Effects of exercise-induced low back pain on intrinsic trunk stiffness
and paraspinal muscle reflexes
Emily M. Millera, Babak Bazrgarib, Maury A. Nussbauma,c, Michael L. Madigana,d,n
aVirginia Tech—Wake Forest School of Biomedical Engineering and Sciences, Blacksburg, VA, USA
bCenter for Biomedical Engineering, University of Kentucky, Lexington, KY, USA
cDepartment of Industrial and Systems Engineering, Virginia Tech, Blacksburg, VA, USA
dDepartment of Engineering Science and Mechanics, Virginia Tech, Blacksburg, VA, USA
a r t i c l e i n f o
Accepted 3 November 2012
Low back pain
a b s t r a c t
The purpose of this study was to (1) compare trunk neuromuscular behavior between individuals with
no history of low back pain (LBP) and individuals who experience exercise-induced LBP (eiLBP) when
pain free, and (2) investigate changes in trunk neuromuscular behavior with eiLBP. Seventeen young
adult males participated including eight reporting recurrent, acute eiLBP and nine control participants
reporting no history of LBP. Intrinsic trunk stiffness and paraspinal muscle reflex delay were
determined in both groups using sudden trunk flexion position perturbations 1–2 days following
exercise when the eiLBP participants were experiencing an episode of LBP (termed post-exercise) and
4–5 days following exercise when eiLBP had subsided (termed post-recovery). Post-recovery, when the
eiLBP group was experiencing minimal LBP, trunk stiffness was 26% higher in the eiLBP group compared
to the control group (p¼0.033) and reflex delay was not different (p¼0.969) between groups. Trunk
stiffness did not change (p¼0.826) within the eiLBP group from post-exercise to post-recovery, but
decreased 22% within the control group (p¼0.002). Reflex delay decreased 11% within the eiLBP group
from post-exercise to post-recovery (p¼0.013), and increased 15% within the control group (p¼0.006).
Although the neuromuscular mechanisms associated with eiLBP and chronic LBP may differ, these
results suggest that previously-reported differences in trunk neuromuscular behavior between
individuals with chronic LBP and healthy controls reflect a combination of inherent differences in
neuromuscular behavior between these individuals as well as changes in neuromuscular behavior
elicited by pain.
& 2012 Elsevier Ltd. All rights reserved.
Low back pain (LBP) continues to be a significant health and
economic problem in the United States (US) and around the
world. An estimated 60–80% of all adults experience LBP at some
point in their lifetime (van Tulder et al., 1995), and annual health
care costs in the US associated with LBP exceed $90 billion (Luo
et al., 2004). Numerous studies have reported differences in trunk
neuromuscular behavior between individuals with and without
LBP. For example, individuals with chronic LBP exhibit longer
paraspinal reflex delays (Radebold et al., 2000; Radebold et al.,
2001; Reeves et al., 2005), increased sway while sitting on an
unstable seat (Radebold et al., 2001), and increased trunk muscle
activity during slow trunk motions and isometric voluntary
contractions while sitting (van Dieen et al., 2003a). While these
descriptive studies suggest altered trunk neuromuscular beha-
viors that adversely affect spinal loads and stability (i.e., reduced
stability and higher spinal loads), and which thereby may
increase the risk of injury and pain, they are unable to discern
whether these alterations were in response to LBP or whether
they existed prior to the development of LBP.
To help understand the relationship between altered neuro-
muscular behavior and LBP, prior work has investigated changes
in neuromuscular behavior after experimentally inducing LBP.
Experimentally-induced LBP, caused by injecting a saline solution
into the lumbar longissimus muscle, leads to decreased trunk
motion during walking (Moe-Nilssen et al., 1999) and quiet
standing (Smith et al., 2005), and altered trunk muscle activation
(delayed onsets and decreased amplitudes) during a postural task
involving rapid arm movements (Hodges et al., 2003). A recent
study induced LBP using noxious heat applied on the skin, which
decreased lumbar spine movement relative to the hip while
performing trunk flexion (Dubois et al., 2011).
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0021-9290/$-see front matter & 2012 Elsevier Ltd. All rights reserved.
nCorresponding author at: Engineering Science and Mechanics (0219), Virginia
Tech, Blacksburg, VA 24061, USA. Tel.: þ1 540 231 1215; fax: þ1 540 231 4574.
E-mail addresses: email@example.com, firstname.lastname@example.org (M.L. Madigan).
