Muscle

Question 1

What Ca2+ pours into when a signal initiated in CNS triggers an AP (can increase in frequency if nerve impulse’s does) in alpha motor neuron that opens the voltage-gated Ca2+ channel

Answer 1

Presynaptic nerve terminal (bouton)

Question 2

Where Ca2+ pours into when increased Ca2+ triggers exocytosis of stored vesicles containing ACh

Answer 2

Synaptic cleft

Question 3

Where Ca2+ pours into when increased Ca2+ triggers exocytosis of stored vesicles containing ACh

Answer 3

Synaptic cleft

Question 4

Once ACh attaches to it, this acts as a ligand-gated nonselective cation channel that allows Na+ & K+ to pass through and depolarizes the postsynaptic membrane

Answer 4

Nicotinic ACh receptor

Question 5

The resulting local depolarization that spreads to the nearby plasma membrane and triggers a muscle AP which propagates down the T-tubules and causes contraction

Answer 5

End-plate potential (EPP)

Question 6

This enzyme rapidly hydrolyzes ACh to acetate & choline in the basal lamina

Answer 6

AChE

Question 7

Transports choline into the presynaptic terminal where choline is then used as a substrate for new ACh synthesis

Answer 7

Choline acetyltransferase

Question 8

When excess ACh is released for triggering muscle AP to ensure that the muscle AP will always be triggered when the nerve AP reaches the presynaptic terminal

Answer 8

Safety factor

Question 9

Where a muscle AP is generated on the sarcolemma by the nerve AP transmission of chain events

Answer 9

Motor end plate (neuromuscular junction)

Question 10

Propagates along the cell surface and reaches deeper inside the myofiber via invaginations of sarcolemma called T-tubules (transverse-tubules) and opens voltage-gated NA+ channel in it linked to Ca2+ channels in terminal cistern

Answer 10

Muscle AP

Question 11

Propagates along the cell surface and reaches deeper inside the myofiber via invaginations of sarcolemma called T-tubules (transverse-tubules)

Answer 11

Muscle AP

Question 12

Part of the sarcoplasmic reticulum (SR), it flanks each side of a T-tubule (this is a triad)

Answer 12

Terminal cisternae

Question 13

Voltage-gated L-type Ca2+ channels activated when the T-tubule is depolarized and allows extracellular Ca2+ to enter the sarcoplasm

Answer 13

DHPRs (dihydropyridine receptors)

Question 14

A Ca2+ channel on the SR membrane opened mechanically by an open DHPRs and allowing large amounts of Ca2+ stored in the SR to enter the sarcoplasm, increase Ca2+, & initiate muscle contraction. Thus, skeletal muscle won’t need to rely on extracellular Ca2+
-in terminal cisterna

Answer 14

Ryanodine receptor (RYR)

Question 15

Troponin T - binds to tropomyosin
Troponin I - binds to actin inhibiting contraction
Troponin C - binds to Ca2+ acting as the regulatory element of Troponin complex

Answer 15

Troponin

Question 16

Has 6 protein subunits, 2 myosin heavy chains form a long helical ‘tail’ and 2 globular ‘heads’.Tail points toward the center of sarcomere to form the M line while the head points to the ends to form the Z disk.

Answer 16

Myosin

Question 17

A very large protein that links the thick myofilament to the Z disks, contributing to the strength & elasticity of the sarcomere.

Answer 17

Titin

Question 18

Actin filaments insert into the Z disk by binding to this

Answer 18

Alpha actinin

Question 19

A specialized plasma membrane region where intermediate filament protein linked Z disks are between. It contains integrin membrane proteins that bind to extracellular matrix proteins (laminin, fibronectin).

Answer 19

Costamere

Question 20

A thick filament that doesn’t change in width throughout the contractile cycle when the sarcomere shortens

Answer 20

A band

Question 21

A non-overlapping region of thin filament that narrows when the sarcomere shortens

Answer 21

I band

Question 22

Non-overlapping region of thick filament that narrows when the sarcomere shortens

Answer 22

H zone

Question 23

Thick and thin filaments slide past each other when sarcomere shortens, pulling the 2 adjacent Z lines closer

Answer 23

Sliding filament theory/ model

Question 24

Hydrolyzes the new ATP and cocks the head

Answer 24

Myosin ATPase

Question 25

A pump using one molecule of ATP to transport 2 Ca2+ molecules into the SR lumen and is the main Ca2+ reduction mechanism distributed throughout the SR membrane.

