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Electromyography (EMG) Modeling

Chapter · April 2006

DOI: 10.1002/9780471740360.ebs0656

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ELECTROMYOGRAPHY (EMG) MODELING
N. A. DIMITROVA
G. V. DIMITROV
Bulgarian Academy of Sciences
Sofia, Bulgaria
1. SOME DEFINITIONS RELATED TO ACTIVATION OF
SKELETAL MUSCLE AND SIGNAL DETECTION
Any skeletal muscle is activated by electrical impulses
coming from alpha-motoneurons through their axons (my-
elinated nerve fibers). Reaching the muscle, each nerve
fiber branches into numerous unmyelinated nerve termi-
nals. They innervate a number of skeletal muscle fibers
(Fig. 1a) through neuromuscular junctions at the end-
plate regions (black ellipses in Fig. 1a). Activation of an
excitable cell results in its depolarization and generation
of transmembrane voltage across its membrane. As the
extracellular potential is much smaller than the intracel-
lular potential the term intracellular action potential
(IAP) is predominantly used instead of transmembrane
voltage. In addition, it is the IAP that is measured under
P1
skin
axon



end-plate region
depolarized zones
(a)
IAP (x) IAP profiles depolarization transition
repolarization transition
b = Tin ·

fiber axis
(b)
IAP (t) rising phase
falling phase
Tin t tive (4–6). Such electrodes are at commensurable dis-
(c)
Figure 1. (a) Schematic presentation of axon of alpha-motoneu-
ron whose nerve terminals innervate a number of muscle fibers
through neuromuscular junctions at the end-plate region. Two
depolarized zones (black rectangulars) propagate along each fiber
from the end-plate region to the fiber ends. (b) The shape of the
intracellular action potential (IAP) spatial profiles within the two
depolarized zones. (c) IAP in temporal domain corresponds to that
detected by a microelectrode.
Wiley Encyclopedia of Biomedical Engineering, Copyright & 2006 John Wiley & Sons, Inc.
experimental conditions. In muscle fiber, the membrane
depolarization excites neighbor regions at both sides from
the end-plate located somewhere in the middle portion of
the fiber. As a result, two IAPs propagate in an all-or-
nothing way (i.e., without decrement) with propagation
velocity v along the muscle fiber to its ends where they
extinguish. At any moment after the fiber activation, two
potential profiles exist across the fiber membrane (Fig. 1b)
that are called waves of excitation or depolarized zones
(Fig. 1a, black rectangles over the fibers). The length of
the IAP profile along the fiber, b, is defined by the product
of the IAP duration, Tin, (Fig. 1c) and propagation velocity
v.
Processes across the muscle fiber membrane produce
electrical currents and potentials in extracellular medium
that is a volume conductor. The functional unit of the mo-
tor system is the motor unit (MU). The MU consists of an
alpha-motoneuron, its axon, and the muscle fibers inner-
vated by this single axon (1). Sum of potentials produced
at the detecting electrode by the muscle fibers belonging to
a certain MU is the motor unit potential (MUP). As the
nerve terminals have different diameters and lengths, and
as the neuromuscular transmission delay is fiber-specific,
the axon impulse reaches individual muscle fibers nonsi-
multaneously. Thus, the potentials produced by individual
P2
muscle fibers belonging to a certain MU are desynchro-
nized.
Detection of extracellular potentials produced by mus-
cles (i.e., electromyography, EMG) is performed either by
intramuscular (needle or wire) or surface (Fig. 1a, P1 and
P2) electrodes. At least two electrodes are necessary for
EMG detection. When one of the electrodes is located at a
remote site where the potential is close to zero, such de-
tection is called monopolar and the voltage between the
two electrodes is the potential produced by the muscle at
another electrode. The EMG recording could also be per-
formed by multielectrodes that represent a set of detecting
electrodes. In this case, the EMG signal could also be the
sum of weighted potentials detected by individual elec-
trodes.
Intramuscular electrode that has a very small detect-
ing surface (25 mm in diameter, i.e., smaller than the fiber
diameter, which is about 60 mm) can detect potentials pro-
x duced predominantly by a single muscle fiber located close
to it (2). Such an electrode is very selective and it is called
single-fiber electrode (SF electrode). Analysis of the po-
tentials from single muscle fibers is the object of single-
fiber electromyography (SF EMG) (3). The monopolar elec-
trodes of larger area or those located at greater distances
from active fibers (e.g., surface electrodes) are not selec-
tances from many active muscle fibers and they detect
the sum of potentials produced by all active MUs. More-
over, they can detect undesired activity produced by mus-
cles other than the muscle of interest. That sort of activity
is called cross talk.
Any motion or force production is accompanied by ac-
tivity of different MUs whose firing is defined by motor
control strategy. Summed activity of desynchronized
MUPs forms the so-called interference EMG. When stim-
ulation of the nerve is performed, the activated MUs are
1
2 ELECTROMYOGRAPHY (EMG) MODELING
fired almost simultaneously. Such a rather synchronized
EMG signal is called muscle- or M-response or M-wave.
2. MODELING OF EMG SIGNALS IN A HOMOGENEOUS
VOLUME CONDUCTOR OF INFINITE EXTENT
2.1. Physical Basis for Modeling Extracellular Potentials
Generated by an Excitable Fiber
Pioneer studies by Helmholtz (7) can help in understand-
ing and calculating potentials produced by excitable fibers
and especially by fibers of finite length, like those of the
skeletal muscles. The author introduced the concept of an
electric double (dipole) layer into the potential theory. He
determined the potential jðPÞ produced by an uniform
double layer at a point P in a volume conductor of infinite
extent as a product of the dipole moment per unit area
(Vdl) and the solid angle (O) subtended by the layer at the
point P (Fig. 2a). The dipole moment per unit area is the
product of charges per unit area and the layer thickness.
Any excitable cell is characterized by potential difference
across its thin membrane. As the membrane can be con-
sidered a capacitor, the amount of charge per unit area is
directly proportional to the transmembrane voltage at any
point.
Wilson et al. (8) were the first who applied the concept
of double layer to analysis of electrical field around excit-
able cells. When the dipole layer is uniform, like a resting
or completely depolarized cell, the potential at any point
outside the closed surface of the cell is zero. In this case,
the identical layers, corresponding to the outer (‘1’ in Fig.
2b) and inner (‘2’ in Fig. 2b) surfaces of the cell, are seen
under the same solid angle O from the point of observation
P. The layers, however, are turned to the P with their dif-
ferent signs and thus produce equal potentials of opposite
sign, the sum of which is zero. The authors also noted that
the potentials produced by a cylindrical uniformly polar-
ized fiber opened at one of its ends (Fig. 2c), and by the
polarized disk that makes the fiber closed are equal in
magnitude but opposite in sign (Fig. 2c1). Indeed, closing
the fiber, the potential produced by such a closed surface is
equal to 0, which means that the disk produces a potential
whose magnitude is identical to that of the open cylindri-
cal fiber. Thus, the double-layer disk can replace the rest
of the uniformly polarized fiber surface.
If a cylindrical uniformly polarized fiber is opened at its
two ends, it could respectively be closed and thus replaced
by two disks of the corresponding polarity located at the
ends (Fig. 2d). An actual potential profile (Fig. 1b) has
gradual depolarization and repolarization transitions that
correspond to the rising and falling phases of IAP (Fig. 1c).
It can be represented (Fig. 2e) through a number of steps
of equal length dx that are opened at their ends and uni-
formly depolarized according to the mean IAP value at the
corresponding membrane portions. The dipole disks have
different polarity (represented by the disks of different,
white and black, color) at the boundaries between two
steps. Their summated effect can be represented through a
disk whose dipole moment is defined by the difference in
IAPs at the corresponding membrane points. As a result,
an actual excitation wave can be represented (8,9) by two
P
ϕ(P)~(-Vdl)·Ω
Ω
−
Vdl
(a) (d)
P IAP profile,
ϕ(P)=Vdl·Ω+(-Vdl)·Ω=0 Vi(x)
Ω
1( )
2(−)
Vdl
dx X
(b) (e)
P
Ω1 IAP profile
ϕ(Ω1)=0
P
c1 Ω2 St1 Stack2
c2
(f)
(c)
Figure 2. Double layer presentation. (a) Helmholtz’s formulation
of potential jðPÞ produced at a point P by a uniform double layer
(dl) whose moment is defined by Vdl. O is the solid angle sub-
tended by the double layer at P. (b) Extracellular potential pro-
duced at P by a resting or uniformly polarized excitable cell is
zero. (c) Extracellular potential produced by a uniformly polarized
fiber membrane open at one of its ends is identical in magnitude
and opposite in sign (c1) to that produced by the polarized disk
that makes the membrane closed. For large distances of P from
the fiber (45 radii), the disk can be replaced (c2) by a lumped
dipole, concentrated over the fiber axis, whose dipole moment is
proportional to the disk area. (d) A uniformly polarized fiber
membrane opened at two of its ends can be replaced by two po-
larized disks in which polarity is opposite to that of the disks that
make the membrane closed. (e) Approximation of IAP profile
through a number of steps of equal length dx that are opened at
their ends and uniformly depolarized according to the mean IAP
value at the corresponding membrane portions. (f) IAP potential
profile along the fiber membrane can be considered as two stacks
of dipole disks oriented in opposite directions (black and white
disks).
stacks of double-layer disks distributed equidistantly
along the fiber axis (Fig. 2f, black and white disks). Ori-
entation of the dipoles is identical in each stack and op-
posite in different stacks. Thus, calculation of the
extracellular potential, j(P), can be reduced to the sum
of the potentials produced by the disks distributed along
the fiber axis (10).
Wilson et al. (8) also made a step to line presentation of
the IAP sources. They noted that the potentials produced
by a disk (Fig. 2c1) and a point dipole whose moment is
proportional to the disk area and whose position coincides
with that of the disk (fiber) axis (Fig. 2c2) are almost iden-
 ELECTROMYOGRAPHY (EMG) MODELING 3

y P1(x o,yo) P2
skin

z
y1 y2
y3 yo

xo x

depolarized zones
(a)

propagation generation propagation extinction

t6 t5 t4 t1÷t3 t4 t5 t6 t7 t8÷t10
P1 P2

fiber end
end-plate region
(b)

MUP
P1
SFP
Figure 3. (a) Peculiarities of single-fiber po-
tential (SFP) detection. Distances from a mus-
cle fiber, yo, from the end-plate region, y1, and
from the fiber ends, y2 and y3, to the observa-
P2 t7
tion point P1 are commensurable. (b) Genera-
tion and extinction of the depolarized zones. (c)
SFP (thin lines) and motor unit potentials,
(c) MUP (thick lines) detected above the fibers
(couple of upper lines, P1) and behind the ends
terminal phases of the fibers (couple of lower lines, P2) at 10 mm
from the fiber or MU axis in isotropic volume
conductor. The potentials are normalized with
respect to the corresponding negative phase
amplitude detected above the fibers. (d) SFP
produced by a fiber with asymmetrical position
of the end-plate with respect to the fiber ends,
leading edges and calculated for different points along the
longer fiber semi-length. Negativity is upward
as is accepted in neurophysiology. The shape of
the IAP used for calculations corresponds to
(d) that of IAP from Fig. 7 (line with a mark).

tical. The error caused by such a source simplification is to the observation point P(xo,yo); and @ð1=rÞ
@x is the potential
less than 5% provided the radial distance is 5 fiber radii or produced by the dipole of unit moment at P(xo,yo).
greater from the fiber axis (9). Dipole presentation of the membrane source (Equation
This idea can be described by the following equations: 1) can also be used for calculating potentials produced by
curve fibers. In this case, the changes in the angle between
Z 1
the axis of each dipole and radius-vector to the point of
@Vi @ð1=rÞ observation (because of the fiber curvature) are taken into
jðxo ; yo Þ ¼ C   dx; ð1Þ

1 @x @x account (11).

2
si d 2.2. Peculiarities of a Skeletal Muscle Fiber as a Source of
where C ¼ 16s ; d is the fiber diameter; si and se are the
e Extracellular Potentials
intracellular and extracellular conductivities; Vi(x) is the
IAP profile along the fiber; @Vi(x)/@x represents distribu- In contrast to long nerve fibers, the distances of the ob-
tionqffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffi
of the dipole ffi moment along the fiber axis x; servation point P1 (Fig. 3a) from the muscle fiber axis, yo,
r ¼ ðxo
xÞ2 þ y2o is the distance from the current dipole end-plate region, y1, and fibers’ ends, y2 and y3, can be
4 ELECTROMYOGRAPHY (EMG) MODELING

commensurable. Thus, correct models of single-fiber po- Lumped (point) dipole

tential (SFP) that are valid for any distance from a muscle Y
fiber should include the processes of generation of two de- a a
polarized zones at the end-plate (Fig. 3b, moments of time y3
t1–t5), their propagation in opposite directions to the fiber y2
y1
ends (Fig. 3b, moments t6–t7), and extinction of the zones
at the fiber ends (Fig. 3b, moments t8–t10, thick lines).
The effects of these processes on SFP are discussed in de- X
tail in the section entitled SFP Produced by a Muscle Fi-
ber of Finite Length.
However, to realize main features of potential field pro-
duced by a muscle fiber, it is useful first to consider basic 0
regularities of potentials produced by a single propagating (a)
depolarized zone and detected by a very small (point)
monopolar electrode. This situation resembles detection 0
of extracellular potentials by a SF electrode located far A A
Y
from the end-plate and ends of fiber (i.e., when y1, y2, and
a y a
y3 (Fig. 3a) are large as compared with yo.

