|
THE EFFECTS OF KNEE JOINT EFFUSION ON QUADRICEPS ELECTROMYOGRAPHY
DURING JOGGING
|
1Biomechanics Research Lab., Steadman"Hawkins Research Foundation
Vail, Colorado, USA
2Steadman Hawkins Sports Medicine Clinic, Vail, Colorado USA
3Department of Orthopedics, Brigham and Women's Hospital, Harvard
University, Boston, MA, USA
| Received |
|
26 October 2004 |
| Accepted |
|
30
November 2004 |
| Published |
|
01
March 2005 |
©
Journal of Sports Science and Medicine (2005) 4, 1 - 8
Search
Google Scholar for Citing Articles
| ABSTRACT |
To
investigate and describe the influence of intra-articular effusion
on knee joint kinematics and electromyographic (EMG) profiles during
jogging. Thirteen individuals underwent a 20 cc 0.9% saline insufflation
of the knee joint capsule and completed 8 jogging trials. Stance phase,
sagittal plane knee joint kinematics and thigh muscular EMG profiles
were compared pre- and post-insufflation utilizing a paired t-test
( = 0.05). Mild knee effusion
caused a reduction in vastus medialis (p = 0.005) and lateralis (p
= 0.006) EMG activity. The rectus femoris, biceps femoris and medial
hamstring muscles did not exhibit changes due to this protocol. There
were no changes in the sagittal plane knee joint kinematic pattern.
Twenty cc effusion can cause quadriceps inhibition in the vastus medialis
and the vastus lateralis in otherwise healthy individuals during jogging.
This study provides baseline data for the effects of mild knee joint
effusion on thigh musculature during jogging.
KEY
WORDS: Electromyography (EMG), kinematics, jogging, muscle inhibition,
knee.
|
| INTRODUCTION |
The
neuromuscular system acts to regulate intra-articular knee joint loading
by acting as a shock absorber, producing and controlling movement
and by providing functional stability via sensory and proprioceptive
valuation (Andriacchi and Alexander, 2000;
Hurwitz et al., 1997;
O'Connor, 1993). Quadriceps inhibition has been suggested to be a causative
factor in quadriceps strength deficits observed in many knee pathologies
(Hurley, 1998; Hurley and Scott, 1998; Itoh et al., 1998; O'Reilly et al., 1998).
Muscular weakness in association with quadriceps inhibition has also
been implicated in the development of functional and structural changes
of the knee joint in some knee pathologies such as patellofemoral
pain (Sakai et al., 2000;
Thomee et al., 1996;
Thomee et al., 1995)
and tibio-femoral osteoarthritis (OA) (Brandt, 2000;
Brandt et al., 1999;
Hurley, 1998;
Hurley and Scott, 1998;
Hurley et al., 1997;
O'Reilly et al., 1998).
Studies that have investigated the neuromuscular performance after
knee injury have shown that quadriceps electromyographic (EMG) amplitude
is reduced compared to healthy controls, implying muscle inhibition
is a consequence of the disease process (Hurley and Newham, 1993;
Hurley and Scott, 1998;
Hurley et al., 1997;
Thomee et al., 1996;
Thomee et al., 1995).
Hurley et al. (1994) investigated the role
of muscle inhibition and isometric and isokinetic muscle strength
in 10 patients with unilateral osteoarthritic (OA) knees. The quadriceps
of all OA legs demonstrated muscular inhibition and were significantly
weaker than the non- diseased legs. The authors suggested that muscular
inhibition may be partially responsible for the unilateral muscle
weakness and thus may be associated with the cause or progression
of OA.
Thomee et al. (1995) assessed muscle function in patients with patellofemoral
pain syndrome (PFP) and healthy controls. Patients with PFP exhibited
lower knee extensor strength in the most symptomatic knee compared
to the least symptomatic knee and less vertical jumping ability compared
to the controls. These findings correlated with lower EMG activity
in the vastus medialis and the rectus femoris muscles in the PFP group.
Other reports support the notion of quadriceps muscular imbalances
as a function of PFP (Cerny, 1995;
Souza and Gross, 1991).
A major limitation of all these reports, however, is that they only
assess the current functional capacity of these individuals under
the influences of the current state of the disease process. Thus,
these studies cannot address the question of whether the observed
muscular inhibition is or was a consequence of the knee pathology
or contributed to its etiology.
