Muscle Flashcards

1
Q

What is the thin filament made of?

A

Actin polymer and troponin and tropomyosin

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2
Q

What is the thick filament made of?

A

Myosin and myosin heads

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3
Q

5 differences between slow (type 1) and fast twitch fibers:

A

slow fibers are small, are high on mitochondria and myoglobin, do oxidative phosphorylation and are slow to fatigue. Fast twitch fibers are larger, have few mitochondria and myoglobin, do glycolytic pathway (anaerobic) and have low resistance to fatigue

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4
Q

What constitutes the motor unit?

A

motor neuron and muscle fibers it inervates

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5
Q

In the muscle the action potential is perceived by:

A

dihydropyridine receptor (DHP) that interacts with ryodine receptors in the SR causing opening of Ca channels

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6
Q

Isometric contraction is when there is tension of muscle fibers and _______

A

no shortening of the muscle

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7
Q

Where does Ca comes from in the skeletal muscle?

A

Solely from the sarcoplasmic reticulum

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8
Q

What happens after action potential in skeletal muscle?

A

T tubules carry it down and spread action potential, DHP receptors engage ryanodine receptor in SR and cause it to open its Ca release channels which increases intracellular Ca, Ca then binds to troponin C, tropomyosin moves and allows interaction of actin and myosin, subsequent cross bridge cycling (pull and detach) and force generation

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9
Q

What breaks down acetylcholine in receptor neuron?

A

acetylcholinesterase

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10
Q

Contraction _________ the affinity of troponin for Ca

A

increases

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11
Q

What happens during relaxation in skeletal muscle?

A

Ca is returned into SR by active transport by sarco/endoplasmic reticulum Ca-ATPase (SERCA) and calsequesterin in the SR binds Ca and allows more Ca to fit in SR

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12
Q

What can affect neuromuscular transmission?

A

Blocking of Ach release from presynaptic terminal (botulism) (paralysis), blocking of reuptake of choline (thus theres no synthesis of Ach), blocking of nicotinic receptors (curare)

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13
Q

What happens in myasthenia gravis?

A

the body’s own antibodies destroy Ach receptors (thus depolarization does not occur and normal action potential doesn occur in muscle) and causes voluntary muscle weakness, it can be releaved with AChE inhibitors (anticholinesterase) e.g. neostigmine that prevent degradation of Ach in synaptic cleft, thus it prolong its action at the motor end plate

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14
Q

What is the difference between multiunit and unitary smooth muscle cells?

A

multiunit cells all have nervous input (normaly autonomic, e.g. eye and circulatory) and can fire separetely, while unitary are interconnected by gap junctions and not all fibers are innervated so the action potential spreads and act as a unit (have slow waves, e.g. GIT).

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15
Q

What are some characteristics of smooth muscle?

A

are involuntary, are not organized into myofibrils but as overlapping filaments, filaments are tied to dense bodies and do not have troponin

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16
Q

What are the three types of smooth muscles?

A

physically active (have peristaltic movements), normally partially contracted muscle (of blood vessels and airways) and normally contracted for prolonged time and only relax transiently(sphincter muscles)

17
Q

Where can Calcium come from in smooth muscle?

A

Stretch causes opening of Ca channels from extracelular fluid and the increase in Ca concentration causes opening of channels from SR as well, also the binding of neurotransmitters to ligand gated channels allows Ca to enter or they can act as 2nd messenger and cause Ca to be released from SR

18
Q

How does contraction take place in smooth muscle?

A

When intracelular Ca concentration increases, it binds to calmodulin (as there is no troponin) and it activates MLCK (myosin light chain kinase) that phosphorylates myosin exposing myosin heads and allowing contraction

19
Q

How is intracelular Ca concentration reduced in smooth muscle?

A

SERCA pumps Ca into SR, in surface membrane Ca ATPase and Na/Ca exchanger remove it to ECF, when Ca is low myosin phosphatase dephosphorylates the myosin heads

20
Q

What are some distinguishing characteristics of cardiac muscle?

A

The fibers are cylindrical branched, have intercalated disks between fibers (holds them together and have gap junctions that allow spread of AP), purkinje system allows spread of action potential, fibers do not fatigue, have a lot of mitochondria as most energy comes from oxidative phosphorylation

21
Q

Where does Ca comes from in cardiac muscle?

A

AP causes opening of channels from extracecular fluid and from SR, and increase in Ca level causes opening of more channels from SR (Ca induced Ca release)

22
Q

Which 2 types of muscles have troponin?

A

Skeletal and cardiac

23
Q

How is Ca removed in cardiac muscle?

A

By SERCA and Na/Ca exchanger

24
Q

How can the sympathetic NS increase heart rate and force of contraction?

A

Releasing norepinephrine that is bound by adrenergic receptors, it phosphorylates Ca channels, opening and increasing IC concentration

25
Q

How can cardiac glycosides increase force of contraction?

A

Inhibiting Na K pump, thus the Na stays at higher concentration intracelularly for longer and the Na/Ca exchanger works slower since it uses the Na gradient (higher extra) to send Ca out as the Na gradient difference will be lower.

26
Q

What are the main differences of the 3 muscle types?

A

Smooth muscle doesnt have T tubule or sarcomeres while both skeletal and cardiac have. Only smooth and cardiac have gap junctions and can stimulated by hormones, only smooth regulates contraction by phosphorylating myosin, and only in skeletal the Ca comes solely from SR

27
Q

Where does depolarization start in the heart?

A

At sino-atrial node