Anatomy/Physiology: Vocab – Chapter 7



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Anatomy/Physiology: Vocab – Chapter 7
Epimysium Perimysium

Fascicles Endomysium

Sarcoplasm Sarcolemma

Transverse tubules (T tubules) myofibrils

Myofilaments thin filaments

Thick filaments sarcoplasmic reticulum (SR)

Sarcomeres Z line

M line A band

I band Tropomyosin

Troponin Cross bridges

Synaptic terminal Acetylcholine (ACh)

Synaptic cleft End plate

Acetylcholinesterase (AChE) Tension

Resistance Compression

Twitch Latent period

Contraction phase Relaxation phase

Summation Incomplete tetanus

Complete Tetanus Motor units

Recruitment Muscle tone

Atrophy Isotonic contraction

Isometric contraction Cretine phosphate

Cretine phosphate kinase (CPK or CK) Glycolysis

Muscle fatigue Recovery period

White muscles Red muscles

Anaerobic endurance hypertrophy

Aerobic endurance Intercalated

Pacemaker cells Origin

Insertion Action

Primary action Prime mover (agonist)

Antagonist Synergist

Fixators Axial musculature

Appendicular musculature Perineum


Anatomy Memorization: Chapter 7
Figure 7-1 page 186

Figure 7-2 page 188

Figure 7-3 page 189

Figure 7-4 page 191

Figure 7-5 page 192-193

Table 7-1 page 194

Figure 7-11 page 205-206

Table 7-3 page 207


Teacher’s Notes: Chapter 7

Types of Muscle tissue

  1. Skeletal

  2. Cardiac

  3. Smooth


Functions of skeletal muscle

  1. Movement of skeleton

  2. Maintain posture and body position

  3. Support soft tissue

  4. Guard entrances and exits (swallowing, defecation, urination)

  5. Maintain temperature (energy releases heat so movement maintains temp)


Anatomy of a skeletal muscle

GROSS Anatomy

  1. Connective tissue organized (SEPERATED)

    1. Epimysium- surrounds entire muscle

    2. Perimysium – divides muscle fibers

    3. Fascicle – Bundle of muscle fibers

    4. Endomysium – IN fascicle divides EACH muscle fiber

    5. Tendon (connective tissue…collagen fibers…where epi, peri, and endomysium come together.)

  2. Blood Vessels and Nerves


Microanatomy (different than other cells…large, multinucleated)

  1. Sarcolemma and Tubules

    1. Sarcolemma (cell membrane)…Sarkos (flesh)

    2. Sarcoplasm (cytoplasm)

    3. Transverse Tubules (T TUBULES) – contain extracellular fluid and help coordinate contractions

  2. Myofibrils (100s to 1000s of these make up the muscle fiber (cell)…myofibrils are bundles of:

    1. Myofilaments (thin and thick)…RESPONSIBLE for muscle contractions

      1. Thick = myosin molecules

      2. Thin = actin, tropomyosin, troponin




  1. Sarcoplasmic reticulum = SMOOTH ER (in specialized form)…network around myofibril

    1. Terminal cistern = ENDS at T tubules (calcium ions stored here…contraction begins when calcium released)

    2. Triad = 2 terminal cistern and 1 T tubule




  1. Sarcomeres – Repeating UNITS on myofibrils…Z line to Z line

    1. Z line = boundaries of sarcomeres (made of thin filaments)

    2. M line = Myosin that connects thick filament to neighbor

    3. A band (thick filaments)…dArk…A is thicker than I

    4. I band (thin filaments)…lIght…I is thinner than A




  1. Thin and Thick filaments

    1. Thin

      1. Actin with ACTIVE site

      2. Tropomyosin (turning)

      3. Troponin (holds tropomyosin together)

    2. Thick

      1. Myosin…each has a tail and head…heads out to interact with active site of actin.

    3. MUSCLE CONTRACTIONS

      1. Calcium unlocks the active site and starts a contraction.

      2. Calcium binds to troponin

      3. Troponin changes shape and swings away from tropomyosin

      4. Tropomyosin then moves to reveal active site

      5. Myosin BINDS and contraction begins.




  1. Sliding filament/Cross bridges (Sliding filament theory)

    1. I band gets smaller because Z lines move closer to each other.

    2. A band does NOT move

    3. Cross bridges are connected myosin heads…it PULLS the thin filaments toward the center of the sarcomeres.

Skeletal muscles fibers ONLY contract under control of nervous system using neuromuscular junctions.


1. Motor neuron – the nerve cell that controls muscle fiber contraction.

a. A single axon branches into perimysium and ends in a

synaptic terminal. (THIS communicates with the

neuromuscular junction)


I. Acetylcholine (ACh) is in terminal (also mitochondria for energy….it is a neurotransmitter (a chemical released to comm. With another cell)
II. Synaptic cleft separates terminal from sarcolemma
III. End Plate – the membrane portion of sarcolemma

that has receptors for ACh.


IV. Acetylcholinesterase (AChE) enzyme in BOTH

cleft and plate to break down ACh.


