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Muscle System Jaime Chavez Per #5 - Coggle Diagram
Muscle System
Jaime Chavez
Per #5
FUNCTIONS
Produce movement; locomotion and manipulation
maintain posture and body position
Stabilize joints
Generate Heat
CHARACTERISTICS
Excitability
: receive and respond to stimuli
contractility
: ability to shorten when stimulated
Extensibility
: ability to be stretched
Elasticity
: Ability to recoil to resting length
TYPE
Skeletal Muscle
Description: long, cylindrical, mulitnucleate cells; obious strations.
Function: Voluntary movement/control; locomotion; manipulation of the environment; facial expression
Location: Attached to bones or skin
Cardiac Muscle
Description: Branching, striated, generally unicelulate cells that connect at specialized junctions (intercalated discs)
Function: as it contracts it propels blood into the circulation, involuntary contriol
Location: walls of heart
Smooth Muscle
Description: cells are spindle shaped with central nucleus; no striations.
Function: propels substances or objects along internal passeways; involuntary
Location: Walls of hollow organs
MUSCLE NAMES
Head
Masseter (A)
Orbicularis Oris (A)
Zygomaticus (A)
Orbicularis Occuli (A)
Temporalis (A)
Frontalis (A)
Occipitalis (P)
Neck
Patysma (A)
Trapezius (A) (P)
Sternocleidomastoid (A) (P)
Chest and Abdomen
Pectoralis Major (A)
Serratus Anterior (A)
Rectus Abdominalis (A)
External Oblique (A)
Upper Limb
Deltoid (A)
Biceps Brachii (A)
Brachialis (A) (P)
Pronator teres (A)
Flexor Carpi Radialis (A) (P)
Brachioradialis (A)
Palmaris Longus (A)
Flexor Carpi Ulnaris (A) (P)
Triceps Brachii (A) (P)
Extensor Digitorum (P)
Extensor Carpi Ulnaris (P)
Lower Limb
Upper
Ilipsoas (A)
Pectineus (A)
Tensor Fasciae Latae (A)
Adductor Longus (A)
Gracilis (A) (P)
Sartorius (A)
Vastus Lateralls (A)
Rectus Femoris (A)
Vastus Mediallis (A)
Illiotibial Tract (A)
Gluteus Medius (P)
Gluteus Maximus (P)
adductor Magnus (P)
Semitendinosus (P)
Biceps Femoris (P)
Semimembranosus (P)
Lower
Fibularis Longus (A) (P)
Tibiallis Anterior (A)
Soleus (A) (P)
Gastrocemius (A) (P)
Extensor Digitorum Longus (A)
Calcaneal Tendon (P)
Back
Trapezius (P)
Infraspinatus (P)
Teres Major (P)
Teres Minor (P)
Rhomboid (P)
Latissimus Doris (P)
SARCOMERE
smallest contractile unit of muscle fiber, in myofibril. It's composed of myofilaments. Contains A band in middle and half of an I band on both ends
Actin (thin) Myofilaments
Thon filament is made up of Protein Actin, composed of Gactin subunits that link together to form two long Factin that twist together.
Proteins
Troponin
: a protein that binds to actin, tropomyosin and calcium ions, responsible for pulling tropomyosin out of the bending sites.
Tropomyosin
: a regulatory protein that covers myosin bending site in actin subunits when a muscle is relaxed
Extends across I band and part way in A band; anchored to Z line
Hexagonal arrangements of one thick filament surrounded by six thin filaments.
Myosin (thick) myofilament
composed of protein myosin that contains two heavy and four light polypeptide chains
Heavy chains: intertwine to form myosin tail
Light Chains: form two myosin heads
Extend length of A band. Connected at M line
titin (elastic) filaments
holds thick filaments in place, helps recoil. attached to Z line
NEUROMUSCULAR JUNCTION
Anatomy
Axon terminal
Axons are elongated extensions of motor neurons that travel from central nervous system to skeletal muscle.
Each Axon divides into many branches as it enters muscle, they end on muscle fiber.
