Skeletal Muscle Mechanics: Implications

for Rehabilitation

Skeletal muscles are the pn'mury organ system responsible for force generation
and motlement. As such, an improved understanding of normal movement can
be obtained by understanding skeletal muscle mechanical propm'es. In this review, we present the basic mechanical properties of skeletal muscle in a way that
relates to their normalfunction. First, isometricforce production is discussed
followed by a presentation of isotonicforce production. Then, skeletal muscle
architectural properties are presented as a strategy for muscles to specialize in
either force production or excursion. Finally, we discm the relationship between
muscles and joints and the signiJicanceof this relationship for undemanding
strength. Based on this presentation, the therapist will have an improved understanding of normal movement and may have imghts into developing rehabilitation protocols that can improvefunction. [LieberRL,Bodine-Fowler SC. Skeletal
muscle mechanics: implicationsfor rehabilitation. Phys Thm 1993;73:844456]

Rlchard L Lleber
Sue C Bodlne-Fowler

Key Words: Movement, Muscle physiology, Muscle structure, Rehabilitation.

Skeletal muscle biomechanical properties have been widely studied since

the 1600s. Because the primary purpose of skeletal muscle is to generate
force and movement, it is important
to understand the mechanical basis of
these properties. When muscle force
or movement is lost due to disease,
trauma, o r disuse, an understanding
of muscle properties can improve our
ability to restore function.

velocities. Clearly, this is technically

not possible in humans. Thus, descriptions of muscle biomechanical properties have relied on experimental studies in model systems. In this review,
we describe muscle contractile properties during either constant-length (isometric) or constant-force (isotonic)
contractions. We will then use this
information to speculate as to how
muscles operate in vivo.

Ideally, muscle contraction would be

studied during normal movement, that
is, under conditions of physiological
activation, experiencing physiological
loads, and contracting at physiological

Length-Tenslon Relatlonshlp:
lsometrlc Muscle Contraction
The original biological experiments
performed by Blixl demonstrated that

RL Lieber, PhD, is Associate Professor, Department of Orthopaedics, Biomedical Sciences Graduate

Group, Universiry of California at San Diego School of Medicine and Veterans Administration Medical Center, 3350 Ia Jolla Village Dr, San Diego, CA 92161 (USA). Address all correspondence to
Dr Lieber.
SC Bodine.Fowler, PhD, is Assistant Professor, Department of Orthopaedics, Biomedical Sciences
Graduate Group, University of California at San Diego School of Medicine and Veterans Administration Medical Center.
This work was supported by the Veterans Administration and National Institutes of Health Grants
AR34192 and AR40050.

Physical Therapy/Volume 73, Number 12December 1993

the force developed by a muscle

during isometric contraction (ie,
when the muscle is not allowed to
shorten) varies with the muscle's
length. Experimentally, isometric
contractions are performed at different lengths (Fig. I), and peak isometric tension is measured at each
length. These tensions are then plotted against length, and a relationship
such as that shown in Figure 2 is
obtained. It has thus been demonstrated that at very long and very
short lengths, muscles generate low
tension, whereas at intermediate or
"optimal" lengths, muscles generate
higher tension. Although a general
description of this relationship was
presented in the 1800s, the precise
structural basis for the length-tension
relationship in skeletal muscle was
not elucidated until the sophisticated
mechanical experiments of the early
1960s were performed.213It was these
experiments that defined the precise
relationship between myofilament
overlap and tension generation, which
we refer to today as the sarcomere

844 / 25

Length = Lo-40%

Length =

length-tension relationship. In its most

basic form, the length-tension relationship illustrates that tension generation in skeletal muscle is a direct
function of the magnitude of overlap
between the actin and myosin
filaments.

Length = Lo-20%

Sarcomere LengthmTenslon
Relatlonshlp
Length = Lo -10%

Length = Lo

Length = Lo+lO%

Length = Lo +20%

Length = Lo +so%

Length = Lo +40%

Sophisticated experiments by Gordon

et a12 defined what might be one of
the most explicit structure-function
relationships in all of biology. In
these experiments, a small segment of
muscle fiber was held at a constant
length (and therefore a region of the
fiber was held at a constant sarcomere length).
The results of these experimentsZare
summarized in Figure 2. In this figure, muscle relative tetanic tension (as
a percentage of maximum) is plotted
as a function of sarcomere length (in
micrometers). This was one instance
in which anatomy met physiology in
dramatic fashion, because knowledge
of the precise anatomic lengths of the
myosin and actin filaments was crucial
for understanding the basis of the
sarcomere length-tension relationship.

Figure 1. Experimental determination of the length-tension curve. Each trace represents a schematic isometric tetanic contraction at a particular length. Lo=optimal
length; AT=active tension; PT=passive tension, shown as the distance between the
dashed line and beginning of curve (only sfgnificant at lengths above Lo). These values
are combined to produce their relationship described in Figure 2.

