Muscle Pt. 7 (Cardiac-EC coupling/relaxation/contracile vs autorythmic)

Question 1

What is the funciton of cardiac muscle?

Answer 1

to contract & create pressure gradient to allow bloodflow

Question 2

Cardiac muscle made of cardiac myocytes, which are __ myofibrils than SM

Answer 2

shoerter fibers, stacked on top of eachother

Question 3

Cardiac myocytes are . . .

Answer 3

branched cells that usually only have 1 nucleus

Question 4

Cardiac muscle is interconnected by _____. What is the benefit? (what 2 parts make these up?)

Answer 4

connected via interclated disks = seperate cells
interclated disks = allows uniform contraction in chamber
1. desmosomes = link cells mechanically
2. gap junctions = links cells electrically

Question 5

T/F Cardiac muscle is not straited

does it have thick/thin filaments?

Answer 5

False - cardiac muscle = striated with similar thin/thick filamnts

Question 6

Do cardiac muscle have T-tubules?

Answer 6

Yes, less abundant (compared to SM) but do form a network

T-tubules run un random directions (unlike SM = only parralel)

Question 7

Cardiac muscle has a ___ SR compared to SM

Answer 7

smaller SR

Cardiac muscle requires the entry of EXTRACELLULAR Ca+ = doesn’t need Ca storage

Question 8

Cardiac muscles relationship to mitochondria

Answer 8

mitochondria make up 1/3 of cell volume
allows cardiac to use oxidative metabolism for ATP protuctino

Question 9

T/F cardiac muscle perform a lot of work contineuosly

Answer 9

True = contact about 3 billion times in lifespan

Question 10

Is contraction started by nueros in cardiac muscle?

Answer 10

No!!! nueral input in cardiac can only MODIFY contraction not CREATE it (unlike SM)

Question 11

Skeletal muscle has a __ AP within its __ period.

Answer 11

SM = brief AP in latent period
allows for multiple AP to be generated and summed for greater tension

Question 12

Cardiac muscle has ___ AP and a ___ period

Answer 12

Cardiac muscle = eleongated AP & refractory period
long AP prevents summation of AP within the same period (would lead to more contraction force) & we need the heart to relax between contractions

Question 13

How does EC coupling in cardiac muscle differ from that of skeletal?

Answer 13

Cardiac = L-type Ca+ channels (DHP channels) are NOT linked to RyR receptors —> DEPENDING on Ca+ entry from EXTRACELLULAR for contraction

SM = they were linked

Question 14

Through what proccess is extracellular Ca+ aquired in cardiac muscles

Answer 14

Ca+ induced Ca release

Question 15

How is relaxation done for cardiac muscle?

Answer 15

Cardiac muscle needs to return about 10% of Ca+ signal it received from the extracellular space
and return 90% of Ca signal it received from SR

Question 16

What is the primary mechanism of cardiac muscle relaxation?

Answer 16

reuptake into the S is still the primary method

Question 17

How does Ca+ uptake into SR differ in cardiac from skeletal?

Answer 17

skeletal = SERCA pump allways highly active
cardiac = SERCA pump controled by phospholamban (phosphorylated = high uptake = fast relax & unphosphorylated = low uptake)

Question 18

How do you enhance contractile force in cardiac muscle?

how does this differ from skeletal muscle?

Answer 18

Cardiac
1. increase in intracellular Ca+ in myocytes = increase force (due to graded single twitch capability, low cystolic Ca+ level, and increased Ca+)
2. Length tension relationship = cardiac muscle generaters a greater force when slighly streched (ulike optimal length of skeletal)

skeletal muscle force was increased via increase in AP = summation/tetanus

Question 19

Exaplain how nueronal input on the Cardiac muscle (the heart) can modify conduction/contraction

Answer 19

Heart is intervated by the autonomic nervous system
Sympathetic activity/input (fight/flight) = controls both autoryhtmic cells (increase heart rate/conduction) and contractile cells (increase in contracility)
Paraysympathetic input (rest) = controls ONLY autorythmic (decrease heart rate/conduction)

symp imput (active) = increase heart rate/conduction (autorythmic) & increase contractility (contractile)
parasymp input (rest) = decrease heart rate/conduction (autorythmic)

Question 20

List 4 mechanisms that create an increase/start sympathetic modulation in Cardiac

Answer 20

1. increased extracellular Ca+ entering (increase conductance via phosphorylation of L-type Ca+ chanels)
2. increase release of Ca+ from SR (via phosphorylization of RyR receptors)
3. Increase rate of myosin ATPase
4. Increase Ca+ reuptake speed (via phosphorylation of SERCA pump)

Question 21

2nd way to increase force in cardiac

What is the Cardiac length tension releationship?

Answer 21

ability of cardiac to make more contraction even when lightly streched (unlike optimal SM length)
1. strech -> smalled diameter –> shortens travel time for Ca+ across
2. strech –> adds more tension on stress-activated Ca= channels = increase Ca+ entry from Extracellular

Question 22

What is the normal instrinsic firing rate of autorythmic cells without autonomic input?

Answer 22

90 AP/min for auto cells in SA node (sympa input = increase ) (parasympa = decrease)
in resting state, parasmpatheitc is more dominant = 70-72 BPM

Question 23

What is the normal instrinsic firing rate of autorythmic cells without autonomic input?

Answer 23

90 AP/min for auto cells in SA node (sympa input = increase ) (parasympa = decrease)
in resting state, parasmpatheitc is more dominant = 70-72 BPM

Question 24

How does parasympathetic input modulate pacemaker activoty?

Answer 24

they decrease frequency of AP at the SA and AV node = decrease heart rate there
= act as decrease in conduction veloiity at AV node

Question 25

parasypathetic modulation of pacemaker activty

Name 3 mechanisms that decrease conduction velocity at AV node?

Answer 25

1. slow opeing of HCN chanenels (vs fast)
2. opening of K+ GIRK channels
3. block T-type Ca+ channels

Question 26

List 3 ways that sympathetic input can modulate pacemaker activity

Answer 26

1. activate beta1 adregenic receptors (by NE/Ep) –> increase Na & Ca entry through channels –> cells reach threshold faster –> with a decreased level of repolarization = RAPID AP firing