Download File - Portfolio - Kelly Nicole Boden

The Anatomy and Physiology of Lifting Your Arm
Kelly Nicole Boden
Human Anatomy and Physiology
January 23, 2013
1
R6
Introduction:
There are many seemingly simple actions your body makes every day that appear to be
easy, effortless, and takes no thought. That would be incorrect. Even the simplest action, like
lifting up your arm, is a complex feat of the finely tuned instrument that is your body. This
apparently simple act of lifting up your arm begins in your brain. Your brain is the command
center of your nervous system (the system in charge of telling the other systems what to do). As
soon as you decide that you want to lift your arm up, your brain sends an electrical impulse
through specific nerves to tell the muscles to contract and lift up your arm.
A nerve cell’s membrane is made up of a lipid bilayer; this is formed with two layers of
phospholipids. The external side of the membrane is slightly positive; its internal side is slightly
negative. The main extracellular ion is sodium (Na+), whereas the main intracellular ion is
potassium (K+). The membrane is relatively impermeable to both ions. However, there are
channels in the cell membrane which allow these ions to pass through the membrane. The size,
shape and charge of each channel allow only a certain type of ion to pass through. Other
channels have gates that do not permit ions to pass through it unless it is stimulated. There are
also sodium-potassium pumps and they work like this:
I. 3 Na+ from the intracellular fluid bind to the pump
II. The pump becomes phosphorylated when the 3rd phosphate on the ATP
III. The Na+ are released in to the extracellular fluid and the pump changes shape
IV. 2 K+ from the extracellular fluid bind to the pump
V. The K+ make the pump dephosphorylate and the K+ ions are released in the
intracellular fluid.
A stimulus comes from the brain and is transported through the neurons and their axons to the
intended destination. This stimulus changes the permeability of a “patch” of the membrane, and
sodium ions diffuse quickly into the cell. This changes the polarity of the membrane so that the
inside becomes more positive and the outside becomes more negative. If the stimulus is strong
enough, depolarization causes membrane polarity to be completely reversed and an action
potential is initiated. When the stimulus gets to be around -55 mV, the sodium gates open up and
let the Na+ ions through. More of the sodium channels open because of this and the cycle of
depolarization is created. This is what passes the electrical signal down the axon. Once this
2
depolarization cycle has begun, it continues until the signal reaches the end of the pre-synaptic
nerve cell. Once the cell membrane reaches about +30 mV, the sodium channels close, like
someone shutting their front gate. This prevents the signal from traveling backwards. After the
sodium channel closes, the potassium channel opens as a delayed response to the original
stimulus. The K+ ions move out of the axon and make the membrane rapidly repolarize and
because the K+ channels are slower to close, the membrane is briefly hyperpolarized. In order to
restore the balance of the cell to the resting state of the cell, the sodium/potassium pumps
actively transport sodium ions out of the cell and potassium ions into it.
Axons that are used more frequently for the same task become myelinated. Myelin
sheaths are formed by Schwann cells, and Schwann cells are pretty much a lipid cell layer
wrapped around the axon multiple times. Neurons that have myelinated axons transmit signals
faster than neurons with unmyelinated axons. This is because the sodium, potassium, and
sodium-potassium pumps are located between each Schwann cell; allowing the signal to travel
farther before activating the channels. Fun fact: myelinated axons are harder to retrain.
There is not a single long nerve that travels from the brain to the destination; there are
many nerve cells that form a chain from the brain to the destination. A synapse is a junction
formed by two neurons and allows the neurons to communicate and pass along the signals. The
transmitting neuron is called the presynaptic neuron, and the receiving neuron is called the
postsynaptic neuron. The axon of the presynaptic neuron ends in a synaptic knob that is
practically touching the postsynaptic neuron, but is separated by the synaptic cleft. When the
action potential arrives at the end of the synaptic knob, it triggers the calcium ion channels and
makes them open. This allows Ca2+ to flood into the synaptic knob. The Ca2+ causes the synaptic
vesicles to fuse with the presynaptic membrane. These vesicles store acetylcholine and ACh is
used as the neurotransmitter molecules. The ACh neurotransmitters move across the synaptic
cleft and attach themselves to the acetylcholine receptors that are in the postsynaptic neuron.
These receptors are channels that have gates that are closed until activated by the ACh
neurotransmitters. When the channels open, sodium and potassium diffuse through the
postsynaptic membrane and change the postsynaptic membrane’s potential. The postsynaptic
neuron’s membrane has potassium leak channels that allow K+ to diffuse freely out of the cell.