Descendlng Llmb of the

Length-Tenslon Curve
As a muscle was highly stretched by

0.5

1.0

1.5

2.0

2.5

3.0

Sarcomere Length (pm)

3.5

4.0

Figure 2. Sarcomere length-tensionrelationship elucidated for frog skeletal muscle.

Schematic at top offigure provides relative actin and myosin filament lengths. Note that
maximum actual force exists when myofilament overlap is optimal. Cartoons above
curve demonstrate relative myofilament overlap. Thin line represents the passive tension
of an unstimulated muscle. (Data from Gordon et aL2)
26 / 845

the investigators2to a sarcomere

length of 3.65 km, the muscle developed no active tension. Why? The
answer lay in the observation that, as
the myosin filament was 1.65-km long
and the actin filament was 2.0 km in
length, at a sarcomere length of 3.65
km, there was no overlap (interdigitation) between the actin and myosin
filaments. Therefore, although fiber
excitation might permit actin-myosin
interaction by removing the inhibition
of the actin filament, because no myosin cross-bridges are in the vicinity of
the actin active sites, no tension generation occurred.

As muscle length decreased, overlap

between actin and myosin was possible, and the amount of tension generated by the muscle increased as sarco-

Physical Therapy/Volume 73, Number 12December 1993

length-tension curve. The word "shallow" distinguishes this region from

the next portion of the length-tension
curve, which is known as the steep
ascending limb, because at these very
short lengths, the myosin filament
actually begins to interfere with shortening as it abuts the sarcomere
Z-disk, reducing force precipitously.

M~osln
Actln

M-lke anchored to lnmrmedlate Rlamenta

lmermedlalefltamems Ilnk bet-

myoRbrlla

Flgure 3. Schematic diagram of the sarcomere including contractileJilammts, and

endosarcomeric cytoskeletal and exosarcomeric cytoskeletal components. (Reprinted
with permission fmm Friden J, Lieber RL. The structural and mechanical bas& of
exercise-induced muscle injury. Med Sci Sports Exerc. 1992;24:521-5.30.)
mere length decreased. Increasing
tension with decreasing sarcomere
length occurred until the muscle
reached a sarcomere length of 2.2
km, because, as sarcomere length
decreased, the number of crossbridge connections between actin and
myosin increased, resulting in increased tension. This region of the
length-tension curve is known as the
descending limb.

The region of the length-tension

curve over which length change results in no change in tension is
known as the plateau region. The
muscle length at which the maximum
tetanic tension (Po) is attained is
known as optimal length (Lo).
Ascending Llmb of the

Length-Tenslon Curve
At a sarcomere length of 2.0 km, the

Plateau Reglon of the

Length-Tenslon Curve
As sarcomere length changed from

2.0 km to 2.2 km, muscle tension

remained constant. Again, this was a
direct result of thick filament structure. Because the myosin filament is a
polymeric arrangement of myosin
molecules arranged in an antiparallel
fashion, many myosin "backbones"
come together in the center of the
myosin filament. Thus, there exists a
bare region of the myosin molecule
that is devoid of cross-bridges. The
length of this bare region was 0.2 km,
Even though sarcomere shortening
over the range of 2.2 to 2.0 km resulted in greater filament overlap, it
did not result in increased tension
generation because no additional
cross-bridge connections were made.

actin filaments from one side of the

sarcomere juxtapose the actin filaments from the opposite side of the
sarcomere (Fig. 2). It might be predicted that shortening past this point
would be impossible. As sarcomere
length decreases below the plateau
region, however, actin filaments from
one side of the sarcomere overlap
with the actin filaments on the opposite side of the sarcomere. That is, at
these lengths, actin filaments overlap
both with the opposing actin filament
and with the myosin filament. Under
these conditions, the actin filament
from one side of the sarcomere interferes with cross-bridge formation on
the other side of the sarcomere, resulting in decreased muscle force
output. This decrease occurs from 2.0
to 1.87 km, and this region is known
as the shallow ascending limb of the

Physical Therapy /Volume 73, Number 12December 1993

The length-tension relationship illustrates that muscle force varies as a

function of sarcomere length (rnyofilament overlap). This is a physiologic
property of the force-generating system and should not simply be viewed
as an anatomic artifact.

