Introduction
Muscle is an organ that specializes in the conversion of chemical energy into movement which if necessary for life. Movement occurs in several forms ranging from cytoplasmic streaming to neuron growth at a cellular level to a sprinter’s explosive performance or albatross distance. Muscles are packed with movement-related proteins. Muscles are characterized into three categories namely skeletal muscle responsible for locomotion or flight, cardiac muscle that has the ability to function for a longer time and smooth muscle that lines arterial walls to control blood pressure or causes intestinal movement to control food digestion. Muscle contraction requires the supply of energy from ATP obtained from metabolism of fatty acids and glucose, but the amount of consumed energy varies depending on the types of muscle. This essay compares the similarities and differences in contraction and excitation of the three types of muscles.
Excitation in Skeletal Muscles
The contact area between a skeletal muscle cell and the end of a motor nerve is known as the motor end plate, and it contains acetylcholine, which transmits excitation. Skeletal muscle cell contains excitable sarcolemma that allows the spread of stimuli to the entire muscle via mediation of voltage-gated ion channels. Sarcolemma invaginations form the T-tubule system that initiates excitation of the muscle fiber near the border between the I- and A-bands of the myofibrils. T-tubules closely oppose cisternae generated by the sarcoplasmatic reticulum, an association known as a triad. The proteins in between the cisternae and the T-tubule mediate the excitation-contraction coupling. These proteins can change shape to open calcium channels and consequently permit calcium to enter the cytoplasm near the myofilaments. Actin and myosin interaction take place in resting muscle cells in tropomyosin. Calcium then binds to troponin-C to induce a change in the troponin-tropomyosin complex thereby allowing myosin and actin interaction leading to contraction (Treves 2009, p. 3074).
The nervous system causes excitation of skeletal muscles. Impulses are transmitted from nerves to skeletal muscle fibers. Every nerve fiber can stimulate from three to hundreds of muscle fibers. The movement of the action potential is on both directions of the ends of the muscle fibers. The nerve terminals secrete acetylcholine. Once in the neuromuscular junction, the nerve impulses stimulate the release of vesicles with acetylcholine into the synaptic space. Acetylcholineesterase either destroys acetylcholine that is present in the synaptic space, or it diffuses. A plate potential produced by acetylcholine at the end can either excite the skeletal muscle fiber or not (Treves 2009, p. 3076).
Excitation in Smooth Muscles
Excitation contraction in smooth muscles takes place through pharmaco-mechanical, mechano-mechanical and electro-mechanical coupling. The nervous system causes excitation or inhibition of smooth muscles. In electro-mechanical coupling, smooth muscles are excited by depolarization of the sarcolemma which opens voltage-gated Ca2+ channels to result in the movement of Ca2+ from the extracellular fluid into the sarcoplasm. The Ca2+ stimulates Ca2t release from the sarcoplasmic reticulum, a phenomenon referred to as Ca2+ induced Ca2+ release (CICR). Excitation of smooth muscles via pharmacochemical coupling is caused by chemical agents when a membrane depolarization is present. Hormones and neurotransmitters bind to ligand-gated Ca2+ channels located on the sarcolemma opening them up to allow inflow of Ca2+ from the ECF. Smooth muscle excitation via mechano-mechanichal coupling occurs from a stretch that opens up stretch-sensitive Ca2+ channels located on the sarcolemma thgus allowing inflow of Ca2+ from the ECF.
Excitation in Cardiac Muscles
Myocardium excitation begins at the sinuatrial node located in the right atrium wall on the lateral side where the superior vena cava opens into the atrium. Excitation reaches the atrioventricular node located at the interatrial base. The atria myocardium is separated from ventricles by the heart’s fibrous body that prevents excitation spread right from the atrial to the ventricular muscles cells (Fisher, Sobie, Thakor & Tuna 1996, p. 1357). The nervous system causes excitation or inhibition of cardiac muscles. Excitation is through the ionic permeabilites and electrogenic active transport including the depletion and accumulation of extracellular potassium. The rapid sodium current that spikes the action potential as well as the slow calcium or sodium inward current that is responsible for the plateau are both controlled by inactivation and activation variables, but the closing and opening of corresponding conductance is variable. This results in slow action potentials from a rapidly ascending phase of partially depolarized fibers. Many components of depolarizing currents, some controlled by intracellular calcium exist. Depolarization in purkinje fibers is more labile as compared to myocardium (Coraboeuf 2005, p. 15).
Contraction in Skeletal Muscles
Contraction in skeletal muscles occurs through a mechanism of sliding filament. The interaction between myosin cross-bridges and the actin filaments generate mechanical forces that lead to the inward sliding of the actin filaments amid the myosin filaments. These forces are inhibited in resting conditions. A travel of an action potential above the fiber membrane causes the sarcoplasmic reticulum to release large amounts of calcium ions, which in turn activates the forces between the myosin and the actin and consequently initiates contraction (Prosser et al. 2008, p. 5050).