V. Action potential electrical impulse in sarcolemma.
PROCESS of muscle contraction initiation:

1. Action potential at synaptic terminal

2. ACh released from terminal when potential reaches terminal

3. ACh binds to motor end plate on sarcolemma…to change permeability to sodium ions and they RUSH into sarcolemma…THIS produces action potential in sarcolemma

4. Action potential at sarcolemma spreads triggers calcium ion release by terminal cisternae.

Next: Calcium initiates exposure of active site on thin

filaments (EVERY cisternae on EVERY myofibril)

Next: Cross bridge with myosin and actin
Contraction Cycle
Resting sarcomere – cross bridges are bound by ADP and a phosphate. (Potential energy here…PRIMED, setting the mousetrap)
1. Active site exposed as calcium binds to troponin

a. Tropomyosin BLOCKS active site and troponin holds it in place. (Calcium makes troponin TURN so that tropomyosin is no longer blocking active site)

2. Myosin cross-bridge forms and attaches to active site

3. Head pivots to center of sarcomere…ADP and P released (energy used)

4. Cross-bridge DETACHES as myosin binds another ATP.

5. Head reactivated as ATP captures released energy and cycle begins again.
NOTE:

Calcium moves to normal levels as it moves back into sacroplasmic reticulum.

Short contraction = a single action potential

Long contraction = numerous action potentials one after another.


Tension = an active force caused by collagen fibers being pulled by muscle cell contraction.
Resistance – must be overcame to apply tension…opposes movement
Compression – a push applied to an object…forces an object away from compression.

NOTE: muscles can only contract and relax they do NOT lengthen


So tension depends on the number of cross-bridges it contains.

1. Frequency of neural stimulation

2. Number of muscles fibers activated.
Tension varies depending on

1. Fiber’s resting length and degree of overlap of thick and thin filaments

2. Frequency of stimulations (amount of calcium present)
Twitch – a single stimulus contraction relaxations sequence in a muscle fiber.
Myogram – graph that plots a twitch
A TWITCH

Latent period – begins stimulation when action potential sweeps sarcolemma but NO tension produced yet.

Contraction phase - tension rises to peak

Relaxation phase – tension decreases as calcium levels drop

NOTE: A twitch does NOTHING, you need repeated stimulation to produce a muscle contraction


Summation – addition of one twitch to another…A SECOND comes before the first relaxation is complete thus BUILDING
Incomplete tetanus – produces ALMOST peak tension during rapid contraction and relaxation….ALMOST ALL contractions involve this
Complete tetanus – relaxation is completely eliminated…action potential comes so fast the sarcoplasmic reticulum has no time to reclaim calcium.
Motor unit – a single motor neuron and the muscle fibers it controls.

1. If we need LOTS of control (eyes) one motor neuron only controls 2-3 muscle fibers

2. If LESS control needed one motor neuron may have 2000 fibers to control.

Motor neurons use recruitment with more and more units being used starting with the smaller units first. THESE are intermingled so forces applied are balanced


Muscle tone – resting tension of muscles
Atrophy – muscle fibers become weak and smaller due to lack of motor neuron stimulation (NO USE)
Isotonic contractions – (iso = equal…tonos – tension) muscles LENGTHEN, Tension remains constant until relaxation…walking, running, and lifting
Isometric contractions (metron – measure)…muscle does NOT change length…tension exceeds resistance (pushing against a wall)
Muscle elongation = passive

Contraction = active

Elongation achieved by:

1. Elastic forces – Fibers of endomysium, perimysium, perimysium, and tendons are elastic and recoil.

2. Opposing muscles – biceps brachii and triceps brachii

3. Gravity – example, pulling arm down after bent contraction.


ATP NOT stored so transfers energy to creatine
ATP + creatine  ADP + creatin phosphate (a high energy molecule)
SO, IT’S LIKE AN EXTRA RESERVE OF PHOSPHATES
Creatine phosphate kinase (CPK or CK) does this….kinases phosphoralate things THAT IS THEIR JOB.
NOTE: When muscles are damaged they leak CPK into bloodstream…this indicates muscle cell damage (heart or skeletal muscles)
Glycolysis is anaerobic…if the mitochondria involved = cellular respiration if NOT is lactic acid fermentation.
AEROBIC metabolism

1. Glycolysis

2. TCA (tricarboxylic acid cycle)…Krebs cycle

3. Electron transport chain…17 ATP for each Pyruvic acid (approx 34 per glucose molecule)


SO, in resting muscles we use fatty acids for ATP production and Glucose becomes glycogen for storage

BUT in activity, Glycogen is broken down to glucose which is broken to Pyruvic acid for more ATP production (cellular respiration)

THIS IS LIMITED BY AVAILABIILTY OF OXYGEN
Glycolysis – breaks glucose to pyruvic acid…SO muscles first use