Structural Basls of the

Passlve Length-Tenslon
CUW~
The thin line in Figure 2 represents
the tension recorded if a muscle is
stretched to various lengths without
stimulation. Note that near the optimal length, passive tension is almost
zero. As the muscle is stretched to
longer lengths, however, passive tension increases dramatically. These
relatively long lengths can be attained
physiologically, and therefore, passive
tension can play a role in providing
resistive force even in the absence of
muscle activity. The structure(s) responsible for passive tension are
obviously outside of the cross-bridge
itself, because muscle activation is not
required. Recent studies have shown
that the origin of passive muscle tension is actually within the myofibrils
themselves.* Interestingly, a new
structural protein has been identified
that is the source of this passive tension. The very large protein, creatively
named "titin" (and formerly termed
"connectin") connects the thick myosin filaments end to end (Fig. 3). This
very large protein is also relatively
fragile and thus has probably been
missed in earlier studies because
laboratory techniques destroyed the
protein. Experiments have now been
performed in which isolated fibers
were bathed in a solution that selectively extracted the titin molecule.5
Under these conditions, the time
course of loss in muscle passive tension is exactly correlated with the

A
Velocity = 40% Vmax

Muscle Length # I

Force = 2590 Po

Muscle Force # I

= 6% Vmax

Muscle Length #2 -Veo

l ctiy

Muscle Force #2

!7

Velocity = -5% Vmax

time course of appearance of titin

protein in the extracting solution. In
addition to passively supporting the
sarcomere, titin stabilizes the myosin
lattice so that high muscle forces d o
not disrupt the orderly hexagonal
array. If titin is selectively destroyed,
normal muscle contraction causes
significant myofibrillar disruption.6
Finally, it appears that titin may act as
sort of a "molecular ruler" during the
formation of sarcomeres (sarcomerogenesis), which occurs during development and following chronic muscle
stretch during immobilization.7

Force = 150% Po

Force-Veloclty Relatlonshlp:
lsotonlc Muscle Contractlon

Force = 75% Po

Muscle Length #3

Muscle Force #3
1s
200-

In contrast to the sarcomere lengthtension relationship, the force-velocity

relationship does not have a precise,
anatomically identifiable basis. The
force-velocity relationship illustrates
that the maximum force generated by
a muscle is a function of its velocity.
This relationship can also be stated in
the reverse; that is, muscle contraction
velocity is dependent on the force
resisting the muscle. Historically, the
force-velocity relationship was used to
define the kinetic properties of the
cross-bridges as well as the precise
form of the force-velocity relationship
itself. The form of this relationship
has been shown to explain the behavior of whole muscle8?9and isolated
single muscle fibers.10

Isometric

I
I
I
I
I
I
I
I

no150 -

g 100-

LL

-a
53

5
0
-100 -75
1

-50

-25

Figure 4. Experimental detennination of the force-velocity relationship: (A)

Schematic illustration of muscle length
and muscle force versus time when muscles are maximally activated and pennitted to shorten against various loads; (B)
initial shortening (or lengthening velocity) plotted as a function of load. Note
the familiar rectangular hyperbolafor
shortening contractions and the very high
forces obtained for eccentric contractions Circled numbers in Figure 4 8 correspond to three traces in Figure 4A.
(Data from Edman.3) Po= maximum
tetanic tension; V=,
maximum contraction velocity.

25

50

75

Contractile Velocity (%Vmax)

100
Experimental elucidation of the forcevelocity relationship was first presented by Hille and Katz? but the
current description of the force-

Physical TherapyIVolume 73, Number 12December 1993

Table. Relative Muscle Force at

Various Muscle Velocities
Relatlve Force

Velocity

(% Po)'

(% Vm=)b

100

0.0

95

1.o

90

2.2

75

6.3

50

16.6

muscle is stimulated maximally and

allowed to shorten (or lengthen)
against a constant load (Fig. 4A). The
muscle velocity during shortening (or
lengthening) is measured and then
plotted against the resistive force. The
general form of this relationship is
plotted in Figure 4B. On the horizontal axis, we have plotted muscle velocity relative to maximum contraction
velocity ,)V
(,,
and on the vertical
axis, we have plotted muscle force
relative to maximum force (Po).

Concentrlc Contractlons-Muscle
Actlvely Shortenlng

aP,,=maxin?um tetanic tension.

%,,=maximum

contraction velocity

velocity relationship has been ascribed to Hill.ll

The force-velocity relationship, like
the length-tension relationship, is a
curve that actually represents the
results of many experiments plotted
on the same graph. Experimentally, a

When a muscle is maximally electrically activated and required to lift a

load that is less than its maximum
tetanic tension, the muscle begins to
shorten. Contractions that permit the
muscle to shorten are known as concentric contractions. In concentric
contractions, the force generated by
the muscle is always less than the
muscle's maximum force (P,). As the
load the muscle is required to lift
decreases, contraction velocity increases. This occurs until the muscle

finally reaches its V,

at which force
generation is zero. Maximum contraction velocity is a parameter we can
use to characterize muscle that is
related to both fiber type distribution
and architecture. The force-velocity
relationship is characterized by a
rectangular hyperbola and is expressed mathematically as

where a and b are constants derived

experimentally (usually about 0.25), P
is muscle force, and v is muscle velocity. This equation can be used to
determine the relative muscle force
that occurs as a muscle is allowed to
shorten. Some of these values are
presented in the Table. The forcevelocity relationship is a steep rectangular hyperbola. In other words, force
drops off rapidly as velocity increases.
For example, in a muscle that is
shortening at only 1% of its maximum
contraction velocity (extremely slow),
tension drops by 5% relative to maximum isometric tension (Table). Similarly, as contraction velocity increases
to only 10% of maximum (easily
attainable physiologically), muscle
force drops by 35%. Even when muscle force is only 50% of maximum,
muscle velocity is only 17% of V.,
As shortening speed increases, force
drops precipitously.