Answer 25

Sarcoplasmic & endoplasmic reticulum Ca2+ ATPase (SERCA)

Question 26

Helps buffer Ca2+ in the SR which allows a large amount of Ca2+ to be stored inside the SR.

Answer 26

Ca2+ binding proteins (calsequestrin)

Question 27

2 transporters on the sarcolemma that are the 2nd mechanism to reduce Ca2+

Answer 27

Na/ Ca2+ exchanger & plasma membrane Ca2+ ATPase

Question 28

Caused by stretching of various structural elements of the muscle

Answer 28

Passive tension

Question 29

Occurs during the increase (to a certain point) of tension of a muscle due to the shortening of sarcomere while the muscle length is fixed (muscle length variation = contraction force variation)

Answer 29

Isometric contraction

Question 30

Causes the length of the whole muscle to change while the tension of the muscle stays the same

Answer 30

Isotonic contraction

Question 31

The length at which the maximum force is generated, length beyond this point decreases the contraction force

Answer 31

Optimal length

Question 32

When sarcomere length gets too long and the thick & thin filaments are no longer overlapped, preventing crossbridge formation to occur (insignificant compared to cardiac muscle preload)

Answer 32

Length-tension relationship (preload)

Question 33

How fast a muscle shortens at zero load which depends on the rate of crossbridge cycling (depending on the muscle being white or red)

Answer 33

Maximum velocity (y-intercept)

Question 34

The load at which the shortening velocity is at its lowest and cause isometric contraction (zero muscle shortening)

Answer 34

Maximum load (X-intercept = initial length)

Question 35

A contraction at loads higher than the maximum load while muscle lengthens

Answer 35

Eccentric contraction

Question 36

Contraction that starts before the muscle fully relaxes from previous contraction

Answer 36

Tetanus

Question 37

When the muscle has a chance to relax before being stimulated to contract further while in a complete tetanus, the muscle never relaxes until the stimulation ends

Answer 37

Incomplete tetanus

Question 38

Frequency summation, temporal summation, or summation from incomplete tetanus

Answer 38

AP frequency change

Question 39

A Method for changing the force of muscle contraction where more motor neurons are stimulated to participate in the contraction by sending APs to muscle fibers they innervate when more force is needed.

Answer 39

Recruitment

Question 40

The smaller motor units will be recruited 1st before larger motor units are recruited when more force is needed (spatial summation)

Answer 40

Size principle

Question 41

Muscles lengthen by adding more sarcomere in series, which increases their length and allows them to shorten more and with a faster velocity

Answer 41

Growth

Question 42

Increase the # of myofibrils in each muscle cell parallel and increase the maximum force that the muscle can achieve without affecting shortening length or velocity

Answer 42

Hypertrophy

Question 43

Increase the # of myofiber in each muscle in parallel and increase the maximum force that the muscle can achieve without affecting shortening length or velocity

Answer 43

Hyperplasia

Question 44

Parallel running mechanorecptors located in the muscle that sense the length and the rate of stretching (triggers AP) of the muscle

Answer 44

Muscle spindles

Question 45

Senses the tension of the muscles in the tendons of muscles and sends the information to the brain. It’s involved in Bisynaptic reflex arc (Inverse myotatic reflex) that prevents muscle injury by inhibiting the contraction of that muscle. This can also be seen in a reflex seen in some patients called clasp-knife reflex.

Answer 45

Golgi tendon organs (GTOs)

Question 46

Random contractions of the muscle fibers occurring when ACh from presynaptic terminals of the damaged nerve is released

Answer 46

Fasciculation

Question 47

Develops several days after as a result of hypersensitivity to ACh (denervation hypersensitivity) due to the spreading of AChR from motor end plate throughout the membrane and manifests as contractions of the muscle.

Answer 47

Fibrillation

Question 48

Caused by denervation of an affected muscle. Can be reversed if reinnervation occurs within a few months. If reinnervation doesn’t occur the muscle will be replaced by adipose & fibrous tissues (contracture).

Answer 48

Atrophy

Question 49

Picking up EMG (not pathognomonic) using 2 electrodes to detect electrical potential differences.

