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Cardiac muscle, also known as myocardium, is one of three types of muscles in the human body, the other two being skeletal and smooth muscles. The myocardium makes up the thick middle layer of the heart and is surrounded by the thin outer layer epicardium and the inner endocardium. The primary function of the cardiac muscle is to pump blood into circulation by generating sufficient force through contraction and relaxation. This process requires a constant supply of oxygen and nutrients to meet the energy demands of the cardiac muscle. The force developed by the cardiac muscle is dependent on several factors, including muscle length, preload, and inotropy.
| Characteristics | Values |
|---|---|
| Primary function | To pump blood into circulation by generating sufficient force |
| Contraction | Requires ATP, which can be obtained through various substrates, including fatty acids, carbohydrates, proteins, and ketones |
| Action potential | Divided into 5 phases: resting, upstroke, early repolarization, plateau, and final repolarization |
| Cardiac muscle | Also called the myocardium |
| Sarcomeres | Allow for contractility |
| Contractile state | Variable and generally less than maxima |
| Maximum force | 2 to 7 g/mm2 |
| Factors affecting force | Muscle length, degree of overlap of thick myosin and thin actin filaments, sympathetic nervous system activity, frequency of contraction, muscle length, preload, inotropy |
| Calcium removal | SERCA (sarco-endoplasmic reticulum calcium-ATPase) pump |
| Hypertrophy | Increase in the mass of the heart |
| Vmax | Represents the intrinsic capability of a muscle fiber to generate force independent of either preload or afterload |
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What You'll Learn
- Cardiac muscle is one of three types of muscle in the body, along with skeletal and smooth muscle
- The primary function of cardiac muscle is to pump blood into circulation by generating sufficient force
- The force developed by heart muscle cells is altered by changes in muscle length
- The force-velocity relationship of cardiac muscle is unique and is altered by changes in preload and inotropy
- The contractile functions of the heart require ATP, which can be obtained through various substrates
Cardiac muscle is one of three types of muscle in the body, along with skeletal and smooth muscle
Cardiac muscle, also known as the myocardium, is one of three types of muscle in the human body, the other two being skeletal and smooth muscle. The myocardium makes up the thick middle layer of the heart and is surrounded by a thin outer layer called the epicardium (or visceral pericardium) and an inner endocardium. Coronary arteries supply blood to the cardiac muscle, and cardiac veins drain this blood. Cardiomyocytes are the individual cells that make up the cardiac muscle, and their primary function is to contract, generating the pressure required to pump blood through the circulatory system.
Cardiac muscle, like skeletal muscle, is made up of sarcomeres that enable contraction. However, unlike skeletal muscle, cardiac muscle is under involuntary control. The contractile functions of the heart require ATP, which can be obtained from various substrates, including fatty acids, carbohydrates, proteins, and ketones. The primary source is aerobic production, although the heart can also use anaerobic processes to a limited extent. The force generated by cardiac muscle fibres varies with preload and inotropy. Increasing the preload enables the muscle to contract faster (increased shortening velocity) against a given afterload. Changes in inotropy also alter the force-velocity relationship, with an increase in the inotropic state resulting in a parallel shift in the force-velocity curve, leading to an increase in both maximal velocity of shortening (Vmax) and maximal isometric force (Fmax).
The force developed by cardiac muscle cells is influenced by several factors, including muscle length and the degree of overlap of thick myosin and thin actin filaments. As muscle length increases, the active force developed reaches a maximum and then decreases, with the maximum point corresponding to the length at which the heart typically functions. Short-term increases in demand on the heart, such as during exercise, lead to an increase in the force and frequency of contraction, mediated by increased sympathetic nervous system activity and changes in muscle length. In contrast, long-term stress, such as hypertension and thyrotoxicosis, results in an increase in heart mass (hytrophy) to meet the elevated demand.
The myocardial action potential, which occurs in five phases, is essential for the contraction and relaxation of cardiac muscle. The five phases are rapid depolarization (Phase 0), initial partial repolarization (Phase 1), a plateau period (Phase 2), rapid repolarization (Phase 3), and stabilization at the resting potential (Phase 4). Phase 2 is unique to cardiac muscle and is absent in skeletal muscle. Lusitropy refers to the relaxation of the myocardium, which is mediated by the SERCA pump, allowing the removal of calcium from troponin-C and returning the myocardium to its relaxed state.