Quadriceps inhibition, particularly of the vastus medialis, has been
demonstrated by simulated knee joint effusion in humans without prior
knee injuries (Kennedy et al., 1982;
Spencer et al., 1984;
Torry et al., 2000).
This inhibition has been reported to alter quadriceps EMG (Stratford,
1981;
Torry et al., 2000)
patterns and decrease quadriceps strength (Fahrer et al., 1988;
Jensen and Graf, 1993;
McNair et al., 1996)
in various isometric and isokinetic exercises. Intra-articular knee
joint effusion has also been shown to cause altered EMG, kinematic
and kinetic characteristics in the stance phase of gait (Torry et
al., 2000)
that are similar to those reported in knee injured groups (Boucher
et al., 1992;
Messier et al., 1992).
While the influences of knee joint effusion have been reported for
slower motions such as gait (Torry et al., 2000),
a specific goal of this research was to investigate and describe the
influence of intra-articular effusion on knee joint kinematics and
EMG profiles during a more dynamic activity such as running. Despite
the plausible mechanical association of the neuromuscular system to
the development of many knee joint pathologies in the active individual,
few studies have investigated the role of muscular weakness, dysfunction
and imbalance on the pathogenesis of these knee injuries. Because
individuals employed in this study did not have confounding pathology
(OA or PFP), the results of this protocol may help explain performance
differences that have been reported in these populations in previous
studies. Furthermore, the results of this study may help researchers
and clinicians begin to understand the relationship muscular inhibition
may possess in the pathogenesis of knee injuries in active individuals
and add to our growing understanding of why strengthening exercises
are effective in safely treating these injuries. |
| METHODS |
|
Subjects
Thirteen healthy subjects (8 male; 5 female) with no history of
lower extremity pathology (mean age = 28.5, SD 5.1 years; mean mass
= 76.50, SD 3.7 kg; mean height = 181.2, SD 5.1 cm) volunteered
for participation in this study. Prior to testing, all participants
provided their written informed consent according to a protocol
approved by an Institutional Review Board retained by Local Ethics
Committee.
Jogging protocol
The subjects were allowed to familiarize themselves with the runway
and testing apparatus prior to testing. Infra-red timing lights
evenly positioned before and after the force plate 1.5 m apart measured
jogging speed. Each participant practiced jogging on the 16 m runway
at a self-selected speed until they could provide a consistent jogging
speed and full foot-strike on the force platform. Upon satisfying
these requirements, the average speed of 5 consecutive, practice
trials was used as the self-selected speed during the testing protocol.
Only the trials within ± 2.5% of the self-selected speed were considered
acceptable for analysis in both the pre and post-test conditions.
Knee effusion and test protocol
After 8 pre-effusion jogging trials were collected, a sub-cutaneous
injection of 1.5 cc of 25% Marcaine and 1.5 cc of 1% Lidocaine was
administered at the supra-patellar portal. After this injection
had taken affect (~ 5 minutes), 20 cc of 0.9% saline were injected
into the joint capsule to simulate knee joint effusion. A physician
(PM) administered all injections using an aseptic sterile technique
identical to the methods described previously (Torry et al., 2000).
To ensure saline was administered into the joint space, an intra-articular
(weight-bearing) pressure reading (mmHg) was recorded via a pressure
transducer aligned in parallel with the syringe (Kennedy et al.,
1982;
Torry et al., 2000).
The needle was withdrawn a sterile dressing applied and the individuals
performed 8 post-effusion jogging trials. All jogging tests were
completed within 10 min to avoid the stretch-relax cycle of the
human knee joint capsule (Levick, 1983).
In accordance with Internal Review Board recommendations, all participants
were instructed to refrain from weight bearing exercises for two-weeks
after testing. This was to promote the return of Donnan's osmotic
pressure gradient within the hyaline cartilage, as increased or
decreased water content has been experimentally shown to have a
strong influence on the mechanical properties of articular cartilage
(Mow and Ateshian, 1997;
Mow and Ratcliff, 1997).
Instrumentation and data processing
Lower extremity kinematic performance during level ground jogging
was recorded using a three-dimensional motion analysis system (Motion
Analysis Corporation, Santa Rosa, CA, USA). A four segment, rigid-link
model of the lower limb was defined by 13 retro-reflective, spherical
markers (diameter = 25 mm) (Kadaba et al., 1990).
