Baronda, Pauline Cristine D.

BSBio-3
A. Movement
1. Non-muscular movement
Amoeboid movement is typically found in amoeba, a unicellular animal. Amoeba
moves by producing pseudopodia, which are cytoplasmic projections. This involves
change in the shape of the cell body and streaming movement of cytoplasm into the
pseudopodium. The movement due to pseudopodia in amoeba is termed as amoeboid
movement. Amoeboid movement is characteristic of certain cells in other organisms.
For example, the movement of white blood cells or leucocytes, in human blood.
Amoeba moves about to obtain food or to avoid dangers or to escape from energy.
Leucocytes like phagocytes or macrophages of the lymph, show amoeboid movements
to engulf antigen or microbes and to immigrate in the circulatory fluid.
Ciliary movement is the method by which ciliated protozoans like paramoecium, move
from plate to place in water medium. Paramoecium uses cilia not only for moving from
one plate to another (locomotion) also to drive water and food into their gullet.
Cilia can perform a variety of functions:
1. In certain molluscs, cilia help to pass water currents over the gills
2. In echinoderms cilia helps to drive water through the water vascular system,
(locomotion)
3. Cilia of the cells lining the respiratory tract of humans help to drive away the
microbes and dust particles towards the nose or mouth
4. Cilia in the oviduct or fallopian tubes of human female transport ova
Flagellum also helps in the movement in certain protozoans like euglena. Flagellum is
a long, thread like cytoplasmic projection. Flagellum in sperms also helps in the
swimming movement.
2.

Different muscle type

Visceral Muscle. found inside organs like the stomach, intestines, and blood
vessels. The weakest of all muscle tissues, visceral muscle makes organs contract to
move substances through the organ. Because visceral muscle is controlled by the
unconscious part of the brain, it is known as involuntary muscle. The term smooth
muscle is often used to describe visceral muscle because it has a very smooth,
uniform appearance when viewed under a microscope. This smooth appearance
starkly contrasts with the banded appearance of cardiac and skeletal muscles.
Cardiac Muscle. Found only in the heart, cardiac muscle is responsible for
pumping blood throughout the body. Involuntary muscle. Cardiac muscle stimulates
itself to contract. The natural pacemaker of the heart is made of cardiac muscle tissue
that stimulates other cardiac muscle cells to contract. Because of its self-stimulation,
cardiac muscle is considered to be autorhythmic or intrinsically controlled.
The cells of cardiac muscle tissue are striatedthat is, they appear to have light
and dark stripes when viewed under a light microscope. The arrangement of protein
fibers inside of the cells causes these light and dark bands. Striations indicate that a
muscle cell is very strong, unlike visceral muscles.
The cells of cardiac muscle are branched X or Y shaped cells tightly connected
together by special junctions called intercalated disks. Intercalated disks are made up
of fingerlike projections from two neighboring cells that interlock and provide a strong
bond between the cells. The branched structure and intercalated disks allow the

muscle cells to resist high blood pressures and the strain of pumping blood throughout
a lifetime. These features also help to spread electrochemical signals quickly from cell
to cell so that the heart can beat as a unit.
Skeletal Muscle. Voluntary. The function of skeletal muscle is to contract to
move parts of the body closer to the bone that the muscle is attached to. Most
skeletal muscles are attached to two bones across a joint, so the muscle serves to
move parts of those bones closer to each other.
Skeletal muscle cells form when many smaller progenitor cells lump themselves
together to form long, straight, multinucleated fibers. Striated just like cardiac muscle,
these skeletal muscle fibers are very strong. Skeletal muscle derives its name from
the fact that these muscles always connect to the skeleton in at least one place.

3. Structural Basis of Contraction

An action potential reaches the axon of the motor neuron.
The action potential activates voltage gated calcium ion channels on the axon, and
calcium rushes in.
The calcium causes acetylcholine vesicles in the axon to fuse with the membrane,
releasing the acetylcholine into the cleft between the axon and the motor end plate of
the muscle fiber.
The skeletal muscle fiber is excited my large mylenated nerve fibers which attach to
the. There is one neuromuscular junction for each fiber.
The acetylcholine diffuses across the cleft and binds to nicotinic receptors on the
motor end plate, opening channels in the membrane for sodium and potassium.
Sodium rushes in, and potassium rushes out. However, because sodium is more
permeable, the muscle fiber membrane becomes more positively charged, triggering
an action potential.
The action potential on the muscle fiber causes the sarcoplasmic reticulum to
release calcium ions(Ca++).
The calcium binds to the troponin present on the thin filaments of the myofibrils. The
troponin then allosterically modulates the tropomyosin. Normally the tropomyosin
physically obstructs binding sites for cross-bridge; once calcium binds to the troponin,
the troponin forces the tropomyosin to move out of the way, unblocking the binding
sites.
The cross-bridge (which is already in a ready-state) binds to the newly uncovered
binding sites. It then delivers a power stroke.
ATP binds the cross-bridge, forcing it to conform in such a way as to break the
actinmyosin bond. Another ATP is split to energize the cross bridge again.
Steps 7 and 8 repeat as long as calcium is present on thin filament.
Throughout this process, the calcium is actively pumped back into the sarcoplasmic
reticulum. When no longer present on the thin filament, the tropomyosin changes
back to its previous state, so as to block the binding sites again. The cross-bridge then
ceases binding to the thin filament, and the contractions cease as well.
Muscle contraction remains as long as Ca++ is abundant in sarcoplasm.

