Chp 6
Muscular System
6-1. Roles of muscles
a- Roles
b- Structure:
6-2. Muscle contraction
a- Sliding filament mechanism:
b- Pathology
c- Sources of energy
d- Oxygen debt
e- Muscle fatigue
f- Types of muscle contraction
6-3. Muscle activity
a1- Twitch
a2- Threshold
a3- All-or-none effect
a4- Wave summation and tetanus
a5- Recruitment
a6- Effect of exercise on muscles
6-4. Cardiac and smooth muscles
6-5. Disorders of the muscular system
6-1. Muscle properties
a- Roles:
-
Produce movement or tension: Body has about 600 muscles. Muscles are attached to bones by tendons.
-
Generate heat: help control body temperature. Shivering produces extra heat.
-
Muscle cells are excitable, can contract and relax

http://www.bmb.psu.edu/courses/bisci004a/muscle/b4muscle.htm
b- Structure:


Muscles
are made of bundles of fibers, the fascicles, enclosed into a fibrous
membrane. The fascicles are made from
many muscle fibers. Muscle fibers run
from one end of the muscle to the other.
Within the muscle fiber are many myofibrils, responsible for the
mechanism of contraction.
Nerves, carrying the fibers from the motor
neurons, connect to the muscles. The
junction between motor neuron and muscle fiber is called the neuromuscular
junction (NMJ). The contact between
muscle and nerve is also called a synapse.
A
motor unit is one motor neuron and all the muscle fibers attached to this motor
neuron. When the motor neuron fires an
impulse, all the muscle fibers have to contract





The myofibrils are formed by myosin and
actin fibers aligned in a distinct pattern.
The myosin is a large fiber with enlargement called head which will bind
with actin. The actin fiber is shaped
like a string with a smaller string, the tropomyosin wrapped around it. A protein, troponin, attached to the
tropomyosin is a binding site for calcium.
When not bound to calcium, troponin prevents myosin from attaching to
the actin. The actin filament will bind to the myosin during contraction.
Myosin
and actin form a repeating pattern, the sarcomere.



6-2. Muscle contraction
a- Sliding filament mechanism:
Contraction
1- The nerve impulse coming from the
motor neuron reaches the synapse.
2- The impulse triggers the release
of the neurotransmitter, acetylcholine, in the
synapse.
3-
The acetylcholine binds to receptors on the surface of the muscle cell and
triggers an impulse along the
membrane of the muscle cell and also deep inside
these cells.
4- Calcium ions, normally present in
special vesicles, move toward the myofibrils
and bind to troponin.
5- Troponin moves out, allowing
actin and myosin to react.
6- The thin actin filaments slides
inside the myosin filaments, shortening the I band (the A band remains
unchanged). This is repeated for each
sarcomere, along the muscle fiber. This
causes a shortening of the entire muscle.

Relaxation
7- An enzyme present in the synaptic
cleft, acetylcholinesterase, destroys Ach shortly after it is bound to the
receptors. The membrane, thus, no longer, respond to impulse.
7- Ca++ goes off troponin
and is transported by into its storage vesicles (using ATP). Therefore,
tropomyosin moves back in place. Actin
and myosin are no longer linked. The
sarcomere slides back into resting position. The I band increases in
width. The muscle relaxes.

b- Pathology
Rigor mortis: After
death, calcium is released into the sarcoplasm, thus lead to binding on
troponin and muscle contraction. Yet,
since no oxygen is being taken in, ATP cannot be regenerated. When ATP supplies from the cell are
exhausted, Ca++ can not be brought back into the sarcoplasmic
reticulum ---> the muscle remains in a state of contraction (rigor
mortis). The muscle will relax several
hours/days later, due to degradation of the proteins, among them actin and
myosin.
On rigor mortis:
http://www.nurseminerva.co.uk/dying.htm
Insecticide poisoning: The active ingredient in some insecticide is an
inhibitor of the enzyme, acetylcholinesterase.
Since acetylcholine in the synapse is no longer degraded, the muscles
remain in a state of constant stimulation, thus contraction. The insects (and sometimes humans) will die
due to lack of breathing (the breathing muscles are paralyzed in a state of
contraction).
Curare use: Curare blocks the acetylcholine receptors on the muscle membrane. Since
acetylcholine can not bind to them, the muscles can not contract, resulting in
flaccid paralysis. Curare is sometimes used
during surgery, to immobilize a person and prevent spontaneous breathing (the
patient must therefore be placed on respirator).
Myasthenia gravis: An autoimmune disease where the Ach receptors are destroyed.
Botulism: The toxin prevents release of Ach
at the synapse.
http://www.tjclarkinc.com/bacterial_diseases/tetanus_and_botulism.htm
http://www.drlera.com/bacterial_diseases/botulism.htm
Animation
on mechanism of toxicity of botulism
http://www.cat.cc.md.us/courses/bio141/lecguide/unit1/bacpath/botox.html
On
the toxicity of the tetanus toxin:
http://www.cat.cc.md.us/courses/bio141/lecguide/unit1/bacpath/tetexo.html
Toxins
of the neuromuscular junction:
http://members.aol.com/Bio50/LecNotes/lecnot12b.html
c- Sources of energy
Muscle
contraction requires ATP, yet, there is only a small amount of ATP in the
muscle fibers. ATP is generated from other
metabolic systems:
c1- Creatine phosphate has a high
energy level and can generate ATP:
But
this source of ATP is quickly exhausted and the muscle must turn to glucose
metabolism.
c2- Aerobic system
If muscle activity lasts too long, stores of energy will be depleted and must be regenerated by aerobic metabolism or cellular respiration. Glucose, fatty acids will be burned in mitochondria with oxygen coming from hemoglobin from the blood.
c3- Glycogen-lactic acid system
When
ATP and creatine reserves are depleted, glucose will be used to generate ATP. If no oxygen is present (anaerobic
conditions), glucose will be converted in pyruvic acid, and under anaerobic
conditions in lactic acid with production of 2 ATP. Lactic acid can be used by muscle, heart,
liver. Glucose can be formed from
reserve of glycogen in the liver and muscle.
Eventually, glucose and glycogen stores must be restored. Glycogen and lactic acid provide energy for
short period of time.

