in the current study, we analyzed the Effect of eccentric exercise on the conduction velocity of individual motor units at two locations of the vastus medialis muscle during sustained contractions.

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Motor Unit Conduction Velocity During
Sustained Contraction Of The Vastus Medialis
Muscle Injured By Eccentric Exercise: 1706
Article in Medicine & Science in Sports & Exercise · May 2009
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Motor Unit Conduction Velocity during
Sustained Contraction after
Eccentric Exercise
NOSRATOLLAHAQ1 HEDAYATPOUR, DEBORAH FALLA, LARS ARENDT-NIELSEN, CAROLINA VILA-CHA˜ ,
and DARIO FARINA
Centre for Sensory–Motor Interaction (SMI), Department of Health Science and Technology, Aalborg University, DENMARK
ABSTRACT
HEDAYATPOUR, N., D. FALLA, L. ARENDT-NIELSEN, C. VILA-CHA˜ , and D. FARINA. Motor Unit Conduction Velocity during
Sustained Contraction after Eccentric Exercise. Med. Sci. Sports Exerc., Vol. 41, No. 10, pp. 00–00, 2009. Background: Eccentric
contractions induce muscle fiber damage that is associated with a decreased capacity to generate voluntary force and increased fiber
membrane permeability. Changes in fiber membrane permeability cause cell depolarization that is expected to have an effect on the
action potential propagation velocity of the muscle fibers. Purpose: The aim of the study was to investigate the action potential
propagation velocity in individual motor units before and 24 and 48 h after eccentric exercise. Methods: Multichannel surface and fine-
wire intramuscular EMG signals were concurrently recorded from two locations of the right vastus medialis muscle of 10 healthy men
during 60-s isometric contractions at 10% and 30% of the maximal force. Results: The maximal force decreased by 26.1 T 16.1%
(P G 0.0001) at 24 h and remained reduced by 23.6 T 14.5% (P G 0.0001) 48 h after exercise with respect to baseline. With respect
to baseline, motor unit conduction velocity decreased (P G 0.05) by (average over 24 and 48 h after exercise) 7.7 T 2.7% (10% maximal
voluntary contraction (MVC), proximal), 7.2 T 2.8% (10% MVC, distal), 8.6 T 3.8% (30% MVC, proximal), and 6.2 T 1.5% (30%
MVC, distal). Moreover, motor unit conduction velocity decreased over time during the sustained contractions at faster rates when
assessed 24 and 48 h after exercise with respect to baseline for both contraction forces and locations (P G 0.05). Conclusions: These
results indicate that the electrophysiological membrane properties of muscle fibers are altered by exercise-induced muscle fiber damage.
Key Words: DOMS, MUSCLE DAMAGE, MUSCLE FIBER, INTRAMUSCULAR EMG
E
ccentric contractions induce muscle fiber injury that
is associated with a decreased ability of the muscle
to generate force (29). Damage to sarcomeres (27)
and failure of excitation–contraction (E–C) coupling are
two prominent signs of damage in skeletal muscles after
eccentric exercise (31,39). Thus, the cause of a force deficit
after an eccentric task has been commonly attributed to a
disturbance in the mechanisms involved in generating force
within the skeletal muscle (1) and action potential conduc-
tion in the E–C coupling pathways (39). Decreased neural
drive to the muscle after eccentric exercise has also been
demonstrated by an increase in force production with
stimulation to the motor cortex or motor nerve with respect
to the force obtained during a maximal voluntary contrac-
tion (MVC) (31).
The sarcolemma, which conducts the action potential, is
subjected to substantial tears during eccentric contractions
(26). Increased sarcolemmal membrane permeability has
been indicated as one of the features of the damaged muscle
fiber, as assessed by loss of soluble intracellular proteins
(e.g., creatine kinase, myoglobin) and uptake of membrane-
impermeant dyes by damaged cells (26). An abnormal
sarcolemmal membrane permeability would also depolarize
the fiber membrane because of increased intracellular
sodium [Na+
] and calcium [Ca2+
] and extracellular potas-
sium [K+
] (23,24).