Axon terminal is the end of an axon where the neuromuscular junction is
Within Axon terminal, there are membrane bound synaptic vesicles that contain neurotransmitters acetylcholine (ACh)
synaptic cleft
Separate muscle fiber and axon terminal
junctional folds
infoldings of sarcolemma that contain millions of ACh receptors
Events
1) An action potential travels down the axon motor neuron into the axon terminal
2) Calcium channels open and calcium defuses into the axon
3)The Calcium causes the synaptic vesicles to release acetylcholine (Ach) neurotransmitters into the synaptic cleft
4)Ach binds to receptors (Na and K channels) on sarcolemma and opens them
5) Sodium ions (Na) enter the muscle fiber, and Potassium Ions (K) exit the muscle fiber
6) An action potential travels into the sarcolemma (resulting in an end plate potential)
7)ACh is removed from the Ach receptors and it is broken down by Acetylcholinesterase into Acetic acid and Choline, choline, then transports back into axon terminal
DISORDERS
muscular dystrophy
Muscle weakness and atrophy
Caused by: genetics,and mutations
The symptoms are: mental retardation, weakness, atrophy and eyelid dropping
fibromyalgia
Muscle pain
Caused by: Unknown, physical trauma, disturbances, infection.
The symptoms are: pain, tenderness, fatigue, depression
myasthenia Gravis
Neuromuscular disorder that blocks neurotransmitters
Causes are: autoimmune, tumor and age
Symptoms are: muscle weakness, breath problems, chewing and swelling difficulty, and paralysis.
Cerebral Palsy
Spatic paralysis causing muscle weakness
Caused by: brain injury, hypoxia during premature pregnancy, infection, and bleeding
The symptoms: delayed development, tightness, abnormal gait, and paralysis
myositis
inflammation of the muscle
caused by being autoimmune, infections, medication induced, and muscle traume
The symptoms are muscle weakness, swealing, tenderness and fatigue.
SLIDING FILAMENT THEORY
During contraction thin filaments slide past tick filaments, causing actin and myosin to overlap
When a calcium ion binds to troponin in thin filaments it pulls tropomyosin off the myosin-binding sites of actin, so myosin can bind to actin and cause contraction
neither filaments change length, just overlap
when nervous system stimulates muscle fiber, myosin heads are allowed to bind to actin forming cross bridges.
Cross bridge attachments form and break several times.
Z discs are pulled toward M line, I bands shorten, Z discs become closer, H zone disappear, A band move closer to each other
ADP and P are released from myosin, which causes the myosin to move. Then ATP binds to myosin causing it to release the Actin reverting ATP into ADP and P.
ACTION POTENTIAL (MF)
1) Generation of end plate potential
1) ACh released from motor neuron binds to ACh receptors on sarcolemma
2) Causes chemically gated ion channels (ligands) on sarcolemma to open
3) 𝑁𝑎 + diffuses into muscle fiber, Some 𝐾 + diffuses outward, but not much
4) Because 𝑁𝑎 + diffuses in, interior of sarcolemma becomes less negative (more positive)
5) Results in local depolarization called end plate potential
2) Depolarization
1) If end plate potential causes enough change in membrane voltage to reach critical level called threshold, voltage-gated 𝑁𝑎 + channels in membrane will open
2) Large influx of 𝑁𝑎 + through channels into cell triggers AP that is unstoppable and will lead to muscle fiber contraction
3) AP spreads across sarcolemma from one voltage-gated 𝑁𝑎 + channel to next one in adjacent areas, causing that area to depolarize
3) Repolarization
1) 𝑁𝑎 + voltage-gated channels close, and voltage-gated 𝐾 + channels open
2) 𝐾 + efflux out of cell rapidly brings cell back to initial resting membrane voltage
3) Refractory period: muscle fiber cannot be stimulated for a specific amount of time, until repolarization is complete
4) Ionic conditions of resting state are restored by 𝑁𝑎 + −𝐾 + pump. 𝑁𝑎 + that came into cell is pumped back out, and 𝐾 + that flowed outside is pumped back into cell
MUSCLE COVERINGS
Epimysium
dense irregular connective tissue surrounding entire muscle; may blend with fascia
perimysium
Fibrous connective tissue surrounding fasciacles, group of muscle fibers
Endomysium
Fine areolar connective tissue surrounding each muscle fiber