Cardiac muscle tissue
It is very easy to overlook and take for granted a particular structure that is not readily visible in the human body. One such example are muscles. It is very easy to observe skeletal muscle tissue, especially if you exercise physically.
This article will start by describing the general classification of muscle tissue. After that, it will focus on the characteristics, components, and briefly on contraction of cardiac muscle tissue.
- Muscle tissue
- Clinical points
- Related diagrams and images
Muscle tissue is one of the four basic types of tissues that make up the human body. It is composed of elongated cells arranged in parallel that are capable of contracting and generating a force. Through this unique ability, muscle tissue allows the body, together with its parts and internal organs, to move and continuously adjust their shapes.
Muscle tissue is categorized according to the presence or absence of striations within myocytes and the location of the muscle itself:
- Striated muscle (exhibits cross striations)
- Skeletal muscle (attached to bones)
- Visceral striated muscle (within specific soft tissues)
- Cardiac muscle (within the heart)
- Smooth muscle (doesn’t exhibit cross striations)
Skeletal muscle is a voluntary type of muscle that acts upon the skeletal system by pulling on the bones and allowing body movements. Visceral striated muscle is identical to skeletal muscle, but restricted to specific areas like the tongue, upper esophagus, the pharynx, and the lumbar part of the diaphragm. Therefore it permits breathing, swallowing, and speaking. Smooth muscle is an involuntary muscle that is less structured and more easily altered compared to striated muscles. It mainly forms part of viscera, blood vessels, arrector pili, and the intrinsic eye muscles.
Cardiac muscle tissue, also known as myocardium, is a structurally and functionally unique subtype of muscle tissue located in the heart, that actually has characteristics from both skeletal and muscle tissues. It is capable of strong, continuous, and rhythmic contractions that are automatically generated. The contractility can be altered by the autonomic nervous system and hormones. In addition, this tissue type has high metabolic, energy, and vascular demands.
Cardiac muscle fibers are long, branched cells, shaped like cylinders joined end-to-end, with one or two nuclei located centrally. The fibers are separated by collagenous tissue that supports the capillary network of cardiac tissue.
The myofilaments of cardiac muscle are arranged in a similar pattern to skeletal muscle, resulting in cross-striations. The fibers are crossed by linear bands called intercalated discs. These structures have two important roles. Firstly, they provide attachment points that provides the tissue with a characteristic branched pattern. Secondly, they allow cardiac muscle tissue to function as a functional syncytium. Essentially, the contractile stimuli is propagated from one cell to the next one, resulting in a synchronous contraction of the entire tissue section.
While the majority of muscle cells within cardiac tissue are physically contracting, there is a special set that performs another role. They are called cardiac conducting cells and they automatically initiate and propagate the contraction impulses.
Cardiomyocytes, also known as cardiac muscle cells, usually contain one elongated nucleus that lies in the centre, which is a distinguishing feature from skeletal muscle. By examining the ultrastructure, it becomes apparent that the myofibrils separate as they approach the nucleus, pass around it and re-assemble in their original pattern on the other side. You can visualize the arrangement by imagining two cones that are joined at their vertices, which represents the nucleus. In fact, cell organelles are also concentrated in this cytoplasmic region around the nucleus. These include mitochondria, Golgi apparatus, lipofuscin filled granules, and glycogen. Lipofuscin is a red-brown pigment, often called the wear and-tear-pigment, which gradually accumulates inside cardiac tissue with age. It is the remnant of lysosomal cell contents. The cytoplasm of cardiomyocytes, called sarcoplasm, is eosinophilic and appears as a 3D network.
Due to the high energy requirements, cardiac muscle tissue contains additional large and elongated mitochondria located between the myofibrils. They can run the full length of the sarcomere and contain many internal cristae. In addition, extra glycogen granules are also located between the myofibrils to store the energy. Threads of collagenous tissue fibers together with capillaries are also present between the muscle fibers to provide the tissue with support and a blood supply.
Cardiac myocytes are joined together via intercalated discs, which coincide with Z lines. They appear as lines that transverse the muscle fibers perpendicularly when examined with a light microscope. However, if the ultrastructure is examined, the discs are far from linear because they have finger-like interdigitations to maximize the contact surface area. The discs also contain two compartments that are orientated transversely and laterally (parallel) in relation to the myofibrils, resembling a flight of stairs.
To accomplish their attachment roles, intercalated discs contain three types of cell junctions:
- Adherens junctions (fascia adherens) are a part of the transverse component and are the ones making the intercalated discs visible in hematoxylin and eosin (H&E) staining. They are responsible for actually connecting the ends of the myocytes together to form a fiber. In addition, they transmit the force of contractions from cell to cell because the actin filaments of terminal sarcomeres insert into these junctions.
- Desmosomes (maculae adherentes) are part of both components and they reinforce adherens junctions. They prevent the separation of myocytes during contractions by anchoring intermediate filaments.
- Communication (gap junctions) are part of the lateral component of intercalated discs. They allow cardiac tissue to function as a syncytium by providing pathways for various ions to pass between adjacent cells, resulting in the propagation of excitation and subsequent contraction.
