Regulation Of Cardiac Contraction Flashcards
Length tension relationship: how does the sarcomere look when tension is at its max and min?
Max: sarcomere is relaxed
Min: sarcomere is shortened for a contracted muscle state. OR over stretching of sarcomere causes titin to break, no overlap between thick and thin filament causes there to be no tension (physiologically impossible condition)
What is the normal length of sarcomere (resting)
LN- 2.2 micro m
What is the optimal length of sarcomere
LO- 2.3 micro m
Name the five factors that effect the length tension relationship
- Overlap of actin and myosin
- Increased myofilament Ca2+ sensitivity
- Geometric changes- decreased spacing between myofilaments ( more likely to form crossbridge)
- Stretch-activated Ca2+ channel activation
- Increased SR Ca2+ release
What do the active and passive length tension curves relate to
Active- contraction of muscle, shortening of sarcomere
Passive- resistance to stretch caused by titin. Sarcomere stiffness
Roles of titin
Increase resistance to stretch
Maintain force generation
Length tension relationship: does the passive component have more tension in cardiac or skeletal muscle? Explain
More tension in cardiac- can not have any overstretch
Skeletal- has more non-contractile components that can be “turned off” (distensible) allows muscle to be stretched more
What are the axis for the frank-starling mechanism graph
Force or stroke volume VS end diastolic volume
Define stroke volume
How much blood is pumped out of the heart by the left ventricle
What is end diastolic volume
Amount of blood in the heart before contraction
Frank-starling (F vs EDV): what kind of tension is provided by systolic and diastolic curves
Systole- active tension
Diastole- passive tension
What creates the active tension
Contraction of heart
What creates passive tension
Titin. Resistance to filling
Frank-starling (F vs EDV): After ejection why does the force not decrease?
Although active tension has dropped, there is an increase in passive tension, thus causing the total force in the heart to remain the same. No descent because of titin and connective tissue
With regards to the frank-starling mechanism, where would you label the preload and after load?
Preload= passive tension = diasole
After load= active tension= systole
What factors increase EDV
Exercise- more active=sarcomeres stretch, larger chamber
Venous constriction- more blood return, greater volume
Decrease in heart rate- more filling time, amount of blood in chamber increases
What things cause passive force in heart
Force of blood on wall and wall on the blood
Titin and non-contractile proteins increasing stiffness
What is preload?
Force that stretches the relaxed muscle cells (ex. Blood filling and stretching walls during diastole)
Preload=end diastolic volume
What is afterload?
Force against which the contracting muscle must act. Aortic pressure must be overcome to open aortic valve and eject blood.
Afterload=blood pressure
Force-velocity curve: why can Vmax not be reached?
To have vmax we much have zero force/load. That would mean having no blood to move which doesn’t occur in living humans
What are the axis of the force-velocity curve
Velocity of shortening VS force/load
What is the name of the condition when max force is generated
Isometric
What happens during isometric contraction
Ventricles contract but the valves are closed so no volume changes occur (isovolumetric). Force is max and velocity of shortening is zero (on force velocity curve)
What is an isotonic contraction
Occurs when the heart muscles shorten and the force generated in greater than the load
When we decrease the force in the heart, what load are we decreasing?
Preload
When we decrease the force in the heart, how does the velocity of shortening change?
Slower velocity, less to push out
How do we determine Vmax values experimentally?
Rate of cross bridge cycling