4. Chemistry of Muscle Contraction

Muscle contraction requires energy, and muscle has been called a machine for
converting chemical energy into mechanical work. The immediate source of this

energy is ATP, and this is formed by the metabolism of carbohydrates and lipids.
PHOSPHORYLCREATINE
ATP is resynthesized from ADP by the addition of a phosphate group. Some of the
energy for this endothermic reaction is supplied by the breakdown of glucose to CO2
and H2O, but there also exists in muscle another energy-rich phosphate compound
that can supply this energy for short periods. This compound is phosphorylcreatine,
which is hydrolyzed to creatine and phosphate groups with the release of considerable
energy. At rest, some ATP in the mitochondria transfers its phosphate to creatine, so
that a store is built up. During exercise, the phosphorylcreatine is hydrolyzed at the
junction between the myosin heads and actin, forming ATP from ADP and thus
permitting contraction to continue.
CARBOHYDRATE & LIPID BREAKDOWN
At rest and during light exercise, muscles utilize lipids in the form of free fatty acids
as their energy source. As the intensity of exercise increases, lipids alone cannot
supply energy fast enough and so use of carbohydrate becomes the predominant
component in the muscle fuel mixture. Thus, during exercise, much of the energy for
phosphorylcreatine and ATP resynthesis comes from the breakdown of glucose to CO2
and H2O. Glucose in the bloodstream enters cells, where it is degraded through a
series of chemical reactions to pyruvate. source of intracellular glucose, and
consequently of pyruvate, is glycogen, the carbohydrate polymer that is especially
abundant in liver and skeletal muscle. When adequate O2 is present, pyruvate enters
the citric acid cycle and is metabolizedthrough this cycle and the so-called
respiratory enzyme pathwayto CO2 and H2O. This process is called aerobic
glycolysis. The metabolism of glucose or glycogen to CO2 and H2O forms large
quantities of ATP from ADP. If O2 supplies are insufficient, the pyruvate formed from
glucose does not enter the tricarboxylic acid cycle but is reduced to lactate. This
process of anaerobic glycolysis is associated with the net production of much smaller
quantities of energy-rich phosphate bonds, but it does not require the presence of O2.
THE OXYGEN DEBT MECHANISM
During exercise, the muscle blood vessels dilate and blood flow is increased so that
the available O2 supply is increased. Up to a point, the increase in O2 consumption is
proportional to the energy expended, and all the energy needs are met by aerobic
processes. However, when muscular exertion is very great, aerobic resynthesis of
energy stores cannot keep pace with their utilization. Under these conditions,
phosphorylcreatine is still used to resynthesize ATP. In addition, some ATP synthesis is
accomplished by using the energy released by the anaerobic breakdown of glucose to
lactate. Use of the anaerobic pathway is self-limiting because in spite of rapid diffusion
of lactate into the bloodstream, enough accumulates in the muscles to eventually
exceed the capacity of the tissue buffers and produce an enzyme-inhibiting decline in
pH. However, for short periods, the presence of an anaerobic pathway for glucose
breakdown permits muscular exertion of a far greater magnitude than would be
possible without it. For example, in a 100-m dash that takes 10 s, 85% of the energy
consumed is derived anaerobically; in a 2-mi race that takes 10 min, 20% of the
energy is derived anaerobically; and in a longdistance race that takes 60 min, only 5%
of the energy comes from anaerobic metabolism. After a period of exertion is over,
extra O2 is consumed to remove the excess lactate, replenish the ATP and
phosphorylcreatine stores, and replace the small amounts of O2 that were released by
myoglobin. The amount of extra O2 consumed is proportional to the extent to which