2.3. Amplitude Characteristics of SFP

2.3.1. Potential Field Produced by a Lumped Di-
pole. Considering the source across the fiber membrane
as two stacks of distributed dipoles (Fig. 2f), it is useful to
remember potential field produced by a lumped (point) di-
pole (Fig. 4a). The dipole produces zero potential every-
where in the plane that is perpendicular to the dipole axis
and passes through its midpoint (Fig. 4a, projection of the
plane, i.e., zero line, is along the dashed y-axis). The plane
divides the space into regions with positive and negative
potentials denoted by ( þ ) and (
). At a certain radial
distance, y, from the dipole axis (Fig. 4a, lines for
y ¼ y1 ; y2 ; y3 ), the maximal potential is produced at the
points a + and a
. They coincide with the tangency points
(depicted by black spots) of the corresponding line and
equipotential lines schematically represented by solid and
dotted circles for positive and negative dipole fields, re-
spectively. The larger the radial distance, the further from
the zero line is the corresponding maximum (Fig. 4a, black
spots and Fig. 4b lines A þ and A
). For any distance y, the
extremes are at points a + and a
that are at distances
x ¼  y=H2  0:7y from the zero line (Fig. 4b). The poten-
tial produced by the dipole along a line located at a certain
distance from the dipole axis, uðxÞjy , is biphasic, positive-
negative (Fig. 4c, uðxÞ for y ¼ y1 ; y3 ).
2.3.2. Extracellular Potentials Produced by a Depolariza-
tion or Repolarization Transition. Consider peculiarities of
extracellular potentials produced by a distributed (not a
point) dipole source of different length. It is the case cor-
responding to depolarization or repolarization transition
(Fig. 5a) distributed between the resting potential (de-
noted by 0) and IAP amplitude, Vm. The total dipole mo-
ment of such a membrane source (i.e., the sum of the
moments
P of individual dipoles distributed equidistantly,
i dVi =dx) is Vm.
If the fiber-electrode distance y is shorter than the
length (b ¼ L) of the shortest transition, than the distances
between the point of observation and individual dipoles
representing the transition differ significantly. The longer
the transition, the larger is the portion of the dipoles
x⬇ -0.7y d x⬇ 0.7y X


(b)
ϕ(x) y
1
y3
0
X
(c)
Figure 4. (a) Schematic drawing of the potential field produced
by a lumped (point) dipole (black point in the center of the figure).
Signs ( þ ) and (
) near the point denote location of the positive
and negative point charges that constitute the dipole. The circles
depict equipotential lines of the positive (solid lines) and negative
(dotted lines) fields produced by the dipole. a þ and a
denote
points of extreme potential along the line y ¼ y3 . See text for more
details. (b) lines denoted by A þ and A
represent position of the
extreme points at different distances from the dipole axis. (c) Po-
tentials produced by a lumped dipole along the lines located at
distances y ¼ y1 and y ¼ y3 from the dipole axis.
whose contribution to the detected potential is weak be-
cause they are far away (as compared with y) from the
point of observation. Moreover, the moment of individual
dipole, which is proportional to dVi/dx (and can be roughly
estimated through Vm/b), is lower in longer transitions
(Fig. 5a). As a result, longer transitions produce potentials
of lower amplitude in spatial (Fig. 5b) and temporal (Fig.
6a and 6b, y ¼ 0.5 mm, curves denoted by 2 and 3) domains
at such distances.
If, however, the fiber-electrode distance y is larger than
the longest transition length, differences in the distances
between the point of observation and individual dipoles
become insignificant. As a result, the sources representing

Distributed dipoles
Stack 1 Stack 2 Stack 3
Vm
0 L b=2L b=4L
(a)
ϕ(x)
X quadrupole character (combination of two dipoles oriented
(b)
A Y(L) A thin curve up to the moment of time t7). Thus, the shape of
2
1 lumped dipole depend on the distance from the dipole axis
0 4 8 12 b (L)
(c)
Figure 5. (a) Schematic presentation of the distributed dipoles,
namely, the dipole stacks of different length, distributed along a
fiber axis. (b) Potentials (relative units) produced by the corre-
sponding stack along a line that is parallel to the fiber axis and is
located at a small radial distance from the axis. (c) Lines denoted
by A þ and A
represent position of the extreme points at differ-
ent distances from the lumped dipole (dotted lines) and from dis-
tributed dipoles whose length b ¼ L (solid lines), b ¼ 2L (dashed
lines), b ¼ 4L (dashed-dotted lines).
transitions of different length are seen from the point of
observation as a lumped dipole (Fig. 5c, solid, dashed, and
dashed-dotted lines approach the dotted lines represent-
ing the lines of extremes A þ and A
corresponding to
point dipole). At such distances, the dipole moment of the
distributed and point dipole sources appears to be identi-
cal and equal in magnitude to Vm. The amplitudes of po-
tentials produced by these transitions are also
approximately identical (Fig. 6c and 6d, y ¼ 5 mm).
2.3.3. Extracellular Potentials Produced by a Propagating
Depolarized Zone. The shape of the IAP typical for muscle
fibers is asymmetrical (i.e., its rising phase is shorter than
the falling one) (Fig. 1c). So is the IAP profile along the
fiber membrane (Fig. 1b). The actual IAP asymmetry is
still more pronounced when the IAP spike is followed by
after-depolarization also called negative after-potential
(Fig. 7). The relative weight of the latter could increase
considerably during prolonged muscle activity resulting in
muscle fatigue (Fig. 7, the curves with lowering ampli-
tude). Thus, the main contribution to the extracellular po-
tential detected in the fiber proximity is that from the
shorter (i.e., depolarizing transition of the IAP profile)
(12). As a result, the potentials detected by SF electrodes
located between the end-plate and fiber ends are mainly
biphasic (2,13–15), positive-negative, like potentials pro-
ELECTROMYOGRAPHY (EMG) MODELING 5
duced by a distributed dipole source (Fig. 6a and 6b). They
are poorly sensitive to a longer repolarization transition
and to negative after-potential that have to produce
smaller potentials (23).
At larger distances from the fiber, typical for noninva-
sive detection by surface electrodes, the rising and falling
phases of the IAP profile can be considered as lumped di-
poles d1 and d2 with opposite orientation (Fig. 8a and 8b).
The distance between the dipoles, b, reflects the length of
the depolarized zone. The source across the membrane has
in opposite directions). In this case, the SFPs have already
three phases (positive, negative, positive) with positive
phases of approximately similar values (Fig. 3c, upper
SFPs (relative magnitude of their positive phases) de-
pends on the fiber-electrode distance.
As positions of extremes of potential produced by a
(Fig. 4b, lines A þ and A
), then for any fiber-electrode
distance, y, an optimal length of the depolarized zone ex-
ists (10), for which the negative maxima of both dipoles
coincide (Fig. 8a, point a12, for dipoles d1 and d2 and Fig.
8b, point a13 for dipoles d1 and d3). As a result, the SFP
amplitude is maximal when b  2y=H2 ¼ yH2  1:41y.
This equation is useful for an approximate classifica-
tion of the depolarized zone as short or long and for as-
sessing the source character and the effect of change in the
zone length at a certain fiber-electrode distance. When the
depolarized zone is shorter than the mean fiber-electrode
distance (as in the case of noninvasive detection), the
source looks like quadrupole and lengthening of the zone
increases the magnitude of the potential detected. How-
ever, in the case of needle detection, when the zone is
longer than 1.41y, the source looks like a distributed di-
pole and the detected potential decreases with the zone
lengthening. Thus, simultaneous detection by needle and
surface electrodes can result in opposite amplitude
changes (16–19) with lengthening the IAP profile. In this
sense, the amplitude characteristics are ambiguous.
Changes in the length of the depolarized zone reflect
changes in propagation velocity and IAP duration. SFP
amplitude remains unchanged only if duration and veloc-
ity changes in such a way that their product (i.e., length of
the depolarized zone) remains also unchanged.
2.3.4. Conclusions. (1) Potential field formation is es-
sentially a spatial problem that relates the asymmetry
and length of the IAP profile with the fiber-electrode dis-
tance. (2) Affecting the amplitude of potentials produced
close and far from active fibers in a different way, the IAP
profile asymmetry and length affect the radial decline of
different phases of SFP and as a consequence the SFP
shape. (3) The increased after-depolarization cannot affect
the potential detected by a SF electrode significantly, but
it can considerably increase potentials detected by surface
electrode (20). (4) Simultaneous detection by needle and
surface electrodes can result in opposite amplitude
changes (16–19) with IAP profile variations. (5) As the
profile length can remain the same under different com-
binations of the IAP duration and propagation velocity, it
6 ELECTROMYOGRAPHY (EMG) MODELING

y = 0.5 mm y = 5 mm

1
= var
= var 1
1
2 0.01 2
3
0 0 3

-0.01
-1

0 1 2 3 4 2 6 10 14 18
Time (ms) Time (ms)
(a) (c)

y = 0.5 mm y = 5 mm

1 1 Tin = var Tin = var

2 Figure 6. Effect of the stack (IAP transition) length
0.01
3 (1, 2, and 4 mm) on potentials produced in infinite
volume conductor at different fiber-electrode dis-
0 0 tances y. Potentials produced by the corresponding
stack when the transition length is increased at the
-0.01 expense of velocity at y ¼ 0:5 mm (a) and y ¼ 5 mm
-1 (c). Potentials produced by the corresponding stack
when the transition length is increased at the ex-
0 1 2 3 4 2 6 10 14 18 pense of duration (Tin) of the transition at y ¼ 0:5 mm
Time (ms) (b) and y ¼ 5 mm (d). The numbers next to the curves
Time (ms)
denote the stacks 1,2,3 of different length schemat-
(b) (d) ically represented in Fig. 5a. Negativity is upward.

IAP for different stages of fatigue (mV)

120
IAP Spike
80 Negative after-potential
or
after-depolarization
40
0 2 4 6
Time (ms)
Figure 7. IAPs used for simulation of changes in muscle fiber
membrane accompanying muscle fatigue. IAPs are represented in
respect of resting potential denoted here by 0.
is not correct to relate SFP amplitude or its radial decline
to changes in only one of these parameters.
2.4. Temporal Characteristics of SFP
2.4.1. Duration of Potentials Detected by an SF Elec-
trode. The peak-to-peak duration of potentials detected
by an SF electrode is determined by the ratio of the dis-
tance between the negative and positive maxima of the
potential field and velocity of the field propagation. If the
membrane source was a lumped dipole, than the field ex-
tremes should lay at the lines denoted A þ and A
(Fig.
4b, solid lines and Fig. 5c, dotted lines). As a result, the
distance between the extremes would increase with the
distance from the dipole and the peak-to-peak duration
would always be inversely proportional to velocity, irre-
spective of the distance (y) from the dipole axis.
This relation is not valid when the dipole source is dis-
tributed and the detection is performed in the fiber prox-
imity. In this case, the transition shape and length (Fig.
5a) determine the positions of the extremes of potential
field (Fig. 5b and Fig. 5c, solid, dashed, and dashed-dotted
lines). Up to a certain distance from the fiber that depends
on the transition length, the fiber-electrode distance prac-
tically does not affect the distances between the negative
8 and positive extremes (Fig. 5c, solid, dashed, and dashed-
dotted lines are almost perpendicular to the axis in the
fiber proximity) (21). As a result, the peak-to-peak interval
of the potentials detected up to 0.15–0.2 mm from the fiber
remains practically unchanged (22).
Let us now assume that the transition length
ðb ¼ Tin :v ¼ LÞ increases twice (Fig. 5a) because of a two-
time increase of the initial velocity v. The distance be-
tween the extremes of the potential field increases about
twice too (Fig. 5b, Fig. 5c, solid and dashed or dashed and
dashed-dotted lines at small y). As such a new two times
longer (2L) transition moves beneath the electrode with
the new velocity that is twice as high (2v) as the initial one
(v), the peak-to-peak duration of the detected potential
(B2L/2v) is approximately the same as under the initial
velocity (BL/v) (Fig. 6a).
If, however, the transition length increases twice at the
expense of the transition duration (2Tin) under velocity v