Eccentrlc Contractlons-Muscle
Actlvely Lengthenlng

ADP

pi

;:E

ATP

.---,

,.-,

,--

'ACTIN

-.
.-

.-

Flgure 5. Relationship between biochemical reactions and mechanical force produced during the cross-bridgecycle (+actin represents association of actin and myosin
filaments; -actin represents dissociation of actin from myosin). ATP=adenosine triphosphate; M=rnyosin; ADP=adenosine diphosphate; P,=inorganic phosphate; A=actin.
(Reprinted with permission fmm Lieber.I8)
Physical Therapy/Volume 73, Number 12December 1993

As the load imposed on the muscle

increases, it reaches a point at which
the external load is greater than the
load the muscle can generate. Thus,
the muscle is activated, but it is forced
to lengthen due to the high external
load. This is referred to as an eccentric contraction (contraction in this
context does not necessarily imply
shortening). There are two main
features to note regarding eccentric
contractions. First, the absolute muscle tensions are very high relative to
the muscle's Po. Second, unlike concentric contractions, the absolute
tension is relatively independent of
lengthening velocity.9 This suggests
that skeletal muscles are very resistant

SOL (6800)

am-

'r
E

lncreasing Excursion ---D

hG

VL

3.000-

&!
2800:

2,000-

to lengthening, a property that comes

in very handy for many normal movement patterns in which muscles hnction as "brakes" to decelerate a limb
(for example, the hamstring muscles
"brake" the tibia during the swing
phase of gait) o r to absorb the momentum of the body during stance
(for example, the quadriceps femoris
muscles absorb body momentum
during heel-strike).

VI
VM

TP

0,

.E

!l

SM

1800-

1,000

m-

BF

RF

PL

TA
POP

AL
EDL

F ~ F H L ~ ~

o
20

.
40

60

OR (277,177)
SAR (455,170)

PEC

EHL

PLT

ST

AB

80

~
120

100

~
140

~
180

160

Fiber Length (mm)

Eccentric contractions are currently a

subject of great interest for two main
reasons. First, much of a muscle's
normal activity occurs while it is actively lengthening; thus, eccentric
contractions are physiologically common.
Second,
and sore~
.
m muscle
~ injury
l
ness are thought to be associated
more with eccentric contractions.

lncreasing Excursion

The Cross-Bridge Cycle

B
cO

FOS (825) FOP (792)

PT

400-

i:
-f

FCU
EDC
E C R 6 ~ ~ ~

200'

.E
0,

300:

Pa

FCR

FPL

FDs (L)
FDP (S)
FDP (1)
FDS (R)

100

EPL

EDC(R)
Pa ED0

FDP (L)
(Rim(I)

ECRL

BR (121)

EDC (L)

CIP
FDS (s)

ED2 (S)

07

20

30

40

50

60

70

80

We alluded to cyclic interaction between actin and myosin in explaining

the force-velocity curve. Much of our
understanding of the mechanism of
muscle contraction has come from
excellent biochemical studies performed from the 1950s to the mid1970s.I2It was during this period that
methods for isolating specific muscle
proteins were developed as well as
the methods for measuring their
physicochemical and biochemical
properties.

Fiber Length (mm)

Figure 6. Architectural properties of the (A) lower limb and (B) upper limb, plotted
in t e r n of physiological cross-sectional area (which is proportional to maximum muscle force) and muscle fiber length (which is proportional to muscle excursion).
AB=adductor breuis;AL=adductor longus; AM=adductor magnus; BF=biceps femoris;
EDL =extensor digitorum longus; EHL =extensor hallucis longus; FDL =flexor digitorum
longus; GR=gracilis;FHL=fexor hallucis longus; MG=medial gastrocnemius;
PEC=pectineus; PB=peroneus breuis; PL=peroneus longus; PLT=plantaris;
POP=politeus; RF=rectusfemoris; SAR=sartorius; SM=semimembranosus;SOL=soleus;
ST=semitendinosus: TA=tibialis anterior; TP=tibialis Dosterior; VI=uastus intermedius;
VL=vastus lateralis;' VM=uastus medialis; BR= brachidradialis;bra extensor carpi ul-'
naris; ECRB=extensor carpi radialis breuis; ECRL=extensor carpi radialis longus; EDC
(I), EDC (L), EDC (R), and EDC (S)=extensor digitorum communis to the index, long,
ring, and small fingers, respectiuely; EDQ=extensor digiti quinti; EIP=extensor indicis
proprius; EPL=extensor pollicis longus; FCU=fexor carpi ulnaris; FCR=flexor carpi
radialis; FDP (I), FDP (L), FDP (R), and FDP (S)=flexor di''torum profundus to the
index, long, ring, and smallfingets, respectively;FDS (I), FDS (L), FDS (R), and FDS
(S)=flexor digirorum supe$cialis to the index, long, ring, and small fingers, respectiuely; FPL =flexor pollicis longus; PQ =pronutor quadratus; PS=palmaris longus;
PT=pronator teres (Datafrom Wickiewicz et alZ1and Lieber and colleag~es.25~26
Reprinted with pennision from Lieber.18)