the energy demands during exertion exceeded the capacity for the aerobic synthesis
of energy stores, ie, the extent to which an oxygen debt was incurred. The O2 debt is
measured experimentally by determining O2 consumption after exercise until a
constant, basal consumption is reached and subtracting the basal consumption from
the total. The amount of this debt may be six times the basal O2 consumption, which
indicates that the subject is capable of six times the exertion that would have been
possible without it. RIGOR When muscle fibers are completely depleted of ATP and
phosphorylcreatine, they develop a state of rigidity called rigor. When this occurs after
death, the condition is called rigor mortis. In rigor, almost all of the myosin heads
attach to actin but in an abnormal, fixed, and resistant way.
HEAT PRODUCTION IN MUSCLE
Thermodynamically, the energy supplied to a muscle must equal its energy output.
The energy output appears in work done by the muscle, in energy-rich phosphate
bonds formed for later use, and in heat. The overall mechanical efficiency of skeletal
muscle (work done/total energy expenditure) ranges up to 50% while lifting a weight
during isotonic contraction and is essentially 0% during isometric contraction. Energy
storage in phosphate bonds is a small factor. Consequently, heat production is
considerable. The heat produced in muscle can be measured accurately with suitable
thermocouples. Resting heat, the heat given off at rest, is the external manifestation
of basal metabolic processes. The heat produced in excess of resting heat during
contraction is called the initial heat. This is made up of activation heat, the heat that
muscle produces whenever it is contracting, and shortening heat, which is
proportionate in amount to the distance the muscle shortens. Shortening heat is
apparently due to some change in the structure of the muscle during shortening.
Following contraction, heat production in excess of resting heat continues for as long
as 30 min. This recovery heat is the heat liberated by the metabolic processes that
restore the muscle to its precontraction state. The recovery heat of muscle is
approximately equal to the initial heat; that is, the heat produced during recovery is
equal to the heat produced during contraction. If a muscle that has contracted
isotonically is restored to its previous length, extra heat in addition to recovery heat is
produced (relaxation heat). External work must be done on the muscle to return it to
its previous length, and relaxation heat is mainly a manifestation of this work.

5. Mechanical Properties of Contraction Muscle

Twitch Contractions
The mechanical response of a single muscle fiber to a single action potential is
known as a twitch. Following the action potential, there is an interval of a few
milliseconds, known as the latent period, before the tension in the muscle fiber begins
to increase. During this latent period, the processes associated with excitationcontraction coupling are occurring. The time interval from the beginning of tension
development at the end of the latent period to the peak tension is the contraction
time. Not all skeletal muscle fibers have the same twitch contraction time. Some fast
fibers have contraction times as short as 10 ms, whereas slower fibers may take 100
ms or longer. The duration of the contraction time depends in part on the time that
cytosolic calcium remains elevated so that cross-bridges can continue to cycle. It is
closely related to the Ca2- ATPase activity in the sarcoplasmic reticulum; activity is
greater in fast-twitch fibers and less in slow-twitch fibers. Moreover, the
characteristics of an isotonic twitch depend upon the magnitude of the load being

lifted: At heavier loads: (1) the latent period is longer, (2) the velocity of shortening
(distance shortened per unit of time) is slower, (3) the duration of the twitch is
shorter, and (4) the distance shortened is less. A closer look at the sequence of events
in an isometric twitch explains this load-dependent behavior. Following excitation, the
cross-bridges begin to develop force, but shortening does not begin until the muscle
tension just exceeds the load on the fiber. Thus, before shortening, there is a period of
isometric contraction during which the tension increases. The heavier the load, the
longer it takes for the tension to increase to the value of the load, when shortening
will begin. If the load on a fiber is increased, eventually a load is reached that the
muscle is unable to lift, the velocity and distance of shortening will be zero, and the
contraction will become completely isometric. Load-Velocity Relation It is a common
experience that light objects can be moved faster than heavy objects. That is, the
velocity at which a muscle fiber shortens decreases with increasing loads. The
shortening velocity is maximal when there is no load and is zero when the load is
equal to the maximal isometric tension. At loads greater than the maximal isometric
tension, the fiber will lengthen at a velocity that increases with load. The shortening
velocity is determined by the rate at which individual cross-bridges undergo their
cyclical activity. Because one ATP is split during each crossbridge cycle, the rate of ATP
splitting determines the shortening velocity. Increasing the load on a crossbridge slows
its forward movement during the power stroke. This reduces the overall rate of ATP
hydrolysis, and thus the velocity of shortening
Frequency-Tension Relation
Since a single action potential in a skeletal muscle fiber lasts 1 to 2 ms but the twitch
may last for 100 ms, it is possible for a second action potential to be initiated during
the period of mechanical activityThe increase in muscle tension from successive
action potentials occurring during the phase of mechanical activity is known as
summation. A maintained contraction in response to repetitive stimulation is known
as a tetanus (tetanic contraction). At low stimulation frequencies, the tension may
oscillate as the muscle fiber partially relaxes between stimuli, producing an unfused
tetanus. A fused tetanus, with no oscilla tions, is produced at higher stimulation
frequencies. As the frequency of action potentials increases, the level of tension
increases by summation until a maximal fused tetanic tension is reached, beyond
which tension no longer increases with further increases in stimulation frequency. This
maximal tetanic tension is about three to five times greater than the isometric twitch
tension. Since different muscle fibers have different contraction times, the stimulus
frequency that will produce a maximal tetanic tension differs from fiber to fiber. Why is
tetanic tension so much greater than twitch tension? Summation of tension can be
explained in part by considering the relative timing of calcium availability and crossbridge binding. The isometric tension produced by a muscle fiber at any instant
depends mainly on the total number of cross-bridges bound to actin and undergoing
step 2 of the cross-bridge cycle. Recall that even a single action potential in a skeletal
muscle fiber releases enough calcium to saturate troponin, and all the myosin-binding
sites on the thin filaments are therefore initially available. But the binding of energized
crossbridges to these sites (step 1 of the cross-bridge cycle) takes time, while the
calcium released into the cytoplasm begins to be pumped back into the sarcoplasmic
reticulum almost immediately. Thus, after a single action potential the calcium
concentration begins to fall and the troponin/tropomyosin complex re-blocks many
binding sites before cross-bridges have had time to attach to them. In contrast, during

