Three Features Of Cardiac Muscles

Comprehensive Introduction to Essential Cardiac Muscles

Cardiac muscles are unique muscle fibers found solely in the heart. They facilitate the mechanical activities necessary to keep blood moving around the body continuously. Heart muscle cells powerfully contract to eject blood from the heart into the arterial circulation and then relax to accept blood into the heart from the venous circulation. 

These muscle cells are involuntary - we cannot consciously control them. When they contract, the results are usually termed contractions or beats. Every time a heart muscle cell relaxes, it becomes ready to contract again. This rhythm continues as long as we are alive, and it never stops. A temporary pause is called deadly, and a prolonged pause is called death.

Cardiac muscle cells constitute the myocardium, which is central to the functioning of the heart and is composed solely of muscle cells. Cardiac muscle cells rhythmically and continuously contract to provide the energy and force required to pump blood throughout the body. 

This ensures that all tissues receive an uninterrupted supply of blood and nutrients and that metabolic wastes are removed from the body. The myocardium is mostly composed of muscle cells and has no neuron- or glial-like supporting cells. Two major cell types can usually be identified in the myocardial cells: contractile cells and non-contractile cells. 

The contractile cells are of paramount importance in cardiac function as they function to contract and relax the myocardium. In general, the term 'myocardial cell' refers to the cardiac muscle cells of the heart. 

Overall, the concept of a 'cell' cannot be strictly restricted to the common cell of the immunohistological anatomy because structural, biochemical, and functional differences occur. The term 'cardiomyocytes' defines morphologically and functionally classical myocardial cells.

Structural Characteristics of Cardiac Muscles

Cardiac muscles have some characteristic features because their function is different from that of other muscle cells. Cardiac muscle cells are called cardiomyocytes. The microscopic images of the cardiomyocyte show us their special structural adaptation. 

Cardiomyocytes are multinucleated and have a lot of mitochondria and myoglobin in their cytoplasm because cardiac muscle is the most energetic tissue in mammals. In addition, cardiomyocytes have a branched and interconnected structure that allows them to be electrically and mechanically connected. 

The length of the cells varies between 20–200 μm, and the diameter changes between 10–25 μm.

The protrusions of the cardiomyocyte can be seen as if they were pricked; these are called T-tubules. The region of the plasma membrane attached to the T-tubules and the two lateral sarcoplasmic reticular is specially called a triad. 

The triads can be seen in close proximity to the Z line in the sarcomeres. Cardiomyocytes have a special membrane structural modification called intercalated disks at the ends. Each intercalated disk is divided into three regions: the zonula adherens or adhering region, the fascia adherens or adhering region, and the gap junction or the coupling region. 

The intercalated disk units end in folds that promote electrical coupling via gap junctions between compartments. The main storage organelle of Ca2+ in cardiomyocytes is the sarcoplasmic reticulum. Besides intensive sarcoplasmic reticulum, cardiomyocytes contain a lot of mitochondria to provide the energy requirement of their working, myofibrils consisting of actin and myosin proteins. 

Cardiomyocytes contain quite a lot of glycogen and lipid both inside the myofibrils and between the myofibrils.

It is arranged in sheets called lamellae. While the longitudinal layer is formed mainly by the continuous lines of myofibrils in the lobes of the endocardium and the outer parts of the epicardium, the cross-sectional myocardium is composed of the intersection of the myofibrils in the central parts of the lobes of the epicardium. 

Cardiomyocytes share a lot of features with the cells of skeletal muscles and smooth muscles. Like skeletal muscle cells, cardiomyocytes can produce contractions, unlike smooth muscle cells, which can create contractions. 

For this reason, skeletal and cardiac muscles contract in a manner, whereas smooth muscles have slower contractile mechanisms. In contrast to striated skeletal muscle cells, the striation distance in a cardiomyocyte is shorter since they are smaller than muscle cells.

Functional Properties of Cardiac Muscles

Functional Properties Automaticity. Frequently, the heart will need to adjust its functioning to reflect changes in the blood that is being sent through the body. Cardiac muscles are myogenic, which means they are able to generate electrical impulses on their own without the need for an external stimulus. 

A single electrical signal can travel through the heart and stimulate the cells to contract. While there are exceptions, it is understood that this excitation usually travels in only one direction. Thus, the cells contract as a single unit.

Mechanism of Contraction. The contraction mechanism in cardiac muscles is produced by the sliding of protein filaments against each other. The sliding filament theory, used to describe the general process, is briefly this: The filaments slide by using the energy released by the breakdown of ATP. 

The position of the troponin-tropomyosin complex on the thin filaments is determined by the movement of calcium into the sarcoplasm. The arrival of calcium triggers the troponin-tropomyosin to move laterally, so the active sites on actin are exposed. 

More cross-bridges now form to produce a contraction. As more calcium moves into the sarcoplasm, more active sites are exposed, and stronger contractions result.

Several variables that contribute to the heart's ability to pump blood effectively are: 

Length-tension relationship. Elasticity allows stretching to a point, providing strong tubing for propulsion. 

Frank-Starling law of the heart. The heart pumps all the blood it receives. 

Cardiac reserve. The ability of the heart to adjust its functioning to meet changes in workload or lifestyle is due to the characteristics of its specialized cells. 

This capability also allows the heart muscle time to recover in between contractions. Diseases affecting the functioning of the cardiac muscle are thus often life-threatening. To prevent this from occurring, it will be necessary to ensure that the functional properties of the heart muscle are preserved.

Interactions with the Autonomic Nervous System

The ANS consists of two branches: the sympathetic and parasympathetic systems. The role of the sympathetic system is to exercise control over the "4 F's", i.e., fight, flight, feeding, and copulation. 

Its action in the heart is to increase the heart rate and contractility by releasing norepinephrine from nerve terminals that act on beta-adrenergic receptors. In contrast, the parasympathetic system has the role of "rest and digest." 

Its influence on the heart is to decrease the heart rate by releasing acetylcholine from terminals that act on muscarinic receptors. The positive and negative inotropic effects operated in the atria and ventricles allow the heart to pump more blood and adapt to the new energetic demands of the body by modifying the ejection fraction of the ventricles. 

Negative inotropy allows the heart to store more blood, while positive inotropy results in increased cardiac output. The balance between these two effects determines the final changes in cardiac output.

A conceptual classification of neurohormonal modulation in the heart is based on the presence of feedback mechanisms. Feed-forward is a control system principle that involves a change in stimulus leading to a direct change in the physiological response. 

In the setting of a healthy heart, these are immediate "powering up" and "powering down" effects triggered by both hormonal factors and chemoreceptors that usually reduce cardiac cycle time and amplitude in a synchronized way. 

With baroreceptors acting as central mediators, these effects are counteracted during long-term increased demands such as exercise stress. Baroreceptors are nerve endings that are positioned primarily in the carotid sinus, arterial wall, lung, heart, and aortic arch to monitor sinus blood pressure. 

When the heart senses high blood pressure or excessive cardiac output above the physiological range, it triggers a signal from the baroreceptors to the brain that describes the "vagus brake." 

The end result of increasing parasympathetic tone to the heart is an intrinsic increase in cardiac contractility and a decrease in heart rate. Overall, therapeutic strategies aiming at modulating the autonomic nervous system through neural circuits overwhelmingly dominate preclinical research. 

Contrariwise, only a handful of these devices have entered clinical trials; thus, it is important to emphasize the limited knowledge of precisely how the heart and kidneys interact with respect to the autonomic nervous system.

Check out:

National Institutes of Health (NIH): https://www.nhlbi.nih.gov/health/heart