d- Oxygen
debt
The oxygen used during strenuous exercise
must be eventually replaced. Heavy
breathing will occur for a while after exercise. Oxygen must be used to 1) convert lactic acid
back into pyruvic acid and glucose; 2) reestablish glycogen stores; 3) restock
creatine phosphate and ATP and 4) replace the oxygen on the myoglobin.
e- Muscle
fatigue
Occurs when the muscle can not synthesize
enough ATP to sustain its contraction.
Factors involved in muscle fatigue are lack of oxygen, depletion of
glucose, glycogen, creatine phosphate, depletion of acetylcholine at the
synapse, and especially build up of lactic acid.
f- Types of
muscle activity
Isotonic contraction: contraction
with movement
Isometric contraction: contraction
without movement (tension present)
6-3. Muscle activity
a1- Twitch
Contraction resulting from all the fibers
innervated by a single motor neuron. A
motor neuron will innervate few muscle fibers if the movement produced is fine
(ex: thumb) and a large number of fibers for gross movement (ex: back).


A myogram can record a twitch. There is a brief delay between the
stimulation and the beginning of contraction, called the latent period. It corresponds to the time it takes for the
nerve impulse to reach deep inside the muscle cell. In the second phase, the contraction phase,
the muscle contracts. Myosin heads bind to actin and slide along it. It lasts
10-100 msec. The third phase or
relaxation period lasts slightly longer than the contraction period. It corresponds to the calcium ions being
shipped back into the storage vesicles.
Shortly after initial stimulation, the muscle fiber can not
contract. It is the refractory period,
lasting a short time in this muscle and is due to the depolarized state of the
muscle membrane.
a2- Threshold
An
action potential must have a minimal strength in order to trigger contraction
of the muscle fibers. This minimal value
is the threshold.
a3- All-or-none
effect
If
the strength of an action potential arriving at the synapse is adequate (above
threshold), all the muscle fibers innervated by the motor neuron will contract
to the fullest.
a4- Wave summation
and tetanus
In wave summation, if a second stimulus comes
before the relaxation phase is complete, the contraction of other muscle fibers
will be added to that of the first one, thus increasing the overall contraction
strength of the muscle. If a muscle is
rapidly stimulated before relaxation can take place, the muscle remains in a
state of constant contraction or tetanus.

a5- Recruitment
During stimulation, various motor units are
being recruited. They do not contract in
unison. The greater the stimulation, the
more motor units are recruited, the stronger the contraction. During a lengthy contraction, recruited motor
units alternate, to avoid fatigue.
.
http://homepages.ius.edu/KEDMONDS/muscles.htm
http://www.mrs.umn.edu/~goochv/HAP/lectures/muscle/muscle.html
Notes:
http://highered.mcgraw-hill.com/sites/0070272352/student_view0/chapter12/chapter_summary.html
http://www.shef.ac.uk/uni/projects/mc/intro2p2.html
a6- Effect of exercise on muscles
Two
types of exercise: strength (resistance) training and aerobic (endurance)
training.
-
Strength training: uses resistance to make muscle work harder. Short, intense à weight training à promote increase in size of fast twitch
myofibrils, rich in glycogen, creatine phosphate
-
Aerobic training: ex: running, bycicling. Promotes development of more muscle
fibers rich in mitochondria (slow twitch fibers), with more blood vessels.
Improves cardiovascular and respiratory system.
Less intense than strength training but more prolonged in time. Best is to exercise in order to increase
heart rate to target rate for 20 minutes three times per week and to practice
also strength training.
6-4. Cardiac and smooth muscles
Cardiac muscle is striated like skeletal
muscle but the cells are not fused and the cell wall is visible as intercalated
disc. Cardiac muscles are involuntary
and can contract without external stimulation.
They have a network of self-depolarizing cells, triggering
contraction. They respond to nerve
impulses, hormonal stimulation (acetylcholine and epinephrine).
Smooth muscles are also involuntary, slow, have
no striations because the myofibrils are not organized like in the other 2
muscles. Smooth muscle is present is the
wall of many viscera (blood vessels, intestines, uterus, iris, bronchioles..). Some fibers can self stimulate and thus
trigger a wavelike motion called peristalsis.
Theses muscles respond to nerve, hormones, chemical conditions (pH...)
6-5. Disorders of the muscular system
-
Muscular dystrophy: muscle proteins are
being destroyed, leading to muscle wasting and death due to cardiac and
respiratory failure
-
Tetanus: disease caused by a bacteria which growth in deep, anoxic wound. The bacteria secretes a toxin in the wound
which travel along the nerve, back to the brain. There, it will trigger a severe contraction
of most of the body muscles. The person
will die of hyperthermia or injury (due to contraction)
-
Muscle cramps: due to ion imbalance in the muscle cell environment, mostly
potassium. Increased blood circulation
decrease cramping.
-
Pulled muscle: torn muscle fibers. very
painful. If a muscle is severly torn
off, muscle cells can not divide thus won't regenerate if there is muscle
damage. They can grow in size under the
influence of exercise.
-
Fasciitis: inflammation of the fascia, the membrane surrounding the muscle.
Painful, slow to heal.
-
Aging: after the 30's, muscle mass is slowly replaced by fat. A principal cause is a decrease in the level
in physical activity in older age.