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The primary function of cardiac muscle is to pump blood into circulation by generating sufficient force
The primary function of the cardiac muscle, or myocardium, is to pump blood into circulation by generating sufficient force. It makes up the thick middle layer of the heart and is one of three types of muscles in the body, the other two being skeletal and smooth muscles. Cardiac muscle, like skeletal muscle, is made up of sarcomeres that allow for contractility. However, unlike skeletal muscle, cardiac muscle is under involuntary control. The rapid contraction and relaxation of the cardiac muscle are vital for pumping blood throughout the cardiovascular system.
The contractile functions of the heart require adenosine triphosphate (ATP), which can be obtained through various substrates, including fatty acids, carbohydrates, proteins, and ketones. Aerobic production is the core utilization process; however, the heart may use anaerobic processes in a limited capacity. The cardiac action potential lasts approximately 200 ms and is divided into five phases: resting, upstroke, early repolarization, plateau, and final repolarization.
The force generated by the cardiac muscle is influenced by several factors, including muscle length and the degree of overlap of the thick myosin and thin actin filaments. As the muscle length increases, the active force developed reaches a maximum and then decreases, with the maximum point corresponding to the length at which the heart normally functions. Short-term increases in demand on the heart, such as during exercise, lead to increases in the force and frequency of contraction, mediated by increased sympathetic nervous system activity and changes in muscle length.
Additionally, the force-velocity relationship in cardiac muscle fibres is altered by changes in preload and inotropy. Increasing the preload enables the muscle to contract faster against a given afterload, resulting in a greater velocity of shortening. Changes in inotropy also impact the force-velocity relationship, leading to increases in both maximal velocity of shortening (Vmax) and maximal isometric force (Fmax). The increase in Vmax is significant as it represents the intrinsic capability of a muscle fibre to generate force independently of preload or afterload.
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The force developed by heart muscle cells is altered by changes in muscle length
Cardiac muscle, also called the myocardium, is one of three major categories of muscles in the human body, the other two being smooth muscle and skeletal muscle. The primary function of cardiac muscle is to pump blood into circulation by generating sufficient force. The force developed by heart muscle cells is altered by changes in muscle length.
There is a relationship between muscle length and the isometric force developed. As the muscle length increases, the active force developed increases to a maximum and then decreases. This maximum point is the length at which the heart normally functions. Changes in muscle length alter the active force by varying the degree of overlap of the thick myosin and thin actin filaments.
The force developed by heart muscle cells also depends on the frequency at which the muscle is stimulated. As the stimulus frequency increases, the force increases until a maximum is reached, after which it decreases. An increase in the level of circulating epinephrine and norepinephrine from the sympathetic nervous system also increases the force of contraction.
Short-term increases in demand on the heart, such as during exercise, are met by increases in the force and frequency of contraction. These changes are mediated by increases in sympathetic nervous system activity, an increase in the frequency of contraction, and changes in muscle length. The response to long-term stress, such as hypertension and thyrotoxicosis, results in an increase in the mass of the heart (hypertrophy), providing more heart muscle to pump blood and meet the increased demand.
Intracellular changes also affect the performance of muscle cells. In pressure-overload hypertrophy (hypertensive heart disease), the pumping system of the sarcoplasmic reticulum responsible for calcium removal is slowed, while the contractile protein myosin shifts toward slower cross-bridge cycling. The outcome is a slower, more economical heart that can meet the demand for pumping against an increase in pressure.
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The force-velocity relationship of cardiac muscle is unique and is altered by changes in preload and inotropy
Cardiac muscle, also called the myocardium, is one of three major categories of muscles in the human body, the other two being smooth muscle and skeletal muscle. The primary function of cardiac muscle is to pump blood into circulation by generating sufficient force. The force-velocity relationship of cardiac muscle is unique and is altered by changes in preload and inotropy.
