Q.9 Give an account of the fine structure of striated muscle fibres and describe the physiology of muscle contraction in brief. (2006, 2008)
Other Related Questions -
Q. Write a short note on striated muscles. (2009)
Q. Describe the mechanism of muscle contraction. (2010, 12 , 14)
Q. Write short note on Muscle contraction. (2015)
Q. Describe the ultra structure of Skeletal of muscle and explain mechanism of muscle contraction. (2016)
Q. Describe the mechanism of muscle contraction with suitable illustrations. (2018)
Ans. Striated muscle is a form of fibers that are combined into parallel fibers. More specifically, it can refer to:
· Skeletal muscle · Cardiac muscle~cardiac referring to the heart.
In practice, the term “striated muscle” is sometimes used to refer exclusively to skeletal muscle when distinguishing it from smooth muscle.
Structure of Skeletal Muscle: -
Skeletal muscles are usually attached to bone by tendons composed of connective tissue. This connective tissue also ensheaths the entire muscle & is called epimysium. Skeletal muscles consist of numerous subunits or bundles called fasicles (or fascicles). Fascicles are also surrounded by connective tissue (called the perimysium) and each fascicle is composed of numerous muscle fibers (or muscle cells). Muscle cells, ensheathed by endomysium, consist of many fibrils (or myofibrils), and these myofibrils are made up of long protein molecules called myofilaments. There are two types of myofilaments in myofibrils: thick myofilaments and thin myofilaments.
Skeletal muscles vary considerably in size, shape, and arrangement of fibers. They range from extremely tiny strands such as the stapedium muscle of the middle ear to large masses such as the muscles of the thigh. Skeletal muscles may be made up of hundreds, or even thousands, of muscle fibers bundled together and wrapped in a connective tissue covering. Each muscle is surrounded by a connective tissue sheath called the epimysium. Fascia, connective tissue outside the epimysium, surrounds and separates the muscles. Portions of the epimysium project inward to divide the muscle into compartments. Each compartment contains a bundle of muscle fibers. Each bundle of muscle fiber is called a fasciculus and is surrounded by a layer of connective tissue called the perimysium. Within the fasciculus, each individual muscle cell, called a muscle fiber, is surrounded by connective tissue called the endomysium. Skeletal muscles have an abundant supply of blood vessels and nerves. Before a skeletal muscle fiber can contract, it has to receive an impulse from a neuron. Generally, an artery and at least one vein accompany each nerve that penetrates the epimysium of a skeletal muscle. Branches of the nerve and blood vessels follow the connective tissue components of the muscle of a nerve cell and with one or more minute blood vessels called capillaries.
Skeletal muscle is the muscle attached to the skeleton. Hundreds or thousands of muscle fibers (cells) bundle together to make up an individual skeletal muscle. Muscle cells are long, cylindrical structures that are bound by a plasma membrane (the sarcolemma) and an overlying basal lamina and when grouped into bundles (fascicles) they make up muscle. The sarcolemma forms a physical barrier against the external environment and also mediates signals between the exterior and the muscle cell.
The sarcoplasm is the specialized cytoplasm of a muscle cell that contains the usual subcellular elements along with the Golgi apparatus, abundant myofibrils, a modified endoplasmic reticulum known as the sarcoplasmic reticulum (SR), myoglobin and mitochondria. Transverse (T)-tubules invaginate the sarcolemma, allowing impulses to penetrate the cell and activate the SR. As shown in the figure, the SR forms a network around the myofibrils, storing and providing the Ca2+ that is required for muscle contraction.
Myofibrils are contractile unit s that consist of an ordered arrangement of longitudinal myofilaments. Myofilaments can be either thick filaments (comprised of myosin) or thin filaments (comprised primarily of actin). The characteristic ‘striations’ of skeletal and cardiac muscle are readily observable by light microscopy as alternating light and dark bands on longitudinal sections. The light band, (known as the I-band) is made up of thin filaments, whereas the dark band (known as the A-band) is made up of thick filaments. The Z-line (also known as the Z-disk or Z-band) defines the lateral boundary of each sarcomeric unit. Contraction of the sarcomere occurs when the Z-lines move closer together, making the myofibrils contract, and therefore the whole muscle cell and then the entire muscle contracts
Muscle contraction: -
(1) Because skeletal muscle is voluntary muscle, contraction requires a nervous impulse. So, step 1 in contraction is when the impulse is transferred from a neuron to the SARCOLEMMA of a muscle cell.