left unchanged, than the twice longer transition (2L)
moves along the point of observation twice as much
(B2L/v). The peak-to-peak duration increases correspon-
dently (Fig. 6b) (21).
2.4.2. Duration of SFP Produced by a Propagating Depo-
larized Zone. At larger distances, where the distributed
dipole sources (representing the IAP transitions) resemble
lumped dipoles, the negative region of the field produced
by the two dipoles widens with fiber-electrode distance y
(Fig. 8c), which reflects the increased degree of interac-
tions between the two dipole fields with y (Fig. 8a, lines of
maximal negative potential, A
, occur deeper in the pos-
itive region of another dipole field that modifies position of
the zero lines in the joint field more strongly with y in-
creasing). Distance between the zero lines defines the
length of the negative potential region. Duration of the
SFP negative phase is defined by this length divided by
velocity v of the field propagation beneath the point of ob-
servation.
Closer to the fiber (Fig. 8c, y ¼ y1), where the interac-
tion between the dipole fields is practically absent (Fig. 8a,
lines of maximal negative potential, A
, are in the prox-
imity of its own dipole), the distance between the zero
lines is in rather close relation to the IAP profile length. As
a result, similar to the peak-to-peak duration of potentials
produced by a single transition (see previous subsection)
duration of the SFP negative phase is proportional to the
IAP duration and is insensitive to changes in the propa-
gation velocity (23).
At large distances from the fiber typical for surface de-
tection, the length of the negative field is practically in-
sensitive to changes in the IAP profile (Fig. 8c, y ¼ y2, the
relative expansion of the negative field in the shaded re-
gion is short). As a result, sensitivity of the SFP negative
phase duration is very high to the fiber-electrode distance
and to changes in propagation velocity and it is much
lower to changes in duration of the IAP (23). After-poten-
tial, however, could also affect the duration of the SFP
negative phase (20), because the fiber-electrode distance
that is large compared with the length of the IAP spike
profile could be short compared with the length of the IAP
after-potential profile.
2.4.3. Conclusions. (1) The peak-to-peak duration of
biphasic extracellular potentials detected by an SF elec-
trode is proportional to duration of the IAP depolarization
phase and is insensitive to changes in propagation velocity
and fiber-electrode distance (21). (2) At a small fiber-elec-
trode distance, typical for detection by conventional mono-
polar or concentric needle electrode, the duration of the
negative phase of triphasic SFP is proportional to the IAP
duration and is insensitive to changes in propagation ve-
locity (23). (3) At a large distance from the fiber, typical for
surface detection, duration of SFP is sensitive to changes
in the fiber-electrode distance, propagation velocity, and
after-potential and is practically insensitive to changes in
the IAP spike duration (20,23).
ELECTROMYOGRAPHY (EMG) MODELING 7
Amplitude characteristics
A2− A1− A3− A1−
P2
a13
P1
a12 y2
y1
d1 d2 X d1 d3 X



(a) (b)
Temporal characteristics


0 0 0
P2
initial negative field
y2
P1
y1
L X
b=2L
(c)
Figure 8. Relationships between the profile length and ampli-
tude (a, b) and duration (c) of the SFP negative phase. Profile
length is represented by two lumped dipoles with different dis-
tance between them. (a) Lines A1
and A2
of the negative field
maxima, corresponding to the dipoles d1 and d2, are crossed (point
a12) at a radial distance y1. Any other distance between the di-
poles cannot provide the optimal field summation at y1. (b) d1 and
d3 are in optimal location to produce maximal potential at P2 lo-
cated at distance y2 (see point a13). (c) Changes in the width of the
negative potential field (distance between zero lines) with dis-
tance y from the fiber axis. (Thick solid lines) are for initial length
b ¼ L of the source along the fiber axis; (dotted lines) are for twice
longer b ¼ 2L source. Relative expansion of the field at a short
distance to the fiber ðy ¼ y1 Þ is much stronger than at a large dis-
tance ðy ¼ y2 Þ (compare expansion of the negative field (dashed
area) with the width of the initial negative field at distances y1
and y2).
2.5. SFP Produced by a Muscle Fiber of Finite Length
Appearing at the end-plate, the two depolarized zones ini-
tially act as a single source (Fig. 3b, t  t5). During this
stage, leading edge (5,6,24,25) is produced in SFP (Fig.
3d). Its duration is about that of the IAP spike (i.e., rather
short). Its amplitude depends on the electrode position.
After separation of the zones (Fig. 3b, t > t5), they continue
to produce joint effect on SFP. The larger the radial dis-
tance and the closer the point of recording to the end-plate
region, the stronger is the effect of the depolarized zone
that moves in the opposite direction. As a result, the shape
and amplitude of SFP detected near the end-plate vary
(Fig. 3d, the first four curves from left to right), which
makes the end-plate region inappropriate (16,26–28) for
noninvasive estimation of propagation velocity that as-
sumes similar shapes of potentials detected by two elec-
trodes located along the fiber direction. The velocity is
estimated by the ratio of the distance between the two
electrodes and latency between the signals. On the other
8 ELECTROMYOGRAPHY (EMG) MODELING
hand, if the electrodes are in symmetrical position in re-
spect to the end-plate, the detected potentials have iden-
tical shapes. They, however, are not suitable for velocity
estimation, because their latency is also identical, which
results in abnormally high velocity estimates. If these
electrodes are poles of a bipolar electrode (that detects
difference in two potentials), the resulting signal is re-
duced to values close to zero, which can be useful for non-
invasive determination of the end-plate position but can
result in wrong estimates of the muscle activity level. To
perform a correct estimate, the poles of a bipolar electrode
have to be located at one side of the end-plate region (it is
often located within the muscle belly) and as far as pos-
sible from it.
During formation of a depolarized zone, the sum of the
moments of all dipoles in one stack is not equal to that of
the dipoles of opposite direction in the other stack (Fig. 3b,
t ¼ t4, one zone). Nevertheless, the total dipole moment of
the fiber as a source comprising the two zones is equal to
zero because the stacks in the two zones are opposite (Fig.
3b, t ¼ t4, the two zones). Zero is also the total dipole mo-
ment of any propagating wave (Fig. 3b, t ¼ t6 and t ¼ t7).
At a large distance from the fiber, the character of such
sources is close to that of axial quadrupole.
After the moment t7, when a depolarized zone reaches
the corresponding fiber end, the total dipole moment of the
depolarized zone (Fig. 3b, moments t8–t10) starts to differ
from zero (17,20,29). If the point of observation P is above
the fiber (Fig. 3b, P ¼ P1 , t ¼ t8), some of the dipoles that
should produce negative potential at P1 if the fiber was
infinite are lacking. As a result (Fig. 3c, P ¼ P1 , thin upper
curve, t > t7), the positive deflection in the SFP is pro-
duced. The maximum of this positive terminal phase cor-
responds to the moment when the maximum of the IAP
profile is at the fiber end (Fig. 3b, moment t9). Then, the
stack of the dipoles facing the point of observation with its
positive sign also starts to disappear, which results in re-
duction of the positive terminal phase. If the point of ob-
servation is behind the fiber end, the terminal phase is
negative (Fig. 3c, P ¼ P2 , thin lower curve, t > t7), as the
disappearing dipoles face the point of observation with
their positive sign and then (after passing the fiber end by
the IAP profile maximum) with their negative sign (Fig.
3b, P ¼ P2 ). If the end-plate is in asymmetrical position in
respect to the muscle fiber ends, then two terminal waves
are produced in SFPs (Fig. 3d).
2.5.1. Conclusions. (1) The leading edge of SFP devel-
ops during IAP generation at the end-plate (5,6,24,25). (2)
When a depolarized zone reaches the fiber end, a terminal
phase develops in the SFPs because of change in the total
dipole moment of the depolarized zone (17,29). The termi-
nal phase is positive in detection above the fiber and neg-
ative in detection behind the end of the fiber (17). (3) The
shape and duration of the SFP terminal phase repeat
those of IAP (20). (4) The duration of the SFP terminal
phase does not depend on propagation velocity (20). (5) In
contrast to duration of negative phase of SFP that in-
creases with radial distance, duration of the terminal
phases is distance-independent (20). (6) As the full dipole
moment of the source producing the terminal phase is not
zero, the source has dipole character and the decline of the
SFP terminal phase with distance from the fiber is smaller
than the decline of the SFP negative phase, induced by
quadrupole-like source (5,17,20). As a result, the terminal
phases are especially pronounced in signals detected from
deeper muscles (5,6,30), which makes these phases re-
lated to the cross talk (5,6,30). (7) The regions near the
end-plate and fiber ends are inappropriate for noninvasive
estimation of propagation velocity (16,26–28).
2.6. Motor Unit Potentials (MUPs) and M-Waves
MUPs and M-waves represent the sum of SFPs produced
in response to a single impulse exciting either a single
nerve fiber or a number of nerve fibers innervating differ-
ent MUs in the muscle. The activated muscle fibers are
located at different distances from the detecting electrode
in these cases. Nevertheless, the distance-dependent fea-
tures of the amplitude and temporal characteristics of
MUPs and M-waves are similar to those described for SFP.
The mean fiber-electrode distance determines their spe-
cific characters (18,19).
Another peculiarity of such muscle activation is related
to scattering of the end-plates, different propagation ve-
locity of IAP along individual muscle fibers as well as to
differences in diameter and length of the nerve terminals
and in time of transmission across individual neuromus-
cular junctions, which causes spatial and temporal dis-
persion of the potential fields produced by IAP profiles
moving along individual fibers. The resulting desynchro-
nization of different SFPs additionally affects the MUP
and M-wave shape, amplitude, and duration (Fig. 9). The
effect is more pronounced (compare Fig. 9b and 9c) in nee-
dle detections, when the distance from active fibers and
thus signal duration are shorter (Fig. 9a and 9b) than
those in surface ones (Fig. 9c), which determines the com-
plex polyphasic shape of signals detected in some patho-
logical cases by needle electrodes (15).
The terminal phases of individual SFPs also have short
duration (Fig. 3c, thin lines, t4t7, Fig. 3d), which is why
the effect of desynchronization on the MUP and M-waves
terminal phases is pronounced (Fig. 3c, thick lines, Fig. 9c)
irrespective of the MU-electrode distances. The desyn-
chronization affecting the terminal phases has an addi-
tional component. It is related to differences in the
moments of arriving of the depolarized zones at the ends
of different fibers. It depends on the fibers’ semi-lengths
and propagation velocity (6,19,31).
2.6.1. Conclusions. (1) The distance-dependent fea-
tures of the amplitude and temporal characteristics of
MUPs and M-waves are similar to those described for SFP.
The mean fiber-electrode distance determines their spe-
cific character. (2) Desynchronisation of individual SFPs
additionally affects amplitude, duration, and the number
of phases in MUPs detected by needle electrodes and in
terminal phases of MUPs and M-waves detected by sur-
face electrode. (3) In contrast to the SFP terminal phases,
the shape, amplitude, and duration of terminal phases
MUPs and M-waves depend also on the fiber semi-length
and propagation velocity.