Journal of Biomechanics 46 (2013) 801–805
The decreased voluntary trunk/spine motion in these studies is
consistent with increased trunk stiffness and may thus represent
a central nervous system response to LBP to help minimize pain
and further injury (Dubois et al., 2011; Hodges and Moseley,
2003; Smith et al., 2005; van Dieen et al., 2003a).
An alternative approach, to further our understanding of the
relationship between trunk neuromuscular behavior and LBP, is to
study individuals who experience recurrent, acute, exercise-
induced LBP (eiLBP). This approach provides the opportunity to
determine whether neuromuscular behavior is altered among
these individuals when they are not experiencing pain, which
would suggest that altered neuromuscular behavior is an inherent
characteristic of selected individuals that may contribute to the
development of LBP. This approach can also determine if/how
neuromuscular behavior changes with pain. Any such changes
would suggest that altered neuromuscular behavior is a response
to LBP. Therefore, the purpose of this study was to compare trunk
neuromuscular behavior between individuals with no history of
LBP and individuals who experience eiLBP when pain free, and to
investigate changes in trunk neuromuscular behavior with eiLBP.
Our general expectations were that neuromuscular behavior
would differ between groups when the eiLBP group was not
experiencing pain, and respond differently to exercise between
groups. The following two specific hypotheses were tested: 1)
neuromuscular behavior differs between an eiLBP group when not
experiencing pain and a healthy control group, and 2) neuromus-
cular behavior responds differently to exercise in an eiLBP group
compared to a healthy control group. Trunk neuromuscular
behavior was quantified using measures of intrinsic trunk stiff-
ness and paraspinal reflex delay, using sudden trunk flexion
perturbations, and differences/changes in either measure were
used to indicate differences/changes in underlying neuromuscular
Seventeen males, all members of the Virginia Tech Triathlon Club, completed
the study. Only males were included to avoid the influence of gender differences
in intrinsic trunk stiffness (Miller et al., 2012) and paraspinal muscle reflex delay
(Miller et al., 2010). Eight of the participants reported experiencing recurrent,
age¼20.7(1.0)yr) and nine control participants reported no history of LBP
(stature¼1.79 (0.03) m; mass¼70.8(7.3) kg; and age¼20.4(1.6)yr). None of the
anthropometric or age differences between groups were significant (p40.05 from
unpaired t-tests). Participants with eiLBP were required to pass a screening by a
chiropractic physician that evaluated their ability to complete the experiment
without further injury and ensured agreement with specific inclusion and
exclusion criteria. Participants were included if they had recurrent acute eiLBP
for at least six months, and excluded based on any neurological deficits, vestibular
or visual disorders, major structural deformities of the spine, genetic spinal
disorders, spinal surgery within the past five years, or spinal mechanical implants.
The study protocols were approved by the Virginia Tech Institutional Review
Board, and written consent was obtained from all participants prior to data
Neuromuscular behavior was characterized in each participant during two
experimental sessions. The first session (post-exercise) was 1–2 days following a
triathlon race or simulated race, when the eiLBP participants were experiencing an
episode of LBP. The second session (post-recovery) was 4–5 days following the
triathlon activity, when eiLBP had subsided. The control group participated in
experimental sessions on the same schedule (although they did not experience
eiLBP). A visual analog scale (Scott and Huskisson, 1976) (VAS) was used for rating
LBP during each session, and which quantified LBP on a numerical scale with text
descriptors from 0 (none) to 10 (agonizing pain). During the first session, the eiLBP
group provided a mean rating of 2.54 (0.91), which was between ‘‘annoying’’
(2) and ‘‘uncomfortable’’ (4), and is similar to that reported by chronic LBP
individuals who exhibited increased sway measures while sitting compared to
controls (Radebold et al., 2001). During the second session, each eiLBP participant
provided lower ratings, and the mean (SD) decrease was 1.16(0.74), which was
significantly a zero (paired t-test, po0.001). All members of the control group
provided ratings of 0 during both sessions.