Five synchronized cameras captured the gait motion at a frequency
of 120 Hz. The cameras were calibrated with mean residual errors
in the range of 1.55 - 2.95 mm over a volumetric space of 1.50 x
1.10 x 1.50 m centered over the force platform.
The coordinate data for each marker trajectory were smoothed using
a fourth-order Butterworth filter with a 9 Hz cut-off frequency
(Wood, 1982).
The smoothed coordinates were used to calculate joint coordinate
system angles for the knee as described previously (Kadaba et al.,
1990;
Kadaba et al., 1989;
Torry et al., 2000). The force plate was used to determine the period of
the stance phase defined as heel strike to toe-off. An average,
stance phase, knee joint angle was calculated for each individual
trial, by summing the values from heel strike to toe-off and dividing
by the total number of values in the series. These values were then
averaged for all 8 trials to yield average knee flexion angles pre-
and post-effusion. For graphical purposes only, custom software
utilizing a cubic spline function was used to time normalize the
kinematic data, expressed as 0 to 100% of the stance phase (Torry
et al., 2000).
The EMG patterns were recorded with pre-gelled, silver-silver/chloride
bipolar surface electrodes (Medicotest A/S, Rugmaken, Denmark) for
the vastus medialis, vastus lateralis, biceps femoris, and the medial
hamstrings (semitendinosus and semimembranosus) according to Basmajiian
and Deluca (1985) and Delagi et al. (1981). After the skin was shaved and cleansed with alcohol,
the electrodes were placed over each muscle belly in line with the
direction of the fibers with a center to center distance of approximately
2.5 cm. Electrode placement was confirmed for each muscle with manual
muscle testing and visual biofeedback monitoring (Torry et al.,
2000). A single ground electrode was placed over the anterior
tibial spine.
EMG data were collected (1200 Hz) with the TeleMyo telemetric hardware
system (Noraxon, USA, Inc., Scottsdale, AZ) on-line with a 16-bit
A/D board (National Instruments, Austin, TX) of the motion capture
system. Each EMG signal had a bandwidth of 3 dB at 16-500 Hz. The
lower cutoff filter is a first order high-pass design and the upper
cut-off filter is a sixth order Butterworth low-pass design. The
differential amplifier has a fixed gain of 1700, an input impedance
of >10 MΩ , and a common mode rejection ratio of 130 dB. Although
the transmitter automatically removes the low frequency noise component
from the EMG signals, a resting trial was collected and used to
remove any additional noise. After removing signal offset, the raw
dynamic EMG, and maximum voluntary contractions (MVCs) for each
muscle, were processed with 15 and 50 ms root mean square (RMS)
smoothing window algorithms, respectively (Deluca, 1997; Lange et al., 1996; Torry et al., 2000).
Five trials of pre-test MVCs were collected using methods previously
described by Lange et al. (Lange et al., 1996).
EMG reference values were calculated for each muscle using the average
of the five peak EMG signals and represented 100% MVC. The mean
peak EMG amplitude derived from the MVC protocol was used to scale
the raw dynamic EMG recorded during each jogging trial (%MVC). The
scaled data were then averaged over the stance phase.
Statistical
analysis
Differences in the average, knee joint flexion angle and the average
EMG (%MVC) of the five muscles were compared pre- and post-insufflation
with a paired t-test with an a priori alpha level set at
0.05.
|
| RESULTS |
Individual
intra-articular pressures, jogging speeds and average knee angles
for pre- and post-insufflation are reported in Table
1. The effusion did not cause a significant change (t=2.00, df=12,
p=0.068, 1-ß=.440) in the average knee angle over the stance phase
(Table 1 and Figure
1).
Table 2 presents EMG values and
standard deviations pre- and post-insufflation for all subjects and
each muscle tested. Eleven of the 13 subjects exhibited EMG inhibition
in the vastus medialis while 10 of the 13 subjects exhibited inhibition
of the vastus lateralis after insufflation. Specifically, vastus medialis
and lateralis activity decreased on average 8.5% (t = 3.42, df = 12,
p = 0.005) and 5.0% (t = 3.33, df = 12, p = 0.006), compared to the
respective pre-effusion values. Although seven of 13 subjects showed
an increase in EMG, rectus femoris activity did not demonstrate significant
changes between conditions (t = -2.16, df = 12, p = 0.052, 1-ß = .500).
