16 Questions
What prevents cardiac muscle from increasing motor unit recruitment or undergoing tetanic contraction?
Lack of spare units to recruit
What is the reason behind the inability of cardiac muscle to undergo tetanic contraction?
Long refractory period
Why is there no force summation during cardiac twitches?
Refractory period
What prevents cardiac myocytes from recruiting more fibers to increase force?
Lack of spare units to recruit
Why can't cardiac muscle increase motor unit recruitment like skeletal muscle?
Lack of spare units to recruit
What characteristic of cardiac myocytes prevents twitch summation?
Long absolute refractory period (ARP)
What triggers the opening of dihydropyridine (DHP) Ca++ channels in cardiac muscle cells?
Action potentials (AP)
What is the primary mechanism by which cardiac muscle cells modify the strength of contraction?
Enhanced calcium channel opening
What is the main role of the DHP channels in cardiac muscle cells?
Facilitate calcium-induced calcium release from the sarcoplasmic reticulum (SR)
What is the function of SERCA2 in cardiac muscle cells?
Pump calcium back into the sarcoplasmic reticulum (SR)
What mechanism can occur independent of changes caused by preload/afterload in cardiac muscle cells?
Enhancement of calcium influx during action potentials
During which phase does ~70% of stroke volume get ejected from the left ventricle?
Period of rapid ejection
What is the primary role of the atria in the cardiac cycle?
Topping up remaining volume in the ventricles
What prevents cardiac muscle from undergoing tetanic contraction like skeletal muscle?
Inability to generate action potentials
'Mucopolysaccharides sequester Ca++ ready for AP' refers to the role of mucopolysaccharides in:
Storing calcium ions for action potentials
What triggers the release of Ca++ from SR in cardiac muscle cells?
Increased intracellular [Ca++]i
Study Notes
Cardiac Muscle Characteristics
- Cardiac muscle cannot increase motor unit recruitment or undergo tetanic contraction due to the absence of motor units and the inability to voluntarily recruit more fibers.
- The lack of tetanic contraction in cardiac muscle is attributed to the asynchronous activation of cardiac myocytes, preventing force summation during cardiac twitches.
Cardiac Muscle Contraction
- The primary mechanism by which cardiac muscle cells modify the strength of contraction is through changes in intracellular Ca++ concentrations.
- Dihydropyridine (DHP) Ca++ channels are triggered to open by depolarization of the cardiac muscle cell membrane.
- The main role of DHP channels in cardiac muscle cells is to regulate the influx of Ca++ ions, which triggers contraction.
Cardiac Muscle Function
- SERCA2 (Sarcoplasmic/Endoplasmic Reticulum Calcium ATPase 2) is responsible for reuptaking Ca++ ions into the sarcoplasmic reticulum, reducing intracellular Ca++ concentrations and allowing for muscle relaxation.
Cardiac Cycle
- During the late rapid ejection phase, ~70% of stroke volume gets ejected from the left ventricle.
- The primary role of the atria in the cardiac cycle is to serve as a primer pump, allowing for the efficient filling of the ventricles.
Calcium Regulation
- Mucopolysaccharides sequester Ca++ ions, making them ready for release during action potentials.
- The release of Ca++ from the sarcoplasmic reticulum (SR) in cardiac muscle cells is triggered by the opening of ryanodine receptors.
Test your knowledge of the contraction of cardiac muscle, events during the cardiac cycle, and the regulation of cardiac output with this quiz. Explore the mechanisms of matching cardiac output to metabolic tissue demands and the unique aspects of heart rate and contractile force.
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