Once the acetycholine activates the process of depolarization in the postsynaptic cell, they are
then broken down by the enzyme acetylcholinesterase. The choline is absorbed back into the
3
presynaptic neuron and made into new acetycholine in the vesicles in the presynaptic cell. Once
the ACh has been broken down, the gated receptors close again. The sodium-potassium pumps
then work to restore the equilibrium of the postsynaptic neuron. This process is the stimulus that
continues the signal from the brain to the destination site. The signal goes from neuron to neuron
this way.
At the neuromuscular junction, a synapse is formed by a motor neuron and sarcolemma
of a muscle fiber. At this junction, the neuron passes the electrical signal to the muscle cell tells
the muscle cell what to do. The transmitting neuron is called the presynaptic neuron, and the
axon of the presynaptic neuron ends in a synaptic knob that is practically touching the muscle
fiber at the axonal terminal, but is separated by the synaptic cleft. When the action potential
arrives at the end of the synaptic knob, it triggers the calcium ion channels and makes them open.
This allows Ca2+ to flood into the synaptic knob. The Ca2+ causes the synaptic vesicles to fuse
with the presynaptic membrane. These vesicles store acetylcholine and ACh is used as the
neurotransmitter molecules. The ACh neurotransmitters move across the synaptic cleft and attach
themselves to the acetylcholine receptors that are in the muscle fiber membrane. These receptors
are channels that have gates that are closed until activated by the ACh neurotransmitters. When
the channels open, sodium ions diffuse through the muscle fiber’s membrane and depolarize the
postsynaptic membrane. The postsynaptic action potential is made and spreads over the muscle
cell membrane. Once the acetycholine activates the process of depolarization in the muscle fiber
cell, they are then broken down by the enzyme acetylcholinesterase. The choline is absorbed
back into the presynaptic neuron and made into new acetycholine in the vesicles in the
presynaptic neuron. Once the ACh has been broken down, the gated receptors close again. This
is the destination of the brain stimulus sent through the nerves to end with the chemical process
of turning an electrical signal in the presynaptic neuron to an electrical signal in the muscle fiber.
It is very similar to what happens between neuron synapses.
All nerve paths begin in your brain then travel down your spinal cord. Your spinal cord is
like a highway for the nerves. If the signal’s destination is somewhere in the arm, the nerve
impulse would leave the spinal cord at any of the exits between the C4 and T2 bones. It depends
exactly where in the arm the signal is going to determine what exit to take. If the signal is to tell
the deltoid to contract and abduct the arm, then the signal would exit at C5 and C6, go through
the C5, C6 roots to the upper trunk. From the upper trunk, the signal would move to axillary
4
nerve via the posterior division. The axillary nerve then transmits the signal to the deltoid via the
neuromuscular junction.
Once the signal has been passed from nerve to nerve, and nerve to muscle via the
neuromuscular junction, the informed muscle cells contract. Skeletal muscle cells, myofibers, are
long and narrow cells. Interesting fact: because the myofibers are so long, they have multiple
nuclei. The muscle cell is surrounded by a lipid bilayer membrane (sarcolemma); this encloses
the sarcoplasm and the myofibrils. Myofibrils are bundles of contractile proteins. The myofibril
is made up repeating subunits called sarcomeres. The lateral boundaries of a sarcomere are made
with the protein plates, Z discs. In between the Z discs, there are thin filaments and thick
filaments. The thin filaments extend from the Z discs towards the center where they partially
overlap with the thick filaments. The thin filaments are made up of G actin (globular actin) that
attach end to end to form two twisted strands. These two strands are called F actin (fibrous actin)
and nebulin span the length of the F actins and act as measuring sticks for the F actin. To prevent
the F actin from unraveling, the strands are capped on the medial end by tropomodulin, and by
Cap Z on the lateral end. The Cap Z is attached to the Z disc by actinin proteins. When the
muscle fiber is at rest, the G actins are covered by a series of tropomyosin proteins. Assositated
with each tropomyosin is a troponin molecule. This molecule is what helps the muscle
contraction to take place. The thick filaments are composed of myosin molecules. These
molecules are made of two heavy chain polypeptides. The tail of each myosin wrap around the
tails of all the other myosins. At the other end of the heavy chains there are two globular heads
that contain a binding site for actin. These heads are used for moving the thin filaments during
contraction. During the contraction, the myosin heads bind to the G actins in the thin filaments
and pull the thin filaments towards the center of the sarcomere. However, the tropomyosins
cover the F actin binding sites. In order to uncover the binding sites, calcium (C2+) must bind to
the troponin protein complex. This makes the troponin complex to change shape and move the
tropomyosin away from the binding sites. The action potential passes from the neurons through
the neuromuscular junction to the muscle fibers and releases the calcium ions into the
sarcolemma to initiate this contraction process.