needle detection
Σ Σ
(a) (b)
surface detection
Main phases
Σ sentation of the membrane source through sequence of
Terminal phases
(c)
Figure 9. Effect of desynchronization on potentials that mimic
needle (a, b) and surface (c) detection. (a) Synchronized activity of
different fibers or motor units results in increase of the summed
potential amplitude. (b) Desynchronization in generation of short
potentials can make the shape of the summed potential polyp-
hasic. (c) Identical to (b) desynchronization has slight effect on
result of summation of the wide main phases and strong effect on
result of summation of the short terminal phases of SFP produced
at the muscle surface, which makes the terminal phases pro-
longed and its relative weight lower in the resulting signal (thick
line).
2.7. Anisotropy of the Volume Conductor
As the muscle fibers can often be considered parallel to
each other, conductivity of the muscle tissue in the longi-
tudinal direction (sl) is higher than in radial (sy) and
transversal (sz) ones (i.e., the volume conductor is aniso-
tropic with anisotropy ratio Kan ¼ s1 =sy ). In the case of
parallel fibers, such an anisotropic volume conductor can
be replaced by an equivalent isotropic one in two different
ways.
One way is to decrease all longitudinal dimensions (fi-
ber length, IAP propagation velocity and thus the length
of the depolarized zones) HKan -times (32,33). Note that
shortening of the depolarized zones decreases the SFP
amplitude at a large distance and increases it at a short
distance to the fiber (see section on Extracellular Poten-
tials Produced by a Propagating Depolarized Zone) that
results in increasing the SFP amplitude radial decline.
Another way is to increase all radial and transversal
dimensions of the volume conductor (9,34–40) and of the
fiber diameter HKan -times (32). The increase in fiber di-
ameter is often not considered in simulation studies. In
such cases, the SFP at short fiber-electrode distances de-
creases (instead of increasing) because the fiber-electrode
ELECTROMYOGRAPHY (EMG) MODELING 9
distance becomes larger in the equivalent volume conduc-
tor. Thus, the results obtained by the two ways are not
identical, which can be a reason the SFP simulated at
short fiber-electrode distances to be of lower amplitude
than the measured ones (34,35,37,40).
2.7.1. Conclusion. The effect of the volume conductor
anisotropy (anisotropy ratio Kan) is equivalent to the cor-
responding increase in all radial and transversal dimen-
sions of the volume conductor (the diameters of the active
fibers included) HKan -times (32).
2.8. SFP and MUP as an Output of a Linear TimeShift-
Invariant System
2.8.1. Single Muscle Fiber Potential (SFP). The above
considerations have physical transparency that helps to
understand electrical phenomena. They are based on pre-
dipoles distributed along the fiber axis. Equation 1 is a
mathematical formulation of such a spatial problem. It is,
however, not convenient for calculation of potentials pro-
duced by an ensemble of different muscle fibers, because
both its terms (IAP spatial profile and the term that take
into account the fiber geometry) are fiber-specific, which
must result in calculation of SFPs for each fiber from the
ensemble. To reduce the number of calculations, it is use-
ful (see the next subsection) to transform the formulation
into the temporal domain when the IAP as a function of
time can be considered identical for fibers of identical
membrane properties.
Assume that a unit dipole originates at the end-plate at
time zero and propagates along a fiber with a constant
velocity v. The potential produced by this dipole at the
point of observation P is IR(t) (Fig. 10a, left). The mem-
brane source, So ðtÞ ¼ dVi =dt can be approximated (Fig.
10a, middle) by n dipole sources of different moment
(an). Each subsequent ith dipole source originates at an
interval of dt. Propagating along the fiber, it produces po-
tential pi whose shape is also IR(t), magnitude is defined
by ai, and it is delayed by (i
1)dt from the potential pro-
duced by the first dipole source [i.e.,
pi ðtÞ ¼ ai  IRðt
ði
1ÞdtÞ]. The total potential is the sum
of n such potentials. As dt tends to zero and n tends to
infinity, the total potential produced at the point P by a
depolarized zone is represented through convolution:
jðP; tÞ ¼ So ðtÞ  IRðtÞ:
Thus, an active fiber can be considered as a linear
timeshift-invariant system of potential generation and
jðP; tÞ is the output of the system with the impulse re-
sponse IR(t) (Fig. 10, left) and input signal So(t) (Fig. 10a,
middle). The latter is the first temporal derivative of the
IAP (Fig. 10a, right).
As a skeletal muscle fiber has two depolarized zones,
IR(t) is the sum of potentials generated at the observation
point by two dipoles moving in opposite directions from
the end-plate to the fiber ends, where they disappear
(25,41), which can be described by the following equations
10 ELECTROMYOGRAPHY (EMG) MODELING

a2 So or IS
P IAP,
a3 dVi(t) Vi(t)
a1
IR dt

t a4 t t Figure 10. Excitable fiber as a linear time-

an
shift invariant system of SFP generation (a)
a5
and result of changes in velocity on tripole
a6
presentation (b). (a) impulse response (IR)


(i.e., potential produced by a moving unit di-
(a) pole) (left); the membrane source, So, or input
signal (IS) in double-layer presentation, qVi(t)/
qt (middle); IAP (i.e., Vi(t)) (right). (b) The IAP
2
potential profile (left, thick line, 1) length is
II Derivative
1 2 shorten (left, thin line, 2) upon two-fold de-
1
I Derivative crease of velocity; (middle) first spatial deriv-
IAP x ative of the two IAP profiles; (right) second
spatial derivatives of the two IAP profiles dem-
x tripole1 onstrating differences in the sources’ strengths
x
x (different phases’ areas) and differences in dis-
tripole 2
tances between the individual poles in the two
(b) approximating tripoles.

for anisotropic volume conductor (41): (15). If the membrane parameters are the same for all fi-
bers, the IAP in time domain could be accepted as identi-
Z t
@fi ðtÞ 1 cal, irrespective of the fiber diameter (44,45). So does the
ji ðt; xo ; yo ; zo Þ ¼ Can   ½IR1 ðt
tÞ input signal (the first temporal derivative of IAP) for all N
0 @t v
ð2Þ fibers of the MU. Then, the MU could also be considered as
@f ðtÞ 1 a linear time shift-invariant system, whose common im-
þ IR2 ðt
tÞdt ¼ Can  i  IRðtÞ;
@t v pulse response (CIR) is the sum of N impulse responses
corresponding to individual muscle fibers. Instead of N
where * means a convolution, IR ¼ IR1 þ IR2 , 0  t  tmax ; convolutions (one for every fiber), the MUP as the output
signal can be calculated as a single convolution between
IR1 the IAP first temporal derivative and CIR.
The properties of the volume conductor (conductivity
@ 1 and anisotropy) are included as a common factor into CIR.
¼ C1
@t ½ðxo
xep
vtÞ2 þ Kan ðyo
yi Þ2 þ Kan ðzo
zi Þ2 1=2 IR of an individual fiber incorporates information (41)
ð3Þ about fiber diameter, propagation velocity, positions of the
end-plate and fiber ends, location of the fiber within the
C1 ¼ 1 for : t  L1 =v and C1 ¼ 0 for : t > L1 =v; MU territory, electrode position, and the effect of a rect-
angular electrode area (see below). Any spatial filtering in
IR2 accordance with multielectrode arrangement can be also
included in IRs of an individual fiber (46). The CIR of an
@ 1 MU is, in fact, the sum of potentials produced at a mono-
¼ C2
@t ½ðxo
xep þ vtÞ2 þ Kan ðyo
yi Þ2 þ Kan ðzo
zi Þ2 1=2 polar or multielectrode by N pairs of propagating dipoles
corresponding to N fibers.
ð4Þ
2.8.3. Conclusions. (1) The presentation of SFP and
C2 ¼ 1 for : t  L2 =v and C2 ¼ 0 for : t > L2 =v;
MUP as an output signal of linear and timeshift-invari-
ant system (Equation 2) results in fast calculation of MUP
tmax is the time during which the excitation passes along
without simplification of the IAP shape. It, however, has
the longer distance from the end-plate (xep) to the proxi-
no such transparent physical interpretation as that
mal (L1) or distal (L2) fiber end (tendon).
through two stacks of distributed double-layer disks. (2)
This approach is convenient also for simulation of SFP
This approach allows better understanding of regularities
produced by muscle fibers inclined to the skin (42) or by
of SFP and MUP spectral characteristics (see below).
fibers with nonuniform propagation (43).
2.9. Spectral Characteristics of SFPs and MUPs
2.8.2. Motor Unit Potentials (MUP). Although fibers in
MUs differ by their length and positions of their end- Attempting to describe the power density spectrum (PS) of
plates and ends as well as by their diameter and thus ve- SFP in terms of well-defined physical parameters, Lind-
locity of IAP propagation, histochemical and biomechani- ström (47,48) related all expressions to the action poten-
cal characteristics of all fibers in a given MU are identical tial just outside the fiber (i.e., IAP did not participate in

the equations). Following Krakau (49), Lindström (47)
proposed a mathematical model of the SFP power density
spectrum (PS), which explicitly depended on propagation
velocity because this term was part of the impulse re-
sponse of their systems. As a result, it was concluded (47–
49) that any change in propagation velocity was reflected
in proportional shift of the power spectrum of the signal.
Convolution in the temporal domain (used to express
SFP and MUP, as described earlier) is transformed into
product of PS of the input signal and impulse response in
the frequency domain. The input signal (as the first tem-
poral derivative of IAP(t)) does not depend on propagation
velocity. However, as the impulse response becomes wider
(and thus lower frequency) with radial distance (Fig. 4),
the interrelation between power spectra of the IAP deriv-
ative and impulse response does depend also on the fiber-
electrode distance (50,51), which means that the effect of
the product of two terms can differ from that of one term
(impulse response) only (19,46,50–52). The PS of the sig-
nal detected in the proximity of muscle fiber is not ex-
pected to shift in accordance with the propagation velocity.
Thus, conclusion that any change in propagation velocity
is reflected in a shift of the power spectrum of the signal
(53,54) could be invalid for detection by SF electrode,
which is in line with the distance-dependent sensitivity
of SFP duration to propagation velocity demonstrated ear-
lier.
Besides, duration of the leading edge and terminal
phases (Fig. 3d) is in close relation to that of the short
IAP spike. It does not depend on the distance from the
source and determine the high-frequency components of
the SFP and MUP power spectra (5,6,46,52). Combination
with the low radial decline of the terminal phases makes
contribution of these components to the cross talk more
significant than that of other signal phases (5,11,30). Con-
sequently, the cross talk from other muscles should dom-
inate in the high- but not in the low-frequency region as is
considered by the most authors (53,54). Thus, mathemat-
ical differentiation and high-pass filtering of the raw sur-
face EMG signal proposed (55) for cross-talk reduction,
could increase the cross talk (6).
The leading edge and terminal phases considerably af-
fect (56) also fmean defined (54) by the ratio R between the
myoelectric signal spectral moments, PSðf Þ  ðf Þk df , of
order k ¼ 1 and order k ¼ 0. As a result, sensitivity of fmean
to changes in propagation velocity only is strongly reduced
(56), which makes fmean proposed (57) and used as a mea-
sure of propagation velocity changes not very reliable. On
the other hand, depolarizing after-potential determines
IAP and SFP low-frequency components (19,50,51). Under
detection by surface electrodes, the relative weight of the
low-frequency components in SFP is especially pro-
nounced (19,50,51). Taking into account this fact as well
as the effects of changes in leading edge and terminal
phases, it is possible to create a sensitive noninvasive
spectral
R Rfatigue index (58,59),
PSðf Þ  ðf Þ
1 df = PSðf Þ  ðf Þk df , where 2  k  5.
2.9.1. Conclusions. (1) The characteristics of the power
spectrum density and their sensitivity to changes in prop-
agation velocity and IAP are defined by distance-depen-
ELECTROMYOGRAPHY (EMG) MODELING 11
dent interrelations between power spectra of the input
signal and impulse response (19,46,50–52). (2) Mathemat-
ical differentiation and filtering of the raw surface EMG
signal with high-pass filters can increase the cross talk (6)
instead of its decreasing.
2.10. Other Ways to Model SFP and MUP
If Equation 1 is integrated by parts, a version of equation
of Lorente de Nó (60) for a fiber of finite (x1–x2) length is
obtained:
 Z 1 2 
@Vi 1  @ Vi 1 @Vi 1 
jðPÞ ¼ þ C dx
: ð5Þ
dx ran x1 dx ran x2
an 2

1 @x ran
It is a single-layer presentation (9). The terms at the ends
x1 and x2 of a very long cylinder are close to zero like at
points remote from the membrane source. Then another
expression for unlimited fibers is obtained:
Z
þ1
@ 2 Vi 1
jðPÞ ¼ Can  dx: ð6Þ