Neither the medial hamstrings (t = -1.74, df = 12, p = 0.107, 1-ß
= .340) nor the biceps femoris (t = -1.89, df = 12, p = 0.083, 1-ß
= .400) muscles exhibited a significant change in EMG activity after
knee effusion. |
| DISCUSSION |
|
The
neuromuscular system is integral in controlling and maintaining
the mechanical environment of the internal knee joint. It is plausible
that alterations in thigh muscular activity patterns may reflect
muscular force adaptations that could have a profound affect on
the internal loading of the joint and its tissues. In the present
study, vastus medialis and vastus lateralis inhibition occurred
with mild knee effusion during jogging without a significant change
in sagittal plane knee joint kinematics. These results are similar
to those reported for walking (Torry et al., 2000), where 20 cc of effusion caused vastus medialis and lateralis
inhibition. In contrast to a previous study (Torry et al., 2000),
the present investigation did not observe significant changes in
the sagittal knee joint kinematic pattern. This was surprising given
the notable changes in the EMG. One possible explanation for this
is that the inertial forces experienced by the lower limb during
jogging are significantly higher compared to walking and may be
of sufficient magnitude to overcome the muscular deficits of the
medialis and lateralis in order to passively extend the leg. This
further implicates the important functional and adaptive role the
bi-articulate rectus femoris muscle may play in knee joint pathology,
as this muscle would beprimarily responsible
for generating the increased inertia for the lower extremity by
acting at the hip.
It is believed that increased fluid in the knee distends the joint
capsule and produces quadriceps inhibition that leads to weakness
and atrophy (Spencer et al., 1984;
Stratford, 1981;
Suter and Herzog, 2000).
Suter and Herzog (2000)
hypothesized that muscle inhibition via knee injuries may lead to
joint degeneration. However, in that study, it was not known whether
the injury itself may have initiated the joint degeneration process
as all participants were injured prior to the start of the study.
The results of this study supports the concept that an otherwise
healthy knee may experience reduced EMG drive to the vastus medialis
and lateralis due to effusion and/or capsular distension as the
individuals in this study were healthy and the observed effects
can not be attributed to a pre-existing injury. Other studies have
also reported reduced EMG drive to the medialis in PFP patients
performing activities of daily life (Souza and Gross, 1991;
Thomee et al., 1996;
Thomee et al., 1995).
These authors suggest that the reduced EMG to the quadriceps may
be due to pain inhibition. The present study also offers an alternative
hypothesis, suggesting that many of the observed changes in EMG
in the pathological knee may also be, in part, due to knee joint
effusion that often accompanies many of these clinical pathologies.
While reduced EMG activity does not necessarily translate into muscle
force reduction during a dynamic contraction, several investigators
have reported reduced EMG in the vastus medialis for knee injured
groups (Boucher et al., 1992;
Cerny, 1995;
Souza and Gross, 1991;
Thomee et al., 1995)
where simultaneous knee extensor strength deficits were also noted.
In support, a study conducted by Boucher et al. (1992)
determined that EMG activity of the vastus medialis was reduced
in patients with PFP syndrome compared to a non-pathological group.
Thus, in addition to pain inhibition, it is plausible that knee
joint effusions may also contribute to those findings.
In vivo function influences the mechanical environment of articular
cartilage. Thus, in vivo function is coupled to the health of a
joint. Muscle weakness has been associated with degenerative joint
disease of the knee (Hurley, 1998;
1999)
and others have suggested its importance in the initiation and progression
of knee OA (Suter and Herzog, 2000).
Recently, Andriacchi et al. (2004)
suggested that the initiation of knee OA is associated with the
kinematic change in tibiofemoral load bearing to areas where cartilage
is not accustom to such loads and breaks down. Based on this data,
it is not unreasonable to infer that similar cartilage breakdown
may occur on the retro surface of the patella when the normal activation
patterns of the quadriceps are interrupted as in the current study;
and this altered quadriceps function will most likely produce some
aberrant patellar tracking. Unfortunately, measuring patellar motion
is not feasible with non-invasive means and thus we cannot determine
if indeed patellar motion was altered in these subjects post-effusion.
The capsular tissue of the knee joint is visco-elastic (Levick,
1983).
