Cardiac And Skeletal Muscle Notes

Skeletal and Cardiac Muscle

Skeletal and cardiac muscle are two main types of muscle in the human body, and although they possess similarities both structurally and physiologically, differing functions have lead to important differences. Skeletal muscle is that found attached to the skeleton via aponeuroses and tendons, and upon contraction normally moves bones. Cardiac muscle is unique to the heart, whose regular contractions act as a pump. Both are striated due to the presence of sarcomeres arranged in myofibrils; both contract via the mechanism of cross-bridge cycling between myosin heads and F-actin filaments, and there are some superficial differences (e.g. skeletal muscle nuclei are peripheral and cardiac muscle nuclei are central in the cell), but they also differ in vital features which relate to their function. Firstly, methods of excitation-contraction coupling differ in the two muscle types. Secondly, cardiac myocytes are electrically coupled whereas skeletal muscle cells must be individually innervated. Thirdly, cardiac muscle must pump continuously to ensure blood supply around the body, and so creates its own action potentials (i.e. it is myogenic), whereas skeletal muscle is neurogenic. Another crucial dissimilarity is the way in which tensile force is increased: in cardiac muscle, an increase in contractility is brought about by a larger intracellular calcium ion concentration, but in skeletal muscle motor unit recruitment and twitch frequency summation are employed. Additionally, only skeletal muscle can be tetanised; this has important consequences for the maintenance of effective heartbeats. The mechanisms of ion exchanges which constitute the action potential also display variation in cardiac and skeletal myocytes. Finally, contractions are terminated by different mechanisms in muscle and heart tissue.

Excitation-contraction coupling in the heart has a different mechanism from that in skeletal muscle. In both muscle types, action potentials propagate along the sarcolemmas and membrane invaginations called transverse tubules (the heart has more of these: it contains axial T tubules in addition to skeletal muscle’s radial T tubules). These action potentials open L-type Ca²⁺ channels (DHP receptors), which are voltage-gated channels in the T tubules. They are mechanically coupled to different calcium release channels (ryanodine receptors) in the sarcoplasmic reticulum, such that opening of the L-type channel causes the Ca²⁺ release channels to open and allows the large amount of stored Ca²+ in the sarcoplasmic reticula to enter the sarcoplasm. In skeletal muscle, this is all that is required to raise [Ca²⁺]_i sufficiently for cross-bridge cycling, as many Ca²⁺-troponin complexes form and move to expose the sites on actin to which myosin heads can bind. Because the opening movement of the DHP receptors results in a large calcium efflux from the sarcoplasmic reticula, it is not necessary for any calcium ions to actually enter through these receptors and so skeletal muscle does not rely upon extracellular calcium ion concentration.

However, the heart is dependent upon extracellular calcium ion concentration; if a heart is placed in a solution containing no Ca²⁺ it stops beating because no calcium enters through the L-type Ca²⁺ channels. This influx is essential in cardiac muscle because here the ryanodine receptor feet, although located near clusters of DHP receptors, are not mechanically coupled to DHP receptor tetrads, and so raised intracellular Ca²⁺ levels are the only trigger for the opening of nearby ryanodine receptors. This is calcium-induced calcium-release (CICR), so called because the large stores of calcium ions in the sarcoplasmic reticulum are released into the sarcoplasm upon the signal of far smaller amounts of calcium entering the sarcoplasm from the T tubules. The influx of calcium ions from the two sources rapidly raises the intracellular calcium concentration, and together they can induce troponin C to bind to calcium and ultimately allow cross-bridge cycling and therefore muscle contraction to commence.

Cardiac myocytes are electrically coupled due to the presence of intercalated disks which connect branches of the myofibrils. These contain desmosomes for mechanical linkage and gap junctions, which connect the cytoplasm of adjacent cells. The gap junctions, or nexuses, are formed from two connexons (hexamers of connexin subunits), one on each membrane; two connexons bind together to form a channel with cytosol in the pore through which ions and other small molecules may travel. An action potential in one cell can therefore excite the next cell, so heart muscle is a functional syncytium. This means contractions are synchronised, so the atria and ventricles can effectively pump out a full stroke volume of blood per beat. Another essential effect is that the cells with the fastest action potentials will set the pace of the entire heartbeat, as when they depolarise this depolarisation will quickly spread to the other heart cells. In mammals this pacemaker region is the sino-atrial node (SAN). The advantage of having one pacemaker region is that there can be greater control of heartbeats. This is evidenced by the SAN’s pacemaker function, and also the effect of hormones e.g. circulating adrenaline, which increases SAN firing frequency and therefore heartbeat, by acting on one area. In contrast, skeletal myocytes do not have intercalated disks and cells must each be stimulated by a motor neuron synapse.

The SAN is able to regulate heartbeat rhythm and initiate action potentials because it is made up of myocytes which have a pacemaker potential; this is the gradual fall in negativity after the hyperpolarisation at the end of the action potential. This slow depolarisation arises from slowly activating sodium channels (there is no fast sodium influx in SAN cells) which allow sodium ions to enter the cell, opposing the...

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