undue reservation.
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Author contributions
This work was equally contributed by KB and WM. MZ: conceptuali-
zation, resources, validation; KB and WM: writing original draft, meth-
odology; MZ, J-M F and R B-S: instructing, review; KB and WM: data
collection and analysis; J-M F and R B-S: instructing; MZ: review. All
authors contributed to the article and approved the submitted version.
Funding
This research received no specific grant from any funding agency in
the public, commercial, or not-for-profit sectors.
Competing of interest disclosure
The authors declare that the research was conducted in the absence
of any commercial or financial relationships that could be construed as a
potential conflict of interest.
Acknowledgments
The authors acknowledge the contribution of the medical staff and
the managers of the “Clinique du Parc de Belleville” for their help in the
recruitment and monitoring of patients and the organization of the con-
duct of the experimental protocol. This study was conducted with the
support of CLINEA group.
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