J Appl Physiol 102: 601– 609, 2007.
First published October 12, 2006; doi:10.1152/japplphysiol.00602.2006.
Muscle pain induces task-dependent changes in cervical agonist/antagonist activity
D. Falla,1 D. Farina,1 M. Kanstrup Dahl,2 and T. Graven-Nielsen1
1
Center for Sensory-Motor Interaction (SMI), Department of Health Science and Technology,
Aalborg University, Aalborg; and 2Sector of Anesthesia, Northern Jutland, Denmark
Submitted 31 May 2006; accepted in final form 5 October 2006
experimental muscle pain; isometric contraction; electromyography;
hypertonic saline
III and IV muscle afferents are
sensitive to noxious mechanical and chemical stimuli (29, 30).
Nociceptive afferents can be elicited in humans by intramuscular injection of chemical substances, such as hypertonic
saline or capsaicin (21, 36). Experimental muscle pain has
often resulted in inhibited activation of the painful muscle.
Pain-induced inhibition of muscle activity has been observed
as decreased surface EMG signal amplitude (21, 37) and motor
unit discharge rate (15, 36).
Because decreased muscle activity has been observed with
unchanged force (14, 21), compensatory mechanisms should
occur to allow similar motor output in painful and non-painful
conditions. A possible adaptation is an acute change in muscle
fiber contractile properties induced by modification of the
extracellular environment with injection of painful substances.
However, injection of hypertonic saline is not associated with
a change in muscle fiber electrophysiological membrane prop-
A LARGE PROPORTION OF GROUP
Address for reprint requests and other correspondence: D. Falla, Center for
Sensory-Motor Interaction (SMI), Dept. of Health Science, and Technology,
Aalborg Univ., Fredrik Bajers Vej 7D-3, DK-9220 Aalborg, Denmark (e-mail:
[email protected]).
http://www. jap.org
erties (15, 21). Thus adaptation of the coordination at the level
of the muscle group acting on the joint seems a more likely
compensatory mechanism.
Results of the effect of local muscle pain on muscle group
coordination are less consistent. In isometric dorsiflexion and
plantarflexion contractions sustained until exhaustion, EMG
amplitude of both the painful and nonpainful synergic muscles
decreased with pain (9). Moreover, the relative activity of
painful and nonpainful muscles changed with fatigue, which
was considered a compensatory mechanism to maintain force
(9). However, group III and IV afferent activity is also influenced by accumulation of metabolic products with fatigue (5,
19); therefore, it is not possible to separate the effects due to
pain and fatigue on muscle coordination during sustained
contractions. The effect of muscle pain on nonpainful synergists and antagonists has also been investigated in dynamic
contractions (2, 21, 40); however, these results cannot be
directly extrapolated to isometric conditions.
The effect of local excitation of nociceptive afferents on
muscle coordination is particularly relevant in joints with
multiple degrees of freedom. The cervical spine is a complex
biomechanical system composed of numerous degrees of freedom of movement about each of its joints and at least 20 pairs
of muscles, many of which are capable of performing similar
functions (26). This system is highly redundant, and specific
forces may be produced by several combinations of muscle
actions (31). Decreased muscle activity due to pain may be
compensated, for example, by decreased antagonist or increased synergic contribution. Given the complexity of the
cervical spine musculature, the effect of pain on muscle coordination may depend on the specific direction of movement and
intensity of contraction. If force maintenance is mainly due to
reorganization among painful and nonpainful muscles, it is
expected that there would be a differential effect on the
antagonist muscles depending on the force direction and thus
the ability to recruit synergic muscles. This hypothesis has
never been tested. Therefore, the aim of the study was to
examine the effect of experimental neck pain on the EMGforce relationship in agonist and antagonist muscles during
cervical flexion and extension.
METHODS
Subjects. Fourteen volunteers (6 women) participated in the study
after providing informed consent. Subjects [age, 26.3 yr (SD 3.6);
height, 1.73 m (SD 0.11); weight, 71.9 kg (SD 14.6)] were free of
neck pain and headache at the time of testing. In addition, subjects
were excluded if they had a history of headache or orthopedic
disorders affecting the cervical spine or a history of neurological
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Falla D, Farina D, Kamstrup Dahl M, Graven-Nielsen T.
