muscle physiology

MUSCLE PHYSIOLOGY
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TYPES OF MUSCLES
SKELETAL MUSCLE
SMOOTH MUSCLE
MUSCLE RECEPTORS
REFLEXES
NEUROTROPHISM

Muscles are broadly classified into 3 types
– Skeletal muscle
– Smooth muscle
– Cardiac muscle
Muscle contains:
– 75% water
– 20% protein
– 5% organic and inorganic compounds

40 % of the body is skeletal muscle
10 % is smooth and cardiac muscle.
40% of adult body weight
50% of child’s body weight

FASCIA
Connective tissue that encases the muscles
Functions of fascia –
– Protect muscle fibers
– Attach muscle to bone
– Provide structure for network of nerves and
blood/lymph vessels

Layers of fascia –
– Epimysium
• Surface of muscle
• Tapers at ends to form tendon
– Perimysium
• Divides muscle fibers into bundles or fascicles
– Endomysium
• Surrounds single muscle fibers

SKELETAL MUSCLE
All skeletal muscles are composed of numerous
fibers ranging from 10 to 80 micrometers in diameter.
In most skeletal muscles, each fiber extends the
entire length of the muscle.
Each fiber is usually innervated by only one nerve
ending, located near the middle of the fiber, except
for about 2 % of the fibers

Sarcolemma- it is the cell membrane of the
muscle fiber.
consists of
• true cell membrane - plasma membrane,
• outer coat made up of a thin layer of
polysaccharide material that contains
numerous thin collagen fibrils
– At the end of the muscle fiber sarcolemma fuses
with a tendon fiber

Sarcoplasm- The spaces between the myofibrils
are filled with intracellular fluid called sarcoplasm,
containing large quantities of potassium, magnesium,
phosphate, and multiple protein enzymes
Large numbers of mitochondria that lie parallel to the
myofibrils are present that provide ATP

Sarcoplasmic Reticulum - surrounding the
myofibrils of each muscle fiber is an extensive
reticulum called the sarcoplasmic reticulum.
This reticulum has a special organization that is
extremely important in controlling muscle contraction.

Myofibrils –
Each muscle fiber contains several hundred to
several thousand myofibrils
Each myofibril is composed of about 1500 adjacent
myosin filaments and 3000 actin filaments, which are
large polymerized protein molecules that cause the
actual muscle contraction.

The thick filaments are myosin and the thin filaments
are actin.
myosin and actin filaments partially interdigitate and
thus cause the myofibrils to have alternate light and
dark bands.

I bands- isotropic to
polarized light.
light bands
contain only actin filaments
A bands- anisotropic to
polarized light.
dark bands
contain myosin and ends of
the actin filaments

Z disc - composed of filamentous proteins, passes
cross wise across the myofibril and also crosswise
from myofibril to myofibril, attaching the myofibrils to
one another across the muscle fiber giving them a
striated appearance.
The ends of the actin filaments are attached to the Z
disc. Filaments extend in both directions to
interdigitate with the myosin filaments

Sarcomere – The portion of the myofibril that lies
between two successive Z discs
When the muscle fiber is contracted, the length of the
sarcomere is about 2 micrometers. The actin
filaments completely overlap the myosin filaments
and the tips of the actin filaments begin to overlap

Steps In Muscle Contraction
Excitation
– Action potential
– Neurotransmitter release
– Muscle fiber depolarization - Ca++
release from
sarcoplasmic reticulum
Coupling
– Ca++
binds to troponin-tropomyosin complex

Contraction
– Ca++
binding moves troponin-tropomyosin complex
– Myosin heads attach to actin
– Crossbridge cycling
Relaxation
– Ca++
removed from troponin-tropomyosin complex
– Cross bridge detachment
– Ca++
pumped into SR – active transport

General Mechanism of Muscle
Contraction
Initiation and execution of muscle
contraction occur in the following
steps
1. An action potential travels along a motor nerve
to its endings on muscle fibers.
2. At each ending, the nerve secretes a small
amount of the neurotransmitter substance
acetylcholine.