1 @x2 ran
The results described in the previous sections could also
be obtained with the model based on Equation 5. It, how-
ever, requires special description of the source change dy-
namics at the end-plate and tendons (61,62). As a result,
SFP and MUP calculation cannot be directly reduced to
single convolution. A fast-computing algorithm is crucial
when a large number of fibers are included in simulation
of MUP or interference EMG signals.
To eliminate the explicit expression of the terms at the
end-plate and fiber ends, Farina and Merletti (63) intro-
duced them implicitly in analytical description of the
source. At a certain moment, the source across the mem-
brane of each fiber semi-length was represented through
the first spatial derivative of the IAP profile. It was mul-
tiplied by the function that takes the value 1 above the
fiber semi-length and 0 otherwise. The transmembrane
current density was then represented through the first
spatial derivative of the sum of two (for two depolarized
zones) sources. Inclusion of anatomical parameters of in-
dividual fiber in the input signal, IS, deprives the IS of
generality. The IS becomes specific for each fiber and cal-
culation of MUP cannot be reduced to single convolution.
Hammarberg and Stålberg (64) overcame the problem
with description of the source change dynamics at the end-
plate and tendons in another way. They transformed the
changes in the source at the end-plate and tendons into
the corresponding changes of the weighting function. In
such a way, they were also able to reduce the formal ex-
pression of SFP to single convolution in temporal domain.
However, the SFP expression is split into six terms; each
term depends on the individual fiber length (i.e., does not
contain a term that could become a common one in calcu-
lations of potentials produced by a number of fibers). The
authors paid attention to the sampling frequency required
for a correct SFP calculation. They noted that the fre-
quency must be defined not by bandwidth of the resulting
SFP but by the transmembrane current that had signifi-
cant high-frequency content. Just the high-frequency con-
12 ELECTROMYOGRAPHY (EMG) MODELING
tent of IS made the authors to apply an antialiasing filter
to remove the excess bandwidth of the transmembrane
current. The dipole presentation (first temporal derivative
of Vi in the IS against the second one) reduces the IS high-
frequency content.
SFP can be obtained also by formal solutions of Pois-
son’s or Laplace’s equation with the corresponding bound-
ary conditions using method of separation of variables
(9,36,38,65–69). The solution is based on Fourier trans-
form technique and modified Bessel functions. The formal
solution, however, gives no chance for transparent phys-
ical interpretations (9).
Taking into account the fact that the transmembrane
current is the primary electric source producing the ex-
tracellular potentials, many authors (36,37,40,68,70–77)
modeled SFPs on the basis of Equation 6, although Lo-
rente de Nó (60) explicitly stressed that it is valid for fibers
of infinite length only. Although different types of MUs can
differ in their IAPs (78), mathematical description of IAP
in space domain most used (27,36,37,63,73–75,79–81) is
either that suggested by Rosenfalck (68) or its modifica-
tion (37). Belonging to one type of MU and thus having
identical IAP as a function of time, the fibers of different
diameters have to differ in their velocity and consequently
in spatial extent of the IAP profiles and thus in trans-
membrane current density.
Thus, to simulate differences in diameters of fibers
through presentation of the source in spatial domain, it
is necessary to calculate the source strength each time
when the IAP spatial profile changes. It is not correct to
move the source, calculated for initial conditions, with dif-
ferent velocity along the fibers. Similar problems develop
when duration of the IAP and its velocity change with the
muscle functional state in such a way that their product
(the length of the depolarized zone) is also changed. The
opposite changes in amplitude of the signals detected si-
multaneously by electrodes located at different distances
from the active fibers (4,81,83–85) is an indirect indication
of the possible changes in the IAP profile length. The only
case when the identical source can be moved along the fi-
bers with different velocity is when the IAP duration is
changed together with velocity in such a way that their
product remains unchanged.
2.10.1. Approximation of the IAP through a Tripole. A
simplification of the above model is replacement of the
distributed source by an equivalent current tripole
(9,36,40,66,68,71,72,76,82). The intensity of the individ-
ual point current source is defined by area of the corre-
sponding phase of the transmembrane current density.
Each point source should be located at the centroid of the
corresponding phase (Fig. 10b, right). Such a presentation
cannot be suitable for a proper approximation of IAP with
after-potential. In addition, variation of the IAP profile
length must involve changes in the tripole parameters.
The lower the velocity, the shorter the depolarized zone
(Fig. 10b, left, thin line, 2) and the distances between the
positive and negative poles (Fig. 10b, right, tripole 2). The
point source intensities must be higher because of larger
areas of the phases (Fig. 10b, right, thin line, 2).
To avoid the problem with simulating the effects of IAP
generation and extinction, some authors (66,71,72,82)
treated the space and time domains separately. Each point
source remained stationary at the end-plate until its de-
parture time, and then it propagated along the muscle
axis until reaching the tendon where it remained station-
ary. The terminal phases and changes in the dipole mo-
ment did not follow the actual IAP time course in this case.
Difficulties with presentation of the IAP tail (IAP depo-
larizing after-potential, whose effect is especially consid-
erable at large fiber-electrode distances) can make the
tripole simplification of the source not correct at large fi-
ber-electrode distances either.
2.10.2. Conclusions. (1) SFP and MUP produced by
muscle fibers of finite length in infinite volume conductor
can be calculated identically correctly on the basis of
Equations 1 or 2, or Equation 5 or by formal solution of
Poisson’s or Laplace’s equations. (2) Calculations of poten-
tials produced by a great number of muscle fibers on the
basis of Equations 1 or 5 either cannot be reduced to a
single convolution or required complication of specific ex-
pression of the equation terms. (3) The simplified model of
SFP through an equivalent current tripole cannot be suit-
able for a proper approximation of IAP with after-poten-
tial. (4) To model changes in propagation velocity only, it is
necessary to change the length and intensity of the source
(Fig. 10b, right). It is not correct just to move the source,
calculated for initial velocity, with the new velocity along
the fibers.
2.11. Effect of Electrode Dimensions
The actual electrodes have a certain contact area that acts
as spatial averager of the extracellular potentials and
background noise. The noise intensity is approximately
inversely proportional to the contact area (86,87). A larger
electrode area, however, reduces the signal detected (88–
90). A useful combination of required noise reduction with
an acceptable signal distortion can be found by a proper
modeling.
Equation 2 provides a possibility for a simple analytical
integration of the SFP over rectangular electrode area.
The temporal derivative of (1/r) in Equations 3 and 4 dif-
fers from the spatial derivative along xo only by the term
7v. Thus, integration along longitudinal xo dimension of a
rectangular electrode is reduced to corresponding multi-
plication of the term 1/r (41). Analytical integration over
another transversal electrode dimension can be performed
by the way described by Griep et al. (71). The effects of
longitudinal and transversal electrode dimensions on SFP
essentially differ (91). The longitudinal dimension affects
the main SFP phases (that reflect the IAP profile propa-
gation along the fiber) more than the transversal one. In
this sense, the rectangular shape has its advantages. Nev-
ertheless, electrodes with circular shape are also used.
Farina and Merletti (63) proposed a transfer function, as a
2D spatial filter in space domain, to simulate the effect of
rectangular, circular, and elliptic electrodes.

2.11.1. Conclusion. As the effects of longitudinal and
transversal electrode dimensions on SFP essentially differ,
the appropriate choice of dimensions and orientation of
rectangular electrodes gives a chance for obtaining useful
information in SFP, MUPs, and EMG signals and sup-
pressing noise and other obstructive information (91).
2.12. Modeling of Interference EMG
To simulate correct interference EMG signals, it is neces-
sary to take into account muscle and MUs anatomy
(61,73,75,92,93) that can be affected in specific ways by
neuromuscular disorders (15), proportion between differ-
ent types of MUs (94,95), their recruitment and firing
rates (61,93,96) as well as adequate MUPs. As was dem-
onstrated above, the effect of IAP profile across the mem-
brane on EMG is distance-dependent. Thus, adequate
interference EMG signals could not be obtained using
samples of individual SFPs or MUPs detected experimen-
tally at a given electrode position (97–101), which is also
valid for the case when analytic functions that mimic such
experimental SFPs or MUPs (12,53,54,90,102–106) or a
band-limited Gaussian random process (107–109) are used
to simulate interference EMG. That type of models cannot
take into account neither distance-dependent relations
between individual phases of SFPs and MUPs nor the ef-
fects of anatomical and physiological parameters of differ-
ent muscles. They are descriptive or phenomenological
with limited validity.
Models by Nandedkar et al. (110,111) and Stashuk (93)
take into account delays in neuromuscular transmission, a
realistic IAP shape, and distribution of muscle fibres
within MUs and muscle territory. The correct effects of
the IAP origin at the end-plate and the IAP extinction at
the fiber ends were not a part of these models. They could
be used for simulation of EMG detected by an SF electrode
(located far from the end-plate and fiber ends), whose ref-
erence electrode is far away from the active fibers and de-
tects no electrical activity. They could also be used for
simulation of EMG detected by a concentric needle elec-
trode although experimental recordings performed sepa-
rately from the central electrode and cannula
demonstrated registration of the terminal phases (related
to the processes at the fiber ends) at both recordings (112).
Simulation of EMG signal detected by a needle mono-
polar, MACRO-, or surface electrode requires inclusion of
the processes at the end-plate and fiber ends. They are
included in models of interference EMG signals proposed
by Duchêne and Hogrel (62), Farina and Merletti (64),
Lowery et al. (76), and by Hamilton-Wright and Stashuk
(92). However, the MUP calculation cannot be directly re-
duced to single convolution in these models and the MUPs
were calculated as the sum of individual SFPs. When a
large number of fibres is included in simulation, a fast-
computing algorithm is important. To reduce the number
of calculations, contribution of the muscle fibres located
only in the so-called detection area is taken into account
(93), the MU or muscle fibers are assumed to be distrib-
uted within a few ‘‘isopotential’’ layers, each fiber of which
produces the same potential (90) or SFPs are calculated
instead of MUPs (27).
ELECTROMYOGRAPHY (EMG) MODELING 13
2.12.1. MU Recruitment and Firing Rates. The regi-
ments of MU recruitment and derecruitment as well as
the firing rates of different MUs are task-specific and have
no general character. The classic approach is related to the
so-called Henneman (113–116) ‘‘size principle,’’ according
to which progressively larger MUs are recruited with in-
creasing muscle force. Larger MUs comprise muscle fibers
of greater diameter, which is why the MUs are often or-
dered by their mean propagation velocity value. It is, how-
ever, found that the order of MU recruitment can depend
also on movement speed and direction (117).
The physiological range of mean firing frequencies is
reported to be within 8–35 Hz (79,118–121). The interpulse
intervals produced by an MU are considered to be inde-
pendent samples of a random variable. Different distribu-
tions of the consecutive interpulse intervals of an MU are
proposed, but a Gaussian distribution appears justifiable
to model them (39,61,73,75,79,92,93,96,122). Usually, con-
stant ranges for the variation of the firings are chosen,
irrespective of the mean interpulse interval. The typical
values for the coefficient of variation are within the 0.1–
0.33 range, which corresponds to a standard deviation of
10–30 ms for mean firing frequency of 10 Hz.
The experimental results on relations between fre-
quency of MU discharge and muscle tension are contra-
dictory (123) even for a simple muscle activity like
isometric contraction when the muscle length is main-
tained unchanged. With the increase of muscle tension,
the frequency of discharge was reported first to increase,
then to be stable and to increase again near the maximum
effort (124,125). Other investigators have found increasing
firing rate at low tension (126) and an almost stable fre-
quency at high tension (126,127). An approximately linear
relation between firing frequency and muscle force was
established by Clamann (128) and many others (see, for
example, Ref. 119). Gydikov and Kosarov (120) found two
types of MUs, one of which demonstrated a linear- and
another one demonstrated a plateau-like dependence. The
discrepancies in the data are because of insufficient selec-
tivity of recordings, difficulties with following activity of
one MU especially under high-level contraction, and bias
of the data collected by different methods. On the other
hand, the loss of force during a sustained maximal volun-
tary contraction is accompanied by a marked decrease in
the MU firing rate, which can be as much as 50% in 1
minute (129,130).
When additional MUs are recruited at a certain force
level, they usually fire at lower rate than the MUs re-
cruited earlier at the same force level (130). No systematic
assessments of the distribution of mean interpulse inter-
vals of the whole pool of active MUs exist. The firing rates
of simultaneously active MUs do not differ by more than
10 Hz. The variability seems to decrease with increasing
force level (131).
When a number of MUs are active, their firing rates
can be synchronized (132,133). A number of authors ana-
lyzed the effect of synchronization on frequency and am-
plitude characteristics of EMG signals (73,134–138). The
degree of this phenomenon is still not clear. Synchroniza-
tion has been implicated as one of the causes of frequency
shifts in the power spectrum during fatigue
14 ELECTROMYOGRAPHY (EMG) MODELING
(134,137,139,140) because a declining propagation veloc-
ity only partly explains the frequency decrease. However,
after many years of discussion, it is still a matter of con-
troversy (141,142). A more pronounced frequency shift
could (19,50,51,56) be because of the end effects and effect
of IAP changes during fatigue (Fig. 7). Attempts to explain
the increase in the EMG amplitude with synchronization
also exist (73,138) although IAP profile lengthening could
also be responsible (10,18,19).
The specific parameters used to model MU recruit-
ments can be found, for example, in Refs. 61,79,92,96.
2.12.2. Conclusions. (1) When intramuscular interfer-
ence EMG is simulated, it is necessary to pay a special
attention to a correct inclusion of parameters of IAP and
propagation velocity in simulation of each SFP as well as
anatomy of MUs. (2) When surface interference EMG is
simulated, it is necessary to include processes at the end-
plate and fiber ends. (3) As no reliable experimental
method exists for studying the firing patterns of the ma-
jority of the MUs in a muscle, the simulations give a
chance for analysis of different regiments of recruitment
and firing rates.
3. MODELING OF EMG SIGNALS IN AN
INHOMOGENEOUS BOUNDED VOLUME CONDUCTOR
An actual volume conductor is inhomogeneous and
bounded because of the presence of bones, vessels, inter-
stitial tissue, and layers of fat, skin, and air contacting
with the skin. The inhomogenities affect the potential field
and EMG signals (143). Together with a complex muscle
structure, they are obstacles for a correct assessment and
interpretation of the detected EMG signals. Thus, propa-
gation velocity is estimated in a few muscles only. The
analysis of the effects of the volume conductor complexity
gives ideas to what extent regularity obtained for homo-
geneous unbounded volume conductor could be distorted.
The parameters, varying with muscle activity, are func-
tional (IAP duration, after-potentials, velocity, whose pro-
nounced effect on regularities of SFP changes was
demonstrated in the first part of the chapter), anatomical
(fiber diameter, curvature, angle between the fibers in
pinnate muscles and thus anisotropy of the volume con-
ductor), and biochemical, affecting conductivity of the vol-
ume conductor. The volume conductor inhomogenities are
subject specific and, fortunately, do not change a lot with
muscle activity.
The effect of air or an insulating plate can be taken into
account by the method of mirror images whose application
show (38,144) that the SFP decline is reduced in direction
to the boundary where the SFP is doubled. The effect of
layers of lower conductivity can be approximated through
corresponding increase of the electrode distance from the
active fibers (145), which can explain expansion of the
signals, increase in the relative weight of the terminal
phases, lower decline of MUPs in transversal direction,
and possibility of a good estimation of the MU axis location
but not of the MU size.
Formal exact mathematical description of potentials in
inhomogeneous and bounded volume conductor differs
from the Poisson’s equations for isotropic infinite volume
conductor only by dependence of conductivities on the
point in the volume conductor. In case of layered geome-
try, the equation is solved in each layer and then the
boundary conditions at the surfaces between the layers
are used for obtaining the final solution.
The clear general idea, however, results in complicated
solutions that can be analytical for certain simple geom-
etries of volume conductor such as half-spaced or circular
cylinders. For more complicated geometries, numerical
techniques are used. As a result of complicity and compu-
tational demands, these models are often accompanied by
a simplified membrane source presentation through a
tripole. Their further development and analysis of the ef-
fects are forthcoming. They will shortly be described be-
low. A wider review of these approaches can be found in a
recent book on EMG (146).
3.1. Effect of Frequency Dependence of Volume Conductor
Strictly speaking, muscle tissue, as a volume conductor, is
frequency-dependent because of the capacitive effect of the
muscle fiber membranes. Starting from a certain fre-
quency, the tissue conductivity increases. The increase
in longitudinal conductivity starts at a higher frequency
than that in the radial conductivity. As a result, anisot-
ropy ratio is also frequency-dependent (147).
Using a model for infinite fiber, Albers et al. (34) found
pronounced effect of tissue conductivities on SFPs at small
distances only, because the distance from the fiber acted as
a low-pass frequency filter widening the SFP. However,
muscle tissue does not act as a low-pass filter on the ter-
minal phases that (together with the leading edge) deter-
minate high frequencies of the signal and its power
spectrum (6). Thus, frequency dependence of tissue con-
ductivities can affect SFPs, MUPs, and M-waves at a large
distance as well. This effect on SFPs was demonstrated
recently (80). However, the actual effect on MUPs or M-
waves should be smaller because the frequency content of
their terminal phases are not as high as in the case of SFP.
3.2. Semi-Infinite Layered Volume Conductor
Following Farina and Rainoldi (148), Farina and Merletti
(63) proposed an approach of surface EMG modeling based
on the spatial and temporal Fourier frequency character-
istics of the signal. It was applied to generate signals in a
layered volume conductor (muscle, fat, skin) with infinite
parallel planes separating the tissues. The signal in the
temporal domain was generated by an equivalent 1D filter
in the time domain. The filter was computed based on the
spatial transfer functions of the volume conductor and de-
tection system and of the spatio-temporal function de-
scribing the evolution in space and time of the IAP. The
effect of electrode shape and size as well as the inclination
of the fibers parallel to the surface in respect to the de-
tecting system can be included in the transfer function of
the filter. The model allows computation of the simulated
potentials using properties of the 2D Fourier transforma-
tion.