Muscle pain induces task-dependent changes in cervical agonist/
antagonist activity. J Appl Physiol 102: 601– 609, 2007. First published October 12, 2006; doi:10.1152/japplphysiol.00602.2006.—
This study examined the effect of experimental neck muscle pain on
the EMG-force relationship of cervical agonist and antagonist muscles. Surface EMG signals were detected from the sternomastoid,
splenius capitis, and upper trapezius muscles bilaterally from 14
healthy subjects during cervical flexion and extension contractions of
linearly increasing force from 0 to 60% of the maximum voluntary
contraction (MVC). Measurements were performed before and after
injection of 0.5 ml hypertonic and isotonic saline into either the
sternomastoid or splenius capitis in two experimental sessions. EMG
average rectified value (ARV) of the sternomastoid, splenius capitis,
and upper trapezius muscles and the muscle fiber conduction velocity
(CV) of the sternomastoid muscle were estimated at 5% MVC force
increments. During cervical flexion with injection of hypertonic saline
in sternomastoid, ARV of sternomastoid was lower on the side of pain
in the force range 25– 60% MVC (P ⬍ 0.05) and was associated with
a bilateral reduction of splenius capitis and upper trapezius ARV (P ⬍
0.01). During cervical extension, injection of hypertonic saline in
splenius capitis resulted in lower estimates of splenius capitis ARV on
the painful side from 45 to 60% MVC (P ⬍ 0.05), which was
associated with a bilateral increase in upper trapezius ARV estimates
from 50 to 60% MVC (P ⬍ 0.001). However, no significant change
was identified for estimates of sternomastoid ARV. Experimentally
induced neck muscle pain resulted in task-dependent changes in
cervical agonist/antagonist activity without modifications in muscle
fiber CV.
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J Appl Physiol • VOL
Questionnaire (28). Pain rating indexes based on rank values of the
word descriptors were calculated (28). In addition, words chosen by
more than 25% of subjects (n ⫽ 4) were noted.
Linear array surface EMG. Multichannel surface EMG signals
were detected from the sternomastoid muscle bilaterally using linear
adhesive arrays of 8 electrodes (bar electrodes, 5-mm ⫻ 1-mm size, 5
mm apart; LISiN-SPES Medica, Torino, Italy). The detection surface
was separated from the skin by a small cavity (⬃1 mm deep) filled
with 20 ␮l of conductive gel. Myoelectric signals were amplified
(ASE16, 16-channel amplifier, LISiN Centro di Bioingegneria, Politecnico di Torino, Torino, Italy; gain: 5,000), filtered (⫺3-dB bandwidth, 10 – 450 Hz), sampled at 2,048 Hz, and converted to 12-bit
digital samples.
Before electrode placement, the sternomastoid muscles were assessed during preliminary test contractions with a dry array of eight
electrodes (silver bars, 10- ⫻ 1-mm size, 10 mm apart) with the
subject positioned in sitting. The innervation zone location of the
sternomastoid muscle was identified from the surface EMG recordings, as described previously (13, 27). The subject’s skin was prepared
by gentle local abrasion using abrasive paste and cleaned with water
and the array electrodes were positioned between the innervation zone
and the caudal tendon region of the sternomastoid muscle. A reference
electrode was placed over the upper thoracic spine.
Bipolar surface EMG. Bipolar surface EMG was recorded with
pairs of electrodes positioned 20 mm apart (Neuroline 72001-k,
Medicotest, Ølstykke, Denmark) over the splenius capitis and upper
trapezius muscles bilaterally following skin preparation. For the
splenius capitis, electrodes were positioned over the muscle belly at
the C2-C3 level between the uppermost parts of trapezius and sternocleidomastoid. For the upper division of trapezius, the electrodes were
positioned 20 mm lateral to the midpoint along the line between the
acromion and the seventh cervical vertebra (23). Signals were bandpass filtered (10 –500 Hz), amplified (EMG amplifier, Aalborg University, Aalborg, Denmark; gain: 5,000 –10,000), and sampled at 2
kHz. Skin temperature (Ellab, Copenhagen, Denmark) over the neck
region was monitored before and after completion of the each set of
contractions throughout the experimental session.
