CARDIAC UNIT: REGULATION OF CARDIAC CONTRACTION Flashcards
What is the cardiac sarcomere’s natural resting length?
What is the cardiac sarcomere’s optimal length for force production?
Sarcomere’s natural resting length is 2.2 um.
Sarcomere’s optimal length of force production is 2.35 um.
Draw and describe the length-tension relationship of cardiac muscle.
As length of sarcomere increases, % tension also increases up to a certain point. Too long, not enough interaction potential for actin and myosin as there is little overlap. Too short, there is no room in the sarcomere for further shortening (contraction) thus little force production
What are the 5 factors that explain the length tension relationship?
- the overlap of actin and myosin. A consequence of extreme shortening is that there is no further potential for myofibrils to contract, and little to no force can be generated. During sarcomere lengthening, actin moves in the opposite direction along the myosin. At extreme lengths, the myosin binding sites on the actin filaments move out of the range of the globular heads of the myosin filaments. As fewer myosin heads can bind with the actin filaments, lower force is generated from myofibril contractions
- When you stretch a muscle, its sensitivity to myofilament ca2+ increases. Now, for the same amount of calcium, you have an increase in force production
Referring to graph shown in lecture, you will see a left shift and steeper curve on the force length curve (displayed in red) - Geometric changes - if you stretch the sarcomere, you decrease the space between myofilaments which facilitates better interaction between actin and myosin for cross-bridge cycling. Myosin heads are better able to interact/have a higher chance of interacting with actin
- Stretch-activated Ca2+ channel areactivated which increases calcium release and increases contraction
- Increased sarcoplasmic Ca2+ release when muscle strectches
What prevents overstretch? This is especially important in cardiac muscle.
Passive tension caused by titin and other non-contractile proteins. Titan and other non-contractile proteins increase sarcomere stiffness which increases resistance to stretch and maintains force generation.
Compare and contrast the length-tension relationship of cardiac muscle with that of skeletal muscle
- see lecture graph
- skeletal muscle can produce tension at a wider range of sarcomere length
- maximum force production for skeletal muscle occurs at a shorter length than cardiac muscle
Skeletal muscle has more distensible (stretchy) non-contractile components than muscle
- EX: different isoform of titan
Draw and describe the force-velocity curve of cardiac myocytes
force velocity curve: physical representation of the inverse relationship between force and velocity
- lower Vmax than force-velocity curve for skeletal muscle
What determines Vmax?
the rate of cross bridge cycling which is slower in cardiac muscle
Also regulated by composition of myosin heavy chains!
ex: V1 has a larger Vmax than V3
Do we ever see an isometric contraction (F-max )in the heart?
Yes - when the heart contracts before the valve opens!
Isovolumetric phase.
Define pre-load; if we decrease pre-load, what happens to the force velocity curve for cardiac myocytes?
Preload: the load the heart sees before it contracts - is the force that stretches the relaxed muscle cells (e.g. blood filling and stretching the myocardium in the ventricular wall during diastole)
If we decrease the preload, we are able to generate less force, and thus change the shape of the graph
Slower velocity of shortening and shorter force production
Describe the physiological importance of pre-load
Preload: the load the heart sees before it contracts - is the force that stretches the relaxed muscle cells (e.g. blood filling and stretching the myocardium in the ventricular wall during diastole).
Maximal systolic pressure is reached at optimal preload (further increases will decrease peak pressure)
Basically the end diastolic volume can be thought of as the preload
What can increase pre-load
Can be increased by greater filling of the left ventricle during diastole (increasing EDV)
Define after-load and discuss its physiological importance
Afterload: the load the heart sees after it contracts - is the force against which the contracting muscle must act (e.g. the aortic pressure that must be overcome to open the aortic valve and eject blood
- Increasing afterload can lead to higher systolic pressure (e.g. by increasing peripheral resistance)
- Continued increases in afterload lead to isovolumetric systole
- The valve only opens if left ventricle pressure is greater than aorta. Thus, if aortic blood pressure increases, then the contraction force must also increase
- Important - afterload is only “felt” once muscle is contracted
How would the velocity force curve change depending on if an organism has predominantly V1, V2, and V3 isoforms of myosin
see graph
- V1: highest velocity
- V3: lowest velocity
Discuss the meaning and importance of the Frank-Starling law
Frank-starling mechanism: length tension relationship in intact heart. reflects combination of active and passive tension. plots force or stroke volume vs end diastolic volume.
- high end diastolic volume means ventricles are more stretched and the sarcomeres are lengthened
- higher EDV, we get a greater stroke volume and force
- we don’t see a decrease in force as we do in the length tension relationship in skeletal muscle because of passive tension. Due to titin and connective tissue protecting the heart from overstretch
- systolic curve= active tension
- diastolic curve: passive tension
What factors increase end diastolic volume
Factors that increase end diastolic volume: exercise, venous constriction, decrease in heart rate (increases filling time)