30 / 849

In its simplest form, biochemical

experiments on muscle contractile
proteins have shown that during the
cross-bridge cycle, actin (A) combines
with myosin (M) and adenosine triphosphate (ATP) to produce force,
adenosine diphosphate (ADP) , and
inorganic phosphate (P,). This can be
represented as a chemical reaction in
the form:
(2)

A+M+ATP+
A + M + A D P + P i +Force

However, we also know that death of

a muscle produces a rigor state
whereby actin and myosin interact to
form a very stiff connection. This
connection can be represented as

Physical Therapy/Volume 73, Number 12December 1993

rate-limiting step of contraction.

The actin-myosin cross-bridge is
now ready for the ATP binding of
step 1.
This is currently an active area of
muscle biophysical research.12One
might imagine the dificulty in confirming these elementary mechanical
and biophysical reactions. A recent
advance in biochemistry, however,
has allowed direct testing and manipulation of this scheme. The adcance
involves the development of "caged
compounds--compounds that are
inactive in their caged form and become active when the cage is instantaneously removed by a pulse of highenergy laser light.'* Using caged ATP,
single muscle fibers have been subjected to experiments such as those
described earlier and found to behave
much as predicted based on the biochemical data.15

VELOCITY

FORCE

VELOCITY

FORCE

Figure 7. General design offunctional musclegroups within the lower limb. Left
to right: hamstrings, quadriceps femoris, dorszjlexors, and plantarflexors. Note that the
plantar-flexor and quadricepsfemoris muscles are designed primarily for high forces,
whereas the dorsflexor and hamstring muscles are designed primarily for high excursions FL =fiber length;ML =muscle length.

(3) A

+ .v + A

. M iM"rigorw
compla

If actin and myosin can interact by

themselves, where does ATP come
into the picture during contraction?
Experiments have demonstrated that
the myosin molecule can hydrolyze
ATP into ADP and Pi. In other words,

The relationship between the LymnTaylor kinetic scheme and the mechanical cross-bridge cycle is not fully
known. Lyrnn and Taylor,'3 however,
proposed that their biochemical data
could be incorporated into a four-step
cross-bridge cycle that could be envis i ~ n e das
(Fig. 5):
1. The actin-myosin bridge very rap-

Scientists now agree that ATP serves

at least two functions in skeletal muscle systems. First, ATP disconnects
actin from myosin. Second, ATP is
hydroly~edby the myosin molecule
to produce the energy required for
muscle contraction. This description
of the different biochemical steps
involved in muscle contraction is
referred to as the Lymn-Taylor actomyosin adenosine triphophatase hydrolysis rnechanism.l2.'3

idly dissociates due to ATP binding

to myosin.
2. The free myosin bridge moves into
position to attach to actin, during
which ATP is hydrolyzed.
3. The free myosin bridge along with
its hydrolysis products rebinds to
the actin filament.

4. The cross-bridge generates force,

and actin displaces the reaction
products (ADP and Pi) from the
myosin cross-bridge. This is the

Physical Therapy /Volume 73, Number 12December 1993

Skeletal Muscle Architecture

All muscles are made of similar contractile units (sarcomeres), but the
arrangement of these sarcomeres
dramatically aiTects whole muscle
contractile properties. The fundamental relationship between muscle architecture and muscle function is that
muscle velocity and excursion are
proportional to the number of sarcomeres in series, whereas muscle
force is proportional to the total
cross-sectional area of ~arcomeres.'6~~~
In practice, it is dificult to determine
these values precisely, so we often say
that muscle velocity and excursion are
proportional to muscle fiber length,
whereas muscle force is proportional
to total fiber cross-sectional area
(PCSA). Physiological cross-sectional
area is a calculated variable's that
estimates the total muscle fiber crosssectional area. It is not necessarily the
same as any area calculated in one of
the traditional anatomical planes as
would be obtained, for example, from
computed tomography or magnetic
resonance imaging. This is because
the PCSA is a calculated amount that
attempts to sum the entire muscle
fiber cross-sectional area. Depending
on the architecture of a particular

850 / 31

pennation angles, large PCSAs, and

short fibers. In terms of design, these
muscles appear suited for the generation of large forces. The hamstring
muscles, however, by virtue of their
relatively long fibers and intermediate
PCSAs, appear to be designed for
large excursions (because excursions
are proportional to fiber length). The
same appears to be true of the plantar
flexors and dorsiflexors.