3.3. Cylindrical Volume Conductor
A model by Gootzen et al. (62) describes cylindrical volume
conductor consisting of two layers (muscle and subcuta-
neous fat). Roeleveld et al. (67) and Blok et al. (149) de-
veloped it and described a three-layered model that
included muscle, fat, and skin. The authors found that
the terminal phases were enhanced significantly because
of the finite limb dimensions.
Recently, Farina et al. (150) proposed a surface EMG
generation model and multilayer cylindrical volume con-
ductor and the source in an internal, intermediate, or ex-
ternal layer. It allows the description of layers (which are
anisotropic in the three directions), sources (traveling ei-
ther in the longitudinal or in the angular direction), and
any detection electrode shape.
3.4. Volume Conductor with Complicated Geometry
Lowery et al. (74) attempted to analyze a potential field in
multiple-layer finite-element model of the upper arm that
incorporates muscle tissue, fat, skin, and bone. Potential
distribution generated by a single fiber was analyzed. The
authors have found that the effect of bone was minor in the
upper arm. Recently, Lowery et al. (80) presented a more
realistic finite-element model based on arm anatomy ob-
tained through magnetic resonance images of human up-
per arm. The model includes resistive and capacitive
tissue properties as well as the effect of finite length of
muscle fibers. Farina et al. (151) presented the possibility
of combining analytical and numerical methods for de-
scription of the complex volume conductor and analytical
methods for modeling the source. Mesin and Farina (152)
analyze the ability to describe surface EMG signals gen-
erated by bi-pinnate muscles analytically.
3.5. Conclusions
Studies of a more actual complicated volume conductor
are of doubtless interest. Complicity of these models and
computational demands often require simplification of the
expression for the membrane source. Further develop-
ment of those models and comprehensive analysis of the
complicated volume conductor effects are forthcoming.
4. GENERAL CONCLUSION
EMG investigations include detection of changes in the
neuromuscular system as a result of pathology, treatment
or changes in muscle functional state, and analysis of rea-
sons for them. Each model reflects only part of reality. The
art of the modeling is in the choice of significant param-
eters and rejection of the secondary ones in answering a
specific question.
BIBLIOGRAPHY
1. C. S. Sherrington, Ferrier lecture: some functional problems
attaching to convergence. Proc. R. Soc. (Lond.) 1929;
105:332–362.
ELECTROMYOGRAPHY (EMG) MODELING 15
2. J. Ekstedt, Human single muscle fiber potentials. Acta
Physiol. Scand. 1964; 61(Suppl 226):1–96.
3. E. Stålberg and J. V. Trontelj, Single Fiber Electromygraphy.
Surrer, UK: Mirvalle Press, 1979: 1–244.
4. J. V. Basmajian and C. J. De Luca, Muscles Alive: Their
Functions Revealed by Electromyography. 5th ed. Baltimore,
MD: William and Wilkins, 1985.
5. G. V. Dimitrov, C. Disselhorst-Klug, N. A. Dimitrova, E.
Schulte, and G. Rau, Simulation analysis of the ability of
different types of multi-electrodes to increase selectivity of
detection and to reduce cross-talk. J. Electromyogr. Kinesiol.
2003; 13:125–138.
6. N. A. Dimitrova, G. V. Dimitrov, and O. A. Nikitin, Neither
high-pass filtering nor mathematical differentiation of the
EMG signals can considerably reduce cross-talk. J. Elect-
romyogr. Kinesiol. 2002; 12:235–246.
7. H. Helmholtz, Uber einege Gesetze der Vertheilung el-
ektrischer Ströme in Körpelischen Leitern mit Anwendung
auf die thierischelektrischen Versuche. Ann. Phys. Chem.
1853; 29:222–227.
8. F. N. Wilson, A. G. MacLeod, and P. S. Barker, The distribu-
tion of the action currents produced by heart muscle and
other excitable tissues immersed in extensive conducting
media. J. Gen. Physiol. 1933; 16:423–456.
9. R. Plonsey, The active fiber in a volume conductor. IEEE
Trans. Biomed. Eng. 1974; 21:371–381.
10. N. Dimitrova, Influence of the length of the depolarized zone
on the extracellular potential field of a single unmyelinated
nerve fibre. Electromyogr. Clin. Neurophysiol. 1973; 13:547–
558.
11. G. V. Dimitrov and N. A. Dimitrova, Modeling of the extra-
cellular potentials generated by curved fibres in a volume
conductor. Electromyogr. Clin. Neurophysiol. 1980; 20:27–40.
12. D. C. Boyd, P. D. Lawrence, and P. J. A. Bratty, On modeling
the single motor unit action potential. IEEE Trans. Biomed.
Eng. 1978; 25:236–243.
13. F. Buchthal and P. Pinelli, Analysis of muscle action poten-
tials as a diagnostic aid in neuromuscular disorders. Acta
Med. Scand. 1952; 142(Suppl 266):315–327.
14. E. Stålberg, Propagation velocity in human muscle fibers in
situ. Acta Physiol. Scand. 1966; 70(Suppl 287):1–112.
15. E. Stålberg, S. D. Nandedkar, D. B. Sanders, and B. Kalck,
Quantitative motor unit potential analysis. J. Clin. Ne-
urophysiol. 1996; 13:401–422.
16. G. V. Dimitrov and N. A. Dimitrova, Extracellular potential
field of a single striated muscle fibre immersed in anisotropic
volume conductor. Electromyogr. Clin. Neurophysiol. 1974;
14:423–436.
17. N. A. Dimitrova, Model of the extracellular potential field of
a single striated muscle fibre. Electromyogr. Clin. Ne-
urophysiol. 1974; 14:53–66.
18. N. A. Dimitrova and G. V. Dimitrov, Amplitude-related char-
acteristics of motor unit and M-wave potentials during fa-
tigue. A simulation study using literature data on
intracellular potential changes found in vitro. J. Elect-
romyogr. Kinesiol. 2002; 12:339–349.
19. N. A. Dimitrova and G. V. Dimitrov, Interpretation of EMG
changes with fatigue: facts, pitfalls, and fallacies. J. Elect-
romyogr. Kinesiol. 2003; 13:13–36.
20. G. V. Dimitrov and N. A. Dimitrova, Influence of the after-
potentials on the shape and magnitude of the extracellular
potentials generated under activation of excitable fibres.
Electromyogr. Cliniol. Neurophysiol. 1979; 19:249–267.
16 ELECTROMYOGRAPHY (EMG) MODELING
21. G. V. Dimitrov and N. A. Dimitrova, Extracellular potentials
produced by a transition between inactive and active regions
of an excitable fibre. Electromyogr. Clin. Neurophysiol. 1989;
29:265–271.
22. C. H. Håkansson, Action potentials recorded intra- and ex-
tracellularly from the isolated frog muscle fibre in Ringer’s
solution and air. Acta Physiol. Scand. 1957; 39:291–312.
23. G. V. Dimitrov, Changes in the extracellular potentials pro-
duced by unmyelinated nerve fibre resulting from altera-
tions in the propagation velocity or the duration of the action
potential. Electromyogr. Clin. Neurophysiol. 1987; 27:243–
249.
24. Z. C. Lateva and K. C. McGill, Estimating motor-unit archi-
tectural properties by analyzing motor-unit action potential
morphology. Clin. Neurophysiol. 2001; 112:127–135.
25. K. C. McGill, Z. C. Lateva, and S. Xiao, A model of the muscle
action potential for describing the leading edge, terminal
wave, and slow afterwave. IEEE Trans. Biomed. Eng. 2001;
48:1357–1365.
26. T. I. Arabadzhiev, G. V. Dimitrov, and N. A. Dimitrova, Sim-
ulation analysis of the ability to estimate motor unit prop-
agation velocity non-invasively by different two-channel
methods and types of multi-electrodes. J. Electromyogr. Kin-
esiol. 2003; 13:403–415.
27. D. Farina, C. Cescon, and R. Merletti, Influence of anatom-
ical, physical, and detection-system parameters on surface
EMG. Biol. Cybern. 2002; 86:445–456.
28. J-Y. Hogrel, J. Duchêne, and J-F. Marini, Variability of some
SEMG parameter estimates with electrode location. J. Elect-
romyogr. Kinesiol. 1998; 8:305–315.
29. N. A. Dimitrova, G. V. Dimitrov, and Z. C. Lateva, Influence
of the fiber length on the power spectrum of single muscle
fiber extracellular potentials. Electromyogr. Clin. Ne-
urophysiol. 1991; 31:387–398.
30. D. Farina, R. Merletti, B. Indini, M. Nazzaro, and M. Pozzo,
Surface EMG crosstalk between knee extensor muscles: ex-
perimental and model results. Muscle Nerve. 2002; 26:681–
695.
31. N. A. Dimitrova, C. Disselhorst-Klug, G. V. Dimitrov, and G.
Rau, Area to amplitude ratio of the terminal phase of the
belly-tendon detected motor unit potentials could be used to
recognize reinnervated motor units. Electromyogr. Clin. Ne-
urophysiol. 2002; 42:267–273.
32. G. V. Dimitrov and N. A. Dimitrova, Extracellular potential
field of an excitable fibre immersed in anisotropic volume
conductor. Electromyogr. Clin. Neurophysiol. 1974; 14:437–
540.
33. O. B. Wilson, J. W. Clark, N. Ganapathy, and T. L. Harman,
Potential field from an active nerve in an inhomogeneous,
anisotropic volume conductor - the forward problem. IEEE
Trans. Biomed. Eng. 1985; 32:1032–1041.
34. B. A. Albers, W. L. C. Rutten, W. Wallinga-de Jonge, and H.
B. K. Boom, A model study on the influence of structure and
membrane capacitance on volume conductor in skeletal mus-
cle tissue. IEEE Trans. Biomed. Eng. 1986; 33:681–689.
35. B. A. Albers, J. H. M. Put, W. Wallinga-de Jonge, and P. Wi-
rtz, Quantitative analysis of single muscle fiber action po-
tentials at known distances. Electroenceph. Clin.
Neurophysiol. 1989; 73:245–253.
36. S. Andreassen and A. Rosenfalck, Relationship of intracel-
lular and extracellular action potentials of skeletal muscle
fibers. CRC Crit. Rev. Bioeng. 1981; 7:267–306.
37. S. D. Nandedkar and E. V. Stålberg, Simulation of single
muscle fibre action potentials. Med. Biol. Eng. Comput.
1983; 21:158–165.
38. R. Plonsey, Bioelectrical Phenomena. New York: Mc-Graw-
Hill, 1969.
39. D. F. Stegeman, R. Merletti, and H. J. Hermens, EMG mod-
eling and simulation. In: R. Merletti and P. A. Parker, eds.,
Electromyography: Physiology, Engineering, and Noninva-
sive Applications. New York: IEEE Press and John Wiley &
Sons, 2004.
40. B. K. van Veen, E. Mast, R. Busschers, A. J, Verloop, W.
Wallinga, W. L. C. Rutten, P. O. Gerrits, and H. B. K. Boom,
Single fiber action potentials in skeletal muscle related to
recording distances. J. Electromyogr. Kinesiol. 1994; 4:37–
46.
41. G. V. Dimitrov and N. A. Dimitrova, Precise and fast calcu-
lation of the motor unit potentials detected by a point and
rectangular plate electrode. Med. Eng. Phys. 1998; 20:374–
381.
42. N. A. Dimitrova, A. G. Dimitrov, and G. V. Dimitrov, Calcu-
lation of extracellular potentials produced by inclined mus-
cle fibres at a rectangular plate electrode. Med. Eng. Phys.
1999; 21:582–587.
43. N. A. Dimitrova, G. V. Dimitrov, and A. G. Dimitrov, Calcu-
lation of spatially filtered signals produced by a motor unit
comprising motor unit with a non-uniform propagation.
Med. Biol. Eng. Compt. 2001; 39:202–207.
44. N. Dimitrova, Mathematical modelling of intra- and extra-
cellular potentials generated by active structures: effects of a
step change in structure diameter. Gen. Physiol. Biophys.
1987; 6:19–34.
45. S. S. Goldstein and W. Rall, Changes of action potential
shape and velocity for changing core-conductor geometry.
Biophys. J. 1974; 14:731–757.
46. N. A. Dimitrova, G. V. Dimitrov, and O. A. Nikitin, Longitu-
dinal variations of characteristic frequencies of skeletal
muscle fibre potentials detected by a bipolar electrode or
multi-electrode. J. Med. Eng. Techn. 2001; 25:34–40.
47. L. Lindström, On the frequency spectrum of EMG signals.
Techn. Rep. 7:70, Res. Lab. Med. Electr. Chalmers Univ.
Technol. Göteborg, Sweden., 1973: 1–39.
48. L. H. Lindström, A model describing the power spectrum of
myoelectric signals. Part I: single fiber signal. Techn Rep.
5:75, Depatr. Appl. Electronics Chalmers Univ. Technol.
Göteborg and Depatr. Clin. Neurophysiol Sahlgern Hospital
Göteborg, Sweden, 1973: 1–30.
49. C. E. T. Krakau, A note on the Fourier transform of Lorente
de Nó’s potential function of the external field of a nerve in a
volume conductor. Kungl. Fysiol. Sällsk I Lund Förhandl.
1957; 27:177–183.
50. G. V. Dimitrov and N. A. Dimitrova, Fundamentals of power
spectra of extracellular potentials produced by a skeletal
muscle fibre of finite length. Part II: Effect of parameters al-
tering with functional state. Med. Eng. Phys. 1998; 20:702–
707.
51. G. V. Dimitrov and N. A. Dimitrova, Effect of parameters al-
tering with muscle fibre functional state on power spectra of
spatially filtered extracellular potentials. J. Med. Eng. Tech-
nol. 2001; 25:74–78.
52. G. V. Dimitrov and N. A. Dimitrova, Fundamentals of power
spectra of extracellular potentials produced by a skeletal
muscle fibre of finite length. Part I: Effect of fibre anatomy.
Med. Eng. Phys. 1998; 20:580–587.