3. The acetylcholine acts on a local area of the muscle
fiber membrane to open multiple acetylcholine gated
channels through protein molecules floating in the
membrane.
4. This allows large quantities of sodium ions to diffuse
to the interior of the muscle fiber membrane. This
initiates an action potential at the membrane.
5. The action potential travels along the muscle fiber
membrane

6. The action potential depolarizes the muscle
membrane, it causes the sarcoplasmic reticulum to
release large quantities of calcium ions that have
been stored within this reticulum.
7. The calcium ions initiate attractive forces between the
actin and myosin filaments, causing them to slide
alongside each other, which is the contractile
process.

8. After a fraction of a second, the calcium ions are
pumped back into the sarcoplasmic reticulum by a
Ca++ membrane pump, this removal of calcium ions
from the myofibrils causes the muscle contraction to
cease.

Muscle Action Potential
Resting membrane potential: about -80 to -90 millivolts
Duration of action potential: 1 to 5 milliseconds
Velocity of conduction: 3 to 5 m/sec-

ACTION POTENTIAL –rapid changes in the
membrane potential that spread rapidly along the
fiber membrane.
Resting Stage- the membrane potential before
the action potential begins. The membrane is
polarized during this stage because of the -90
millivolts negative membrane potential that is
present.

Depolarization Stage – membrane becomes
very permeable to sodium ions, allowing diffusion of
the ions.
Repolarization Stage.- after a few 10,000ths
of a second the sodium channels begin to close and
the potassium channels open more than normal.
Rapid diffusion of potassium ions to the exterior re-
establishes the normal negative resting membrane
potential.

Voltage-Gated Sodium and Potassium
Channels

At rest, virtually all of the voltage-gated channels are
closed, potassium and sodium can only slowly move
across the membrane, through the passive "leak"
channels
The first thing that occurs when a depolarizing
graded potential reaches the threshold is that the
voltage gated Na+
channels begin to open and Na+
influx into the cell exceeds K+
efflux out of the cell

Two things happen next:
1. As the membrane depolarizes further and the cell
becomes positive inside and negative outside, the
flow of Na+
will decrease.
2) Even more importantly, the voltage- gated Na+
channels close
When the inactivation gates close, Na+
influx stops and
the repolarizing phase takes place.

Next, the voltage gated K+
channels are activated at
the time the action potential reaches its peak. At this
time, both concentration and electrical gradients
favour the movement of K+
out of the cell.
These channels are also inactivated with time but not
until after the efflux of K+
has returned the membrane
potential to, or below the resting level (after
hyperpolarization /positive afterpotential).

The Neuromuscular Junction
Each nerve ending makes a junction, called the
neuromuscular junction, with the muscle fiber near its
midpoint
The action potential initiated in the muscle fiber by
the nerve signal travels in both direction toward the
muscle fiber ends.
With the exception of about 2 % of the muscle fibers,
there is only one such junction per muscle fiber.

Motor end plate -
Branching Nerve Terminals - nerve fibers
invaginate into the surface of the muscle fiber but lie
outside the plasma membrane.
Covered by Schwann cells that insulate it from the
surrounding fluids.

Subneural clefts – numerous small folds of the
muscle membrane which increase the surface area at
which the synaptic transmitter can act.
Synaptic trough - invaginated membrane
Synaptic cleft - space between the terminal and the
fiber membrane (20 to 30 nanometers wide.)

Acetylcholine is stored in synaptic vesicles (300,000)
which are in the terminals of a single end plate
When a nerve impulse reaches the neuromuscular
junction, about 125 vesicles of acetylcholine are
released from the terminals into the synaptic space

During the action potential the calcium channels open
and calcium ions to diffuse from the synaptic space to
the interior of the nerve terminal.
The calcium ions attract the acetylcholine vesicles,
drawing them to the neural membrane
The vesicles fuse with the neural membrane and
empty their acetylcholine into the synaptic space by
exocytosis.