Changes in membrane depolarization are expected to have
an effect on the action potential propagation velocity of the
muscle fibers. A recent animal study has shown that eccentric
contractions did not affect muscle fiber conduction velocity
measured during evoked twitch contractions via electrical
stimulation (34). However, there are no human studies that
have investigated action potential conduction velocity at the
level of the single motor unit during sustained voluntary
contraction of a muscle injured by eccentric exercise. The
extent of damage to the muscle fiber depends on the mor-
phological and architectural characteristics of the muscle
fibers within the skeletal muscle (3,37). The vastus medialis
muscle is characterized by varying fiber-type composition
with a greater proportion of IIb fibers and lower proportion
of Type I fibers in distal region compared with proximal
Address for correspondence: Dario Farina, Ph.D., Center for Sensory–
Motor Interaction (SMI), Department of Health Science and Technology,
Aalborg University, Fredrik Bajers Vej 7 D-3, DK-9220 Aalborg, Denmark;
E-mail: df@hst.aau.dk.
Submitted for publication November 2008.
Accepted for publication February 2009.
0195-9131/09/4110-0000/0
MEDICINE & SCIENCE IN SPORTS & EXERCISEÒ
Copyright Ó 2009 by the American College of Sports Medicine
DOI: 10.1249/MSS.0b013e3181a3a505
1
Copyeditor: Jamaica Polintan

3. Copyright @ 2009 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
regions (35). In addition, the fascicle angle is significantly
greater in more distal than proximal regions of the vastus
medialis muscle (2), which may contribute to nonuniform
changes in muscle fiber membrane properties after eccentric
exercise. Therefore, in the current study, we analyzed the
effect of eccentric exercise on the conduction velocity of
individual motor units at two locations of the vastus
medialis muscle during sustained contractions.
METHODS
Subjects. Ten healthy men (age (mean T SD) 25 T 4.4 yr,
body mass 72.4 T 7.6 kg, height 1.80 T 0.06 m) participated
in the study. All subjects were right leg-dominant and
were not involved in regular exercise of their knee extensor
muscles for at least 1 yr before the experiment. The study
was conducted in accordance with the Declaration of
Helsinki and was approved by the local ethics committee
(N-20070019). Subjects provided informed written consent
before participating in the study.
Procedures. Torque produced during MVC, subjective
pain ratings, and intramuscular and surface EMG signals
were recorded before and 24 and 48 h after an eccentric
exercise protocol. A KinCom Isokinetic Dynamometer
(Chattanooga Corp., Chattanooga, TN) was used to measure
knee extension torque. The subject was seated comfortably
on the adjustable chair of the KinCom with the hip in 90-
flexion. The chair position was modified until the knee axis
of rotation (tibiofemoral joint) was aligned with the axis of
rotation of the dynamometer’s attachment arm. The subject
was fixed with straps secured across the chest and hips. The
right leg was secured to the attachment arm in 90- knee
flexion with a Velcro strap. Visual feedback of torque was
provided on a screen positioned in front of the subject. The
subject was asked to perform three maximal isometric knee
extensions of 3 to 5 s in duration in 90- knee flexion, with
2-min rest intervals between contractions. The subject was
encouraged verbally during each trial to exceed the pre-
viously obtained torque level. The highest MVC value was
used as a reference for the definition of the submaximal
torque level for the subsequent sustained contractions. The
submaximal torque was relative to the MVC measured on
the same day of the test. Subjects were asked to maintain a
constant torque at 10% and 30% MVC for 60 s with 30 min
of rest between the two contractions. Visual feedback of the
torque produced was provided to the subject. The torque
signal was sampled at 2048 Hz concurrently with the
surface and intramuscular EMG signals.
Eccentric exercise. The eccentric exercise was per-
formed with a KinCom Isokinetic Dynamometer (Chatta-
nooga Corp.). Subjects resisted against the dynamometer’s
attachment arm from È170- of knee extension to 90- knee
flexion. Angular velocity was set at 60-Isj1
, and the load
was set to twice the value of the maximal voluntary iso-
metric torque produced during the eccentric exercise phase.
The exercise consisted of a series of four sets of 25 repeti-
tions with 3-min rest between each set. During the exercise,
the subject was provided with visual feedback of torque and
was encouraged to maintain maximal torque.
Sensory assessment of muscle pain. The subjects
were asked to rate the average pain intensity of their quad-
riceps during regular activities of daily living (e.g., climbing
stairs) since their last visit to the laboratory (during the past
24 h). Pain was rated on a continuous 10-cm visual analog
scale, where ‘‘0’’ represented ‘‘no pain’’ and 10 represented
the ‘‘worst pain imaginable.’’
EMG recordings. Surface and intramuscular EMG
signals were recorded from two locations of the right vastus
medialis muscle. Intramuscular signals allowed the identi-
fication of single motor unit action potentials, which were
used as triggers for averaging the multichannel surface EMG
signals (9). The length from the anterior superior iliac
spine to the medial border of the patella was measured as
an anatomical reference for positioning the electrodes (40).
