Biomechanics of the muscle. Model of sliding threads. Hill's equation.

Modeling of
muscle contraction. Electromechanical coupling.

The best-known feature of skeletal muscle is its ability to contract and cause movement.
Skeletal muscles act not only to produce movement but also to stop movement, such as
resisting gravity to maintain posture. Small, constant adjustments of the skeletal
muscles are needed to hold a body upright or balanced in any position. Muscles also
prevent excess movement of the bones and joints, maintaining skeletal stability and
preventing skeletal structure damage or deformation. Joints can become misaligned or
dislocated entirely by pulling on the associated bones; muscles work to keep joints
stable. Skeletal muscles are located throughout the body at the openings of internal
tracts to control the movement of various substances. These muscles allow functions,
such as swallowing, urination, and defecation, to be under voluntary control. Skeletal
muscles also protect internal organs (particularly abdominal and pelvic organs) by
acting as an external barrier or shield to external trauma and by supporting the weight of
the organs.
Skeletal muscles contribute to the maintenance of homeostasis in the body by
generating heat. Muscle contraction requires energy, and when ATP is broken down,
heat is produced. This heat is very noticeable during exercise, when sustained muscle
movement causes body temperature to rise, and in cases of extreme cold, when
shivering produces random skeletal muscle contractions to generate heat.
Skeletal muscles are organized multinucleated myofibers, whose function is to
generate length and velocity dependent forces for movement or stability. They are
controlled by the nervous system, thus movement or stability is a mechanical event
produced by skeletal muscles and controlled by a complex system of voluntary,
spinal and sensory control. Muscle function depends on their intrinsic properties and
extrinsic arrangement.

Extensibility and Elasticity

The properties of extensibility and elasticity are common to many biological tissues.
The muscle simultaneously has the property of elasticity and viscosity, that is, it is a
viscoelastic medium.

Extensibility is the ability to be stretched or to increase in length, and elasticity is the

ability to return to normal length after a stretch. Muscle's elasticity returns it to normal
resting length following a stretch and provides for the smooth transmission of tension
from muscle to bone. Deformation - relative change in length

where: l - initial length, - elongation value.

Mechanical stress is a measure of the internal forces that occur when a material is
deformed. For a homogeneous rod

where: F- force applied to the rod and S - cross-sectional area.

The elastic deformation arises and disappears simultaneously with loading and is not
accompanied by energy dissipation. Hooke's law is valid for elastic deformation

E- Young's modulus, determined by the nature of matter.

A contraction is defined simply as the generation of tension within a muscle fiber.

Muscle fibers generate tension through actin and myosin cross-bridge cycling. Under
tension, a muscle belly can either lengthen, shorten, or remain the same length. The
names of contractions are based upon how the muscle belly length changes during this
tension.
Isokinetic contractions are those in which there is a consistent rate of speed.
Isotonic contractions are those in which there is consistent tension as the muscle length
changes. These can be either concentric (muscle shortening) or eccentric (muscle
elongation).
Isometric contractions are those in which the length of the muscle does not change
(Figure 1).
 Figure 1. Types of muscle contractions.

In biomechanics, Hill's muscle model refers to either Hill's equations

for tetanized muscle contraction or to the 3-element model. They were derived by the
famous physiologist Archibald Vivian Hill.

The three-element Hill muscle model is a representation of

the muscle mechanical response. The model is constituted
by a contractile element (CE) and two non-linear spring
elements, one in series (SE) and another in parallel (PE).
They were derived by the famous physiologist Archibald
Vivian Hill.
This is a popular state equation applicable to skeletal
muscle that has been stimulated to show Tetanic contraction.
It relates tension to velocity with regard to the
internal thermodynamics.

The equation is

(+b)(F+a)=b( +a) (1)

where

 is the tension (or load) in the muscle;

  is the velocity of contraction;
 is the maximum isometric tension (or load) generated in the muscle;
 a is a coefficient of shortening heat;

 b=a
  is the maximum velocity, when F=0.
Although Hill's equation looks very much like the van der Waals equation, the former
has units of energy dissipation, while the latter has units of energy. Hill's equation
demonstrates that the relationship between F and υ is hyperbolic. Therefore, the higher
the load applied to the muscle, the lower the contraction velocity. Similarly, the higher
the contraction velocity, the lower the tension in the muscle. This hyperbolic form has
been found to fit the empirical constant only during isotonic contractions near resting
length.
The muscle tension decreases as the shortening velocity increases. This feature has been
attributed to two main causes. The major appears to be the loss in tension as the cross
bridges in the contractile element and then reform in a shortened condition. The second
cause appears to be the fluid viscosity in both the contractile element and the connective
tissue. Whichever the cause of loss of tension, it is a viscous friction and can therefore
be modeled as a fluid damper.
Skeletal Muscle Fibers

