Excitation and Contraction in Muscles

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.