Two adhesive arrays of eight equispaced electrodes
(ELSCH008; SPES Medica, Salerno, Italy; interelectrode
distance 5 mm, electrodes 5 mm  1 mm) were placed at
a distance from the patella of 10% and 30% (distal and
proximal site) of the measured anatomical length, distant
from innervation zones. The muscle innervation zones
were identified during test contractions with a dry array
of 16 electrodes (silver bars, 5 mm long, 1 mm diameter,
5 mm interelectrode distance). Before placing the adhesive
electrode arrays, the skin was shaved, lightly abraded, and
cleansed with water. The positions of the electrodes were
marked on the skin during the first session (day 1),
enabling to replace the electrodes in a similar location at
24 and 48 h after exercise. The surface EMG signals were
amplified (EMG16; LISiN – Ottino Bioelettronica, Torino,
Italy; bandwidth 10–500 Hz), sampled at 2048 Hz, and
stored after 12-bit A/D conversion.
Pairs of wire electrodes made of Teflon-coated stainless
steel (A-M Systems, Carlsborg, WA) were used to record
intramuscular EMG signals at each location. The wires were
cut to expose only the cross-section and were inserted with
25-gauge needles, 10–20 mm proximal to each array of
surface electrodes. The depth of insertion of the needles was
a few millimeters below the muscle fascia. The needles
were removed with the wire electrodes left inside the
muscle. Intramuscular EMG signals were amplified (Coun-
terpoint EMG; DANTEC Medical, Skovlunde, Denmark),
band-pass–filtered (500 Hz to 4 kHz), sampled at 10,240 Hz,
and stored after 12-bit A/D conversion.
Data analysis. The intramuscular EMG signals were
decomposed with an algorithm that has been previously
validated (25). For each contraction, only motor units active
for the entire duration of the contraction were analyzed. The
discharge times of the motor unit action potentials were
used as a trigger for averaging the multichannel surface
EMG signals (20 triggers in each case AQ2; F1Fig. 1). Conduction
velocity of single motor units was estimated from each
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4. Copyright @ 2009 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
averaged surface potential by a multichannel technique
previously described (9). The channels of the surface array
selected for conduction of velocity estimation were the
same for all motor units recorded from the same subject.
The percent change in muscle fiber conduction velocity
over time was calculated by subtracting the final value from
the initial value of conduction velocity and dividing by the
initial value. Variability was calculated as the coefficient of
variation (SD/mean) for both discharge rate and force over
the sustained contractions.
Statistical analysis. Three-way ANOVA was applied
to assess changes in the initial values of motor unit conduction
velocity, discharge rate, and coefficient of variation of dis-
charge rate. The factors were time (before and 24 and 48 h
after exercise), torque level (10%, 30% MVC), and electrode
location (distal, proximal). A three-way ANOVA was also
applied to the percent change in conduction velocity and with
factors time, torque level, and electrode location. For the
sustained contraction, a two-way repeated-measures ANOVA
was used to analyze the coefficient of variation of force with
time (before and 24 and 48 h after exercise) and torque level
(10%, 30% MVC) as factors. A one-way ANOVA with factor
time (before and 24 and 48 h after exercise) was applied to the
MVC torque and pain intensity scores.
Pairwise comparisons were performed with the Student–
Newman–Keuls post hoc test when ANOVA was signi-
ficant. The significance level was set to P G 0.05. Results
are reported as mean and SD in the text and SE in the
figures.
RESULTS
Force production and sensory assessment. The
eccentric exercise protocol reduced the maximal voluntary
isometric torque produced by the knee extensors (F = 19.2,
P G 0.0001) and induced delayed-onset muscle soreness
(DOMS). The MVC decreased from 541.7 T 41.7 NIm at
baseline to 400.8 T 48.9 NIm at 24 h after exercise (26.1 T
16.1%, P G 0.0001) and 413.3 T 41.1 NIm at 48 h after
exercise (23.6 T 14.5%, P G 0.0001). The soreness level
during activities of daily living (e.g., climbing stairs) was
graded 3.8 T 1.4 and 3.6 T 1.3 at 24 and 48 h after eccentric
exercise, respectively.
Motor unit discharge rate. The total number of
analyzed motor units in the distal location was 111 (10%
MVC = 42, 30% MVC = 69) before exercise, 116 (10%
MVC = 45, 30% MVC = 71) 24 h after exercise, and 149
(10% MVC = 51, 30% MVC = 98) 48 h after exercise.