Signal analysis. The force signal was low-pass filtered (anticausal
Butterworth filter of order 4, cutoff frequency 10 Hz) and normalized
with respect to maximum force. Muscle fiber conduction velocity
(CV) (17) and average rectified value (ARV) (16) were estimated
from the EMG signals over 250-ms windows in which the average
force was 5– 60% MVC (5% MVC increments). Thus, in all conditions, the analyzed average force levels corresponded to the same
percentage of the maximum force measured without pain. Conduction
velocity was estimated from the array channels (double differential)
that showed propagation of the action potentials with minor shape
changes (visual inspection). The average cross-correlation over all
signal pairs after alignment with the estimated delay was larger than
0.8 in all cases, indicating reliable estimates of CV (16). Estimates of
ARV were computed from the central channels of those chosen for
CV estimation. All comparisons between painful and nonpainful
conditions were performed on estimates selected from the same set of
channels.
Statistical analysis. The Wilcoxon test was used to identify differences between parameters of pain intensity, duration, area, and quality
of sternomastoid and splenius capitis muscle pain. A three-way
ANOVA was applied to the values of ARV for the sternomastoid and
splenius capitis with condition (baseline, isotonic saline, and hypertonic saline), side (ipsilateral and contralateral to the injection), and
force (5% MVC intervals; 5– 60% MVC) as repeated measures. In
addition, a three-way ANOVA was applied to the values of CV for
sternomastoid with condition (baseline, isotonic saline, and hypertonic saline), side (ipsilateral and contralateral to the injection) and
force (5% MVC intervals; 5– 60% MVC) as repeated measures.
Significant differences revealed by ANOVA were followed by post
hoc Student-Newman-Keuls pairwise comparisons. Results are re-
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disorders. Ethical approval for the study was granted by the Ethics
Committee (VN 2005/38), and all procedures were conducted according to the Declaration of Helsinki.
Procedures. Subjects were comfortably seated in a height-adjustable chair of a cervical force-measuring device (4) with their back
supported, their knees and hips in 90° of flexion, and their head
positioned in a padded head support. The adjustable head support was
fastened across the forehead, which stabilized the head and provided
resistance during cervical isometric contractions. The electrical signals from the load cells incorporated into the device were amplified
(strain gauge amplifier, Aalborg University, Aalborg, Denmark),
and their output was displayed on an oscilloscope as visual feedback
to the subject.
Subjects performed three maximum voluntary isometric contractions (MVCs) of 3- to 4-s duration in cervical flexion and extension.
The order of the MVCs was randomized between movement directions, and an interval of 5 min was provided between each set of three
contractions. Verbal encouragement was provided to induce the subject to reach a higher level in each trial. The highest value of force
recorded over the three MVCs for each direction was selected as the
reference MVC and used to calculate the submaximal targets.
A rest of 30 min followed the maximal contractions. The subject
then performed cervical flexion and extension ramped contractions,
linearly increasing the force from 0 to 60% MVC in 2 s. Visual
feedback on the oscilloscope was provided to the subject. A rest of 1
min was provided between the two movement directions. Following a
rest of 10 min, the subject repeated the ramped contractions after the
injection of isotonic saline into either the sternomastoid or splenius
capitis muscle. Following a further 10-min rest, the subject performed
the final set of ramped contractions following the injection of hypertonic saline into the same muscle as injected with isotonic saline, on
the opposite side. The order of flexion and extension was randomized
throughout the experimental session. Injections for sternomastoid and
splenius capitis muscles were conducted in two experimental sessions
separated by a minimum of 7 days. The entire experimental procedure
was repeated on the second day.
Experimental muscle pain. Experimental muscle pain was induced
by injection (27-gauge cannula) of 0.5 ml of sterile hypertonic saline
(5.8%) into the sternal head of the sternocleidomastoid and the
splenius capitis muscle. Isotonic saline (0.5 ml, 0.9%) was used as a
control injection. For all injections, subjects were positioned in
comfortable sitting. For the injection into the splenius capitis, the
needle was inserted in a caudal direction at the level of the third
cervical spinous process approximately midway between the posterior
boarder of the sternocleidomastoid and the lateral boarder of the
trapezius muscle (35). For the sternomastoid, the subject’s head was
positioned in ipsilateral lateral flexion with slight contralateral rotation. The needle was inserted into the muscle belly 2 cm cephalad to
the midpoint between the sternum and the mastoid process (35). The
bolus was injected over a 10-s period. The location and side of
injection were randomized for each experimental session. The participants were blinded to each injection and were told that one or both
might be painful.
