Myocardial contractility or force of contraction represents the heart muscle, myocardium, or cardiac muscle’s inherent capability.
There exists a gradational level of irrevocability within various kinds of tissue. An example is the binding between the filaments of thick myosin and the thin actin tissue. This irrevocability results in the ability to develop changes in the force of contraction.
Calcium ions available in the cell are amenable to the degree of binding between different tissue types. The release of catecholamine within an intact heart at a specific time operates the sympathetic nervous system’s reaction or response.
This procedure regulates the concentration of calcium ions available inside the cytosol of cardiac muscle cells. The factor responsible for the increment in force of contraction is a rise in the level of intracellular calcium ions (Ca++) during muscle contraction.
This frequency helps in the stimulation of the muscles. When the stimulus frequency increases, the force of contraction rises to its maximum limit and then decreases rapidly.
Another factor responsible for the increment of the force of contraction is the rise in the circulation level of epinephrine and norepinephrine. These two are the neurotransmitters, belonging to a class of catecholamines; these two neurotransmitters also function as hormones. Both Epinephrine and Norepinephrine are responsible for the increased contractility.
All these factors are responsible for developing a force of contraction in the heart when required. A thick filament called cardiac myosin-binding protein-C (cMyBP-C) is a protein-associated filament. It contributes to the rate and force of contraction through interactions with both actin and myosin or either of these.
Increase in the Force of Contraction
During an action potential, the maintenance of higher calcium levels or increase in the influx of calcium in the cytosol of cardiac myocytes is responsible for the rise in the force of contraction.
A phenomenon called excitation-contraction coupling is responsible for the contraction of cardiac muscle fibres. The mechanism used behind this phenomenon is known as calcium-induced calcium release.
Several mechanisms are responsible for the increase in the force of contraction. These various mechanism are listed below:
- Sympathetic initiation
- Phosphorylating phospholamban
- Troponin C-mediated calcium sensitisation
- Phosphorylating L-type calcium channels
- Instantaneous increase in afterload
- Increased heart rate
- Drugs
- Increased level of calcium in the sarcoplasm
Sympathetic initiation
Sympathetic activation is a cause of sudden anger or fear, further resulting in arousal of physiological vigilance, increased heart rate, and increment in blood flow to the skeletal muscles.
The sympathetic nerves stimulate and increase the circulating levels of catecholamines. This aspect results in the rendering of adenylate cyclase by the Gs subunit of the receptor.
The cyclase activation results in increased cAMP. cAMP is responsible for Various effects, including phosphorylation of phospholamban.
Phosphorylating phospholamban
Phospholamban, also known as PLB or PLN, is a protein encoded by the PLN gene. It is responsible for regulating calcium (Ca2+) pumps in cardiac muscle cells.
The calcium stores in the sarcoplasmic reticulum get increased, resulting in a rise in the rate of myocardial relaxation. The expanded rate of calcium ions leads to increased levels of lusitropy.
Troponin C-mediated calcium sensitisation
Levosimendan induces Troponin C-mediated calcium sensitisation which does not impair relaxation.
Phosphorylating calcium channels
Phosphorylation of L-type calcium channels raises its porous property to calcium. It permits the association of more calcium within the myocyte cells, increasing the force of contraction.
Instantaneous increase in afterload
A rapid rise in systemic vascular resistance can cause a slight surge in inotropy.
A Rise in heart rate
Stimulation of inotropy also depends upon the increase in heart rate. This increase is due to the incapacity of Na+/K+-ATPase to cope with sodium influx at raised heart rates.
Drugs
Several drugs, such as Digitalis, are responsible for the increase in the force of contraction. These drugs inhibit the Na+/K+ pump and act as a positive inotropic representative.
Due to the reluctance of the Na+/K+, extra sodium is assembled in the cell. This fact will cause a slight decrease in the outlying of the cell. Calcium ions will be quadriplegic to pull out the cell by dint of the Na+/Ca++ antiporter.
Increased level of calcium in the sarcoplasm
An increased calcium level in the sarcoplasm will enable Troponin to utilise more calcium, resulting in increased force.
Decrease in the Force of Contraction
Maintaining a low calcium level in myocytes’ cytosol or decreasing the calcium influx reduces the force of contraction. A decrease various mechanisms do decrease the force of contraction:
- Hypercapnia, Anoxia or acidosis
- Parasympathetic activation
- Forfeiture in the bit of the myocardium
What Controls the Force of Heart Contraction?
The development of cardiac force of concentration and contraction coupling calcium ions is essential for cardiac excitation. Two major systems responsible for the intracellular concentration of Ca2+ are:
- The sarcoplasmic reticulum
- The sarcolemma reticulum
Protein dephosphorylation and phosphorylation are responsible for regulating the process of Ca2+ control in the cell. Protein dephosphorylation and phosphorylation are mediated by phosphatases and protein kinases, respectively.
Conclusion
The force of contraction in cardiac muscle is an essential function in the body. There are mainly five factors responsible for myocardial performance: conduction velocity, heart rate, afterload, preload, and force of contraction. If all these five factors are held constant, we can conclude that the force of contraction causes the change in myocardial performance.
Increased sympathetic excitement to the heart causes a rise in contractility and heart rate. A surge in contractility consequently increases stroke volume and thus causes an increase in preload, resulting in raised contraction force.