For the proximal location, 113 (10% MVC = 44, 30%
MVC = 69) motor units were analyzed before exercise, 119
(10% MVC = 46, 30% MVC = 73) 24 h after exercise, and
139 (10% MVC = 51, 30% MVC = 88) 48 h after exercise.
The range of analyzed motor units per subject was 3–6 (10%
MVC; distal location), 3–8 (10% MVC, proximal location),
5–10 (30% MVC, distal location), and 4–9 (30% MVC,
FIGURE 1—Example of
AQ3
intramuscular and surface EMG signals
concurrently detected at the beginning (left) and the end (right) of
sustained contractions from the distal portion of the right vastus
medialis muscle of one subject during 30% MVC isometric contraction
before the eccentric phase (A) and 24 (B) and 48 h after the eccentric
phase (C).
TABLE 1. Mean discharge rate (mean T SD, pps AQ4, n = 10 subjects) of vastus medialis
motor units detected at two locations (distal: 10% distant from patella; proximal: 30%
distant from patella) at the beginning of 10% and 30% MVC sustained contractions
performed before and 24 and 48 h after exercise.
Location
Before
Eccentric Exercise
(pps)
24 h after
Eccentric Exercise
(pps)
48 h after
Eccentric Exercise
(pps)
Distal (10% MVC) 9.3 T 1.6 9.1 T 1.3 8.9 T 1.5
Proximal (10% MVC) 9.1 T 1.4 8.7 T 1.2 8.8 T 1. 3
Distal (30% MVC) 11.1 T 1.2 10.7 T 1.6 10.8 T 1.4
Proximal (30% MVC) 10.9 T 1.5 10.6 T 1.8 10.5 T 1.7
* P G 0.05. AQ5
TABLE 2. Mean coefficient of variation of interspike interval (mean T SD, mIsj1
, n = 10
subjects) of vastus medialis motor units detected at two locations over the vastus
medialis muscle (distal: 10% distant from patella; proximal: 30% distant from patella)
during 10% and 30% MVC sustained contractions performed before and 24 and 48 h
after exercise.
Location
Before
Eccentric Exercise
(%)
24 h after
Eccentric Exercise
(%)
48 h after
Eccentric Exercise
(%)
Distal (10% MVC) 11.9 T 3.4 12.1 T 3.4 11.8 T 3.2
Proximal (10% MVC) 11.8 T 2.5 12.2 T 2.8 12.1 T 3.1
Distal (30% MVC) 12.8 T 2.8 13.1 T 4.1 12.9 T 3.8
Proximal (30% MVC) 12.7 T 3.6 13.1 T 3.5 12.8 T 3.4
* P G 0.05. AQ6
MOTOR UNIT CONDUCTION VELOCITY AND DOMS Medicine & Science in Sports & Exercised 3

5. Copyright @ 2009 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
proximal location). Motor unit discharge rate at the begin-
ning of the sustained contraction depended on the level of
torque (F = 30.3, P G 0.0001). Discharge rate increased by
16.5 T 4.2% (P G 0.0001) from 10% to 30% MVC in the
proximal location and by 16.2 T 5.2% (P G 0.0001) in the
distal location (T1 Table 1). Motor unit discharge rate at the
beginning of the posteccentric contractions was not signif-
icantly different from that at the beginning of preeccentric
contractions (Table 1).
In all conditions (before eccentric exercise and 24 and 48 h
after eccentric exercise), motor unit discharge rate at the end
of the sustained contraction was not significantly different
from that at the beginning of the sustained contraction. The
coefficient of variation for both interspike interval and force
was not significantly different between the two contraction
levels and across the three testing days (T2 Tables 2 andT3 3).
Motor unit conduction velocity. Motor unit conduc-
tion velocity at the beginning of the sustained contraction de-
pended on torque (F = 44.3, P G 0.0001) and time (F = 9.1,
P G 0.001). Initial values of conduction velocity increased
(P G 0.05) by 15.3 T 1.5% from 10% MVC to 30% MVC in
the proximal location and by 11.4 T 1.1% in the distal
location. The initial value of conduction velocity at 10%
MVC decreased at 24 and 48 h with respect to baseline by
5.7 T 1.9% and 9.7 T 3.5% (proximal location) and by 6.6 T
2.1% and 7.8 T 3.4% (distal location), respectively (P G
0.05). Similarly, at 30% MVC, conduction velocity was
reduced 24 and 48 h after exercise with respect to baseline
by 7.1 T 3.6% and 10.1 T 4.1% (proximal location) and
by 6.1 T 1.1% and 6.3 T 1.8% (distal location), respectively
(P G 0.05; F2Fig. 2).