Pain measurements. Participants were asked to verbally rate their
level of perceived pain on an 11-point numerical rating scale (NRS)
anchored with “no pain” and “the worst possible pain imaginable.”
Pain intensity ratings were obtained immediately following the injection and every 30 s until pain was no longer reported. Peak pain
intensity, time to peak pain (time point at which the maximum pain is
first reached), duration of pain, and area under the NRS-time graph
were extracted.
Participants documented the area of pain on a body chart. Pain
drawings were subsequently digitized (ACECAD D9000⫹, Taipei,
Taiwan), and pain areas were estimated. Area of local and referred
pain were calculated. Pain areas that were isolated from the area of
local pain caused by injection were selected as referred pain areas.
Quality of the pain was assessed by completion of the McGill Pain
PAIN AND NECK MUSCLE ACTIVITY
603
ported as means (SD) in the text and means and SE in the figures.
Statistical significance was set at P ⬍ 0.05.
RESULTS
Sensory characteristics of experimental neck muscle pain.
Peak pain intensity was 5.5 (SD 1.9) and 4.9 (SD 1.7) following injection of hypertonic saline into the sternomastoid and
splenius capitis muscles, respectively (P ⬍ 0.05; Fig. 1). No
significant differences were identified between the injection
sites for time to peak pain [sternomastoid, 30.0 s (SD 34.3);
splenius capitis, 34.3 s (SD 28.5 s)], duration of pain [sternomastoid, 379.2 s (SD 28.5); splenius capitis: 413.5 s (SD
26.9)], and area under the NRS-time graph [sternomastoid,
1,252.5 (SD 563.6); splenius capitis: 1,276.1 (SD 591.3)].
Fig. 2. Area of pain following the injection of hypertonic saline
into the sternomastoid and splenius capitis muscles. Sternomastoid muscle pain caused more frequent and larger area of
referred pain compared with splenius capitis pain (7 vs. 4
subjects, respectively; P ⬍ 0.05).
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Fig. 1. Pain intensity scores (mean and SE) following the injection of isotonic and hypertonic saline into the sternomastoid and splenius capitis muscles.
Significantly greater peak pain intensity was reported following injection of hypertonic saline into the sternomastoid muscle.
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Fig. 3. Representative force and EMG data from 1 subject
performing a linearly increasing cervical flexion force contraction from 0 to 60% of the maximum voluntary contraction
(MVC). Data are presented before (baseline) and during (pain)
hypertonic saline-induced sternomastoid muscle pain. A: force.
B: sternomastoid EMG ipsilateral to the injection. C: sternomastoid EMG contralateral to the injection. D: splenius capitis EMG
ipsilateral to the injection. E: splenius capitis contralateral to the
injection.
J Appl Physiol • VOL
Muscle activity during flexion. Representative force and
EMG data from sternomastoid and splenius capitis are presented in Fig. 3. During the cervical flexion ramped contraction, significantly lower estimates of ARV were identified for
the sternomastoid muscle on the side of pain from 25 to 60%
MVC following injection of hypertonic saline into the sternomastoid muscle compared with baseline values (F22 ⫽ 1.9,
P ⬍ 0.05; Fig. 4A). In addition, at force levels of 50% and
above, sternomastoid ARV was lower on the side contralateral
to the injection (F22 ⫽ 1.9, P ⬍ 0.05; Fig. 4B). In association
with reduced sternomastoid ARV at higher force levels, lower
estimates of ARV were identified for the splenius capitis (F22
⫽ 2.0, P ⬍ 0.01; Fig. 4, C and D) and upper trapezius (F22 ⫽
2.1, P ⬍ 0.01; Fig. 4, E and F) muscles bilaterally.