Acetylcholine-gated ion channels, are located almost
entirely near the mouths of the subneural clefts. Has
5 subunit proteins, two alpha and one each of beta,
delta, and gamma proteins.
After the Ach attaches a conformational change
occurs that opens the channel

the principal effect of opening channels - allows
sodium ions to pour to the inside of the fiber, carrying
with them positive charges creating a local positive
potential change inside the muscle fiber membrane,
called the end plate potential.
this end plate potential initiates an action potential
that spreads along the muscle membrane and thus
causes muscle contraction.

Most is destroyed by the enzyme acetylcholinesterase,
which is attached to the spongy layer of the connective
tissue that fills the synaptic space between the
presynaptic nerve terminal and the postsynaptic
muscle membrane.
A small amount of acetylcholine diffuses out of the
synaptic space and is then no longer available to act
on the muscle fiber membrane.
Destruction of the Released Acetylcholine

Safety Factor of Transmission at the
Neuromuscular Junction
– Each impulse at the neuromuscular junction
causes about 3 times as much end plate potential
as that required to stimulate the muscle fiber.
– Stimulation of the nerve fiber at rates greater than
100 times/sec for several minutes diminishes the
number of acetylcholine vesicles so that impulse
fail to pass into the muscle fiber- called fatigue

A new action potential cannot occur in an excitable
fiber as long as the membrane is still depolarized
from the preceding action potential.
Shortly after the action potential the sodium channels
(or calcium channels, or both) become inactivated,
and any amount of excitatory signal applied to these
channels at this point will not open the inactivation
gates.

Absolute Refractory Period - period during which a
second action potential cannot be elicited, even with
a strong stimulus. Large myelinated nerve fibers -
1/2500second.
Relative Refractory Period - lasts about ¼ to ½ as
long as the absolute period. During this time, stronger
than normal stimuli can excite the fiber.

Cause of relative refractoriness :
1. During this time, some of the sodium channels still
have not been reversed from their inactivation state
2. the potassium channels are usually wide open at
this time, causing greatly excess flow of positive
potassium ion charges to the outside of the fiber
opposing the stimulating signal

Excitation-Contraction Coupling
Skeletal muscle fibers are so large that action
potentials spreading along its surface membrane
cause almost no current flow deep within the fiber.
This is achieved by transmission of action potentials
along transverse tubules (T tubules)

T tubules
– Very small
– transverse to the myofibrils.
– Penetrate muscle fibers from one side to the other
– They branch among themselves
– They are open to the exterior of the muscle fiber at
their point of origination and so basically are
internal extensions of the cell membrane.
– The action potential spreads along the T tubules to
the interior of the muscle fiber.

Sarcoplasmic reticulum-
– Terminal cisternae
– Long longitudinal tubules
The vesicular tubules have calcium ions in high
concentration, and are released from each vesicle
when an action potential occurs in the adjacent T
tubule.

Molecular Mechanism of Muscle
Contraction
Sliding Filament Mechanism of
Muscle Contraction.

Myosin Filament -The myosin filament is
composed of multiple myosin molecules, each having
a molecular weight of about 480,000.
myosin molecule - 6 polypeptide chains-
– 2 heavy chains- molecular weight 200,000
– 4 light chains - molecular weights 20,000 each.

heavy chains wrap spirally around each other to form
a double helix, called the tail of the myosin molecule.
One end of each of these chains is folded bilaterally
into a globular polypeptide structure called a myosin
head.
4 light chains are also part of the myosin head. These
light chains help control the function of the head
during muscle contraction.

Myosin Filament - Made up of 200 or more
individual myosin molecules. (Length -1.6
micrometers.)
Tails of the myosin molecules bundle together to form
the body of the filament,
Heads of the molecules hang outward to the sides of
the body.

Arm- part of the body of each myosin molecule
along with the head,
Cross bridges- protruding arms and heads
together. It is flexible at the hinges-
– where the arm leaves the body of the myosin
filament,
– where the head attaches to the arm.