Intrinsic trunk stiffness and paraspinal muscle reflex delay were determined
using trials of sudden trunk flexion position perturbations (Bazrgari et al., 2011a;
Bazrgari et al., 2011b; Hendershot et al., 2011; Miller et al., 2012). Participants sat
upright in a rigid metal frame (Fig. 1), were strapped in at the pelvis, and were
attached to a servomotor (Kollmorgen AKM53K, Radford, VA, USA) at the T8 level
of the spine via a rigid harness/rod system. The motor height, foot height, and rod
length were adjustable, and were configured so that the rod was horizontal, the
trunk was upright, and the included hip angle was 90 degrees. During each
40-second perturbation trial, the motor applied a series of 12 anterior and 12
posterior position perturbations, each moving the rod 10 mm over ?40 ms (peak
velocity of 360 mm/s), which is faster than typical erector spinae reflex delays
(Granata et al., 2004; Hwang et al., 2008). Pseudorandom delays between each
perturbation minimized participant anticipation, and participants were instructed
to maintain an upright trunk and otherwise not attempt to resist or intervene with
the perturbations. A real-time visual display of erector spinae (ES) and rectus
abdominus (RA) electromyographic activity (EMG, see below) was used to
minimize muscle activity during the perturbations. One practice trial was
completed prior to a subsequent trial used for analysis.
During each perturbation trial, motor displacement was sampled at 1000 Hz
using an encoder on the motor shaft, and trunk position was sampled at 1000 Hz
with a CCD laser displacement sensor (Keyence LK-G 150, Osaka, Japan) focused
on the midline of the dorsal aspect of the harness just above the rod (Fig. 2). To
account for the vertical offset between the laser sensor and the connecting rod,
laser measurements were multiplied by the ratio of these heights (relative to
L5S1). Forces in the connecting rod were sampled at 1000 Hz using an in-line load
cell (Interface SM2000, Scottsdale, AZ, USA). Muscle activity was monitored using
EMG electrodes (bipolar Ag/AgCl) placed bilaterally over the ES (?3 cm from the
midline at the L1 level) and RA muscles. Raw EMG signals were amplified and
bandpass filtered (20–500 Hz) in hardware (Measurement Systems Inc., Ann
Arbor, MI, USA), sampled at 1000 Hz, then full-wave rectified and smoothed using
a 25 Hz zero-phase-lag low-pass Butterworth filter. Displacement and force data
were low-pass filtered at 10 Hz (7th-order, zero-phase-lag Butterworth filter).
Intrinsic trunk stiffness was estimated with a two degree-of-freedom model of
the trunk and harness/rod connection as described elsewhere (Bazrgari et al.,
Fig. 1. Experimental set up for measurements of trunk neuromuscular behavior in
a seated posture.
Fig. 2. Representative data illustrating motor displacement as measured by
encoder, trunk displacement as measured by laser, perturbation force as measured
by load cell (LC), and EMG from ES. Figure adapted from Bazrgari et al., 2011b.
E.M. Miller et al. / Journal of Biomechanics 46 (2013) 801–805
2011a; Bazrgari et al., 2011b; Hendershot et al., 2011). Briefly, inputs to the model
were the displacements collected from the motor encoder and laser sensor along
with their numerically-calculated 1st and 2nd derivatives. The model output was
an estimated force response. Model parameters of stiffness, damping, and effective
mass (i.e. the driving point mass) were determined for each degree of freedom,
using a curve fit routine in MATLAB (MathWorks, Natick, MA, USA) that minimized
the sum of squared differences between estimated and measured force time series
for each anterior perturbation. Initial efforts revealed an inability to consistently
differentiate stiffness and damping, likely due to the short time interval over
which the analysis was conducted. As such, trunk damping was set to zero, similar
to previous studies (Bazrgari et al., 2011a; Gardner-Morse and Stokes, 2001;
Hendershot et al., 2011). Therefore, changes in trunk mechanical behavior here
were represented by changes in stiffness and effective mass. The model was fit to
each of the 12 anterior trunk position perturbations within each trial using only
data when the load cell measured a tensile force (i.e. when the trunk was being
pulled forward by the motor). Only the value of trunk stiffness derived from the
best model fit within each trial was used. The between-day reliability of stiffness
estimates using this approach is very good, as demonstrated by an ICC¼0.82
(Hendershot et al., 2012). Paraspinal reflex delay was determined for the same
perturbation, and was defined as the time between motor position onset and the
onset of L1 level ES muscle activity (averaged across left and right sides). Motor
position onset and ES muscle activity onset were determined as the instant that
each signal exceeded its mean baseline (over 40 ms) plus two standard deviations,
and all onsets were visually confirmed. Baseline paraspinal EMG amplitude was
defined as the mean muscle activity over the 400 ms prior to the onset of the
Separate two-way, mixed-factor analyses of variance were used to investigate
the effects of group, session, and their interaction on intrinsic stiffness, reflex
delay, effective mass, peak trunk velocity, and baseline paraspinal EMG amplitude.
Significant interaction effects were explored using simple effects testing. All
statistical tests were conducted using JMP 8 (SAS Software, Cary, NC, USA) with
a significance level of pr0.05.