Following the injection of hypertonic saline into the splenius
capitis muscle, lower estimates of ARV were identified for the
splenius capitis muscle ipsilateral to the side of the injection
across all force levels during ramped cervical flexion compared
with baseline values (F2 ⫽ 2.9, P ⬍ 0.05; Fig. 5C). Moreover,
lower estimates of ARV were identified for the sternomastoid
muscle bilaterally from 15 to 60% MVC (F22 ⫽ 3.0, P ⬍
0.001; Fig. 5, A and B).
The average number of channels from which conduction
velocity was estimated was 5.6 (SD 1.5). Sternomastoid muscle fiber conduction velocity increased with increasing cervical
flexion force [across all conditions 5% MVC: 3.96 m/s (SD
1.6), 60% MVC: 5.3 m/s (SD 1.2); F11 ⬎ 6.1, P ⬍ 0.001];
however, no significant changes in CV were identified following injection of hypertonic saline in either muscle. Skin tem-
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Isotonic saline injection of the sternomastoid and splenius
capitis produced lower scores on all measured pain parameters
compared with hypertonic saline injection of the same sites
(P ⬍ 0.05; Fig. 1).
Total mapped pain areas were similar between the two
muscles [sternomastoid, 6.09 arbitrary units (SD 5.16); splenius capitis, 4.90 arbitrary units (SD 5.25); Fig. 2]. Sternomastoid muscle pain caused more frequent (number of participants,
n ⫽ 7) and larger area of referred pain [3.16 arbitrary units (SD
5.14)] compared with splenius capitis [number of participants,
n ⫽ 4; area, 1.69 arbitrary units (SD 5.24); P ⬍ 0.05; Fig. 2].
In addition, the area of referral was more commonly in the
territory of trigeminal innervation for sternomastoid muscle
pain (sternomastoid, n ⫽ 7; splenius capitis, n ⫽ 2).
For sternomastoid muscle pain, the most commonly chosen
word from the McGill Pain Questionnaire was “pressing” (n ⫽
5). The words “sharp,” “taut,” “tight,” and “annoying” were
each selected by 29% of participants (n ⫽ 4). For splenius
capitis muscle pain, the most commonly chosen word was
“tiring” and “tight,” both 36%, and the second most common
word was “taut,” at 29%. The overall pain rating index was
10.5 (SD 5.3) for sternomastoid and 9.8 (SD 8.6) for splenius
capitis pain. For the individual pain categories, the rating index
for sternomastoid and splenius capitis pain were 7.6 (SD 3.9)
vs. 7.0 (SD 5.5) for the sensory, 0.4 (SD 0.7) vs. 0.6 (SD 0.7)
for the affective, 1.0 (SD 1.4) vs. 1.1 (SD 1.5) for the evaluative, and 1.6 (SD 1.5) vs. 1.1 (SD 1.9) for the miscellaneous
category. The overall number of words chosen was 4.9 (SD
2.6) for sternomastoid pain and 4.6 (SD 3.2) for splenius
capitis pain.
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perature did not significantly change during both experimental
sessions [average, 33.5°C (SD 0.9)].
Muscle activity during extension. During the cervical extension ramped contraction, significantly lower estimates of ARV
were identified for the splenius capitis muscle on the side of
injection from 40 to 60% MVC following injection of hypertonic saline into the sternomastoid muscle compared with
baseline values (F22 ⫽ 1.7, P ⬍ 0.05; Fig. 6C).
Following injection of hypertonic saline into the splenius
capitis muscle, significantly lower estimates of ARV for the
splenius capitis muscle on the painful side were identified
during cervical extension from 45 to 60% MVC (F22 ⫽ 1.6,
P ⬍ 0.05; Fig. 7C). Reduced splenius capitis ARV was
associated with a bilateral increase in upper trapezius ARV
estimates from 50 to 60% MVC (F22 ⫽ 2.5, P ⬍ 0.001; Fig. 7,
E and F).
Cervical flexion and extension MVC force were not significantly different between days.
J Appl Physiol • VOL
DISCUSSION
Experimentally induced neck muscle pain changed cervical
agonist/antagonist activity without modification in muscle fiber
membrane properties. EMG activity was consistently reduced
in the painful agonist muscle, whereas modulation of antagonist activity depended on the task.
Subjective characteristics of experimental neck muscle pain.