1. Available ATP

2. Then CP

3. THEN break glycogen to glucose and Pyruvic acid.

4. When NO more oxygen available then glycolysis WITHOUT mitochondria for ATP

a. Problem…pyruvic acid is converted to lactic acid

b. his lowers pH and alters key enzymes in body

c. Because of alteration, muscle fibers cannot continue to contract

d. causes muscle soreness

e. Also can’t produce as much ATP


Muscle fatigue – exhaustion of energy reserves OR lactic acid build up
Recovery period – time for muscle to return to normal levels of energy reserves (heat generated during this time)
Lactic Acid Recycling – presence of incoming oxygen helps convert lactic acid BACK to pyruvic acid….Oxygen demands remain elevated because of oxygen debt…more needed by liver (to produce ATP) more by sweat glands
Heat loss – muscles generate heat…shivering keeps us warm
Muscle performance described in terms of

1. force – max amount of tensions produced

2. endurance – max time of performance

These are determined by types of muscle fibers


TYPES of skeletal muscle fibers:

1. Fast twitch fibers – contract quickly following stimulation

a. They are LARGE in diameter

b. Densely packed myofibrils

c. large glycogen reserves

d. FEW mitochondria

e. Sprinters have more of these

2. Slow twitch fibers

a. ½ the diameter of fast

b. 3 times longer to contract after stimulation

c. continue contracting for extended periods

d. THREE things make oxygen use more effective

I. Oxygen supply (larger network of capillaries)

II. Oxygen storage (have red pigment myoglobin for oxygen

carrying.

III. Oxygen use – MORE mitochondria

e. Long distance runners have more of these


White muscles = more fast twitch (chicken have more because of wing use to flee)

Red muscle - slow fibers – Chickens walk all day so dark meat on legs
Anaerobic endurance – supported by glycolysis, ATP and CP (50 yard dash) – Fast twitch muscles to perform brief intense work (weight lifting)…Hypertrophy – BULKING of muscles and fiber increase in diameter
Aerobic endurance – length of time while supported by mitochondrial activity…sustained low levels of muscular activity, swimming, jogging (glucose the preferred energy source so carbs or energy drinks used
Muscle tissue

  1. Cardiac

    1. Small

    2. Single nuclei

    3. Intercalated discs (gap junctions for communication and contraction)

    4. Striated (not as organized as skeletal)

    5. Automaticity (contract WITHOUT neural stimulations – instead have pacemaker cells)

    6. Contractions are 10 times longer than skeletal muscles

    7. Membranes different so don’t undergo tetanus VERY important

    8. Action potential triggers calcium AND increases permeability to extracellular calcium

    9. AEROBIC metabolism for CONSTANT energy requirements

    10. Lots of myoglobin for oxygen storage

  2. Smooth

    1. Smaller

    2. Single nuclei

    3. Spindle shaped cells

    4. NOT striated

    5. Regulate blood flow through vital organs (remember they surround vital organs

    6. Sphincters in RINGS for passage in internal digestive and urinary systems

    7. Structural differences

      1. Lack myofibrils, sarcomeres (so no striations)

      2. Thick filaments are scattered

      3. Thin filaments are anchored to Sarcolemma

      4. Cells are bound together are anchoring sites to transmit contractile forces

    8. Functional differences

      1. MOST calcium from extra cellular fluid

      2. Can contract over greater rang of lengths than others muscles because actin/myosin NOT rigidly organized…GREAT for large volume changes. (Bladder, stomach)

      3. PACESETTER CELLS – not MOTOR NUERONS FOR CONTRACTION….in response to environment

      4. NOT voluntary control

  3. Skeletal (studied previously)


Anatomy of Muscular system

Muscles begin at:

  1. Origins

  2. Insertions…determine the specific

  3. ACTION

Almost all originate or insert on the skeleton
Actions are described in two main ways

  1. Terms of BONE effect…biceps brachii “Flexion on forearm”

  2. Terms of human movement…biceps brachii “flexion at the elbow” (used by specialists)


Primary actions

  1. Prime mover (agonist) – muscles that are chiefly responsible for producing a particular movement (ex. Biceps brachii)

  2. Antagonists - oppose the movements of other muscles….may be prime movers (triceps brachii)

  3. Synergist – HELPS prime movers

    1. Can provide additional pull.

    2. Fixators – stabilize origin of prime movers to prevent joint movement


POSSIBLE ESSAY Questions – Ant Phy Chapter 7

  1. Mary wants to enter a weight-lifting competition and consults you as to what type of muscle fibers she needs to develop and how she should go about it. What would you suggest to her?




  1. When unloading her trunk, Amy pulls a muscle and as a result has difficulty moving her arm. The doctor in the emergency room tells her that she pulled her pectoralis major. Amy tells you that she thought the pectoralis major was a chest muscle and doesn’t understand what that has to do with her arm. What would you tell her?




  1. An unidentified body is found outside of Ely and a forensic specialist determines the time of death was as recent as 15-25 hours before discovery of the body. When asked how they can determine such accurate measurements, the specialist explains that the time of a murder victim’s death is commonly estimated by the flexibility of the body. Your friend is still confused over this response. Explain why this is possible.



  1. Many ions, fibers, molecules are involved in the contraction of a muscle fiber. Explain what you would expect to happen to a resting skeletal muscle if the sarcolemma suddenly became very permeable to calcium ions particularly.










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