53. L. Lindström and R. Magnusson, Interpretation of myoelec-
tric power spectra: a model and its application. Proc. IEEE.
1977; 65:653–662.
54. L. Lindström and I. Petersén, Power spectrum analysis of
EMG signals and its application. In: J. E. Desmedt, ed.,
Computer-aided Electromyogr. Prog. Clin. Neurophysiol. Ba-
sel: Karger, 1983; 10:1–51.
55. D. A, Winter, A. J. Fuglevand, and S. E. Archer, Crosstalk in
surface electromyography: theoretical and practical esti-
mates. J. Electromyogr. Kinesiol. 1994; 4:15–26.
56. T. I. Arabadzhiev, G. V. Dimitrov, and N. A. Dimitrova, In-
tracellular action potential generation and extinction affect
strongly the sensitivity of M-wave characteristic frequencies
to changes in the peripheral parameters with muscle fa-
tigue. J. Electromyogr. Kinesiol. 2005; 15:159–169.
57. L. Lindström, R. Kadefors, and I. Petersén, An electromyo-
graphic index for localized muscle fatigue. J. Appl. Physiol.
1977; 43:750–754.
58. T. I. Arabadzhiev, G. V. Dimitrov, and N. A. Dimitrova, Sim-
ulation analysis of the performance of a novel high sensitive
spectral index for quantifying M-wave changes during fa-
tigue. J. Electromyogr. Kinesiol. 2005; 15:149–158.
59. N. A. Dimitrova, J-Y. Hogrel, T. I. Arabadzhiev, and G. V.
Dimitrov, Estimate of M-wave changes in human biceps bra-
chii during continuous stimulation. J. Electromyogr. Kin-
esiol. 2005; 15:341–348.
60. R. Lorente de Nó, A study of nerve physiology. Studies from
the Rockefeller Inst. Med. Res. 1947; 132.
61. J. Duchêne and J-Y. Hogrel, A model of EMG generation.
IEEE Trans. Biomed. Eng. 2000; 47:192–200.
62. T. H. J. M. Gootzen, D. F. Stegeman, and A. van Oosterom,
Finite limb dimensions and finite muscle length in a model
for the generation of electromyographic signals. Elect-
roenceph. Clin. Neurophysiol. 1991; 81:152–162.
63. D. Farina and R. Merletti, A novel approach for precise sim-
ulation of the EMG signal detected by surface electrodes.
IEEE Trans. Biomed. Eng. 2001; 48:637–646.
64. B. Hammarberg and E. Stålberg, Novel ideas for fast muscle
action potential simulations using the line source model.
IEEE Trans. Biomed. Eng. 2004; 51:1888–1897.
65. A. Heringa, D. F. Stegeman, G. J. H. Hijen, and J. P. C. de
Weerd, Solution methods of electrical fields problem in phys-
iology. IEEE Trans. Biomed. Eng. 1982; 29:34–42.
66. R. Plonsey, Action potential sources and their volume con-
ductor fields. Proc. IEEE. 1977; 65:601–611.
67. K. Roeleveld, J. H. Blok, D. F. Stegeman, and A. van Ooste-
rom, Volume conduction models for surface EMG; confron-
tation with measurements. J. Electromyogr. Kinesiol. 1997;
7:221–232.
68. P. Rosenfalck, Intra- and extracellular fields of active nerve
and muscle fibers. A physico-mathematical analysis of dif-
ferent models. Acta Physiol. Scand. 1969; (Suppl. 321):1–
168.
69. D. F. Stegeman, J. P. C. de Weerd, and E. G. J. Eijkman, A
volume conductor study of compound action potentials of
nerves in situ: the forward problem. Biol. Cybern. 1979;
33:97–111.
70. V. M. Bernshtein, Modelling of electric signal of muscle fi-
bers group. Biophysics (in Russian). 1967; 12:1059–1063.
71. P. A. M. Griep, K. L. Boon, and D. F. Stegeman, A study of
the motor unit action potential by means of computer sim-
ulation. Biol. Cybern. 1978; 30:221–230.
ELECTROMYOGRAPHY (EMG) MODELING 17
72. P. A. M. Griep, F. L. H. Gielen, H. B. K. Boom, K. L. Boon, L.
L. W. Hoogstraten, C. W. Pool, and W. Walinga-de-Jonge,
Calculation and registration of the same motor unit action
potential. Electroenceph. Clin. Neurophysiol. 1982; 53:388–
404.
73. M. M. Lowery and M. J. O’Malley, Analysis and simulation of
changes in EMG amplitude during high-level fatiguing con-
tractions. IEEE Trans. Biomed. Eng. 2003; 50:1052–1062.
74. M. M. Lowery, N. S. Stoykov, A. Taflove, and T. A. Kuiken, A
multiple-layer finite-element model of the surface EMGsig-
nal. IEEE Trans. Biomed. Eng. 2002; 49:446–454.
75. M. M. Lowery, C. L. Vaughan, P. J. Nolan, and M. J. O’Mal-
ley, Spectral compensation of the electromyographic signal
due to decreasing muscle fiber conduction velocity. IEEE
Trans. Rehabil. Eng. 2000; 8:353–361.
76. B. K. van Veen, N. J. M. Rijkhoff, W. L. C. Rutten, W. Wall-
inga, and H. B. K. Boom, Potential distribution and single
fiber action potentials in a radially bounded muscle model.
Med. Biol. Eng. Comput. 1992; 30:303–310.
77. B. K. van Veen, H. Wolters, W. Wallinga, W. L. C. Rutten, and
H. B. K. Boom, The bioelectrical source in computing single
muscle fiber action potentials. Biophys. J. 1993; 64:1492–
1498.
78. W. Wallinga-de Jonge, F. L. H. Gielen, P. Wirtz, P. de Jong,
and J. Broenink, The different intracellular action potentials
of fast and slow muscle fibers. Med. Biol. Eng. Comp. 1985;
60:539–547.
79. D. Farina, M. Fosci, and R. Merletti, Motor unit recruitment
strategies investigated by surface EMG variables. J. Appl.
Physiol. 2002; 92:235–247.
80. M. M. Lowery, N. S. Stoykov, J. P. A. Dewald, and T. A. Kui-
ken, Volume conduction in an anatomically based surface
EMG model. IEEE Trans. Biomed. Eng. 2004; 51:2138–2147.
81. A. Gydikov, N. A. Dimitrova, D. Kosarov, and G. V. Dimitrov,
Influence of frequency and duration of firing on the shape of
potentials from different types of motor units in human
muscles. Exp. Neurol. 1976; 52:345–355.
82. R. Merletti, L. Lo Conte, E. Avignone, and P. Guglielminotti,
Modelling of surface myoelectric signals. Part I: Model im-
plementation. IEEE Trans. Biomed. Eng. 1999; 40:810–829.
83. T. Moritani, M, Muro, and A. Kijima, Electromechanical
changes during electrically induced and maximal voluntary
contractions: electrophysiologic responses of different mus-
cle fiber types during stimulated contractions. Exp. Neurol.
1985; 88:471–483.
84. F. B. Stulen and C. J. De Luca, The relation between the
myoelectric signal and physiological properties of constant
force isometric contractions. Electroenceph. Clin. Ne-
urophysiol. 1978; 45:681–698.
85. I. Zijdewind, D. Kernell, and C. G. Kukulka, Spatial differ-
ence in fatigue-associated electromyographic behaviour of
the human first dorsal interosseus muscle. J. Physiol.
(Lond.) 1995; 483.2:499–509.
86. D. T. Godin, P. A. Parker, and R. N. Scott, Noise character-
istics of stainless-steel surface electrodes. Med. Biol. Eng.
Comput. 1991; 29:585–590.
87. A. Nightingale, Background noise in electromyography.
Phys. Med. Biol. 1959; 3:325–338.
88. J. Ekstedt and E. Stålberg, How the size of the needle elec-
trode leading-off surface influences the shape of the single
muscle fiber action potential in electromyography. Comput.
Progr. Biomed. 1973; 3:204–213.
18 ELECTROMYOGRAPHY (EMG) MODELING
89. A. H. Flastersten, Voltage fluctuation of metal-electrolyte
interfaces. Med. Biol. Eng. 1966; 4:583–588.
90. A. J. Fuglevand, D. A. Winter, A. E. Patla, and D. Stashuk,
Detection of motor unit action potentials with surface elec-
trodes: influence of electrode size and spacing. Biol. Cybern.
1992; 67:143–153.
91. N. A. Dimitrova, G. V. Dimitrov, and V. N. Chihman, Effect of
the electrode dimensions on the motor unit potential. Med.
Eng. Phys. 1999; 21:479–485.
92. A. Hamilton-Wright and D. W. Stashuk, Physiologically
based simulation of clinical EMGsignals. IEEE Trans. Bio-
med. Eng. 2005; 52:171–183.
93. D. W. Stashuk, Simulation of electromyographic signals. J.
Electromyogr. Kinesiol. 1993; 3:157–173.
94. R. E. Burke, Motor units: anatomy, physiology and func-
tional organization. In: V. B. Brooks, ed., Handbook of Phys-
iology – The Nervous System II, Part I. Bethesda, MD:
American Physiological Society, 1981, pp. 345–422.
95. D. Kernell, Organization and properties of spinal motoneur-
ones and motor units. In: H-J. Freund, U. Büttner, B. Cohen,
and J. Noth, eds., Prog. in Brain Res. Elsevier Science Pub-
lishers B.V. (Biomedical Division), 1986; 64:21–30.
96. A. J. Fuglevand, D. A. Winter, and A. E. Patla, Models of
recruitment and rate coding organization in motor-unit
pools. J. Neurophysiol. 1993; 70:2470–2488.
97. G. Brody, R. N. Scott, and R. Balasubramanian, A model for
myoelectric signal generation. Med. Biol. Eng. 1974; 12:29–
41.
98. Z. S. Pan, Y. Zhang, and P. A. Parker. Motor unit power
spectrum and firing rate. Med. Biol. Eng. Comput. 1989;
27:14–18.
99. P. A. Parker and R. N. Scott, Statistics of the myoelectric
signal from monopolar and bipolar electrodes. Med. Biol.
Eng. 1973; 11:491–496.
100. R. S. Person and M. S. Libkind, Modelling of interfering bio-
electrical activity. Biofizika (in Russian) 1967; 12:127–134.
101. R. S. Person and M. S. Libkind, Simulation of electromyo-
grams showing interference patterns. Electroencephalogr.
Clin. Neurophysiol. 1970; 28:625–632.
102. V. M. Bernshtein, Statistical parameters of the electrical
signal of a muscle model. Biofizika (in Russian) 1967;
12:693–703.
103. K. Blinowska and M. Piotrkewicz, A study of surface elect-
romyograms by means of digital simulation. II. Spectral
analysis of simulated and experimental electromyogram.
Electromyogr. Clin. Neurophysiol. 1978; 18:95–105.
104. R. E. George, The summation of muscle fiber action poten-
tials. Med. Biol. Eng. 1970; 8:357–365.
105. P. Lago and N. B. Jones, Effect of motor unit firing time sta-
tistic on EMG power spectra. Med. Biol. Eng. Comput. 1977;
15:648–655.
106. M. Piotrkewicz, A study of surface electromyograms by
means of digital simulation. I. The principles of a model of
surface electromyogram. Electromyogr. Clin. Neurophysiol.
1978; 18:83–94.
107. E. A. Clancy and N. Hogan, Single site electromyograph
amplitude estimation. IEEE Biomed. Eng. 1994; 41:159–
167.
108. N. Ostlund, J. Yu, and J. S. Karlsson, Improved maximum
frequency estimation with application to instantaneous
mean frequency estimation of surface electromyography.
IEEE Trans. Biomed. Eng. 2004; 51:1541–1546.
109. N. Rababy, R. E. Kearney, and I. W. Hunter, Method for
EMG conduction velocity estimation which accounts for in-
put and output noise. Med. Biol. Eng. Comput. 1989; 27:125–
129.
110. S. D. Nandedkar, D. B. Sanders, and E. V. Stålberg, Simu-
lation and analysis of electromyographic interference pat-
tern in normal muscle. Part I: Turns and amplitude
measurements. Muscle Nerve. 1986; 9:423–430.
111. S. D. Nandedkar, D. B. Sanders, and E.V. Stålberg, Simula-
tion and analysis of electromyographic interference pattern
in normal muscle. Part II: Activity, upper centile amplitude,
and number of small segments. Muscle Nerve. 1986; 9:486–
491.
112. D. Kosarov and A. Gydikov, The influence of the volume
conduction on the shape of the action potentials recorded by
various types of needle electrodes in normal human muscle.
Electromyogr. Clin. Neurophysiol. 1975; 15:319–335.
113. E. Henneman, Relation between size of neurons and their
susceptibility to discharge. Science. 1957; 126:1345–1347.
114. E. Henneman and C. B. Olson, Relations between structure
and function in the design of skeletal muscle. J. Ne-
urophysiol. 1965; 28:581–598.
115. E. Henneman, G. Somjen, and D. Carpenter, Functional sig-
nificance of cell size. J. Neurophysiol. 1965; 28:560–580.
116. E. Henneman, G. Somjen, and D. Carpenter, Excitability
and inhabitability of motoneurons of different sizes. J. Ne-
urophysiol. 1965; 28:599–620.
117. B. M. Van Bolhuis, W. P. Medendorp, and C. C. A. M. Gielen,
Motor-unit firing behaviour in human arm flexor muscles
during sinusoidal isometric contractions and movements.
Brain Res. 1997; 117:120–130.
118. P. Christova, A. Kossev, and N. Radicheva, Discharge rate of
selected mototr units in human biceps brachii at different
muscle lengths. J. Electromyogr. Kinesiol. 1998; 8:287–294.
119. A. J. Fuglevand and D. A. Keen, Re-evaluation of muscle
wisdom in the human adductor pollicis using physiological
rates of stimulation. J. Physiol. (Lond.) 2003; 549.3:865–875.
120. A. Gydikov and D. Kosarov, Some features of different motor
units in human biceps brachii. Pflügers Arch. 1974; 347:75–
88.
121. D. Kosarov and A. Gydikov, Dependence of the discharge
frequency of motor units in different human muscles upon
the level of the isometric muscle tension. Electromyogr. Clin.
Neurophysiol. 1976; 16:293–306.
122. H. P. Clamann, Statistical analysis of motor unit firing pat-
terns in a human skeletal muscle. Biophys. J. 1969; 9:1233–
1259.
123. A. A. Gydikov, K. G. Kostov, and P. G. Gatev, Mechanical
properties and discharge frequencies of single motor units in
human m. biceps brahii. In: M. Kumamoto, ed., Neural and
Mechanical Control of Movement. Kyoto: Yamaguchi Shoten,
1984, pp. 19–36.
124. B. Bigland and O. C. Y. Lippold, Motor unit activity in the
voluntary contraction of human muscle. J. Physiol. (Lond.)
1954; 125:322–335.
125. K. Kanosue, M. Yoshida, K. Akazawa and K. Fujii, The
number of active motor units and their firing rates in vol-
untary contraction of human brachialis muscle. Jap. J.
Physiol. 1979; 29:427–443.
126. F. Brachi, M. Decandia, and T. Gualtierotti, Frequency sta-
bilization in the motor centres of spinal cord and caudal
brain stem. Am. J. Physiol. 1966; 210:1170–1177.