The hinged arms allow the heads either to be
extended far outward from the body of the
myosin filament or to be brought close to the
body. The hinged heads participate in the
actual contraction process

There are no cross-bridge heads in the center of the
myosin filament for a distance of 0.2 micrometer
because the hinged arms extend away from the
center.
The myosin filament itself is twisted so that each
successive pair of crossbridges is axially displaced
from the previous pair by 120 degrees.
This ensures that the cross-bridges extend in all
directions around the filament.

ATPase Activity of the Myosin Head
-the myosin head functions as an ATPase enzyme.
This allows the head to cleave ATP and to use the
energy for the contraction process.

Actin Filament- composed of 3 protein
components: actin, tropomyosin, and
troponin.

Actin - double stranded F-actin protein molecule.
– The two strands are wound in a helix. Each strand
is composed of polymerized G-actin molecules,
(molecular weight 42,000).
– Attached to each one of the G-actin molecules is
one molecule of ADP which are the active sites on
the actin filaments with which the cross bridges of
the myosin filaments interact to cause muscle
contraction.

Actin filament - length -1 micrometer
The bases of the actin filaments are inserted strongly
into the Z discs; the ends of the filaments protrude in
both directions
Troponin- Attached intermittently along the sides
of the tropomyosin molecules
complexes of three loosely bound protein subunits
– troponin I - affinity for actin,
– troponin T - for tropomyosin,
– troponin C - for calcium ions

Tropomyosin Molecules- molecular weight
70,000
length - 40 nanometers.
These molecules are wrapped spirally around the
sides of the F-actin helix
In the resting state, the tropomyosin molecules lie on
top of the active sites of the actin strands, so that
attraction cannot occur between the actin and myosin
filaments

Activation of the Actin filament
The active sites on the normal actin filament of the
relaxed muscle are inhibited or physically covered by
the troponin tropomyosin complex.
When calcium ions combine with troponin C, the
troponin complex undergoes a conformational
change that moves it deeper into the groove between
the two actin strands. This uncovers the active sites
of the actin

What Keeps the Myosin and Actin
Filaments in Place?
The side-by-side relationship between the myosin
and actin filaments is achieved by a large number of
filamentous molecules of a protein called titin.
(molecular weight- 3 million)

It is filamentous, and very springy. These molecules
act as a framework that hold the myosin and actin
filaments in place
The titin molecule itself acts as template for initial
formation of portions of the contractile filaments of
the sarcomere, especially the myosin filaments.

The Walk-Along Theory of
Contraction

When a head attaches to an active site, changes in
the intramolecular forces between the head and arm
of its cross-bridge occur. The head tilts toward the
arm and drags the actin filament along with it (power
stroke)
Immediately after tilting, the head automatically
breaks away from the active site.
The head returns to its extended direction, it
combines with a new active site farther down along
the actin filament.

Chemical Events In the Motion of
the Myosin Head
1. Before contraction -the heads of the crossbridges
bind with ATP. The ATPase activity of the myosin
head immediately cleaves the ATP but leaves the
cleavage products, ADP plus phosphate ion, bound
to the head.
In this state, the head extends perpendicularly toward
the actin filament but is not yet attached to the actin

2. When the troponin - tropomyosin complex binds with
calcium ions, active sites on the actin filament are
uncovered, and the myosin heads then bind with
these.
3.For the power stroke the energy that activates it
already stored, like a "cocked" spring, by the
conformational change that occurred in the head
when the ATP molecule was cleaved earlier.

4. Once the head of the cross-bridge tilts, it allows
release of the ADP and phosphate ion. At the site of
release of the ADP, a new molecule of ATP binds.
This binding of new ATP causes detachment of the
head from the actin.
5. After the head has detached from the actin, the new
molecule of ATP is cleaved to begin the next cycle,
leading to a new power stroke.

The process proceeds again and again until
the actin filaments pull the Z membrane up
against the ends of the myosin filaments or
until the load on the muscle becomes too
great for further pulling to occur.

RELAXATION –muscle contraction continues as
long as the calcium ions remain in high concentration
and thus
A continually active calcium pump located in the walls
of the sarcoplasmic reticulum pumps calcium ions
away from the myofibrils back into the sarcoplasmic
tubules. This pump can concentrate the calcium ions
about 1O,OOO-fold inside the tubules.
Inside the reticulum is a protein called calsequestrin
that can bind up to 40 times more calcium.