Previous researchers have demonstrated that saline is absorbed or
the stretch-relaxation of the capsular tissues can accommodate to
the increase in joint volume (Levick, 1983;
Wood et al., 1988).
In a case study, Spencer et al. (1984)
examined the prolonged effect of 60 cc of saline injected into the
knee joint on H-reflexes and pressures by leaving the fluid in the
joint for 20 min. After 20 min, Spencer et al. (1984)
noted a 3.0 mm Hg drop in intra-articular pressure but a continued
decrease in the magnitude of the H-reflex. In the present study,
all trials were conducted in a short time period (under 10 min from
the time of insufflation) to help negate the confounding effects
absorption and the capsular stretch-relaxation cycle may have had
in this study design (Levick, 1983).
Likewise, this study investigated the immediate effects of effusion
and did not address the effects prolonged exposure may have on quadriceps
or hamstring EMG values during jogging. We chose a volume of 20
cc to represent a mild effusion as it constitutes a clinical representation
of knee effusions (see Table 3),
and has been reported as having an inhibitory effect in previous
studies and did not cause pain (Shakespeare et al., 1985;
Spencer et al., 1984;
Torry et al., 2000).
This study demonstrated the effects of a simulated knee effusion
on the quadriceps and hamstring musculature during jogging. Vastus
medialis and lateralis inhibition were observed in EMG data during
jogging. It is speculated that this inhibition was caused by joint
capsular distension as reported by previous authors (Kennedy et
al., 1982; Spencer et al., 1984; Torry et al., 2000).
Because the subjects employed in this study were healthy, these
results can be considered the isolated effects knee joint effusion
may have on knee joint function during jogging as no other factor
(injury, surgery or rehabilitation) could have caused these adaptations.
Thus, these data suggest that knee effusion may be one factor that
causes vastus medialis and lateralis EMG deficits that are often
associated with knee joint pathologies such as OA or PFP. The results
of this study may used as a baseline when comparing the functional
capabilities of pathological groups who exhibit knee joint effusions.
|
| CONCLUSIONS |
| Previous
research conducted on knee injured individuals is limited as these
reports can only assess the current functional capacity of these individuals
under the influences of the current state of their disease process.
Thus, these studies cannot address the question of whether the observed
muscular inhibition is or was a consequence of the knee pathology
or contributed to its etiology. This study has shown that knee effusion
can cause reductions in the vastus medialis and lateralis EMG output
potentially altering patello-femoral kinematics. These effects may,
in part, help to explain results obtained in injured or diseased knees. |
| KEY
POINTS |
- 20
cc of knee effusion can cause vastus medialis and lateralis inhibition
as noted by decreases in EMG amplitude.
- This
effusion does not appear to alter sagittal plane knee joint kinematics
during jogging.
- This
finding if different from previous work investigating knee joint
kinematic changes during a less dynamic activity (gait) with 20
cc of effusion.
|
| AUTHORS
BIOGRAPHY |
Michael R. TORRY
Employment: Director of Research in the Biomechanics Research
Lab of the Steadman Hawkins Research Foundation. Dr. Torry holds
Adjunct Faculty positions in the Depart. of Bioengineering at
the Univ. of Pittsburgh, at Colorado State Univ. in the Depart.
of Veterinary Medicine and Biomedical Engineering and in the
Depart. of Integrative Physiology at the Univ. of Colorado at
Boulder.
Degree: PhD
Research interests: Knee and shoulder biomechanics.
E-mail: mike.torry@shsmf.org |
|
Michael J. DECKER
Employment: PhD student at the University of Texas-Austin.
Degree: MS
Research interests: Neuromuscular mechanics. |
|
Peter J. MILLETT
Employment: The Depart. of Orthopedics, Brigham and Women's
Hospital, Harvard Univ. Boston, MA.
Degree: MD
Research interests: Knee and shoulder surgery and function. |
|
J.
Richard STEADMAN
Employment: Executive Director, Steadman Hawkins Research
Foundation in Vail, Colorado.
Degree: MD
Research interests: Knee surgery and mechanics. |
|
William
I. STERETT
Employment:
The Head Team Physician for the United States Women's Alpine
Ski Team and a Partner at the Steadman Hawkins Clinic in Vail,
Colorado. He is also the United States Medical Consultant to
the International Federation of Skiing (FIS).
Degree: MD
Research interests: Knee surgery and mechanics.
|
|
|
|
|