Intrinsic trunk stiffness exhibited a significant group ? session
interaction (p¼0.032; Fig. 3a). Trunk stiffness was not different
(p¼0.978) between eiLBP and control groups post-exercise, but was
26% higher in the eiLBP group compared to the control group post-
recovery (p¼0.033). In addition, trunk stiffness did not change
(p¼0.826) within the eiLBP group from post-exercise to post-
recovery, but decreased 22% within the control group (p¼0.002).
Paraspinal muscle reflex delay exhibited a significant group ?
session interaction (p¼0.001; Fig. 3b). Reflex delay was 29%
longer in the eiLBP group compared to the control group post-
exercise (p¼0.006), but was not different (p¼0.969) between the
eiLBP and control group post-recovery. In addition, reflex delay
decreased 11% within the eiLBP group from post-exercise to post-
recovery (p¼0.013), and increased 15% within the control group
Effective mass decreased 14.5% from post-exercise to post-
recovery (post-exercise: 15.973.25 kg; post-recovery: 13.67
3.98 kg; p¼0.010), but there was not a main effect of group (eiLBP:
15.773.70 kg; control: 13.973.74 kg; p¼0.268) or group?session
interaction (p¼0.415). Peak trunk velocity did not differ between
groups (eiLBP: 276725 mm/s; control: 271713 mm/s; p¼0.674),
or between sessions (post-exercise: 275720 mm/s; post-recovery:
273720 mm/s; p¼0.697), and there was no group?session inter-
action (p¼0.808). Paraspinal EMG amplitude prior to perturbations
did not differ between groups (eiLBP: 5.4672.88% MVC; control:
7.5173.75% MVC; p¼0.225), decreased 14.3% from post-exercise to
6.0473.33%MVC; p¼0.027), and exhibited no group?session inter-
Participants in the current study were in a phase of their
triathlon training during which they performed exercise sessions
every weekend and used the weekdays to recover prior to the next
exercise session the following weekend. Thus, our post-recovery
measurements can also be considered pre-exercise measurements
for the following weekend exercise, assuming there are no cumu-
lative effects across subsequent weekend exercise sessions. Hence,
the response of each group to exercise can be inferred by
considering changes from post-recovery to post-exercise measure-
ments. Our first hypothesis was that neuromuscular behavior
would differ between the eiLBP group when not experiencing pain
and the control group. This hypothesis was supported because the
eiLBP group exhibited higher trunk stiffness (but not reflex delay)
post-recovery. Our second hypothesis was that neuromuscular
behavior would respond differently to exercise in the eiLBP group
compared to the control group. This hypothesis was supported
because exercise increased reflex delay (but had no effect on
stiffness) in the eiLBP group, but increased stiffness and decreased
reflex delay in the healthy control group. Overall, these results
suggest inherent differences in neuromuscular behavior in indivi-
duals with eiLBP when not experiencing pain, and distinct changes
in neuromuscular behavior with eiLBP.
Some important comments on the methods employed here are
warranted. The trunk response to perturbations is non-linear and
known to vary with the operating state of the joint (defined by the
mean torque, perturbation magnitude, mean joint angle, and muscle
activity) (Kearney and Hunter, 1990). Linear biomechanical models,
as used here, provide valid estimates of trunk stiffness, but only over
a relatively narrow range of operating states (Granata et al., 2002).
Moreover, differences in experimental methods between studies can
have a large influence on stiffness measurements (Bazrgari et al.,
2011b). As such, it is difficult to compare stiffness values directly
Fig. 3. Mean values of intrinsic trunk stiffness (a) and paraspinal reflex delay (b), by group and session. Asterisks indicate a significant group difference within session, and
lines indicate a significant session difference within group. Error bars indicate standard deviation.
E.M. Miller et al. / Journal of Biomechanics 46 (2013) 801–805
between studies. For example, intrinsic stiffness estimated here
among individuals without eiLBP post-recovery (7.05 N/mm) was
similar to those reported by Miller et al. (2012) among healthy
individuals using similar experimental methods (6.29 N/mm), but
3–4 times higher than the effective stiffness reported by Hodges et al.
(2009) using force perturbations among individuals with no history
of LBP (1.64 N/mm). Despite the difficulty with estimating trunk
stiffness, forces predicted by the model in the current study were
highly correlated with those measured directly (mean r¼0.976),
suggesting that the model provided a reasonable system representa-
tion. Reflex delay, estimated here without the model among indivi-
duals with eiLBP post-recovery (61 ms), was similar to those
obtained from force perturbations (62–69 ms) (Radebold et al.,
2000; Radebold et al., 2001; Reeves et al., 2005).