a tetanic contraction, the successive action potentials each release calcium from the
sarcoplasmic reticulum before all the calcium from the previous action potential has
been pumped back into the reticulum. This results in a persistent elevation of
cytosolic calcium concentration, which prevents a decline in the number of available
binding sites on the thin filaments. number of binding sites remains available, and
many more cross-bridges are bound to the thin filaments at any instant. Other causes
of the lower tension seen in a single twitch are elastic structures, such as muscle
tendons and the protein titin, which delay the transmission of crossbridge force to the
ends of a fiber. Because a single twitch is so brief, cross-bridge activity is already
declining before force has been fully transmitted through these structures. This is less
of a factor during tetanic stimulation because of the much longer duration of
crossbridge activity and force generation Length-Tension Relation The springlike
characteristics of the protein titin, which is attached to the Z line at one end and the
thick filaments at the other, is responsible for most of the passive elastic properties of
relaxed muscles. With increased stretch, the passive tension in a relaxed fiber
increases, not from active cross-bridge movements but from elongation of the titin
filaments. If the stretched fiber is released, its length will return to an equilibrium
length, much like releasing a stretched rubber band. The critical point for this section
is that the amount of active tension developed by a muscle fiber during contraction
can also be altered by changing the length of the fiber. The length at which the fiber
develops the greatest isometric active tension is termed the optimal length, lo. When
a muscle fiber length is 60 percent of lo, the fiber develops no tension when
stimulated. As length is increased from this point, the isometric tension at each length
is increased up to a maximum at lo. Further lengthening leads to a drop in tension. At
lengths of 175 percent lo or beyond, the fiber develops no tension when stimulated.
When all the skeletal muscles in the body are relaxed, the lengths of most fibers are
near lo and thus near the optimal lengths for force generation. The length of a relaxed
fiber can be altered by the load on the muscle or the contraction of other muscles that
stretch the relaxed fibers, but the extent to which the relaxed length can be changed
is limited by the muscles attachments to bones. It rarely exceeds a 30 percent
change from lo and is often much less. Over this range of lengths, the ability to
develop tension never falls below about half of the tension that can be developed at
lo.The relationship between fiber length and the fibers capacity to develop active
tension during contraction can be partially explained in terms of the slidingfilament
mechanism. Stretching a relaxed muscle fiber pulls the thin filaments past the thick
filaments, changing the amount of overlap between them. Stretching a fiber to 1.75 lo
pulls the filaments apart to the point where there is no overlap. At this point there can
be no cross-bridge binding to actin and no development of tension. Between 1.75 lo
and lo, more and more filaments overlap, and the tension developed upon stimulation
increases in proportion to the increased number of cross-bridges in the overlap region.
Filament overlap is greatest at lo, allowing the maximal number of cross-bridges to
bind to the thin filaments, thereby producing maximal tension. The tension decline at
lengths less than lo is the result of several factors. For example, (1) the overlapping
sets of thin filaments from opposite ends of the sarcomere may interfere with the
cross-bridges ability to bind and exert force, and (2) at very short lengths the Z lines
collide with the ends of the relatively rigid thick filaments, creating an internal
resistance to sarcomere shortening