Myofibrils and sarcomeres
Sarcomeres are the functional subunits of myofibrils and the contractile units of cardiac muscle tissue. They are arranged into a branched pattern, forming a 3D network in the cytoplasm. Sarcomeres are specific portions of myofibrils located between two Z lines and are responsible for the striated appearance of cardiac tissue. They are composed of thick and thin filaments. Thick filaments are composed of polymerised myosin type II protein and are attached to band called the M line that is situated in the middle of the sarcomere. Thin filaments consist of polymers of the protein alpha actin and are attached to the Z lines. These two lines, together with the A band that corresponds to the length of the myosin filaments, are electron rich and appear darker in electron microscopy. The I and H bands appear lighter and they represent regions which consist of only thin or thick filaments respectively, but not both.
The cytoplasmic regions between the sarcomere branches are filled with mitochondria and smooth endoplasmic reticulum (sER) called sarcoplasmic reticulum, which envelopes each myofibril. The membranous network of sarcoplasmic reticulum is transversed by structures called T tubules, which are extensions of the sarcolemma (plasma membrane of muscle cells). They form the T tubule system and their lumens are communicating directly with the extracellular space. Their course follows the Z lines of the sarcomeres, resulting in a single T tubule for every sarcomere. The region formed by the pair of flat terminal cisternae of the sarcoplasmic reticulum and a portion of a T tubule is called a triad.
Cardiac conducting cells
Contractions are initiated and propagated throughout the heart by specialised cardiac cells called cardiac conducting cells (they are not neurons). Collectively, they form the conducting system of the heart. These cells form specific structures like nodes, bundles, and conducting fibers. The initial, spontaneous stimulus starts from the sinoatrial node located in the wall of the right atrium at the level of the entry point of the superior vena cava. The impulses travel through the walls of the atria, resulting in contraction. They are then picked up by the atrioventricular (AV) node situated above the tricuspid valve in the medial wall of the right atrium. These two nodes are enveloped by collagenous tissue that is full of capillaries and autonomic nerves. After the AV node, the impulse passes through the bundle of His, the right and left bundle branches, and finally through the Purkinje system. The three bundles stain quite pale due to their high content of glycogen granules and mitochondria. The Purkinje fibers also contain a central area that stains pale. Cardiac conducting cells are connected strictly via desmosomes and gap junctions only. They also don’t have a T tubule system.
As you can see, the contraction of the heart is spontaneous. However, despite their autonomy, conducting cells are not isolated from the nervous system. The sympathetic branch increases the impulse frequency from the nodes to the conducting system, while the parasympathetic branch decreases it. As every impulse is followed by a contraction in normal situations, the rate of contraction is increased or decreased, respectively.
The contraction mechanism is similar to that of skeletal muscle. Basically, the depolarization of the sarcoplasm travels through the system of T tubules, all the way to the sarcoplasmic reticulum. Voltage gated channels open and calcium ions are released in the sarcoplasm. These ions allow the myosin and actin filaments to form cross-bridges and subsequently slide past each other (sliding filament mechanism). The excitation and contraction are passed on to the next myocytes via intercalated discs and cell-to-cell junctions.
Despite the close similarities between cardiac and skeletal muscle tissue, there are several significant differences. Firstly, the depolarization of the sarcoplasm lasts longer in cardiac tissue. In addition, calcium channels are also present in the walls of the T tubule system, rather than being limited strictly to the sarcoplasmic reticulum. In turn, the released calcium ions bind to calcium sensitive channels in the sarcoplasmic reticulum, which results in a large and fast release of further calcium ions required for contraction.
As you have seen previously, cardiac tissue requires a high and continuous supply of energy and oxygen. The heart’s oxygen supply is brought to the heart via the coronary arteries, which are highly susceptible to atheromas. These are abnormal deposits of fatty acids, cholesterol, and various cell debris. If these atheromas keep increasing in size, they eventually occlude the coronary arteries, resulting in a reduction of oxygen supply to the tissue. This lack of oxygen leads to a condition called myocardial infarction, which represents the death of cardiac tissue. As part of a normal physiological response, the affected area is repaired and replaced with fibrous tissue that interrupts the propagation of the excitatory stimuli and subsequent contraction of the heart. Such asynchronous contractions can cause arrhythmias, or disturbances of cardiac rhythm, an example being ventricular fibrillation.
Cardiac hypertrophy means an increase in size of cardiomyocytes. To accommodate this large size, the cells need to assemble more sarcomeres and synthesize more mitochondria. They are also marked by enlarged nuclei and greater protein production. Hypertrophy has several possible causes, each one leading to a particular pattern or type.
- Pressure overload hypertrophy is often caused by hypertension. It involves an increase in the myocyte cross-sectional area due to the assembly of new sarcomeres, in a parallel fashion to the old ones. It usually affects the ventricles by increasing the thickness of their walls.
- Volume overload hypertrophy is caused by an abnormally high blood return to the heart. It involves new sarcomeres being formed at the end of old ones, increasing their length of the myocyte rather than their thickness. This type dilates the ventricles and makes the heart heavier.
Cardiac hypertrophy results in a heart that has very high metabolic and oxygen demands, but insufficient supply due to the extremely high consumption and lack of new capillaries. In turn, the workload is increased and ischemia is possible, eventually resulting in cardiac failure and death.
It is important to realise that cardiac hypertrophy is a completely different condition compared to myostatin-related muscle hypertrophy. The latter is rare and genetic in nature. In addition, it does not cause any medical problems for the affected individual.