The contracting muscles move the bones they are attached to and complete the desired
motion, in this case, lifting your arm up from your side with your palm to the ground. The nerves
5
tell the muscles what to do, but the nerves do not give the energy or nutrients to the muscles that
the muscles need to do their jobs. That is the blood’s job.
Blood is made up of three basic parts. The first part is the red blood cells (RBCs), or
erythrocytes. RBCs make up about 45% of the total blood volume. The second part is the white
blood cells (WBCs), or leukocytes. They only make up about 1% of the blood volume. The final
part is the plasma. Plasma makes up about 55% of the blood volume and is mostly water with
dissolved solutes. These solutes are proteins, nutrients, electrolytes, nitrogenous wastes,
respiratory gases, and regulatory compounds. The RBCs are the oxygen transporters, the WBCs
are the disease fighters, and the plasma is the liquidy thing the RBCs and WBCs travel around
the body through. RBCs have no nuclei or organelles; they are merely temporary hemoglobinfilled vehicles that transport the much-needed oxygen throughout the body. In order for the
RBCs to do their job of exchanging oxygen and carbon dioxide, they need hemoglobin proteins.
These proteins are made up of two alpha subunits and two beta subunits. Each of the subunits
have a heme group surrounded by a long globin polypeptide; two histidine molecules hold the
heme group in place. The hemoglobin bind and release oxygen molecules; this process is what
makes the RBCs red and purple. When the hemoglobin has oxygen, the RBC is red. Once the
hemoglobin releases the oxygen, it turns purple. The RBCs also create and store an enzyme
called carbonic anhydrase. This enzyme converts the CO2 to HCO3. The HCO3 is water soluble
and is released into the plasma until the blood goes back through the lungs where the HCO3 is
converted back into CO2 and exhaled.
The blood travels through arteries to get from the heart to the destination and gets back to
heart through the veins. The arteries branch off and the branches become narrower arterioles.
The arterioles begin branching off and become even narrower capillaries. The capillaries are one
blood cell wide and tiny muscle contractions massage the cells through the capillary network. It
is at the capillary networks that the exchanging of wastes, oxygen, and nutrients occur between
the blood cells and the muscle cells. The blood passes from the arterial capillaries, through the
endothelium, and out the venous capillaries. The venous capillaries converge into venules, and
venules converge into veins which transport the blood back to the heart. There are two
exceptions. They are the pulmonary artery and veins. The pulmonary artery carries unoxygenated
blood from the heart to the lungs, and the pulmonary veins bring the oxygenated blood back to
the heart. So while generally arteries carry oxygenated blood and veins carry unoxygenated
6
blood, the defining factor of what is an artery and what is a vein is whether the blood it carries is
moving away (arteries) or towards (veins) the heart. The heart is a very complex bio-machine
that mixes and controls the oxygenation of the blood. Unoxygenated blood enters the heart
through the superior vena cava and inferior vena cava. The superior vena cava and inferior vena
cava empty the unoxygenated blood into the right atrium. The A-V tricuspid valve opens and the
unoxygenated blood passes from the right atrium to the right ventricle. From the right ventricle,
the blood flows through the pulmonary artery to the lungs. The now oxygenated blood goes back
to the heart through the pulmonary veins. The pulmonary veins empty the oxygenated blood into
the left atrium. The A-V bicuspid valve opens and the oxygenated blood passes into the left
ventricle. The oxygenated blood then leaves the heart via the aorta artery to be sent throughout
the body. Once the oxygen is used up, the blood returns to the heart to repeat the cycle.
7
Summary
The movement in question is the abduction of the arm (it does not matter which) from the
neutral position at the side of the body to the point where the
arm is pronated (palm faces the ground) and parallel to the
floor. In order to do this, the muscles in ‘Table 1: Muscles’ in
the Appendix must be used. A message is sent from your brain
through your motor neurons to the muscles desired. In this case,
the message is for the deltoid and the teres major to contract
and abduct the humerus. The other muscles are used mostly for
stabilization and to keep the forearm pronated.
