Force Generation by the Heart

How Does the Heart Generate Force?

• 
• of cardiac muscle is striated, which is caused by the regular arrangement of contractile protein
• cardiac muscle have no neuromuscular junctions
• cardiac myocytes are electrically coupled by gap junctions
• gap junctions are protein channels, which form low resistance electrical communication pathways between myocytes
• they make sure each electrical excitation reaches all the cardiac myocytes
• desmosomes, within the intercalated discs, provide adhesion between cells
• they make sure tension developed by one cell is transmitted to the next

Structure of Striated Muscle Fiber

• 
• myofibrils are the contractile units of muscle
• myofibrils have alternating segments of thick and thin protein filaments
• ACTIN (thin)
• MYOCIN (thick)
• actin and myocin are arranged into sarcomeres (one section of a fibril)
• muscle tension is produced by sliding of actin filamnets on myocin filaments
• http://bigpictureeducation.com/animation-sliding-filament-theory

Contraction and Relaxation

• myocin head is energised using ATP
• Ca++ must also be present
• if both are present, a crossbridge can form
• actin slides under the myocin and shortening (contraction) occurs
• ATP must also be availble to break the crossbridge. It attaches to the myocin head and it is broken.
• if there is no calcium, myosin binding sites are covered by tropomyosin/troponin
• when Ca++ binds to this, it is pulled aside and binding sites are uncovered
• this allows cross bridge formation to occur
• a stroke pulls the thin myocin filament inward during contraction

Excitation Contraction Coupling

• Ca++ is released from the sarcoplasmic reticulum
• in cardiac muscle, release is dependent on the presence of extra cellular Ca++
• more Ca++ must go into the cell in order for more to be released by the SR
• 

Excitation Contraction Coupling

• DIASTOLE (relaxation)
• When the action potential has passed, Ca++ influx stops
• it is removed and stored in the SR by a Ca++ ATPase
• this means less is available, so relaxation can occur
• SYSTOLE (contraction)
• Ca++ influx occurs during the plateau phase of the action potential
• Ca++ activates the contractile machinery
• Calcium coming into the cell causes more to be released from the SR, causing more contraction

Long Refractory Period

• 
• the ventricular muscle action potential (red) triggers contraction (blue) in cardiac muscle cells
• the long refractory period prevents generation of tetanic contraction, which is sustained muscle contraction
• the refractory period is a period following an action potential where another cannot be produced
• in the plateau phase, Na+ channels are depolarised (closed)
• during the descending phase, K+ channels are open so cannot be depolarised
• this stops them from closing and causing a decrease in K+ efflux, so no more action potentials can occur here

Stroke Volume

• contraction of ventricular muscle ejects the stroke volume, which is the blood ejected by each ventricle per heart beat
• SV is regulated by intrinsic and extrinsic mechanisms
• intrinsic is within the heart muscle itself
• extrinsic is nervous and hormonal control

Intrinsic Control of SV

• changed are brought about by changes in the diastolic length of the myocardial fibers
• these lengths are determined by the end diastolic volume, which determines cardiac preload
• end diastolic volume is determined by the venous return to the heart

Frank Starling Curve

• this describes the relationship between venous return, EDV and SV
• it states "
• a healthy heart does not operate on the descending curve
• it states that "the more the ventricle is filled
• with blood during diastole (END DIASTOLIC VOLUME), the greater the volume of ejected blood will be during the
• resulting systolic contraction (STROKE VOLUME)"
• stretch also increases the affinity of troponin fro Ca++
• 

Frank Starling Mechanism

• if venous return to the RA is increased, EDV of the right ventricle increases
• there will be an increased SV into the pulmonary artery, due to starling's law
• if venous return to the left atrium from pulmonary vein increases, EDV of the left ventricle increases
• there is an increased SV into the aorta, due to starling's law
• starling can also compensate for decreased SV caused by an increase in afterload
• afterload is the resistance into which the heart is pumping, and the extra load is imposes after the heart has contracted
• at first the heart cannot eject the full SV, so EDV increases
• force of contraction rises via starling mechanism
• if increased afterload continuous, ventricular hypertrophy would occurs to try to reach the SV

Extrinsic Control of SV

• this involves nerves and hormones
• the ventricular muscle is supplied by sympathetic nerve fibres, with noradrenaline as the neurotransmitter
• stimulation of the sympathetic nerves increases the force of contraction (positive inotropic effect - increases CONTRACTION)
• greater force of contraction activates more Ca++ channels
• the effect is cAMP mediated
• peak ventricular pressure rises
• rate of pressure change during systole increases, which reduces the duration of systole
• rate of ventricular relaxation increases, which causes an increased rate of Ca++ efflux
• this reduces the duration of diastole

Cardiac Output

• this is the volume of blood pumped by each ventricle per minute
• resting CO is usually 5 litres per minute
• if we regulate HR and SV, we will regulate CO