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Length dependency of a muscle:

1. the longer the muscle is: the more force it generates.
2. In isolated muscle fibers and also in the heart.
3. This is called the preload dependency.


Integrated cardiac performance:

1. pressure volume loop.
2. When cardiac muscle LV increases volume, the amount of blood ejected increases


PKA functions to

1. phosphorylate TnI and influences actin and myosin relationship to allow for more actin and myosin interactions can take place ,
2. also increase the amount of Ca influx from the Ca2+ channel
3. PKA inhibits PLB, which inhibits SERCA, to allow for CA2+ to cycle out of the SR more rapidly.


B adrenergic signal causes

an increase in extracellular ca2+ AND intracellular Ca2+


Major coordinate responses of hear muscle to beta adrenergic stimulation:

phosphorylation of:
1. Ca channels (SAN cells)
2. Ca channels (ventricular cells)
3. Na pump
4. phospholamban
5. FKB
6. troponin I


phosphorylation of Ca channels (SAN cells) will result in

1. ↑ Heart rate
2. Improved CO
(CO=HR x SV)


Phosphorylation of Ca channels
(ventricular cells) will result in

1. ↑ Ca entry
2. ↑ Force of contraction
3. improved EF (+ inotropy)


Phosphorylation of Na pump
will result in

1. ↑ Ca efflux (via Na-Ca exchange)
2. Enhanced relaxation and diastolic filling


Phosphorylation of Phospholamban will result in

1. Disinhibition of SR calcium pump (SERCA2)
2. Increased SR calcium load
3. improved diastolic filling


Phosphorylation of FKB
will result in

1. Enhances Ryr receptor mediated calcium release
2. enhanced contractility


Phosphorylation of troponin I
will result in

1. ↓ Ca affinity for TnC
2. enhanced relaxation


bigger hearts result in

bigger contractions


SV is a measure of

end diastolic volume
because of the length/tension relationship


short contractions (muscle shorter) means the interactions between myosin and actin are



big contractions (muscle longer) means the interactions between myosin and actin are



muscle can increase force of contraction by

1. getting longer
2. if exposed to inotrope and shift Frank starling curve


myosin alpha vs beta

α myosin has greater ATPase activity than β

this means that α has more activity, so it would be more prevalent in a mouse, whose heart beats 400 times a minute (all alpha) , than in an elephant whose is more like 40 and would have all β


ATPase is proprtional to

resting HR per minute


how does LV hypertrophy lead to Chronic HF?

1. heart develops LVH, decrease CO because heart is ejecting against an increased afterload
2. heart falls apart, the frank starling curve shifts down
3. volume increases and the ability to eject decreases


LVH : Cellular mechanisms

1. Likely increase in Ca current via
L-type Ca channel
2. Reduced SR pump fxn
(↑ PLB/SERCA2 ratio)
3. Impaired myofilament relaxation
4. Altered (increased) cytosolic calcium and new steady-state
5. post transcriptional and post translational modifications


LVH: Early/acute modification:

1. PKA
2. PKCβ


LVH: Late/Chronic modification:

1. PKCε / PKD
2. CAMκ
3. calcineurin


triggers for LVH are

1. neurohormonal modulators
2. genetic factors
3. exercise
4. stretch
5. hypertension


Hypertrophic remodeling results in

1. ↑βMHC
2. ↑ ANF
3. ↓ αMHC
4. ↓ SERCA2


Hypertrophic heart is not only different in the appearance, but it also

handles calcium differently and signals differently



1. is activated by calcium
2. It is a phosphatase.
3. It takes a super long time (hours) for it to be activated.
4. When it becomes activated,it dephosphorylates Nfat and nfat is activated and it goes into the nucleus.


how can you make a mouse have dilated cardiomyopathy?

1. dephosphorylate NFAT or
2. chronically activate calceneurin,
3. they contract poorly and have txn factors like human with dilated cardiomyopathy


______ is one of the key markers in dilated cardiomyopathy

Increase in cytosolic calcium


Adaptations to a chronic load is

complex, coordinated and involved changes at the txn level which cause the heart to be reconfigured.


How do you measure heart function?

using ejection