A
1

Tendon

Force-Generating Properties of
Muscles With Different
Archltectures

Flgure 8. Schematic drawing of two muscles with direrent architecture: (A) muscle
with short fibers and large cross-sectional area; (B) muscle with long fibers and small
cross-sectional area. FL =fiber length; ML= muscle length; CSA=muscle physiological
cross-sectional area. (Reprinted with permission from Lieber.I8)
muscle, all fibers will not be present
in a given anatomical plane.

sions indicates that muscles are constructed of various designs, which

enable them to produce high forces
Muscle fiber length must be deterand/or high excursions. For example,
mined experimentally by microdissecthe vastus muscles, with their relatively short, pennated fibers, appear
tion of isolated skeletal muscles. Such
to be specialized for high force promicrodissection has been performed
for numerous animal and human
duction, whereas the sartorius muscle,
with its longer fibers and smaller
m u s ~ l e s . l As
9 ~architecture
~~
is a major
cross-sectional area, appears to be
determinant of muscle function, it
better suited for high excursions and
helps to have a "feel" for the architeclow force. Such specialization is not
tural properties of various human
necessarily an either/or proposition,
muscles. These properties have been
measured in the lower e ~ t r e m i t y ~ ~ ~ ~aszsome muscles generate large forces
(due to large size) and produce high
and upper e ~ t r e m i t y and
~ r ~are
~
presented in graphical form in Figure
excursion.
6. Because muscle fiber length is
proportional to muscle excursion and
In the lower limb, inspection of funcmuscle PCSA is proportional to Po,
tional muscle groups (eg, hamstrings,
the architectural specialization shown
quadriceps femoris, dorsiflexors,
in Figure 6 suggests a wide range of
plantar flexors) permits a number of
generalizations to be made (Fig. 7).
forces and excursions that can be
The quadriceps femoris muscles are
produced by the various skeletal muscharacterized by their relatively high
cles. This range of forces and excur32 / 851

If we had two muscles with dramatically different designs but identical

muscle mass, as illustrated in Figure
8, both muscles would have the same
amount of contractile material (mass),
but the arrangements would be quite
different. The muscle in Figure 8B has
relatively long fibers that extend almost the entire length of the muscle
and are parallel to the muscle's forcegenerating axis (ie, the axis formed
by connecting the line from muscle
origin to insertion). This is the classic
parallel-fibered muscle. The muscle
shown in Figure 8A has relatively
short fibers that extend a very short
length relative to the muscle and are
tilted by about 30 degrees to the
muscle's force-generating axis. This is
the classic pemated muscle.
In Figure 9A, we have plotted the
length-tension curves of the two muscles. Note that the muscle with the
longer fibers has a greater absolute
working range than the muscle with
the shorter fibers. This is because, for
a given length change, each sarcomere in the long-fibered muscle
lengthens less, the length change
being distributed over a greater number of sarcomeres. However, note
also that the long-fibered muscle
generates a lower tension than the
short-fibered muscle because the
muscle with the shorter fibers contains a much greater PCSA. Generally,
muscles with short fibers and a large
PCSA are designed for force production, whereas muscles with long fibers are designed for excursion. This
concept is well illustrated by the
force-velocity curves plotted in Figure

Physical Therapy/Volume 73, Number 12December 1993

that can be quantitatively described

using the equation for torque (7):

Short Fibers, Large PCSA

t\

10

Long Fibers, Small PCSA

15

20

25

Muscle Length (cm)

(6)

10

15

20

25

Muscle Velocity (cmls)

Flgure 9. Isometric and isotonic properties of muscles with diferent architecture

shown in Figure 8: (A) length-tension relationship; (B) force-velocity relationship. Note
that maximum tetanic tension is the common point between force-velocity and lengthtension curves. PCSA =physiological cross-sectional area.
9B. Note that the muscle with long
that is much greater
fibers has a V,
than that of the muscle with short
fibers. Each sarcomere within the
fiber contracts at the same velocity,
regardless of fiber length. However,
by placing more sarcomeres in series
in the muscle with long fibers, the
overall ~nusclevelocity is greater.
Again, note that the Po for the muscle
with short fibers is much greater than

that observed for the muscle with

long fibers due to its greater PCSA.