6. Neural Control of Muscle Contraction

I. The somatic motor neurons that innervate the muscles are called lower motor neurons.
A. Alpha motoneurons innervate the ordinary, or extrafusal, muscle fibers.
These are the fibers that produce muscle shortening during contraction.
B. Gamma motoneurons innervate the intrafusal fibers of the muscle spindles.
II. Muscle spindles function as length detectors in muscles.
A. Spindles consist of several intrafusal fibers wrapped together. These spindle
fibers are in parallel with the extrafusal fibers.
B. Stretching of the muscle stretches the spindles, which excites sensory endings
in the spindle apparatus.
1. Impulses in the sensory neurons travel into the spinal cord in the dorsal roots of spinal
nerves.
2. The sensory neuron makes a synapse directly with an alpha motoneuron within the
spinal cord, which produces a monosynaptic reflex.
3. The alpha motoneuron stimulates the extrafusal muscle fibers to contract, thus
relieving the stretch. This is called the stretch reflex.
C. The activity of gamma motoneurons tightens the spindles, thus making them
more sensitive to stretch and better able to monitor the length of the muscle, even during
muscle shortening.
III. The Golgi tendon organs monitor the tension that the muscle exerts on its tendons.
A. As the tension increases, sensory neurons from Golgi tendon organs inhibit the
activity of alpha motoneurons.
B. This is a disynaptic reflex, because the sensory neurons synapse with
interneurons, which in turn make inhibitory synapses with motoneurons.
IV. A crossed-extensor reflex occurs when a foot steps on a tack.
A. Sensory input from the injured foot causes stimulation of flexor muscles and
inhibition of the antagonistic extensor muscles.
B. The sensory input also crosses the spinal cord to cause stimulation of extensor
and inhibition of flexor muscles in the contralateral leg.
V. Most of the fibers of descending tracts synapse with spinal interneurons, which in turn
synapse with the lower motor neurons.
A. Alpha and gamma motoneurons are usually stimulated at the same time, or
coactivated.
B. The stimulation of gamma motoneurons keeps the muscle spindles under
tension and sensitive to stretch.
C. Upper motor neurons, primarily in the basal nuclei, also exert inhibitory effects
on gamma motoneurons.
VI. Neurons in the brain that affect the lower motor neurons are called upper motor
neurons.
A. The fibers of neurons in the precentral gyrus, or motor cortex, descend to the
lower motor neurons as the lateral and ventral corticospinal tracts.
1. Most of these fibers cross to the contralateral side in the brain stem, forming structures

called the pyramids; this system is therefore called the pyramidal system.
2. The left side of the brain thus controls the musculature on the right side, and vice
versa.
B. Other descending motor tracts are part of the extrapyramidal system.
1. The neurons of the extrapyramidal system make numerous synapses in different areas
of the brain, including the midbrain, brain stem, basal nuclei, and cerebellum.
2. Damage to the cerebellum produces intention tremor and degeneration of
dopaminergic neurons in the basal nuclei produces Parkinson's disease.

B. Circulation
1. General Plan of Circulation
In the vertebrates the circulatory system is of closed type as blood flows through
the closed blood vessels, while in most invertebrates it is of open type. It is very
simple in fishes but it is of complex type in birds and mammals. In fishes the heart is
two chambered but sinus venosus and conus arteriosus are also found attached to the
heart. Blood from the tissues enters a sinus venosus through the veins.It passes
through a sinu-auricular aperture to the auricle, a relatively thin-walled but large
chamber, thence it is propelled through auriculo-ventricular valve to the ventricle.
Vigrous ventricular contraction forces the blood into the bulbous (or conus) arteriosus
through a third set of valves. In elasmobranchi and dipnoi fishes there are several sets
of valves in the conus.
Blood from the conus arteriosus goes into the gills for oxygenation through blood
vessels and then into dorsal aorta for distribution. Blood from the tissues is collected
by the veins and comes back into the heart. Blood passes through the heart only once
in its complete circuit so this is known as simple circuit
of circulation.
Dipnoi or lung fishes show some advancement in the
circulatory system. In them the heart has become
three chambered as auricle has become partially
divided into right and left auricles. Deoxygenated
blood coming to the sinus venosus enters the right
auricle, while the oxygenated blood coming from the
air bladder enters the left auricle.
In Amphibia and reptiles the heart is three chambered
but to some extent double circulation is maintained.
Birds and mammals have a complete double
circulation. This situation is achieved by the development of the complete ventricular septum, with the pulmonary artery originating
from the right ventricle and a single arota originating from the left.
In birds and mammals the heart is four chambered consisting of two auricles and two
ventricles. From the left ventricle aorta takes its origin which is divided into different
arteries which supply different parts of the body.
Blood from different parts of the body is collected by tiny veins which in turn join to
form larger veins. The veins of the posterior part of the body empty into the inferior
vena-cava, while of anterior region empty into the superior vena-cava.
Both these larger veins empty into the right auricle. The blood from the right auricle