Answer 49

Compound muscle action potential

Question 50

A pathway for ATP synthesis in muscle cells that uses creatinine phosphate (cp) by converting between cp and ATP. It’s reversible.

Answer 50

Phosphagen system

Question 51

Catalyzes the short conversion of CP to ATP

Answer 51

Creatine kinase

Question 52

Glucose + 2ATP -> 6CO2 + 6H2O + 40ATP

Answer 52

Oxidative phosphorylation

Question 53

Decline in muscle contraction and speed due to changes in the CNS that is related to motor control

Answer 53

Central fatigue

Question 54

Decline in muscle contraction strength and speed due to abnormal transmission of motor command from the motor neuron to the muscle that could be a defect in the motor nerve or the neuromuscular junction

Answer 54

Neuromuscular fatigue

Question 55

Decline in muscle contraction strength and speed due to something inside the muscle itself such as accumulation of metabolites, depleted SR Ca2+ store, diminished energy substrates

Answer 55

Muscular fatigue

Question 56

Contains myosin ATPase that hydrolyzes ATP at a fast speed

Answer 56

White fiber (quick burst of power)

Question 57

Fast oxidative fiber that’s not very susceptible to fatigue but can contract with a faster speed and stronger contraction than type I fibers, utilizing larger motor neurons forming larger motor units.

Answer 57

Type IIa (postural stability)

Question 58

Fast glycolytic fiber that’s very susceptible to fatigue but can contract with a faster speed and stronger contraction than type I fibers, utilizing larger motor neurons forming larger motor units.

Answer 58

Type IIb (postural stability)

Question 59

Actin is anchored by it instead of Z discs located in both the cytoplasm and the plasma membrane.

Answer 59

Dense bodies

Question 60

Small invaginations of the plasma membrane that serve as the equivalent of T-tubules

Answer 60

Caveolae

Question 61

A series of swelling where neurons synapse onto smooth muscle cells at multiple sites

Answer 61

Varicosities

Question 62

Contract independently of its neighbors due to the lack of electrical connection via gap junction. They need neurons that provide fine control to the iris, the ciliary muscles, the vas deferens & the piloerector muscles.

Answer 62

Multiunit smooth muscle

Question 63

Electronically coupled myocytes coupled via gap junctions to perform functional syncytium by the diffusion of ions (and depolarization) for coordinated but less specific contraction of the urinary bladder and GI

Answer 63

Unitary smooth muscle

Question 64

Maintain a level of contractile force for sphincters, airways, and blood vessels

Answer 64

Tonic smooth muscles

Question 65

Contract rhythmically or transiently upon stimulation for the GI, urinary bladder, & uterine wall

Answer 65

Phasic smooth muscle

Question 66

Can be simple spike, post plateau spike, or slow wave and it’s depolarization relies on Ca2+ current (slower) instead of Na+

Answer 66

Smooth muscle APs

Question 67

Post stretch-causing initial contraction gradual relaxation

Answer 67

Stress relaxation

Question 68

Step1 it enters through voltage-gated channels on the membrane

Answer 68

Extracellular Ca2+

Question 69

Step2 it’s released by the binding of Ca2+ RYR (ryanodine receptor), Ca2+ induced Ca2+ release

Answer 69

Sarcoplasmic Ca2+

Question 70

Step3 it’s released from SR by inositol triphosphate (IP3), why the muscle can contract without a change in membrane potential.

Answer 70

2nd messenger-mediated Ca2+

Question 71

Site on the myosin molecule

Answer 71

Smooth muscle regulatory site

Question 72

A Ca2+ binding molecule in the cytoplasm that’s closely related to Troponin C that increases when 4 Ca2+ bind to it

Answer 72

Calmodulin

Question 73

It binds to and activates an enzyme called myosin light-chain kinase (MLCK)

Answer 73

Ca2+-calmodulin complex (CaCM)

Question 74

Phosporylates the regulatory light chin on the neck of myosin which causes confirmational change of the myosin molecule and increases its ATPase activity, allowing it to form crossbridge and the concentration to occur (slow rate myosin ATPase activity)

Answer 74

Myosin light-chain kinase (MLCK)

Question 75

Enzyme required for muscle relaxation by dephosphorylation of the regulatory light chain of myosin

Answer 75

Myosin light-chain phosphatase (MLCP)

Question 76

Can sustain tonic muscle at a high level of tension while keeping the energy expenditure low

Answer 76

Latch state