(2) The impulse travels along the SARCOLEMMA and down the T-TUBULES. From the T-TUBULES, the impulse passes to the SARCOPLASMIC RETICULUM.
(3) As the impulse travels along the Sarcoplasmic Reticulum (SR), the calcium gates in the membrane of the SR open. As a result, CALCIUM diffuses out of the SR and among the myofilaments.
(4) Calcium fills the binding sites in the TROPONIN molecules. As noted previously, this alters the shape and position of the TROPONIN which in turn causes movement of the attached TROPOMYOSIN molecule.
(5) Movement of TROPOMYOSIN permits the MYOSIN HEAD to contact ACTIN.
(6) Contact with ACTIN causes the MYOSIN HEAD to swivel.
(7) During the swivel, the MYOSIN HEAD is firmly attached to ACTIN. So, when the HEAD swivels it pulls the ACTIN (and, therefore, the entire thin myofilament) forward. (Obviously, one MYOSIN HEAD cannot pull the entire thin myofilament. Many MYOSIN HEADS are swivelling simultaneously, or nearly so, and their collective efforts are enough to pull the entire thin myofilament).
(8) At the end of the swivel, ATP fits into the binding site on the cross-bridge & this breaks the bond between the cross-bridge (myosin) and actin. The MYOSIN HEAD then swivels back. As it swivels back, the ATP breaks down to ADP & P and the cross-bridge again binds to an actin molecule.
(9) As a result, the HEAD is once again bound firmly to ACTIN. However, because the HEAD was not attached to actin when it swivelled back, the HEAD will bind to a different ACTIN molecule (i.e., one further back on the thin myofilament). Once the HEAD is attached to ACTIN, the cross-bridge again swivels, SO STEP 7 IS REPEATED.
As long as calcium is present (attached to TROPONIN), steps 7 through 9 will continue. And, as they do, the thin myofilament is being “pulled” by the MYOSIN HEADS of the thick myofilament. Thus, the THICK & THIN myofilaments are actually sliding past each other. As this occurs, the distance between the Z-lines of the sarcomere decreases. As sarcomeres get shorter, the myofibril, of course, gets shorter. And, obviously, the muscle fibers (and entire muscle) get shorter.
Skeletal muscle relaxes when the nervous impulse stops. No impulse means that the membrane of the SARCOPLASMIC RETICULUM is no longer permeable to calcium (i.e., no impulse means that the CALCIUM GATES close). So, calcium no longer diffuses out. The CALCIUM PUMP in the membrane will now transport the calcium back into the SR. As this occurs, calcium ions leave the binding sites on the TOPONIN MOLECULES. Without calcium, TROPONIN returns to its original shape and position as does the attached TROPOMYOSIN. This means that TROPOMYOSIN is now back in position, in contact with the MYOSIN HEAD. So, the MYOSIN head is no longer in contact with ACTIN and, therefore, the muscle stops contracting (i.e., relaxes)
So, under most circumstances, calcium is the “switch” that turns muscle “on and off” (contracting and relaxing). When a muscle is used for an extended period, ATP supplies can diminish. As ATP concentration in a muscle declines, the MYOSIN HEADS remain bound to actin and can no longer swivel. This decline in ATP levels in a muscle causes MUSCLE FATIGUE. Even though calcium is still present (and a nervous impulse is being transmitted to the muscle), contraction (or at least a strong contraction) is not possible.
Q.10 What is nerve impulse? How does it originate and travel upto the synapse. (2006)
Related Questions -
Q. Mention the structure of a chemical synapse and explain the transmission of nerve impulse across these. (2008)
Q. Write a short note on nerve conduction. (2007, 11, 14)
Q. Describe the transmission of nerve impulse along a nerve fibre. (2009)
Q. Give an account of transmission of nerve impulses at synapses. (2010)
Q. Give an account of transmission of nerve impulses at synapses. (2015)
Q. Write short note on transmission of nerve impulses. (2016)
Q. What is action potential? How does it form and travel from presynaptic to postsynaptic neurons? Explain with suitable diagrams. (2018)
Ans. Nerve signals are transmitted from one neuron to the next through interneuronal junctions called synapses. There are two types of synapses-
(1) The chemical synapse (2) The electrical synapse
Almost all the synapse used for signal transmission in the central nervous system of the human beings are chemical synapses. In these the first neuron secretes a chemical substance called a neurotransmitter at the synapse and this transmitter in turn acts on receptor proteins in the membrane of the next neuron to excite the neuron, inhibit it or modify its sensitivity in some other way. For example acetylcholine, dopamine, norepinephrine, histamine, serotonin, glycine etc.