Torque Deflnltlon
We have discussed isolated muscle
properties, but in the musculoskeletal
system, muscles generate force and
transmit the force, via tendons, to the
bones. If muscles generate sufficient
force, bones rotate about joint axes.
We thus have a mechanical system

Physical Therapy/Volume 73, Number 12December 1993

7=

lrl JFI sine

where the vertical bars around r and

F represent the vector magnitudes,
and 8 is the angle between the direction of force application and the axis
of rotation. The basis for this expression can be seen in Figure 10B,
where the line of force (F) is applied
at an angle (8) relative to the axis of
the moment arm. The component of
force that causes rotation is the short
side of the triangle (F sine).

Short Fibers, Large PCSA

where r is the moment arm, F is the

applied force (due to muscle tension), and x represents the vector
cross-product of the two quantities
(Fig. 10A). Thus, a force (F) is applied
a distance (r) away from an axis
(open circle, Fig. 10A) that is free to
rotate. The arrows above the moment
arm and force variables signlfy that
they are vector quantities. That is,
both have magnitude as well as direction. This is another way of saying that
the orientation between r and F is
important. If we expand this equation,
we can express torque as

The moment arm is measured in

distance units such as meters. Because
the sine term is dimensionless, torque
has units of newton-meters (forcedistance units). Another common unit
of torque is foot-pounds (such as are
used in the automobile industry and,
interestingly, on many isokinetic dynamometers used in rehabilitation).
The word "strength," as we use it,
clinically actually represents torque.
All real-world performance (eg,
sprinting, lifting weights, getting out
of bed, writing) represents manifestations of torque by the musculoskeletal
system. If we grasp the implications of
this statement, it is clearly incorrect to
conclude that a person is strong only
because his or her muscles generate
large forces. It would be just as ridiculous to conclude that a person is
strong only because that person has

852 / 33

Force (F)

large moment arms. Based on this

discussion, it is clear that at least
three strategies exist for changing
torque: (1) changing force magnitude
(tension-producing capability of a
muscle), (2) changing moment arm
magnitude (changing the insertion of
a muscle), and (3) changing the angle
between force magnitude and moment arm magnitude. Two of these
strategies require surgical changes,
whereas the third (changing tension)
is amenable to training.

1
,

Muscle Force Produclng the

Moment

Radius (r)-I

Torque (z)

Figure 10. Physical representation of torque generation. Torque (7) is produced

when a force (F) is applied to a moment arm (r) to produce a rotational torque. (A)
Force applied perpendicularly to moment arm. (B) Force applied in an angle (8) relative to the axis of the moment arm. Component of force causing rotation is shown as
Fssine. (Reprinted with permission from Lieber.I8)

Flgure 11. Schematic illustration of change in moment arm as a function of elbow joint angle rotation: (A) Elbow almost fully extended (8=20); (B) elbow flexed
(8=50). (Reprinted with permission from Lieber.I8)
34 / 853

Determination of the muscle force

that produces a joint moment is simple in principle but extremely difficult
in practice. As discussed previously, if
muscle is fully activated, muscle force
varies with muscle length (lengthtension relationship) and muscle
velocity (force-velocity relationship). If
we know the muscle's length and
velocity, we theoretically can predict
muscle force.

,
I

I
j

Moment Arm Produclng the

Moment
Determination of joint moment arm
requires an understanding of the
anatomy and movement (kinematics)
of the joint of interest. For example,
some joints can be considered to
rotate about a fixed point. A good
example of such a joint is the elbow.27 At the elbow joint, where the
humerus and ulna articulate, the resulting rotation occurs primarily
about a fixed point, referred to as the
center of rotation. In the case of the
elbow joint, this center of rotation is
relatively constant throughout the
joint's range of motion (ROM).Z7 In
other joints (eg, the knee), however,
the center of rotation moves in space
as the knee joint rotates, because the
articulating surfaces are not perfect
circles.28 In the case of the knee, it is
not appropriate to discuss a single
center of rotation-rather, we must
speak of a center of rotation corresponding to a particular joint angle,
or, using the terminology of joint
kinematics, we must speak of the
instant center of rotation (ICR), that is,

Physical Therapy/Volume 73, Number 12Pecember 1993

I
I

Full Flexion

Full Extension

joint surface, not rotate it. Contrast

this situation with the conditions
shown in Figure 11B, in which the
joint has now been flexed so that
8=50 degrees. Now, the moment arm
equals 5 cmxsin(50")4.3 cm. We
see that for a simple hinge joint (a
joint with a fixed ICR), the maximum
moment arm is attained at 8=90 degrees. If we plotted moment arm
versus joint angle for this simple
hinge joint, we would obtain a simple
sine function that has a maximum of
5 cm occurring at 8=90 degrees.
Such a curve can be generated for
any joint. In general, the experimental
curves are not quite as simple as the
one previously discussed.