Injection of 0.5 ml of hypertonic saline in the sternomastoid
and splenius capitis resulted in muscle pain of moderate
intensity, consistent with previous reports of hypertonic
saline-induced muscle pain (e.g., Refs. 22, 38). Pain evoked
in the sternomastoid muscle was of significantly greater
intensity than in the splenius capitis muscle. The difference
may reflect the smaller average cross-sectional area of
sternocleidomastoid (3.72 cm2) relative to the splenius muscle (4.26 cm2) (25). However, pain following injection of
isotonic saline in sternomastoid and splenius capitis was
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Fig. 4. Mean and SE of EMG average rectified value (ARV) of the sternomastoid (A and B), splenius capitis (C and D), and upper trapezius (E and F) muscles
across a linearly increasing cervical flexion force contraction from 0 to 60% of the MVC. Results are presented for each muscle ipsilateral and contralateral to
the side of the injection at baseline (preinjection), and following the injection of isotonic (control) and hypertonic (pain condition) saline into the sternomastoid
muscle. Significant difference of hypertonic saline condition compared with baseline: *P ⬍ 0.05; ^ P ⬍ 0.001.
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comparable, indicating that changes in intramuscular pressure due to the injection were not the main reason for the
difference in pain sensitivity. Compared with splenius capitis, the sternomastoid muscle has lower pressure pain
thresholds (33), which may reflect a greater density of
afferent fibers.
Pain areas drawn by the subjects confirmed previous
experimental studies demonstrating that splenius and sternomastoid muscle pain is frequently referred in the distribution of both cervical and trigeminal innervated areas and
may mimic the clinical representation of headache (3, 33).
Previous work has identified a correlation between pain
intensity and occurrence of referred pain (20, 24, 39).
Accordingly, a greater number of subjects (7 vs. 4) reported
referred pain and a greater area of referred pain following
noxious stimulation of the sternomastoid muscle compared
with splenius capitis. In addition, the distribution of referred
pain associated with sternomastoid muscle pain frequently
J Appl Physiol • VOL
included the oculo-fronto-temporal region, which is consistent with the distribution of the ophthalmic division of the
trigeminal nerve. Experimental studies (1, 32) and clinical
observations of headache associated with the cervical spine
(10) suggest that predominately the ophthalmic division of
the trigeminal nerve is involved in the mechanism of cervicogenic headache attributed to the convergence of cervical
afferents and the trigeminal nerve (7). Therefore, experimental sternomastoid muscle pain may be superior to splenius capitis as an experimental model of cervicogenic headache.
Effect of pain on agonist muscle activity. Injection of hypertonic saline into either the sternomastoid or splenius capitis
muscle resulted in decreased EMG amplitude when the muscle
was acting as an agonist, in agreement with previous work (21,
36). Decreased muscle activation likely reflects decreased
motoneuron discharge rate (15, 36) due to reflex inhibition
mediated by small-diameter muscle afferents. Inhibition of
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Fig. 5. Mean and SE of EMG ARV of the sternomastoid(A and B), splenius capitis (C and D), and upper trapezius (E and F) muscles across a linearly increasing
cervical flexion force contraction from 0 to 60% of the MVC. Results are presented for each muscle ipsilateral and contralateral to the side of the injection at
baseline (preinjection), and following the injection of isotonic (control) and hypertonic (pain condition) saline into the splenius capitis muscle. Significant
difference of hypertonic saline condition compared with baseline: *P ⬍ 0.05; #P ⬍ 0.01; ^ P ⬍ 0.001.
PAIN AND NECK MUSCLE ACTIVITY
607
motoneuron discharge rates is also observed as a consequence
of fatigue-induced excitation of group III and IV muscle
afferents (5, 19).
The decrease in EMG activity following hypertonic saline
injection depended on the exerted force, which may suggest
different sensitivity of motoneurons to nociceptive input depending on their size. In agreement, a differential effect of
fatigue on the discharge rate of low- and high-threshold motor
units has been observed previously (8, 11).