Effect of Amount of Actin and Myosin
Filament Overlap on Tension Developed by
the Contracting Muscle

Point D- no actin-myosin overlap. Tension
developed by the muscle - 0.
Point C- actin filament has overlapped all the
cross-bridges of the myosin filament but not reached
the center. Length -2.2 micrometers.
Point B- two actin filaments begin to overlap each
other. Length -2 micrometers.
Point A- the two Z discs of the sarcomere abut the ends of
the myosin filaments. Length - 1.65 micrometers

Effect of Muscle Length on Force of
Contraction in the Whole Intact Muscle.
Other factors to be
considered –
– connective tissue
– different parts of the muscle
do not contract the same
amount.
Active tension decreases
as the muscle is stretched
beyond its normal length

Relation of Velocity of Contraction to
Load
Against no load-skeletal muscle
contracts in about 0.1 second
When loads are applied, the
velocity of contraction becomes
progressively less
When load is equal to the
maximum force of the muscle,
the velocity of contraction is zero
and no contraction results

Work Output During Muscle Contraction
Sources of energy for muscle contraction
– Phosphocreatine
– Glycolysis of glycogen
– Oxidative metabolism.
The percentage of the input energy to muscle is less
than 25 % with the remainder becoming heat.

Types Of Contraction
Isometric Contraction- when
the muscle does not shorten during
contraction
Isotonic Contraction- when
muscle shortens but the tension on the
muscle remains constant throughout the
contraction.

Fast And Slow Muscle Fibers.
Muscles that react rapidly are composed mainly of
fast fibers with small numbers of slow fibers.
Muscles that respond slowly but with prolonged
contraction are composed mainly of slow fibers

Fast Fibers Slow Fibers
Large fibers Smaller fibers.
Less extensive blood supply Extensive blood vessel
Supply
Fewer mitochondria, Increased numbers of
mitochondria,
No myoglobin present in fibers Large amounts of myoglobin
Large amounts of glycolytic
enzymes
Less amounts of glycolytic
enzymes
Extensive sarcoplasmic
reticulum
Less extensive sarcoplasmic
reticulumwww.indiandentalacademy.com

Motor neurons
Small muscles that react rapidly and whose control
must be exact have more nerve fibers for fewer
muscle fiber
Large muscles that do not require fine control may
have several hundred muscle fibers in a motor unit.

Force Summation.
Summation - adding together of individual twitch
contractions to increase the intensity of overall
muscle contraction.
– Types
• Multiple fiber summation
• Frequency summation

Multiple Fiber Summation- When the CNS
sends a weak signal to contract a muscle, the smaller
motor units of the muscle are stimulated in
preference to the larger motor units. As the strength
of the signal increases, larger motor units begin to be
excited (size principle.)
Cause -smaller motor units are driven by small motor
nerve fibers, and are more excitable than the larger
ones

Frequency Summation and
Tetanization
As frequency increases, a new contraction occurs
before the preceding one is over. As a result, the 2nd
contraction is added partially to the 1st
, so that the
total strength of contraction rises with increasing
frequency.

Tetanization - When the frequency reaches a
critical level, the successive contractions fuse
together, and the whole muscle contraction appears
to be smooth and continuous

The Staircase Effect (Treppe)
When a muscle begins to contract after a long period
of rest, its initial strength of contraction is as little as
½ its strength 10 to 50 muscle twitches later.
Cause – increase in calcium ions in the cytosol
because of the release of more and more ions from
the sarcoplasmic reticulum with each successive
muscle action potential and failure of the sarcoplasm
to recapture the ions immediately.

Skeletal Muscle Tone.
Muscle tone- Even when muscles are at rest, a
certain amount of tautness remains. It results entirely
from a low rate of nerve impulses coming from the
spinal cord.

Muscle Fatigue.
Prolonged and strong contraction of a muscle leads
to the state of muscle fatigue. It results mainly from
inability of the contractile and metabolic processes of
the muscle fibers to continue supplying the same
work output.