Conduction velocity decreased during the sustained con-
tractions. The percent decrease depended on the level of
torque (F = 4.9, P G 0.05) and was higher at 30% MVC
(j7.1 T 4.5%) than at 10% MVC (j4.8 T 4.1%). The per-
cent decrease also depended on time (F = 2.7, P G 0.05) with
a greater reduction in conduction velocity observed in both
posteccentric conditions with respect to baseline. In addition,
the percent decrease in conduction velocity depended on the
interaction among time, electrode location, and torque level
(F = 2.4, P G 0.05; F3Fig. 3). At 24 and 48 h after exercise, a
greater reduction in conduction velocity was observed at the
distal location during the contraction at 30% MVC compared
with that at the proximal location (P G 0.05).
DISCUSSION
The study demonstrates lower values of motor unit con-
duction velocity and greater conduction velocity rate of
change over sustained contractions of the vastus medialis
muscle at 24 and 48 h after eccentric exercise as compared
with the preexercise condition.
TABLE 3. Coefficient of variation of knee extension force (mean T SD, n = 10 subjects)
during sustained isometric contractions at 10% and 30% MVC analyzed before and 24
and 48 h after exercise.
Force Level
Before
Eccentric Exercise
(%)
24 h after
Eccentric Exercise
(%)
48 h after
Eccentric Exercise
(%)
10% MVC 1.7 T 0.5 1.8 T 0.3 2.1 T 0.6
30% MVC 2.2 T 0.8 2.4 T 0.9 2.3 T 0.7
* P G 0.05.AQ7
FIGURE 2—Initial values of motor unit conduction velocity (MUCV;
mean T SE, mIsj1
, n = 10 subjects) for the vastus medialis muscle at
two locations (distal: 10% distant from patella; proximal: 30% distant
from patella) recorded before the eccentric exercise (baseline) and 24
and 48 h after the eccentric exercise. Contraction levels: 10% MVC
(dashed line) and 30% MVC (solid line). *P G 0.05.
FIGURE 3—Percent decrease in motor unit conduction velocity
(MUCV; mean T SE, %, n = 10 subjects) for the vastus medialis
muscle at two locations (distal: 10% distant from patella; proximal:
30% distant from patella) during sustained contractions performed at
10% MVC (dashed line) and 30% MVC (solid line) recorded before the
eccentric exercise (baseline) and 24 and 48 h after the eccentric
exercise. *P G 0.05.
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6. Copyright @ 2009 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
Muscle performance. A significant reduction in MVC
of the knee extensors was observed 24 h after eccentric ex-
ercise and persisted 48 h after exercise, in agreement with
pervious studies (10,14,15). The observation of reduced iso-
metric strength after eccentric exercise indirectly suggests
that the muscle was damaged by the exercise, most likely
because of the mechanical disruption of sarcomeres and/or
the sarcolemma membrane (10,19). Reduced neural drive to
the muscle may also partly explain the decrease in maximal
force generation capacity. However, the relative role of
peripheral and central factors in the reduction in MVC
cannot be estimated from the present results because
measures of central drive, such as twitch interpolation, were
not performed. Subjects also reported soreness in the
quadriceps muscle 24 and 48 h after exercise, which may
be related to damage of the contractile elements and
connective tissue (30).
Motor unit discharge rate. As in previous studies,
the mean motor unit discharge rate increased with the
increasing force level of the sustained contractions, whereas
the coefficient of variation of the interspike interval and of
force did not change between the two force levels (12,17).
There were no significant changes in either discharge rate
or variability of discharge at the end of the sustained con-
tractions with respect to the beginning of the contractions.
These results are in agreement with previous findings on
motor unit behavior over sustained fatiguing contractions at
the same or at different force levels (20–22). The motor unit
discharge rate, the coefficient of variation in interspike
interval, and the coefficient of variation in force were not
different across the testing days. Accordingly, Dartnall et al.
(5) reported no significant changes in the coefficient of
variation of the interspike interval and force 24 h after
eccentric exercise of the biceps brachii muscle.