In order for the muscles to contract, they need nutrients and oxygen. The muscles get
both of these things from the blood supply that flows from the heart to the muscles. The
oxygenated blood flows through arteries to get to the muscles, disperses it’s cargo to the muscle
and get their wastes in the capillary networks. The unoxygenated blood exits the capillary
networks in veins and travels back up to heart to get oxygenated again and repeat the cycle.
8
Appendix
Table 1: Muscles
Muscle Name
Origin
Insertion
Action
Nerve
Blood
Deltoid
tuberosity of
humerus
Abducts arm;
flexion and medial
rotation; extension
and lateral rotation
Axillary
nerve C5,
C6
Posterior
humoral
circumflex
artery; deltoid
branch of
thoracoacromial
artery
Teres Major
Inferior lateral
margin of scapula
Crest of lesser
tubercle
Assists in adduction
of arm, assists in
medial rotation of
arm, assists in
extension of arm
from flexed position
Lower
subscapular
nerve C5,
C6
Thoracodarsal
artery
Teres Minor
Middle half of
scapula’slateral
margin
Lowest of 3
facets of
greater
tubercle of
humerus
Lateral rotaion of
humerus; stabilizes
glenohumeral joint
Axillary
nerve C5,
C6
Scapular
circumflex
artery
Pronator Teres
Humeral head;upper
portion of medial
eicondyle via CFT;
medial brachial
intermusclar septa
ulnar; coronoid
process of ulna;
antebrachial fascia
Laterl aspect
of radius at the
middle of the
shaft
Pronates forearm
Medial
nerve C6,
C7
Muscular
branches of
ulnar and radial
arteries
Triceps Brachii
Long Head: inferior
glenoid tubercle of
scapula
Lateral Head: upper
half of posterior
surface of humerus;
upper half of lateral
intermuscular
septum
Medial Head:
posterior humerus
Posterior
surface of
olecranon
process of
ulna; deep
fascia of the
antebrachium
Long Head: adducts
arm; extends arm at
shoulder; elbow
flexion
Lateral Head:
extends forearm at
elbow
Medial Head:
extends forearm at
elbow
Radial
nerve C6,
C7
Muscular
branches of
brachial artery,
superior ulnar
collateral
artery, profunda
brachii artery
Deltoid
Lateral, anterior 1/3
of distal clavicle,
lateral border of
acromion scapular
spine
9
Base of
proximal
phalanx of
thumb
Extends the
proximal phalanx
and 1st metacarpal
of thumb
Posterior
interosseous
nerve of
radial nerve
C6, C7, C8
Posterior
interosseous
artery
Extends distal
phalanx of thumb,
extends proximal
phalanx of thumb,
assists to extend
hand at wrist
Posterior
interosseous
nerve of
radial nerve
C6, C7, C8
Posterior
interosseous
artery
Extends hand at
wrist
Posterior
interosseous
nerve of
radial nerve
C6, C7, C8
Posterior
interosseous
artery
Extensor
Pollicis Brevis
Posterior surface of
radius, intrerosseous
membrane,
anterbrachial fascia
Extensor
Pollicis
Longus
Posterior surface of
ulna, intrerosseous
membrane,
anterbrachial fascia
Distal phalanx
of thumb
Extensor Carpi
Ulnaris
Lateral epicondyle;
posterior body of
ulna; antebrachial
fascial
Medial side of
base of 5th
metacarpal
10
Works Cited
Mickenberg, Mike. drmikeshap.weebly.com. Web.
http://www.getbodysmart.com/ap/nervoussystem/neurophysiology/menu/menu.html. Web.
http://www.sumanasinc.com/webcontent/animations/content/actionpotential.html. Web.
http://phet.colorado.edu/en/simulation/neuron. Web.
http://www.sumanasinc.com/webcontent/animations/content/synapse.html. Web.
http://msjensen.cehd.umn.edu/1135/Links/Animations/Flash/0009-swf_function_of_th.swf.
Web.
http://bcs.whfreeman.com/thelifewire/content/chp44/4403s.swf. Web.
http://www.youtube.com/watch?v=ZscXOvDgCmQ&safety_mode=true&persist_safety_mode=
1&safe=active. Web.
http://www.getbodysmart.com/ap/muscletissue/fibers/menu/menu.html. Web.
http://www.sumanasinc.com/webcontent/animations/content/muscle.html. Web.
http://www.youtube.com/watch?feature=fvwp&NR=1&v=NRzJjx3ANuE&safety_mode=true&p
ersist_safety_mode=1&safe=active. Web.
http://www.getbodysmart.com/ap/circulatorysystem/menu/menu.html. Web.
11