contraction strength at any given fiber length
The ability of heart muscle cells to shorten in response to an electrical stimulus is known as contractility. This property allows the heart to pump blood effectively throughout the body. Contractility is influenced by various factors, including the availability of calcium ions and the overall health of the heart muscle. It is a crucial aspect of cardiac function, impacting stroke volume and cardiac output.
Cardiac contractility is the force of contraction possible for any given length of the cardiac muscle. It is related to the intracellular calcium levels.
It doesn't - "contractility" refers to the force generated at any given length of muscle. Therefore although the force of contraction does increase with filling, the contractility does not.The reason the force of contraction increases with filling is because filling stretches the heart muscles. Increased stretch causes an increase in force of contraction.Contractility changes because of changes in the level of intracellular calcium. This can be changed by things such as adrenalin (epinephrine), which increases contractility and β blockers, which decrease contractility.
Muscle fiber stretch affects myocardial contractility through the Frank-Starling mechanism, which states that an increase in the length of cardiac muscle fibers (due to increased venous return) enhances their contractile force. When myocardial fibers are stretched, the optimal overlap between actin and myosin filaments occurs, leading to more effective cross-bridge formation during contraction. This results in stronger heart contractions and improved stroke volume. However, excessive stretching can lead to decreased contractility and heart dysfunction.
When muscle cells are oxygen deprived, the heart must work harder to deliver enough oxygenated blood to the tissues. It may increase heart rate or contractility to compensate for the decreased oxygen supply. If oxygen deprivation persists, it can lead to tissue damage or even a heart attack.
Stroke volume is primarily regulated by three factors: preload, afterload, and contractility. Preload refers to the degree of stretch of the cardiac muscle fibers before contraction, influenced by venous return. Afterload is the resistance the heart must overcome to eject blood, primarily determined by arterial pressure and vascular resistance. Contractility refers to the intrinsic strength of the heart muscle's contraction, which can be affected by factors such as sympathetic stimulation and the availability of calcium.
A change in cardiac output without any change in the heart rate, pulmonary artery wedge pressure (PAWP = equated to preload) or systemic vascular resistance (SVR = afterload) would have to be due to a change in the contractility of the heart. Cardiac output (CO) is roughly equal to stroke volume x heart rate. Stroke volume is related to preload, contractility, and afterload. As you can see, the only variables you have not controlled for is cardiac contractility.
increased contractility
Calcium slow channels, also known as L-type calcium channels, play a crucial role in regulating the duration of cardiac muscle contraction. Activation of these channels leads to an influx of calcium ions into the cardiac muscle cells, which triggers contraction. Inhibition of these channels can result in decreased contractility and lengthening of the contraction phase of the heart muscle.
Jozef Zachar has written: 'Electrogenesis and contractility in skeletal muscle cells' -- subject- s -: Excitation - Physiology -, Muscle cells, Muscle contraction
Stretchability does not belong to the functions of muscle tissue. While muscle tissue is stretchable to a certain extent, its primary function is not related to stretching or elongating. The main functions of muscle tissue are the ability to shorten or contract (known as contractility) and to pull on bones (known as pulling or moving bones).
ACE inhibitors primarily work by reducing blood pressure and decreasing the workload on the heart, which can improve cardiac filling by alleviating symptoms of heart failure. While they do not directly decrease contractility, they can lead to improved ventricular function and efficiency, allowing the heart to fill more effectively. This can result in better overall cardiac performance, especially in patients with heart failure, without significantly impairing contractility.