Motor unit conduction velocity. After eccentric
exercise, the conduction velocity of single motor units
decreased with respect to baseline in both the distal and the
proximal locations of the vastus medialis muscle. In add-
ition, conduction velocity decreased at a faster rate during
the sustained contractions after eccentric exercise with
respect to the preexercise condition. A recent animal study
showed that eccentric contractions changed the integrated
EMG and action potential waveforms but did not affect
muscle fiber conduction velocity measured during evoked
twitch contractions via electrical stimulation (34). However,
the current study is the first human study in which
conduction velocity is measured in vivo in single motor
units during sustained voluntary contractions after eccentric
exercise. The observed change in motor unit conduction
velocity after eccentric exercise may indicate membrane
depolarization most likely because of alteration in the
resting membrane permeability of the injured fibers (24).
Ruff et al. (32) proposed that muscle fiber depolarization is
associated with impairment of propagation velocity because
of slow inactivation of a proportion of the voltage-gated
Na+
channels. In the damaged muscle fibers, an increase in
the leak conductance to K+
would further contribute to the
slow inactivation process of the voltage-gated Na+
channels
(38) and consequently lead to a further reduction of action
potential propagation velocity over a sustained contraction.
In addition, the elevated K+
in the interfiber space as result
of membrane damage may expose further muscle fibers to a
reduced membrane excitability and conduction velocity
during a sustained task (11).
The reduction in motor unit conduction velocity may also be
due to an insufficient activity of the Na+
–K+
pump and/or
decreased muscle fiber volume. It is apparent from the
increase in extracellular potassium ([K+
]o) and intracellular
sodium ([Na+
]i) that the pump capacity is not sufficient to
fully compensate for the ionic fluxes during sustained
fatiguing contractions (18). In the injured muscle fiber, an
increase in fiber ionic membrane permeability would further
decrease the capacity of the Na+
–K+
pump to maintain the
normal concentration gradients for Na+
and K+
during
sustained fatiguing contractions (4) and thus lead to a further
reduction in propagation velocity over time. In addition, an
insufficient activity of the Na+
–K+
pump to recover the
normal ionic gradient across the cell membrane within 24 to
48 h after exercise (8) would cause cell shrinkage because of
the net loss of cellular cations and anions (mostly K+
and
Clj
) and an osmotic equivalent of water (6). This process
would also decrease muscle fiber diameter and the absolute
initial value of conduction velocity (6). The increased [Na+
]i
as result of impairment in Na+
–K+
pump activity has been
suggested to increase the degree of phosphorylation of the
Na+
–K+
pump on the fiber membrane after exercise (4,36).
Taken together, the results of this study indicate that the
adaptation of the muscle fiber to eccentric exercise is asso-
ciated with membrane dysfunction within the first 24 to 48 h
after exercise. The prolonged cell depolarization after eccen-
tric exercise may provide a safety mechanism to protect the
cell against Ca2+
accumulation and thus further protein
degradation (7). This observation may partly explain why
performance can remain depressed for days after eccentric
exercise, although all the known fatigue agents (e.g., lactic
acid, inorganic phosphate, creatinine) have long since
recovered (13).
The distal location of vastus medialis muscle showed a
greater decrease in motor unit conduction velocity over the
sustained contraction. This may be related to more ex-
tensive damage of this area (14,15) because of differences
in fiber-type composition (35) and/or high force production
in this area to stabilize the patella during eccentric exercise
(33). This finding may explain preferential muscle soreness
and hypertrophy of the distal region of the quadriceps after
exercise training (14,15,28).
Limitations. In addition to muscle fiber membrane dys-
function, a reduction in the initial value of motor unit con-
duction velocity could be partly explained by the reduction in
MVC or by a predominant damage of fast twitch motor units.
However, at the contraction forces analyzed, all motor units
recruited were probably of the same type (slow twitch) (34).
MOTOR UNIT CONDUCTION VELOCITY AND DOMS Medicine & Science in Sports & Exercised 5

7. Copyright @ 2009 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
The effects of other factors on conduction velocity, such
as muscle fiber swelling, change in fiber pennation angle,
and changes in muscle temperature after eccentric exercise
and across the experimental days, cannot be excluded from
the present results and may have accounted for some of the
changes observed.
Conclusions. Heavy knee extensor exercise results in a
reduction of vastus medialis single motor unit conduction
velocity in low submaximal isometric contractions, proba-
bly due to alterations in muscle cell membrane dynamics
and inhomogeneous damage of muscle fibers.
This study was supported by the Ministry of Science, Research
and Technology of Iran (N.H.) and the Danish Technical Research
Council (project: Centre for Neuroengineering (CEN), contract no.
26-04-0100) (D.F.).
The authors state that the results of the present study do not
constitute endorsement by ACSM.
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