The percentage difference in stiffness found between groups
post-recovery—presumably when neither group was affected by
LBP or any exercise effects—was also consistent with previous
studies. Here, intrinsic stiffness in the eiLBP group post-recovery
(8.90 N/mm) was 26% higher than in the control group post-
recovery (7.05 N/mm). This difference is comparable to a reported
22% higher effective trunk stiffness among individuals with a
history of recurrent, acute LBP when not experiencing LBP
(2.00 N/mm) compared to individuals with no history of LBP
(1.64 N/mm) (Hodges et al., 2009). Researchers have suggested
that the higher stiffness among individuals with LBP, even when
not experiencing pain, may result from higher baseline EMG
levels in the trunk musculature, and may reflect a compensatory
technique to increase spinal stability (Lee et al., 2006; Radebold
et al., 2000; van Dieen et al., 2003b; Wilder et al., 1996). Although
we found no difference in reflex delay between groups post-
recovery (again, presumably when neither group was affected by
LBP or any post-exercise effects), alterations in this aspect of trunk
neuromuscular behavior following exercise were quite opposite in
the eiLBP vs. control groups. Such a difference is interesting given
earlier findings of longer reflex delays in individuals with chronic LBP
compared to healthy individuals (Radebold et al., 2000; Radebold
et al., 2001; Reeves et al., 2005), although this finding is not without
exception (Lariviere et al., 2010).
The control group responded to exercise with an increase in
stiffness and a decrease in reflex delay while the eiLBP group
responded to exercise/eiLBP with no change in stiffness and an
increase in reflex delay. The increase in stiffness in the control
group after exercise is consistent with other studies on eccentric
exercise (Green et al., 2012; Hoang et al., 2007), although it is not
clear how much eccentric activity of the trunk musculature
occurred during triathlon exercise training. The eiLBP group
exhibited higher stiffness than the control group prior to exercise
(i.e. post-recovery). This higher stiffness has been associated with
increased muscle activation (Gardner-Morse and Stokes, 2001;
Lee et al., 2006), and may have limited this group’s ability to
further increase stiffness through increased muscle activation
after exercise. However, no group difference in baseline para-
spinal muscle activity was detected in the present study. It is
interesting to note that reflex delay in the control group
decreased with exercise and increased with exercise/eiLBP in
the eiLBP group. The decrease in reflex delay in the control group
with exercise may be related to the increase in stiffness with
exercise, in that higher stiffness would lead to a larger/faster
change in muscle length of muscle that could lead to quicker
reflex responses. The increased reflex delay after exercise may
have resulted from proprioceptive deficits associated with the
presence of pain (Radebold et al., 2001).
While the use of individuals with eiLBP is a convenient alter-
native to prospective studies for studying changes in neuromuscular
behavior with LBP, there are two notable limitations. First, neuro-
muscular behavior among individuals with eiLBP may differ from
individuals with chronic LBP or acute LBP with varying etiology. As
such, caution should be exercised when generalizing these results to
other populations with LBP. Second, the changes in neuromuscular
behavior with eiLBP are due to the combined effects of pain and
exercise. These changes may differ from the effects of LBP alone.
In conclusion, differences in neuromuscular behavior between
individuals with no history of LBP and individuals with eiLBP
when pain free suggest that altered neuromuscular behavior
contributes to the development of eiLBP with exercise. Also,
differences found among individuals with eiLBP after exercise
suggest that altered neuromuscular behavior is also a response to
eiLBP. Although the neuromuscular mechanisms associated with
eiLBP and chronic LBP may differ, these results suggest that
previously-reported differences in trunk neuromuscular behavior
between individuals with chronic LBP and healthy controls reflect
a combination of inherent differences in neuromuscular behavior
between these individuals as well as changes in neuromuscular
behavior elicited by pain.
Conflict of interest statement
We have no conflict of interest to report.
This work is dedicated to the late Dr. Kevin P. Granata. This
work was supported by awards R01AR046111 from the National
Institute of Arthritis and Musculoskeletal and Skin Diseases of the
National Institutes of Health (NIH), and R01OH008504 from the
National Institute for Occupational Safety and Health of the
Centers for Disease Control and Prevention (CDC). Its contents
are solely the responsibility of the authors and do not necessarily
represent the official views of the NIH or CDC.
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