Muscle Hypertrophy
– When the total mass of a muscle increases
– When muscles are stretched to greater than
normal length causing new sarcomeres to be
added at the ends of the muscle fibers
– Results from an increase in the number of actin
and myosin filaments
– Rate of synthesis of muscle contractile proteins is
far greater

When a muscle loses its nerve supply, it no longer
receives the contractile signals that are required to
maintain normal muscle size and atrophy begins
If the nerve supply grows back rapidly, return of
function can occur in 3 months. Beyond that the
capability of functional return becomes less, with no
further return of function after 1 to 2 years.

Rigor Mortis
Several hours after death, the muscles contract and
become rigid, even without action potentials. This
rigidity results from loss of all the ATP, which is
required to cause separation of the crossbridges from
the actin filaments during the relaxation process.

SMOOTH MUSCLE
Smooth Muscle -1 to 5 micrometers – diameter
20 - 500 micrometers in length
Two major types-
– Multi-unit smooth muscle
– Unitary smooth muscle.

Multi-Unit Smooth Muscle-
– Composed of discrete, separate smooth muscle
fibers.
– Each fiber operates independently
– Innervated by a single nerve ending
– Outer surfaces are covered by a thin layer of
basement membrane
– Each fiber can contract independently of the
others, and their control is exerted mainly by nerve
signals.

Unitary Smooth Muscle-
– smooth muscle fibers that contract together as a
single unit.
– fibers are arranged in sheets or bundles, and their
cell membranes are adherent to one another
– cell membranes are joined by gap junctions
through which ions can flow freely
– Syncytial interconnections among fibers.

Smooth muscle have actin and myosin filaments
having chemical characteristics similar and interact
with each other in much the same way to those of the
skeletal muscle
They do not not contain the normal troponin complex

Actin filaments are attached to dense
bodies.
Some dense bodies of adjacent cells are
bonded together by intercellular bridges
which transmit the force of contraction from
one cell to the next.
Ends of actin filaments overlap a myosin
filament located midway between the
dense bodies.
Myosin filaments have sidepolar cross-
bridges - bridges on both sides hinge in the
opposite direction.www.indiandentalacademy.com

The rapidity of cycling of the myosin cross-bridges in
smooth muscle cycle is much, much slower than in
skeletal muscle (1/10 to 1/300)
Reason- The cross-bridge heads have far less
ATPase activity than in skeletal muscle.
But the fraction of time that the cross-bridges remain
attached to the actin filaments, which determines the
force of contraction, is increased in smooth muscle
- 4 to 6 kg/cm2

Only 1/10 to 1/300 as much energy is required to
sustain the same tension of contraction in smooth
muscle as in skeletal muscle.
smooth muscles -
– begin to contract 50 - 100 milliseconds after
excitation
– reach full contraction - 0.5 second later,
– decline in contractile force -another 1 to 2 sec
– total contraction time - 1 to 3 sec.

Visceral unitary type of smooth muscle of many
hollow organs, have the ability to return to nearly its
original force of contraction seconds or minutes after
it has been elongated or shortened.

Regulation of Contraction by Calcium
Ions-
– the initiating stimulus for most smooth muscle
contraction is an increase in intracellular calcium
ions.
– Caused by –
• nerve stimulation
• hormonal stimulation,
• stretch of the fiber
• change in the chemical environment of the fiber.

Contraction-
1. The calcium ions bind with calmodulin.
2. The calmodulin-calcium combination joins with and
activates myosin kinase, a phosphorylating
enzyme.
3. In response the regulatory chain of the myosin
head becomes phosphorylated and the head now
binds with the actin filament and proceeds through
the entire cycling process causing muscle
contraction.

Cessation of Contraction-
When the calcium ion concentration falls below a
critical level, the contraction processes automatically
except for the phosphorylation of the myosin head.
Reversal of this requires enzyme myosin
phosphatase, which splits the phosphate from the
regulatory light chain. Then the cycling stops and
contraction ceases.

