Victor Forge
Cardiac muscle is a unique tissue that forms the wall of the heart. Its cells are relatively small and usually have a single, centrally placed nucleus. The question of whether cardiac muscle can tetanize has been the subject of various studies, with researchers developing methods to tetanize cat papillary muscle and conducting experiments on tetanus in the shrew myocardium. These studies have provided insights into the length dependence of the force-velocity characteristic of cardiac muscle and the correlation between mechanical properties and myosin type in heart muscle. Understanding the tetanization of cardiac muscle contributes to our knowledge of the complex functioning of the heart and its contractile behaviour.
| Characteristics | Values |
|---|---|
| Can cardiac muscle be tetanized? | Yes, according to studies on cat papillary muscle and shrew myocardium. |
| Methods of tetanization | Repetitive electrical stimulation, increased calcium concentration, and the presence of caffeine. |
| Effects | Delay in the onset of relaxation, increased tension, and changes in calcium concentration and contractility. |
| Applications | Understanding force-velocity relationships and the mechanics of the heart muscle. |
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What You'll Learn
Tetanus in the mammalian heart
The shrew ventricular muscle can be tetanized because the action potential is very short (3 to 4 ms) and ends before any mechanical activity begins. The tension during tetanus usually reached a steady state and exceeded the tension of the regular twitch preceding the train. Tetanus was also observed during an arrhythmic train, which was occasionally triggered spontaneously by a regular stimulus.
These findings advance our understanding of an as-yet uncharacterized mammalian heart and further demonstrate the correlation between mechanical properties and myosin type in heart muscle. The shrew ventricular muscle's twitch duration, tension development, and relaxation are much shorter than in the guinea pig. It also has a high Ca2+-activated ATPase activity and is composed of α-type heavy chains.
In addition, a method of tetanizing cat papillary muscle has been developed to determine the length dependence of the force-velocity characteristic of cardiac muscle when activation is independent of time in the contraction cycle. This was achieved through repetitive electrical stimulation in the presence of 10mM-caffeine and an increased calcium concentration (7.5–12.5 Mm).
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Calcium and contraction kinetics
Calcium is a divalent cation that is essential for molecular signalling in the body. Calcium ions (Ca2+) play a crucial role in the contraction kinetics of cardiac muscle. The process of excitation-contraction (E-C) coupling links the electric excitation of the surface membrane (action potential) to contraction.
Cardiac contractility is regulated by changes in intracellular Ca2+ concentration ([Ca2+]i). For normal cardiac function, [Ca2+]i must be sufficiently high in systole and low in diastole. The calcium required for contraction comes primarily from the sarcoplasmic reticulum and is released through calcium-induced calcium release. This process is regulated by the relationships between the various channels and pumps involved.
The structural coupling aspect involves the organization of transporters within the dyad, linking the transverse tubule and sarcoplasmic reticulum to ensure the proximity of Ca2+ entry to release sites. Functional coupling, on the other hand, requires that the fluxes across all membranes are balanced, maintaining a steady state where Ca2+ influx equals efflux during each cardiac cycle.
The binding of Ca2+ to troponin results in the sliding of thick and thin filaments, leading to cell shortening, pressure development within the ventricle, and the subsequent ejection of blood. The force generated depends on the amount of Ca2+ bound to troponin, which is influenced by the magnitude and duration of the rise in [Ca2+]i, as well as the strength of Ca2+ binding. This binding strength can be modified genetically and is also controlled by factors such as phosphorylation.
Additionally, muscle cells employ calcium handling and transport proteins that work to rapidly restore Ca2+ concentrations to resting levels following contraction. SERCA, for example, is the dominant Ca2+ transport protein in cardiomyocytes, contributing significantly to the decay of Ca2+ transients during E-C coupling. Impairments in Ca2+ transport can lead to the development of skeletal muscle myopathies and cardiomyopathies.
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Action potential and tension
The action potential of cardiac muscle cells is a result of the movement of ions and small molecules through gap junctions. This movement creates a simultaneous contraction of cardiac muscle cells, allowing them to "pull together" efficiently. The action potential plays a crucial role in controlling the contraction of the heart muscle, ensuring that it contracts and relaxes more than 100,000 times a day without stopping or tiring.
Cardiac myocytes, or cardiac muscle cells, can be classified into two types: work cells and pacemaker cells. Work cells have a large and stable resting membrane potential, while pacemaker cells have smaller, unstable resting potentials and spontaneously depolarize, generating the heart's intrinsic electrical activity. The cardiac action potential differs from that of nerves, with a prolonged plateau phase lasting around 300 ms compared to 1 ms in nerves.
