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Contraction of Cardiac Muscle
VCU PHIS 501 Setember 30, October 1, 2010

Additional Physiology Flashcards




Basic differences between cardiac and skeletal muscle contraction

1) Action potential duration is much longer in the heart

2) fewer myofibrils so force per cross sectional area is less

3) Cardiac sarcoplasmic reticulum has a smaller volume, but cardiac muscle has more mitochondria

4)  Tranverse tubules form diads and are much wider, present at each z-line in the ventricle, sparse in the atria, and absent in the purkinje fibers

5) cardiac fibers are interwoven, fibers run circumferentially, app. 45° (helically arranged)

Excitation-Contraction Coupling

1) Action potentional spreds over surface and comes down t-tubules

2) Ca enters during the plateau of the action potontial (DHP receptors)

3) Ca induced Ca release- RyR allows SR to release Ca- amount dependent on amount of Ca that came into the cell and the amount of Ca stored in the SR

4) Intacellular Ca concentration  increases- primarily due to SR release

5) Ca binds to Trop-C

6) contraction occurs

7) Ca reaccumulation by SR

8) Relaxation

Ca regulation

Influx: Ca Current

Efflux: Na-Ca exchanger is high capacity low efficiency, and sarcolemmal Ca pump is low capacity, high affinity


The SR uses the Ca-ATPase to pump Ca back into the SR.  Increasing the cytoplasmic Ca will increase the SR Ca store.  The efflux mechanisms become overloaded and the SR makes up the differece by taking up more than it released.


Mitochondria can also take up SR, but its physiologically insignificant.

Action potential duration and contraction

-Action potential duration less than ≈150msec decreases contractile force

-Decreased action potential duration means that less Ca comes into the cell; so there is a smaller trigger for SR Ca release and also less Ca for the SR to take up so a smaller SR Ca store

-Further shortening results in a graded decrease in force.

Mechanisms modulating contractile force

-Length of the muscle

-Contractility (ability of the muscle to increase force independent of muscle length)


-Contractile force is proportional to the number of cross-bridges that cycle and therefore split ATP.  Which depends on the number of strong actin-myosin complexes (length) and the function of tropinin-C bound to Ca (contractility)


Contractile force= length x contractility

Mechanisms that alter contractility

1) amount of calcium released by the SR which is a function of the size of the SR store and trigger (magnitude of Ca current)

2) Amount of Ca stored in SR depends on rate of reuptake, influx, and efflux of Ca


Sympathetics: positive inotropy

Parasympathetics: negative inotropy

Heart rate: increased HR increases contractility

Discuss effects of HR on contractility

Increasing the HR increases the frequency that Ca enters the cell, which increases the intracellular Ca level.  This means that the SR must take up more Ca to achieve a new steady-state. (NE also increases amount of Ca current per beat and the rate of SR uptake)  This means the SR has more Ca to release for contraction.


Ascending staircase: first beat is lower force, but after a few beats a new steady state is achieved

Rest Potentiation: after a pause the next beat will be more forceful and then come back to normal

Post Extrasystolic potentiation: early beat is suboptimal followed by more forceful beat

Resting, Active, and Total tension

-Resting tension is passively developed by applying preload.  So, preload elongates the cardiac muscle.  Remember cardiac muscle is less compliant.

-Active tension is the developed tension during a twitch and can be calculated by subtracting the resting tension from the total tension


The length at which maximum tension is generated is Lmax

Discuss where and why cardiac muscle functions on the length-tension curve

-there is significant resting tension at Lmax in the heart

-cardiac muscle is stiffer due to the less elastic isomer of titin

-resting tension increases more rapidly with increasing muscle length

-Cardiac muscle operates on the ascending limb of the active length-tension curve

-We never reach Lmax because it takes so much force to stretch the muscle to that length, venous return and contraction of the atria do not produce enough force.

Developed tension as a function of resting sarcomere length

-sarcomere Lmax is 2.2 µm

-sarcomere working length is 1.9-2.0 µm

-force falls near 0 at 1.6 µm (thick filament length)

-Tension is proportional to # of cross-bridges


-Increasing length favors formation of actin-myosin complexes cooperatively, and increases SR release of Ca

Contractions with afterload

-Preload still sets the length of the muscle- so there is an isometric contraction until the force overcomes preload and afterload

-After force overcomes preload and afterload combined there is an isotonic contraction

-Graphically, the upstroke represents the isometric contraction and the plateau represents the isotonic contraction.

Tension-length curves

-predicts the amount of shortening which is effected by:


preload: increased preload increases shortening, and decreased preload decreases shortening (you start at a longer length, but still go to the same point on the tension curve)


Afterload: increased afterload decreases the amount of shortening, and decreased afterload increases the amount of shortening (you start at the same length, but go to a new point on the tension curve which is at a longer length)


Contractility: increased contractility increases shortening and decreased contractility decreases shortening (You start at the same length, but the tension curve is steeper, so the point of intersection occurs at a shorter length)

Force Velocity Relationship

Vmax occurs under 0 load (which never happends physiologically) and velocity is 0 when the load is equal to the isometric tension (Po)


This curve is shifted and up and to the right by increasing length, increasing contractility, and increasing HR.  So, they allow the muscle to produce more isometric tension.


Increased afterload= decreased velocity of shortening

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