Regulation of contraction in skeletal muscles is voluntary through axon terminals located in the somatic nervous system. In skeletal muscles, contractile strength increases depending on the degree of stretch. Contraction is non-rhythmic while the speed of contraction is slow to fast.
Contraction in Smooth Muscles
The sliding filament mechanism that involves thin and thick filaments occurs during contraction of smooth muscles to generate tension, which is transmitted to the intermediate filaments. The latter creates tension on the dense bodies joined to sarcolemma hence shortening the length of the muscle fiber. A contracting smooth muscle fiber rotates the same way a corkscrew turns. Smooth muscles depend on two primary sources of calcium to initiate contraction. These include calcium located in the S.R. of the smooth muscle cell and extracellular calcium entering the muscle cell through calcium channels located on the membrane of the smooth muscle cell (Devine & Somlyo 2006, p. 677).
Regulation of contraction in smooth muscles is involuntary via autonomic nerves, stretch and hormones. Stretch in smooth muscles causes a stress-relaxation response. In smooth muscles, contractions are slower as compared to the skeletal and cardiac muscles. However, smooth muscles have the ability of maintaining a forceful contraction for a longer period with a specific amount of ATP. The prolonged contractions are facilitated by the ‘latch mechanism’; a process reduces the extent of muscle activation to a lesser level than the initial while still maintaining its full contraction force. The advantage of the latch mechanism is its ability to prolong tonic contractions for hours with minimum energy use. Smooth muscles are able to contract when half to twice its resting length (Mikawa et al. 1978, p.1634). Furthermore, smooth muscles can change in fiber length with no change in tautness. This allows smooth muscles, for example, in the blood vessels and the gall bladder to change lumen diameters to become either large or small. The mechanism allows these organs to store contents temporarily. Another special feature of smooth muscles is hyperplasia, the ability of its cells to divide and multiply like estrogenic effects during pregnancy.
Contraction in Cardiac Muscles
Contraction in cardiac muscles occurs because of inward sliding of myosin myofilaments in order to increase the length of sarcomere. Calcium release from the sarcolemma mediates excitation contraction coupling. Polarization of the sarcolemma of an activated muscle takes place. The resting potential, which refers to unstimulated state of a muscle cell, is produced through the presence intracellular nucleic acids and negatively charged proteins. Therefore, polarization occurs when there is a balance between intracellular K+ and extracellular Na+. An action potential depolarizes the cell by upsetting the balance of K+ and Na+. During and after an action potential, a series of events in contractile muscle fibers is the same as in skeletal muscles (Balke & Goldman 2003, p. 350).
Regulation of contraction in cardiac muscles is involuntary through the intrinsic system regulation, stretch, hormones as well as autonomic nervous system control. The contractile strength of cardiac muscles increases depending on the degree of stretch. Contraction is rhythmic, but the speed of contraction is slow (Lakatta 1987, p.528). Cardiac muscles cannot maintain a contraction, therefore; they are able to beat constantly. It contracts and relaxes promptly with a contraction period of half the relaxation period to give it plenty of rest. Smooth muscles have strictly programmed rest and contraction periods. Thus, the cardiac muscle is the only muscle unable to attain a sustained contraction state, except in cases of disease (Johansson & Somlyo 2011, p. 311).
Similarities
The nervous system causes excitation or inhibition of smooth and cardiac muscles. The speed of contraction is relatively slow in both cardiac and smooth muscles as compared skeletal muscles. Contractile strength in skeletal and cardiac muscles increases depending on the degree of stretch. Cardiac and smooth muscles have rhythmic contractions. Contraction in all the three muscles consists of reactions between action and myosin via the sliding filament mechanism. In addition, their activation is via a rise in intracellular calcium ions and membrane impulses. All types of muscles utilize energy from Adenosine Tryphosphate (ATP). Smooth and cardiac muscles have the ability to contract without stimulation by the nervous system. On the other hand, contraction in both muscles can be stimulated by the autonomic nervous system but with moderating effects on the strength and rate of muscle contraction (Caputo 1978, p. 71).
| Summary of Excitation and Contraction in Skeletal, Cardiac and Smooth Muscles | |||
| Characteristic | Skeletal | Cardiac | Smooth |
| Nervous system stimulation effect | Excitation | Excitation or inhibition | Excitation or inhibition |
| Contraction speed | Slow to fast | Slow | Extremely slow |
| Rhythmic contraction | No | Yes | Yes in the single unit muscle |
| Stretch response | The degree of stretch determines the contractile strength | The degree of stretch determines the contractile strength | Stress-relaxation response |
| Regulation of contraction | Voluntary through axon terminals of the somatic nervous system | Involuntary via stretch, hormones, autonomic nervous system and intrinsic system regulation | Involuntary via local chemicals, stretch and autonomic nerves |
Table 1 Summary of Excitation and Contraction in Skeletal, Cardiac and Smooth Muscles
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