goes into the right ventricle through auriculo-ventricular valve. From the right
ventricle it is pumped into the lungs through the pulmonary artery where it is
oxygenated. After oxygenation blood through pulmonary vein comes into the left
auricle from where it is transferred into the left ventricle from where it is pumped into
the aorta. The blood thus circulates continuously. This type of circulation in which the
blood passes twice through the heart during one complete circuit is called a double
circulation.

2. Types of heart and circulatory patterns

1. Blood moves through the body in a continuous fashion: Left ventricle systemic
circulation (body) right atrium right ventricle pulmonary circulation (lungs)
left atrium left ventricle.
2. Deoxygenated blood is pumped from the right ventricle into the lungs through the
pulmonary arteries the only arteries to carry deoxygenated blood.
3. Blood returns to the heart through the pulmonary veins, the only veins to carry
oxygenated blood.
4. The systemic circulation starts at the left ventricle and ends at the right atrium.
It carries blood to and from the rest of the body.
5. The heart itself receives its supply of blood from the two coronary arteries
leading from the aorta. Blood enters into capillaries that lead to veins through
which blood returns to the right atrium.
6. There are three parts of the systemic circulation that you need to know:
A. coronary circulation - supplying blood to the heart muscle (coronary
artery).
B. renal circulation supplying blood to the kidneys (renal artery). Nearly
25% of the blood leaving the heart flows to the kidneys, which are pressure filters
for waste.
C. hepatic portal circulation- nutrients picked up by capillaries in the
small intestines are transported directly to the liver in the hepatic portal vein,
where excess nutrients are stored. This is about 70% of the livers blood supply.
The liver also receives oxygenated blood from the hepatic artery, which
branches off the aorta, and provides 30% of its blood. All blood leaves the liver
through the hepatic vein

3. Physiologic Properties of the heart

1) Automatic Function = ability to work also after an isolation
Principle - existence of primary centre of automatic function the sino-atrial node
special excitatory system of the heart
Necessity to fulfil some condition (temperature, humidity, supply O2, energ.
substances, transport away- metabolites...)
2) Conductivity
The special conductive system of the heart:
SA node Keith-Flacks node (1907) pacemaker
3 mm wide, 1 cm long in the posterior wall of the right atrium (at the junction of v.
cava sup. with RA). The fibers are only 3-5 microns in diameter.
In atria conductive tissue atrial muscle cells. Velocity 1 m/s +
3 bundles of atrial fibers conducting SA-AV node imp.

Internodal tracts of: 1. Bachman

2. Wenckebacnh
3. Thorel
AV node the atrioventricular node. Conduction in AV node (secondary centre of
automatic function) is slow delay of 0.1 s), velocity of conduction 20 mm/s.
Principle: Existence of junctional fibers and transitional fibers. Principle of a
convergence ansd divergence. Reverberation circuits.
Physiological role: It allows time for the atria to empty their contents into the
ventricles before ventricle contraction begins.
His bundle (v- 4-5 m/s), right/left bundle branches, Purkinje system
Very large fibers. This allows quick - immediate transmission of the cardiac impulse
throughout the entire ventricular system.
Excitation of the myocardium from endocardium to epicardium.
3) The excitability = ability to react to a stimulus
Phases: 1. Normal
2. Absolute refractory period
3. Relative refractory period
4. Supranormal excitability
Refractory phases condition for alternation systole diastole against tetanization
Extrasystoles compensated
- interpolated
Vulnerable period just at the end of the action potential, because stimulation at
this time will sometimes initiate flutter or fibrillation.
Flutter/fibrillation - atrial - ventricular fatal
Defibrillation defibrillator 5-7 kV
4) The contractility = ability of the myocardial fibres to contract
Myosin actin filaments
Tropomyosin, troponin
Excitation Contraction Coupling:
Depolarization - electrical charges, T-tubules, release of calcium ions from the
longitudinal sarcoplasmatic reticulum to promote sliding of the actin and myosin
filaments along each other muscle contraction
All or Nothing Principle of the Heart = stimulation of any single atrial muscle fiber
causes the action potential in entire atrial muscle mass. The same in ventricles.
Syncytial nature of cardiac muscle.
5) Rhythmicity = regular alternation of contraction and relaxation The
HR reflects metabolic rate/weight
birds 800/min
mice 500
men 70
elephant 25-30
whale 10/min

4. Cardiac cycle / Conduction system of the heart

1. The cardiac cycle is the sequence of events in one heartbeat. In its simplest
form, the cardiac cycle is the simultaneous contraction of both atria, followed a
fraction of a second later by the simultaneous contraction of both ventricles.
2.