Latch Mechanism
Once smooth muscle has developed full contraction,
the amount of continuing excitation usually can be
reduced to far less than the initial level, yet the muscle
maintains its full force of contraction.
Importance - can maintain prolonged tonic contraction
in smooth muscle for hours with little use of energy.

When the myosin kinase and myosin phosphatase
enzymes are activated, the cycling frequency of the
myosin heads and the velocity of contraction are
great.
As the activation of the enzymes decreases, the
cycling frequency decreases
But the deactivation of these enzymes allows the
myosin heads to remain attached to the actin filament
for a longer proportion of the cycling period.

Therefore, the number of heads attached to the actin
filament at any given time remains large. Because
the number of heads attached to the actin determines
the force of contraction, tension is maintained, yet
little energy is used by the muscle, because ATP is
not degraded to ADP.

Neuromuscular Junctions of Smooth
Muscle
The autonomic nerve fibers that innervate smooth
muscle generally branch diffusely on top of a sheet of
muscle fibers,
These fibers do not make direct contact with the
smooth muscle fiber cell membranes but instead
form diffuse junctions that secrete their transmitter
substance into the matrix a few nanometers to a few
micrometers away

The fine terminal axons have multiple varicosities
distributed along their axes. At these points the
schwann cells are interrupted so that transmitter
substance can be secreted through the walls of the
varicosities. These are called as contact junctions
In the varicosities are vesicles which contain
acetylcholine and norepinephrine

When acetylcholine excites a muscle fiber,
norepinephrine ordinarily inhibits it. Conversely, when
acetylcholine inhibits a fiber, norepinephrine usually
excites it
Reason -the type of receptor determines whether the
smooth muscle is inhibited or excited and also
determines which of the two transmitters,
acetylcholine or norepinephrine, is effective in
causing the excitation or inhibition.

Action Potentials in Smooth Muscle
The normal resting membrane potential is usually
about -50 to -60 millivolts
The action potentials of visceral smooth muscle occur
in one of two forms:
– Spike potentials
– Action potentials with plateaus.

Spike Potentials
similar to the skeletal muscles
occur in most types of unitary smooth muscle
duration -10 to 50 milliseconds

Action Potentials with Plateaus-
The repolarization is delayed for several hundred to
as much as 1000 milliseconds (1 second).
Importance - can account for the prolonged
contraction that occurs in the ureter, the uterus etc

Smooth muscle cell membrane have more voltage-
gated calcium channels than does skeletal muscle
but few voltage gated sodium channels.
Thus calcium ions are mainly responsible for the
action potential.
They open more slowly than sodium channels, and
remain open much longer accounting for the
prolonged plateau action potentials
Calcium ions act directly on the smooth muscle
contractile mechanism to cause contraction.

Slow Wave Potentials
Some smooth muscle are self-excitatory. ie: action
potential arises within the smooth muscle cell without
an extrinsic stimulus.
Often associated with a basic slow wave rhythm of the
membrane potential.
It is not a self regenerative process that spreads
progressively over the membranes of the muscle fibers

Cause
– The membrane potential becomes more negative
when sodium is pumped rapidly and less negative
when the sodium pump becomes less active.
– Or - the conductance of the ion channels increase
and decrease rhythmically.
When they are strong enough, they can initiate action
potentials.

Source of Calcium Ions
Almost all the calcium ions that cause contraction
enter the muscle cell from the extracellular fluid at the
time of the action potential. There is a rapid diffusion
of the calcium ions into the cell from the extracellular
fluid when the calcium pores open.
Time required - 200 to 300 milliseconds and is called
- latent period
This latent period is about 50 times as great for
smooth muscle as for skeletal muscle contraction.