127. H. S. Milner-Brown, R. B. Stein, and R. Yemm, Changes in
firing rate of human motor units during linearly changing
voluntary contractions. J. Physiol. 1973; 230:371–390.
128. H. P. Clamann, Activity of single motor units during isomet-
ric tension. Neurology. 1970; 20:254–260.
129. L. Grimby, J. Hannerz, and B. Hedman, The fatigue and
voluntary discharge properties of single motor units in man.
J. Physiol. 1981; 316:545–554.
130. V. G. Macefield, A. J. Fuglevand, J. N. Howell, and B.
Bigland-Ritchie, Discharge behaviour of single motor units
during maximal voluntary contractions of a human toe ex-
tensor. J. Physiol. (Lond.) 2000; 528.1:227–234.
131. C. J. De Luca and Z. Erim, Common drive of motor units in
regulation of muscle force. Trends Neurosci. 1994; 17:299–
305.
132. C. J. De Luca, A. M. Roy, and Z. Erim, Synchronization of
motor unit firings in several human muscles. J. Ne-
urophysiol. 1993; 70:2010–2023.
133. S. F. Farmer, D. M. Halliday, B. A. Conway, J. A. Stephens,
and J. R. Rosenberg, A review of recent applications of cross-
correlation methodologies to human motor unit recording. J.
Neurosci. Meth. 1997; 74:175–187.
134. B. Bigland-Ritchie, E. F. Donovan, and C. S. Roussos, Con-
duction velocity and EMG power spectrum changes in fa-
tigue of sustained maximal efforts. J. Appl. Physiol. 1981;
51:1300–1305.
135. P. B. Matthews, Relationship of firing intervals of human
motor units to the trajectory of post-spike after-hyperpolar-
ization and synaptic noise. J. Physiol. (Lond.) 1996;
492:597–628.
136. J. L. F. Weytjens and D. van Steenberge, Spectral analysis of
the surface electromyogram as a tool for studying rate mod-
ulation: a comparison between theory, simulation and ex-
periment. Biol. Cybern. 1984; 50:95–103.
137. J. L. F. Weytjens and D. van Steenberge, The effects of motor
unit synchronization on the power spectrum of the elect-
romyogram. Biol. Cybern. 1984; 51:71–77.
138. W. Yao, R. J. Fuglevand, and R. M. Enoka, Motor-unit syn-
chronization increases EMG amplitude and decreases force
steadiness of simulated contractions. J. Neurophysiol. 2000;
83:441–452.
139. H. J. Hermens, T. A. M. van Bruggen, C. T. M. Baten, W. L.
C. Rutten, and H. B. K. Boom, The median frequency of the
surface EMG power spectrum in relation to motor unit firing
and action potential properties. J. Electromyogr. Kinesiol.
1992; 2:15–25.
140. W. H. J. P. Linssen, D. F. Stegeman, E. M. G. Joosten, M. A.
van ’t Hof, R. A. Binknorst, and S. L. H. Notermans, Vari-
View publication stats
ELECTROMYOGRAPHY (EMG) MODELING 19
ability and interrelationships of surface EMG parameters
during local muscle fatigue. Muscle Nerve. 1993; 16:849–
856.
141. G. Kamen and G. E. Caldwell, Physiology and interpretation
of the electromyogram. J. Clin. Neurophysiol. 1996; 13:366–
384.
142. D. F. Stegeman, J. H. Blok, H. J. Hermens and K. Roeleveld,
Surface EMG models: properties and applications. J. Elect-
romyogr. Kinesiol. 2000; 10:313–326.
143. J. Schneider, J. Silny, and G. Rau, Influence of tissue inho-
mogeneities on noninvasive muscle fiber conduction velocity
measurements investigated by physical and numerical mod-
eling. IEEE Trans. Biomed. Eng. 1991; 38:851–860.
144. G. V. Dimitrov, Extracellular potential field of striated mus-
cle fibre immersed in an anisotropic volume conductor, lim-
ited by a dielectric wall. Compt. Rend. Bulg. Acad. Sci. 1974;
27:1133–1136.
145. G. V. Dimitrov, C. Disselhorst-Klug, N. A. Dimitrova, A.
Trachterna, and G. Rau, The presence of unknown layer of
skin and fat is an obstacle to correct estimation of the motor
unit size from surface detected potentials. Electromyogr.
Clin. Neurophysiol. 2002; 42:231–241.
146. R. Merletti and P. A. Parker, Electromyography: Physiology,
Engineering, and Noninvasive Applications. New York:
IEEE Press and John Wiley & Sons, 2004.
147. F. L. H. Gielen, W. Wallinga-de-Jonge, and K. L. Boon, Elec-
trical conductivity of skeletal muscle tissue: experimental
results from different muscles in vivo. Med. Biol. Eng. Com-
put. 1984; 22:569–577.
148. D. Farina and A. Rainoldi, Compensation of the effect of sub-
cutaneous tissue layers on surface EMG. A simulation study.
Med. Eng. Phys. 1999; 21:487–496.
149. J. H. Blok, D. F. Stegeman, and A. van Oosterom, Three-
layer volume conductor model and software package for ap-
plications in surface electromyography. Ann. Biomed. Eng.
2002; 30:566–577.
150. D. Farina, L. Mesin, S. Martina, and R. Merletti, A surface
EMG generation model with multilayer cylindrical descrip-
tion of the volume conductor. IEEE Trans. Biomed. Eng.
2004; 51:415–426.
151. D. Farina, L. Mesin, and S. Martina, Advances in surface
electromyographic signal simulation with analytical and nu-
merical descriptions of the volume conductor. Med. Biol.
Eng. Comput. 2004; 42:467–476.
152. L. Mesin and D. Farina, Simulation of surface EMGsignals
generated by muscle tissues with inhomogeneity due to fiber
pinnation. IEEE Trans. Biomed. Eng. 2004; 51:1521–1529.