The heart consists of cardiac muscle cells that connect with each other they
are branched and so when one contracts, they stimulate their neighbours and
they all contract. The heart is an all-or-nothing muscle, getting its rest between
beats. It can only respire aerobically.

3.

A heartbeat has two phases:

Phase 1 - Systole is the term for contraction. This occurs when the
ventricles contract, closing the A-V valves and opening the Semi-Lunar valves to
pump blood into the two major vessels leaving the heart.
Phase 2 Diastole is the term for relaxation. This occurs when the
ventricles relax, allowing the back pressure of the blood to close the semi-lunar
valves and opening the A-V valves.

4.

The cardiac cycle also creates the heart sounds: each heartbeat produces two
sounds, often called lub-dup, that can be heard with a stethoscope. The first
sound is caused by the contraction of the ventricles (ventricular systole) closing
the A-V valves. The second sound is caused by the snapping shut of the Aortic
and Pulmonary Valves (Semi-lunar valves). If any of the valves do not close
properly, an extra sound called a heart murmur may be heard.

5.

Although the heart is a single muscle, it does not contract all at once. The
contraction spreads over the heart like a wave, beginning in a small region of
specialized cells in the right atrium called the Sino-Atrial Node (SAN). This is
the hearts natural pacemaker, and it initiates each beat

6. The impulse spreads from the SAN through the cardiac muscle of the right and
left atrium, causing both atria to contract almost simultaneously.
7. When the impulse reaches another special area of the heart, right in the centre
of the septum, known as the AtrioVentricular (or AV) Node, the impulse is
delayed for approximately 0.2 s. This allows time for the ventricles to fill
completely.
8.

The AV Node relays the electrical impulse down the septum, along the
Bundle of His, to the base of the ventricles. The ventricles then contract
simultaneously, from the bottom upwards, thus allowing them to empty
completely with each beat.

9.

The heartbeat is initiated by the Sino-Atrial Node and passes through the AtrioVentricular Node, remaining at the same rhythm until nerve impulses cause it to
speed up or to slow down. Unlike other muscles, it does not require a new nerve
impulse for each contraction.

10. The autonomic nervous system controls heart rate. The accelerator nerve
of the sympathetic nervous system increases heart rate and the vagus nerve
of the parasympathetic nervous system decreases heart rate.
11. For most people, their resting heart rate is between 60 and 80 b.p.m. During
exercise that can increase to as many as 200 beats per minute for an athlete;
for the rest of us, 150 b.p.m. is about all we can safely manage!
5.

The blood
We have between 4 and 6 litres of blood, the liquid connective tissue that is
the transport medium of the circulatory system. The two main functions of blood are
to transport nutrients and oxygen to the cells and to carry CO2, urea and other wastes
away from the cells. Blood also transfers heat to the body surface and plays a role in
defending the body against disease.
1. Blood is composed of 55% liquid - plasma and 45% cells, almost all of which
are Red Blood Cells (RBCs). together, they transport all the materials around our
bodies that every cell needs to function and the hormones that are an important part
of coordination.
2. Blood also regulates body temperature, pH, and electrolytes, so it is important
in homeostasis.
3. Blood helps to protect us from infection and reduces fluid loss when we are
injured.
BLOOD PLASMA
1. Approximately 55% of blood is made up of plasma, the straw-coloured liquid
portion of blood; it is 90% water and 10% dissolved molecules (mainly plasma
proteins).
2. These can be divided into three types:
a) Albumins - these help to regulate water potential, by maintaining
normal blood volume and pressure. They are the most common plasma protein.
b) Immunoglobins (antibodies) These are very large proteins that
target infection and so cause infected or foreign cells to be attacked by white blood
cells (WBCs). Together with the WBCs they form the immune system.
c) Fibrinogen these are tightly coiled proteins that unwind to form a
blood clot.
BLOOD CELLS
These comprise Red Blood Cells RBCs (also known as haemocytes or
erythrocytes); White Blood Cells (WBCs) of several different types and platelets.
Together, they make up 45% of blood.
RED BLOOD CELLS (RBCs)
1. RBCs are by far the most numerous. One cubic millimetre (one microlitre, or
1l) contains roughly 5 million RBCs. This figure can rise to over 8 million as an
adaptation to living at high altitudes the reason why endurance athletes train at
altitude. The liver destroys excess RBCs on returning to sea-level, so training must
continue until immediately before the event, if possible.
2. RBCs are biconcave disks about 8 across, thus giving them a larger