Because skeletal muscle cells are long and cylindrical, they are commonly referred to as
muscle fibers. Skeletal muscle fibers can be quite large for human cells, with diameters
up to 100 μm and lengths up to 30 cm (11.8 in) in the Sartorius of the upper leg. During
early development, embryonic myoblasts, each with its own nucleus, fuse with up to
hundreds of other myoblasts to form the multinucleated skeletal muscle fibers. Multiple
nuclei mean multiple copies of genes, permitting the production of the large amounts of
proteins and enzymes needed for muscle contraction.
Some other terminology associated with muscle fibers is rooted in the Greek sarco,
which means “flesh.” The plasma membrane of muscle fibers is called the sarcolemma,
the cytoplasm is referred to as sarcoplasm, and the specialized smooth endoplasmic
reticulum, which stores, releases, and retrieves calcium ions (Ca ++) is called
the sarcoplasmic reticulum (SR) (Figure 2). As will soon be described, the functional
unit of a skeletal muscle fiber is the sarcomere, a highly organized arrangement of the
contractile myofilaments actin (thin filament) and myosin (thick filament), along with
other support proteins.
Figure 2. Muscle fiber. A skeletal muscle fiber is surrounded by a plasma membrane called the
sarcolemma, which contains sarcoplasm, the cytoplasm of muscle cells. A muscle fiber is composed of
many fibrils, which give the cell its striated appearance.

The sliding filament theory explains the mechanism of muscle contraction based on
muscle proteins that slide past each other to generate movement. According to the
sliding filament theory, the myosin (thick filaments) of muscle fibers slide past
the actin (thin filaments) during muscle contraction, while the two groups of filaments
remain at relatively constant length.

What Is a Sarcomere?
When muscle cells are viewed under the microscope, one can see that they contain a
striped pattern (striations). This pattern is formed by a series of basic units called
sarcomeres that are arranged in a stacked pattern throughout muscle tissue (Figure 3).
There can be thousands of sarcomeres within a single muscle cell. Sarcomeres are
highly stereotyped and are repeated throughout muscle cells, and the proteins within
them can change in length, which causes the overall length of a muscle to change. An
individual sarcomere contains many parallel actin (thin) and myosin (thick) filaments.
The interaction of myosin and actin proteins is at the core of our current understanding
of sarcomere shortening. How does this shortening happen? It has something to do with
a sliding interaction between actin and myosin.
 Figure 3. Structure of sarcomere.

The Sliding Filament Theory

In 1954, scientists published two groundbreaking papers describing the molecular
basis of muscle contraction. These papers described the position of myosin and
actin filaments at various stages of contraction in muscle fibers and proposed how
this interaction produced contractile force. Using high-resolution microscopy, A. F.
Huxley and R. Niedergerke (1954) and H. E. Huxley and J. Hanson (1954)
observed changes in the sarcomeres as muscle tissue shortened. They observed that
one zone of the repeated sarcomere arrangement, the "A band," remained relatively
constant in length during contraction. The A band contains thick filaments of
myosin, which suggested that the myosin filaments remained central and constant
in length while other regions of the sarcomere shortened. The investigators noted
that the "I band," rich in thinner filaments made of actin, changed its length along
with the sarcomere. These observations led them to propose the sliding filament
theory, which states that the sliding of actin past myosin generates muscle tension.
Because actin is tethered to structures located at the lateral ends of each sarcomere
called z discs or "z bands," any shortening of the actin filament length would result
in a shortening of the sarcomere and thus the muscle.

Calcium and ATP are cofactors that needed for the muscle cells contraction.
Energy is supplied by ATP. Two proteins, troponin and tropomyosin, which
 control muscle contraction by preventing the binding of myosin to filamentous
actin, need calcium to function. Tropomyosin prevents the binding of myosin to
actin in a sarcomere that is at rest.
Tropomyosin must spin around the actin
filaments to reveal the myosin-binding sites
before myosin can bind actin. To be more
precise, tropomyosin is moved away from the
myosin-binding sites on actin by troponin (the
smaller protein), so clearing the binding site
(Figure 4). If there is enough ATP and the
myosin-binding sites are exposed, myosin binds
to actin to start the cross-bridge cycling process.
The muscle contracts as the sarcomere shortens.
Since this binding cannot take place in the
absence of calcium, free calcium is a crucial
regulator of muscle contraction.

6 steps of muscle contraction:

Step 1: Calcium ions. Calcium ions are released by the sarcoplasmic
reticulum in the actin filament. Myosin head does not move.

Step 2: cross bridge forms. Calcium ions cause cross bridges (bond) to
form between act filament and myosin head.

Step 3: Myosin head slides. ATPase produced by the myosin head

filament produces ATP causing the myosin head to slide in the direction
of the actin filament.

Step 4: skeletal muscle contraction has occurred. The contraction caused

by the release of ATP allows the actin filament to slide past the myosin,
which shortens.

Step 5: Cross bridge breaks. Excess ATP disconnects the myosin head
from the actin filament.

Step 6: troponin. Troponin resets the actin to its original position, ATP
converts back to ADP via ATPase. Myosin head reverts back to its
original position.

Considering some structural similarities between skeletal and heart muscle cells it
appears that electromechanical coupling follows the same principle in both muscle types
and that different responses upon activation are rather due to modifications of the same
principle and not an expression of completely different processes in electromechanical
coupling. The situation may be different in other muscle types.

References:

1. PATRICK F. DILLON. Biophysics. A Physiological Approach. Published in the

United States of America by Cambridge University Press, New York. 2012.