The force-velocity relationship in cardiac muscle examines how changes in preload affect isometric tension development. When a muscle fibre contracts, it also shortens so that external work can be performed. The greater the afterload, the slower the velocity of shortening. Therefore, there is an inverse relationship between shortening velocity and afterload, termed the force-velocity relationship.
If preload is increased, cardiac muscle fibres will have a greater velocity of shortening at a given afterload. This occurs because the length-tension relationship dictates that as the preload is increased, there is an increase in active tension development. Once the fibre shortens, the increased tension-generating capability at the increased preload results in a greater velocity of shortening. Therefore, increasing the preload enables the muscle to contract faster (increased shortening velocity) against a given afterload. Conversely, if preload decreases, the velocity of shortening decreases at a given afterload.
Changes in inotropy also alter the force-velocity relationship. If the inotropic state of the cardiac fibre is increased, there is a parallel shift in the force-velocity curve, resulting in an increase in both Vmax and Fmax. The increase in velocity at any given preload results from the increased inotropy enhancing force generation by the actin and myosin filaments, and increasing the rate of cross-bridge cycling. The increase in Vmax is noteworthy because it represents the intrinsic capability of a muscle fibre to generate force independent of either preload or afterload. Therefore, Vmax is sometimes used experimentally as an index or measure of inotropy for cardiac muscle fibres.
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The contractile functions of the heart require ATP, which can be obtained through various substrates
The primary function of the cardiac muscle, or myocardium, is to pump blood into circulation by generating sufficient force. The contractile functions of the heart require ATP, which can be obtained through various substrates, including fatty acids, carbohydrates, proteins, and ketones. The heart has a high rate of ATP production and turnover, which is necessary for its continuous mechanical work. This ATP is produced through aerobic production, with anaerobic processes being used in a limited capacity.
ATP is generated from substrate oxidation, and this process is integral to the contractile functions of the heart. The myocardial contractile cells, which make up 99% of the cells in the atria and ventricles, conduct impulses and are responsible for the contractions that pump blood through the body. The myocardial conducting cells, which make up 1% of the cells, form the conduction system of the heart and are responsible for initiating and propagating the action potential that triggers the contractions.
The force generated by the cardiac muscle is less than that of skeletal muscle. This is due to a few factors, including the fact that cardiac muscle cannot be tetanized, the contractile state of the heart muscle is variable, and a large proportion of the myocardium consists of non-contractile structures such as mitochondria and nuclei. However, the force and frequency of contraction can increase in response to short-term demands on the heart, such as exercise, through increases in sympathetic nervous system activity and changes in muscle length.
Calcium ions play a critical role in the physiology of cardiac muscle. Their influx through slow calcium channels enables the cardiac muscle to function properly by prolonging the plateau phase and absolute refractory period. Calcium ions also combine with troponin-C in the troponin-tropomyosin complex, which allows the heads of the myosin molecules to form cross-bridges with the active sites on actin, providing the power stroke of contraction. The SERCA (sarco-endoplasmic reticulum calcium-ATPase) pump is responsible for removing calcium from troponin-C and returning the myocardium to its relaxed state.
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Frequently asked questions
Cardiac muscle, also called the myocardium, is one of three major categories of muscles found in the human body, the other two being smooth muscle and skeletal muscle.
The primary function of cardiac muscle is to pump blood into circulation by generating sufficient force through contraction and relaxation. This process requires a constant supply of oxygen and nutrients to meet the energy demands of the cardiac muscle.
The force-velocity relationship in cardiac muscle refers to the interplay between the muscle fiber shortening velocity (Vmax) and the maximal isometric force (Fmax). The relationship is influenced by changes in preload and inotropy, with preload referring to the muscle length and inotropy representing the contractile state.
Cardiac muscle has less strength compared to skeletal muscle. This difference may be due to factors such as the inability of cardiac muscle to be tetanized, the variable contractile state of heart muscle, and the presence of non-contractile structures in the myocardium.
The sympathetic nervous system can increase the force and frequency of contraction in response to short-term increases in demand, such as during exercise. It also enhances lusitropy, promoting relaxation of the cardiac muscle through beta-1 adrenergic stimulation and phosphorylation of phospholamban.
