Justin Cabrera P.6
Muscular system

Major functions of the muscular system

Names of all the skeletal muscles(including the facial muscles)

Neuromuscular junction

Action potential in a muscle fiber

Muscle coverings

3 types of muscles & their functions

Sliding filament theory of muscle contraction

Sarcomere

Disorders

Cardiac

Smooth

Skeletal

Location: Bones, Facial muscles, and skin.

Functions: Propels substance/objects; involuntary control

Description: Single, very long, cylindrical, multinucleate cells with obvious striations

Functions: Propels blood into circulation; involuntary control

Locations: Walls of hearts

Characteristics: Has intercalated discs

Functions: Voluntary movement, locomotion; voluntary control

Description: Multinucleate cells

Locations: Attached to bone or skin

Facial Muscles

Orbicularis Oculi

Frontal Belly

Covers forehead & dome of skull; no bony attachments

Temporalis

Function: Raises the eyebrows, wrinkles forehead skin horizontally

Function: closes jaw, elevates and retracts mandible

Thin, flat, muscle eyelid

Function: Closes eye, blinking, & squinting

Zygomaticus Minor & Major

Muscle pair extending from cheekbone to mouth

Function: Raises lateral corner of mouth

Masteer

Covers lateral aspect of mandibular ramus

Function: Prime mover of jaw closer; elevates mandible

Buccinator

Function: Compresses the cheek

Keeps food between grinding surfaces of teeth

Orbicularis Oris

Multilayered muscle of the lips

Function: Closes lips, protrudes lips

Platysma

thin, sheet like superficial, neck muscle

Function: Tenses skin of neck, helps depress mandible

Covers temporal, frontal, & parietal bones

Skeletal Muscles

Upper half

Lower half

Pectoralis major

Deltoid

Trapezius

Serratus Anterior

Sternocleidomastoid

Rectus Abdominis

Biceps Brachii

Brachioradialis

tricep brachii

Flexor carpi radialis

external oblique

infraspinatus

teres major

latissimus dorsi

extensor carpi radialis

flexor carpi ulnaris

extensor digitorum

bicep femoris

semitendinosus

vastus medialis

semimembranosus

vastus lateralis

tibialis anterior

rectus femoris

extensor digitorum longus

gracilis

fibularis longus

sartorius

gastrocnemius

adductor longus

soleus

iliopsoas

Maintain posture & body position

Stabilize joints

Produce movement: responsible for all locomotion & manipulation

Generate heat as they contract

Duchenne muscular dystrophy

  1. Nervous system stimulates muscle fiber, myosin heads are allowed to bind to actin, forming cross bridges, which cause sliding (contraction)
  1. Cross bridge attachments form and break several times, each time pulling thin filaments a little closer toward center of sarcomein a ratcheting action
  1. During contraction, thin filaments slide past thick filaments, causing actin and myosin to overlap more
  1. Z discs are pulled toward M line
  1. I bands shorten
  1. Z discs become closer
  1. H zones disappear
  1. A bands move closer to each other

Neck muscle

Back muscle

Pectoral muscle

Shoulder Muscle

Abdominal muscle

Abdominal muscle

Bicep muscle

Forearm muscle

Triceps muscle

Forearm muscle

Abdominal Muscle

External Abdominal muscle

Back muscle

Back Muscle

Forearm muscles

Forearm muscles

Forearm muscles

Quadricep muscle

Quadriceps muscle

Quadricep muscle muscle

Quadricep muscle

Quadricep muscle

Quadricep muscle

Quadricep muscle

Hamstring muscle

Epimysium

Endomysium

Perimysium

Contains A band with half of an I band at each end

Consists of area between Z discs

Smallest contractile unit (functional unit) of muscle fiber

Individual sarcomeres align end to end along myofibril, like boxcars of train

Leg muscle

Leg muscle

Leg muscle

Leg muscle

Leg muscle

Leg muscle

Leg muscle

muscle-destroying disease

generally appear during childhood

Disease progresses from extremities upward, finally affecting head, chest muscles, and cardiac muscle.

Caused by defective gene for dystrophin, a protein that links thin filaments to extracellular matrix and helps stabilize sarcolemma

Sarcolemma of DMD patients tear easily, allowing entry of excess calcium which damages contractile fibers

Inflammation follows and regenerative capacity is lost resulting in increased apoptosis of muscle cells and drop in muscle mass

dense irregular connective tissue surrounding entire muscle; may blend with fascia

fibrous connective tissue surrounding fascicles(groups of muscle fibers)

fine areolar connective tissue surrounding each muscle fiber

3.Calcium entry causes release of ACh neurotransmitter into synaptic cleft

4.ACh diffuses across to ACh receptors (𝑁𝑎+chemical gates) on sarcolemma

5.ACh binding to receptors, opens gates, allowing 𝑁𝑎+to enter resulting in end plate potential

  1. AP arrives at axon terminal

6.Acetylcholinesterase degrades ACh

2.Voltage-gated calcium channels open, calcium enters motor neuron

  1. Depolarization

3.Repolarization: restoration of resting conditions

1.Generation of end plate potential

auses chemicallygatedion channels (ligands) on sarcolemma to open

𝑁𝑎+diffuses into muscle fiber

ACh released from motor neuron binds to ACh receptors on sarcolemma

Because 𝑁𝑎+diffuses in, interior of sarcolemma becomes less negative (more positive)

Results in local depolarization called end plate potential

Large influx of 𝑁𝑎+through channels into cell triggers AP that is unstoppable and will lead to muscle fiber contraction

AP spreads across sarcolemma from one voltage-gated 𝑁𝑎+channel to next one in adjacent areas, causing that area to depolarize

If end plate potential causes enough change in membrane voltage to reach critical level called threshold, voltage-gated𝑁𝑎+channels in membrane will open

𝐾+efflux out of cell rapidly brings cell back to initial resting membrane voltage

Refractory period: muscle fiber cannot be stimulated for a specific amount of time, until repolarization is complete

𝑁𝑎+voltage-gated channels close, and voltage-gated 𝐾+channels open

Ionic conditions of resting state are restored by 𝑁𝑎+−𝐾+pump