When the extracellular fluid calcium ion concentration
falls to 1/3 to 1/10 normal, smooth muscle contraction
usually ceases.
Calcium ions are removed by a calcium pump that
pumps calcium ions out into the extracellular fluid, or
into a sarcoplasmic reticulum

Smooth Muscle Sarcoplasmic Reticulum-
caveolae – analog of the transverse tubule system of
skeletal muscle. They excite calcium ion release from
the abutting sarcoplasmic tubules

Receptors provide information regarding:
– Chemical changes (i.e., O2, CO2, H+)
– Tension development: Golgi Tendon Organs
– Muscle length: Muscle spindles
Information from these receptors provides information
about the energetic requirements of exercising muscle
and about movement patterns
MUSCLE RECEPTORS

Muscle spindle –
– Detect dynamic and static changes in muscle
length– Stretch reflex
– Stretch on muscle causes reflex contraction
Golgi tendon organ (GTO) –
– Monitor tension developed in muscle – Prevents
damage during excessive force generation
– Stimulation results in reflex relaxation of muscle

Muscle spindles respond to muscle stretch -
Gamma motor neurons are co activated during
contraction
– Cause contraction of fibers within muscle spindle
– Deviations in consistency signal excessive stretch

Golgi Tendon Organ
Located in tendon
Monitor muscle tension
Activation causes inhibition of alphamotor neuron
Is a safety mechanism against excessive force during
contraction

MYOTACTIC / STRETCH REFLEX

Causes contraction of stretched muscle
Receptor – proprioceptive nerve endings called
muscle spindles
Impulses are conducted by group 1A sensory nerve
endings
Impulse carried by motoneurons / alpha efferent

Functional significance – serves as a mechanism for
upright posture
In mandible it acts to maintain the postural rest
position in reln to the maxilla

CLASP KNIFE REFLEX /AUTOGENIC INHIBITION

Resistance is encountered as soon as the muscle is
stretched throughout the initial part of the bending.
This resistance is due to the hyperactive reflex
contraction of the muscle in response to the
myotactic reflex
If flexion is forcibly carried further, a point is reached
at which all resistance stops, and the previously rigid
limb collapses readily
"clasp-knife" reaction

functional significance - to protect the overload by
preventing damaging contraction against strong
stretching forces.
The stimulus to elicit the clasp-knife reflex is
excessive stretch and, when elicited, inhibits
muscular contraction, thus causing the muscle to
relax.

Receptors - Golgi tendon organs
impulses are conducted by the Group 1B sensory
nerve fiber
Impulses act on the motor neuron, or alpha efferent.

NEURO TROPHISM
Definition - interaction between nerves and other
cells which initiate or control molecular modifications
in other cells (Guth 1969)
Or is a non impulse transmitting neural function that
involves axoplasmic transport and provides from long
term interactions between the nervous and
innervated tissue that homeostatically regulate the
morphological, compositional and functional integrity
of those tissues.

Three types -
Neuro epithelial trophism
Neuro visceral trophism
Neuro muscular trophism
NEURO-MUSCULAR TROPHISM: Skeletal muscle
ontogenesis normally requires motor neuron
innervation to proceed past the stage of myotubes
Embryonic myogenesis is independent of neural
innervation and trophic control.

Approximately at the myoblast stage of
differentiation, neural innervation is established
without which further myogenesis cannot continue.
Neurotrophic influences are involved rather than
conductive influences

Cross-innervation experiments show that many
significant morphologic, biochemical and functional
parameters of the re-innervated muscle come to
resemble those of the muscle formerly innervated by
the now ectopically implanted nerve. Therefore,
these parameters of skeletal muscle are nerve-
specific, not muscle specific

Conformational features of myosin are determined by
the nature of the innervation and that the complex
chain of events leading to particular expression of the
genetic – embryonic potential is not wholly within the
cell, but also includes informational elements
contributed by the nerve

Research shows that a qualitatively different myosin
that resembles that of the muscle, formerly
innervated by the nerve, is synthesized in cross-
innvervated muscle, which indicates that a new
species of protein has been synthesized, and it is
therefore, suggested that the nerve influences gene
expression in the cell.

Implication of these data:
Since periosteal functional matrices regulate the size
and shape of specifically related skeletal units, it is
apparent that the genetic control of the structural,
chemical and functional attributed of these same
matrices cannot reside solely in the matrices
themselves, but rather reflect constant
neurotrophically regulated homeostatic control of
genome.

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muscle physiology

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