Jolnt Angle Corresponding to

Maxlmum Muscle Force

Full Flexion

Full Extension

Figure 12. Change in muscle range of motion as a function of changing moment

arm: (A) With "shrter"fibers,the range of motion is approximately 40 degrees (0
changesfrom 40" to 80") (B) increasedfiber lengtb increases active range of motion to
about 75 degrees (0 changesfiom 70"to 149). Schematic representation only; this is
not meant to represent any specific muscle-joint combination. (Reprinted with permission fiom Lieber.18)
the center of rotation at any "instant"
in time o r space.
Having defined a joint ICR, the mo-

ment a m is defined as the perpendicular distance from the line of force

application to the axis of rotation. The
moment arm is illustrated in Figure
11 for a simulated elbow joint. In
Figure 114 the elbow joint is almost
fully extended. The angle (8) between
the brachialis muscle and the ulna is
relatively small (ie, 8=20") The dis-

tance between the brachialis muscle

insertion site and the elbow ICR is 5
cm. In this example, the perpendicular distance between the line of force
application and the elbow ICR is
shown by the dashed line and is
equivalent to 5 cm X sin(20") 1.7 cm.
Thus, because the joint is nearly fully
extended, this presents an unfavorable mechanical advantage to the
muscle-the moment arm is relatively
small. Much of the force generated by
the muscle will simply compress the

Physical Therapy/Volume 73, Number 12December 1993

Examination of current physiology

texts reveals a good deal of uncertainty regarding the definition of the
joint angle that corresponds to maximum muscle force. Recent studies of
torque generation in animals and
humans have generally agreed that
the joint angle at which the muscle
generates maximal force is not the
same angle at which the moment arm
is maximum. Thus, during normal
joint rotation, both the moment arm
and muscle force are constantly
changing, which results in the "shape"
of the strength or torque curve. This
concept has recently been addressed
in detail by experimental and theoretical m0deling.~~31

Range of Motlon as a Function

of Architecture
We can now "combine" the muscle
architectural discussion with the joint
moment arm concept. We stated that
muscles with longer fibers have a
longer functional ROM than muscles
with shorter fibers. Does this imply
that muscles with longer fibers are
associated with joints that have larger
ROMs? No! A muscle with longer
fibers does have a longer working
ROM. The amount of muscle length
change that occurs as a joint rotates,
however, is very strongly dependent
on the muscle's moment arm (the
perpendicular distance from the mus-

cle insertion to the axis of joint rotation). This idea is illustrated in Figure
12, in which we have attached a simulated "muscle" using two different
moment arms. In Figure 12A, the
moment arm is much less than in
Figure 12B. This means that in Figure
12.4, the muscle will change length
much less for a given change in joint
angle compared with the same
change in joint angle in Figure 12B.
As a result, the active ROM for the
muscle-joint system shown in Figure
1% will be much greater than that
shown in Figure 12B in spite of the
fact that their muscular properties are
identical. In this example, increasing
the moment arm decreased the ROM
from 40 degrees (Fig. 1%) to only 25
degrees (Fig. 12B).
We should now qualify the previous
statement about muscle design and
architecture. Muscles that are, for
example, designed for speed because
of their very long fibers may not actually produce large velocities of contraction if they are placed in position
with a very large moment arm. The
increased moment arm causes a
greater joint moment, and the muscle
is actually best suited for torque production. Similarly, a muscle that appears to be designed for force production due to the large PCSA, if
placed in position with a very small
moment arm, may actually produce
high joint excursions o r angular velocities. Thus, muscle design may o r
may not be a reflection of its actual
use in the physiologic muscle-joint
torque-generating system. In general,
muscle fiber length and muscle moment arm are positively correlated.32
Thus, muscles with long fibers tend to
have long moment arms, but this is
not necessarily the case. Muscle architectural features may represent muscle adaptation to kinematic criteria.

Summary
Skeletal muscles represent a clear
example of a structure function relationship. Isometric contractile properties result from the relative overlap of
actin and myosin contractile filaments.
Isotonic force results from the timing
of the interaction between actin and

myosin during the cross-bridge cycle.

Sarcomere arrangement in whole
muscles dramatically affects contractile
properties and is termed "architecture." Muscle architecture is highly
specialized for the various upper- and
lower-extremity muscles.
The interaction between these muscles and the joint provides flexibility
and specialization, which are required
for normal movement. It can now be
seen that normal movement represents the culmination of complex
interaction between the nervous system, muscles, and joints. Evaluation of
a phenomenon as complex as "movement" or "strength" requires an understanding of the role of each component of this system in producing
the movement o r the force. As diagnostic procedures improve in their
specificity, rehabilitation may be directed toward the particular physiological component that does not function as desired. In this way, treatments
can be developed that have a rational
physiological basis and that result in
measurable physiological changes.
Acknowledgment

We thank Becky Chamberlain for her

artistic work.
References
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856 / 37