The process of depolarization in cardiac myocytes is characterized by the absence of an inward movement of sodium ions. Instead, it is triggered by the opening of L-type calcium channels, allowing calcium ions to enter the cell. Repolarization, on the other hand, is facilitated by an increase in potassium permeability. The rate of firing can be reduced by vagal stimulation, which further enhances potassium permeability and hyperpolarizes the cell.
The action potential in cardiac conductive cells differs significantly from that in cardiac contractive cells. The contractive cells exhibit a more stable resting phase, with a voltage of approximately −80 mV in the atria and −90 mV in the ventricles. When stimulated by an action potential, voltage-gated channels rapidly open, initiating the positive-feedback mechanism of depolarization. This is followed by a plateau phase and then repolarization, resulting in long refractory periods that enable the cardiac muscle cells to pump blood effectively.
The influx of calcium ions during the plateau phase contributes to the extended refractory period, which is essential for proper cardiac muscle function. The absolute refractory period for cardiac contractile muscle lasts approximately 200 ms, followed by a relative refractory period of about 50 ms, totaling 250 ms. This extended period ensures that the heart muscle contracts effectively to pump blood and prevents premature contractions that could be life-threatening.
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Repetitive electrical stimulation
Cardiac muscle, unlike skeletal muscle, is not under direct control of the central nervous system. However, tetanic contractions in skeletal muscle are achieved through repetitive electrical stimulation. This involves stimulating the muscle with multiple impulses at a sufficiently high frequency. Each stimulus causes a twitch, and if the stimuli are delivered at a high frequency, the twitches will overlap, resulting in a tetanic contraction.
Tetanic contractions can be unfused or fused. An unfused tetanus occurs when muscle fibres are stimulated at a fast rate, not allowing them to completely relax before the next stimulus. In a fused tetanus, there is no relaxation of the muscle fibres between stimuli, and it occurs during a high rate of stimulation.
In the laboratory, muscle shortening is usually constrained, and the contraction intensity is measured as force output. The intensity of skeletal muscle contraction is proportional to the frequency of fibre stimulation and the number of muscle fibres activated. During volitional exercise, intact muscles are stimulated by the central nervous system using a complex pattern of activation. In experimental systems, muscles are activated by electrical stimulation, and the intensity of contraction is altered by varying the stimulation frequency.
In one study, a method was developed to tetanize cat papillary muscle by using repetitive electrical stimulation in the presence of caffeine and an increased calcium concentration. These agents delayed the onset of relaxation, allowing repetitive stimulation to reactivate the muscle before relaxation began.
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Mechanical properties of heart muscle
Cardiac muscle is a unique tissue that forms the wall of the heart. It is made up of relatively small muscle cells, each with a single, centrally placed nucleus. These cells are branched and connected to several others at intercalated discs, allowing for the rapid passage of action potentials and simultaneous contraction.
The mechanical properties of the heart muscle, or myocardium, are of significant interest in understanding cardiac function and disease. One of the principal concerns is elucidating the relationship between the contractile properties of the whole heart and the myofilaments that comprise it. This relationship is influenced by the three-dimensional complexity of the heart, which cannot be fully captured by one-dimensional analyses of papillary muscles or trabeculae.
The contractile and mechanical properties of the myocardium can be studied through various ex vivo methods, including whole heart preparations, isolated muscle preparations, and skinned cardiomyocyte preparations. These techniques allow researchers to assess cardiac function at different levels, from the whole organ down to individual protein-protein interactions. For example, by employing techniques that maintain intact multicellular interactions, researchers can gain insights into abnormalities in the calcium handling properties of the muscle.
The mechanical properties of the heart muscle are also influenced by the concentration of calcium ions (Ca2+). Experiments have shown that the initial stiffness of cardiac muscle preparations increases as the Ca2+ concentration in the bathing solution is raised. This suggests that the short-range mechanical properties of activated muscle are due to the stretching of myosin cross-bridges attached between thick and thin filaments. Additionally, the free Ca2+-concentration required to significantly increase passive myocardial stiffness is substantially higher than the concentration typically assumed for working hearts.
Furthermore, studies have investigated the effects of protein kinase C activation on the function of sarcoplasmic reticulum and the calcium sensitivity of myofibrils in intact and skinned muscles from normal and diseased human myocardium. Other areas of exploration include the cross-bridge versus thin filament contributions to force development in cardiac muscle, as well as the simultaneous optical mapping of intracellular free calcium and action potentials.
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Frequently asked questions
Yes, tetanus can occur in the shrew myocardium, a mammalian heart.
Cardiac muscle can be tetanized by repetitive electrical stimulation in the presence of 10mM-caffeine and an increase in calcium concentration.
Tetanizing cardiac muscle allows researchers to determine the length dependence of the force-velocity characteristic of the muscle in conditions where activation is independent of time in the contraction cycle.