Effect of muscle pain on synergist and antagonist muscle
activity. The activity of muscles other than the painful muscle
was also affected, indicating a redistribution of load in the
muscle group contributing to the task. Change in muscle
coordination with pain has been shown in previous work,
although results are often contradictory. Injection of hypertonic
saline in the gastrocnemius muscle resulted in decreased gastrocnemius EMG and increased tibialis anterior EMG when it
acts as an antagonist during the gait cycle (21). However, other
J Appl Physiol • VOL
studies have identified no effect on the antagonist (6, 34) or
even decreased antagonist muscle activity during muscle pain
(12). Such opposing results may reflect different methodologies or variability in the change of motor strategy depending on
the task performed, as hypothesized in this study.
For cervical flexion, decreased sternomastoid EMG activity
following noxious stimulation of the sternomastoid muscle was
associated with a bilateral reduction of splenius capitis and
trapezius motor output that may explain the maintenance of
constant force. This strategy seems necessary considering that
sternocleidomastoid muscle is the main producer of torque in
the cervical flexor muscle group. Similarly, reduced splenius
capitis EMG activity during cervical flexion corresponded to a
bilateral reduction of sternomastoid EMG activity.
The strategy to maintain cervical extension force in the
presence of muscle pain appeared less dependent on the coordination between agonist and antagonist muscles. Pain in
splenius capitis resulted in reduced EMG activity of splenius
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Fig. 6. Mean and SE of EMG ARV of the sternomastoid (A and B), splenius capitis (C and D), and upper trapezius (E and F) muscles across a linearly increasing
cervical extension force contraction from 0 to 60% of the MVC. Results are presented for each muscle ipsilateral and contralateral to the side of the injection
at baseline (preinjection), and following the injection of isotonic (control) and hypertonic (pain condition) saline into the sternomastoid muscle. Significant
difference of hypertonic saline condition compared with baseline: #P ⬍ 0.01; ^ P ⬍ 0.001.
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capitis and a force-dependent increase in trapezius EMG activity (synergist) in the absence of changes in sternomastoid
EMG activity. Thus, for cervical extension, the observed strategy for maintaining force output in the presence of an inhibited
agonist appears to be recruitment of synergistic muscles and
not modification of antagonistic muscle activity. A contribution of cross-talk cannot be entirely excluded; however, it is
unlikely to have a major influence on the conclusions because
the results have been obtained by comparison to control conditions.
Reorganization of synergistic and antagonistic muscle activity is a response to the inhibition of the painful muscle and may
be mediated by reflex mechanisms or changes in the descending drive from higher centers to the motoneuron pool. In a
previous study, percutaneous stimulation of the motor cortex
resulted in a bilateral response for the sternocleidomastoid but
only a unilateral response for the splenius capitis muscle (18).
In agreement with this observation, during cervical flexion the
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agonist (sternomastoid) demonstrated bilateral inhibition to
muscle pain, whereas during cervical extension, the agonist
(splenius capitis) demonstrated a unilateral inhibition.
In conclusion, this study showed that local excitation of
nociceptive afferents has an inhibitory effect on the painful
muscle that is counteracted by a complex reorganization of the
motor strategy at the level of the muscle group involved in the
task. This change in muscle coordination depends on the task
so that the motor output is maintained unchanged in the painful
condition (22, 38).
ACKNOWLEDGMENTS
The authors acknowledge Per Tesch and Marco Pozzo from Karolinska
Institute for the availability of the neck force measurement device.
GRANTS
This study was supported by the Danish Technical Research Council and by
the European project “Cybernetic Manufacturing Systems” (CyberManS; con-
102 • FEBRUARY 2007 •
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Fig. 7. Mean and SE of EMG ARV are shown for the sternomastoid (A and B), splenius capitis (C and D), and upper trapezius (E and F) muscles across a linearly
increasing cervical extension force contraction from 0 to 60% of the MVC. Results are presented for each muscle ipsilateral and contralateral to the side of the
injection at baseline (preinjection), and following the injection of isotonic (control) and hypertonic (pain condition) saline into the splenius capitis muscle.
Significant difference of hypertonic saline condition compared with baseline: #P ⬍ 0.01; ^ P ⬍ 0.001.
PAIN AND NECK MUSCLE ACTIVITY
tract no. 016712). D. Falla is supported by a Fellowship received from the
National Health and Medical Research Council of Australia (ID 351678) and
a John J. Bonica Fellowship received from the International Association for the
Study of Pain.
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