surface area (Ficks Law), and allowing them to fold up and pass through the
smallest capillaries.
3. They are produced from stem cells in the bone marrow; are full of haemoglobin;
have no nucleus or mitochondria and their function is to transport respiratory
gases. A mature RBC becomes little more than a membrane sac containing
haemoglobin and this gives blood its red colour.
4. RBCs stay in circulation for about 120 days before they are destroyed in the
liver and spleen, giving a turnover rate of about 2 million per second!
WHITE BLOOD CELLS (WBC)
1. These are outnumbered by RBCs approximately 500 to 1 and their numbers
fluctuate, rising during infection and falling at other times. Like the RBCs, they are
formed from stem cells in the bone marrow, but may also reproduce in the lymph
nodes, thymus and spleen. They are larger than RBCs, almost colourless, and do not
contain haemoglobin.
2. WBCs have a nucleus and whilst most live for a few days, others can live for
many months or years, thus providing us with life-long immunity from repeat
infections (memory cells)
3. WBCs protect us from infection and invasion by foreign cells or substances.
Whilst lymphocytes produce antibodies, the other two types of WBC can also engulf
bacteria, in a process called phagocytosis (a form of active transport!).
Granulocytes also produce histamine, which is important in allergies.
PLATELETS AND BLOOD CLOTTING
1. Platelets are not true cells; they are tiny fragments of other cells
megakaryocytes - that were formed in the bone marrow; their lifespan is 7-11 days.
2. Platelets play an important role in blood clotting, by adhering to the site of the
wound and releasing clotting factors known as prothrombin.
3. Clotting factors are part of a cascade reaction which begins with chemicals
released by injured cells and ends with a sticky meshwork of fibrin stop bleeding by
producing a clot.
4. A genetic disorder of Factor VII is called haemophilia, suffers (all male why?)
may bleed extensively from even a small cut or scrape.
5. Unwanted clotting of blood within blood vessels can block the flow of blood a
thrombosis. If this happens in the brain, brain cells may die, causing a stroke; in the
coronary artery, it may cause the death of heart cells a coronary thrombosis.
BLOOD TYPES
1. Blood group is determined by the antigens present on the surface of RBCs.
2. An antigen is a molecule (in this case a carbohydrate) that acts as a signal,
enabling the body to recognize foreign substances in the body.
3. Human blood is classified into 4 main groups: A, B, AB and O. Each can be either
Rhesus +ve or Rhesus ve, giving 8 groups in all.
4. Blood typing is the identification of the antigens in a blood sample. The ABO
system is based on the A and B antigens. It classifies blood by the antigens on the
surface of the RBCs and the antibodies circulating in the plasma.
5. An individual's RBCs may carry an A antigen, a B antigen, both A and B
antigens, or no antigen at all. These antigen patterns are called blood types A, B, AB
and O, respectively.

6. Type AB is known as a universal recipient, meaning that they can receive any
type blood, whilst O is the universal donor, meaning they can donate blood to anyone.
Rhesus system
1. An antigen that is sometimes on the surface of RBC is the Rh factor named
after the Rhesus monkey in which it was first discovered. Of the UK population, 85%
are Rh+ ve, meaning that Rh antigens are present. The other 15% are Rh-ve.
2. If an Rh- person receives a transfusion of blood that has Rh+ antigens, anti-Rh+
antibodies will be formed and will react with the Rh+ antigen and agglutination
(clumping) will occur.
3. The most serious problem with Rh incompatibility occurs during pregnancy. If
the mother is Rh and the father is Rh+, the child may inherit the dominant Rh+ allele
(gene) from the father. The babys Rh+ blood will then get into the mothers blood
during delivery, causing her to develop antibodies to the Rh factor.
4. If a second Rh+ child is later conceived, the mother's antibodies will cross the
placenta and attack the blood of the fetus, causing a condition known as rhesus baby
syndrome. The symptoms include damaged liver and so fewer RBCs, brain (due to
lack of oxygen) and skin.
5. To prevent this, any Rh mother will automatically be given an injection of antiRh+ antibodies (known, confusingly, as anti-D) at childbirth. These antibodies attack
and destroy all Rh+ antigens in the mothers blood, thus preventing her from
becoming sensitised to the Rh+ antigen. This tricks her body into believing she has
not had a Rh+ve child, and so the next pregnancy will be protected from attack, since
she will have no antibodies to Rh+ve blood.