Chemical synapse always transmit the signals in one –direction that is from the neuron that secretes the transmitter called the presynaptic neuron to the neuron on which the transmitter acts called the postsynaptic neuron.
Presynaptic terminals have varied anatomical forms such as-terminal knobs, boutons or synaptic knobs. It is separated from the post synaptic neuronal soma by a synaptic cleft having a width usually of 200 to 300 angstroms. The transmitter vesicles contain a transmitter substance that when released into the synaptic cleft either excites or inhibits the postsynaptic neuron. The mitochondria provide ATP which supplies the energy to synthesize new transmitter substance.
When an action potential spreads over a presynaptic terminal the membrane depolarization causes emptying of a small number of vesicles into the cleft.
Nerve Action Potential: -
Nerve signals are transmitted by action potentials which are rapid changes in the membrane potential. Each action potential begins with a sudden change from the normal resting negative potential to a positive membrane potential and then ends with an almost equally rapid change back to the negative potential. To conduct a nerve signal the action potential moves along the nerve fibres until it comes to the fibre‘s end.
The successive stages of the action potential are as follows-
Resting Stage: -
This is the resting membrane potential before the action potential occurs. The membrane is said to be polarized during this stage because of the large negative membrane potential that is present.
The resting membrane potential is about -65 millivolt of the soma of a motor neuron.This is somewhat less than the -90 millivolt found in large peripheral nerve fibres and skeletal muscle fibres.
The immediate cause of the -65 mv RMP is the high concentration of potassium ions inside the neuronal cell membrane and its low concentration outside. In the resting stage the membrane is much more permeable to potassium ions than to sodium ions, therefore the high potassium concentration inside the membrane multiplied by the high permeability for potassium causes large numbers of the positively charged potassium ions to diffuse outward. Because there are large numbers of negatively charged ions still inside the soma that cannot diffuse outward through the membrane –protein ions, phosphate ions and many others –extrusion of the excess positive potassium ions to the exterior leaves these non diffusible negative ions inside the cell unbalanced by positive ions. Therefore the interior of the neuron becomes negatively charged as the result of the potassium diffusion.
Depolarization Stage: -
At this time the membrane suddenly becomes permeable to sodium ions allowing tremendous numbers of positively charged sodium ions to flow to the interior of the axon. The normal polarized state of -90 millivolt is lost with the potential rising rapidly in the positive direction. This is called depolarization. In large nerve fibres the membrane potential overshoots beyond the zero level and becomes somewhat positive but in some smaller fibres as well as many central nervous system neurons the potential merely approaches the zero level and does not overshoot to the positive state.
Repolarization State: -
Within a few 10,00ths of a second after the membrane becomes highly permeable to sodium ions the sodium channels begin to close and the potassium ions to the exterior re establishes the normal negative resting membrane potential. This is called repolarization of the membrane.
Action Potential: -
First as long as the membrane of the nerve fibres remains undisturbed no action potential occurs in the normal nerve. However if any event causes enough initial rise in the membrane potential from -90 mv up toward the zero level, the rising voltage itself will cause many voltage gated sodium channels to begin opening. This allows rapid inflow of sodium ions which cause still further rise of the membrane potential thus opening still more voltage gated sodium channels and allowing more streaming of sodium ions to the interior of the fibre. This process is a positive feedback vicious circle that once the feedback is strong enough will continue until all the voltage gated sodium channels have become activated. Then within another fraction of a millisecond the rising membrane potential causes beginning closure of the sodium channels as well as opening of potassium channels and the action potential soon terminates.
Threshold for Initiation of the Action Potential: -
An action potential will not occur until the initial rise in membrane potential is great enough to create the vicious circle described above. This occurs when the number of sodium ions entering the fibre becomes greater than the number of potassium ions leaving the fibres. A sudden rise in membrane potential of 15 to 30 mv usually is required. Therefore a sudden increase in the membrane potential in a large nerve fibre from -90 mv upto about -65mv usually causes the explosive development of the action potential. This level of -65 mv is said to be the threshold for stimulation.
All or None Law: -
Once an action potential has been elicited at any point on the membrane of a normal fiber the depolarization process will travel over the entire membrane if conditions are right or it might not travel at all if conditions are not right. This is called the all or none law and it applies to all normal excitable tissues. Occasionally the action potential will reach a point on the membrane at which it does not generate sufficient voltage to stimulate the next area of the membrane. When this occurs the spread of depolarization stops. Therefore for continued propagation of an impulse to occur. The ratio of action potential to threshold for excitation must at all times be greater than 1. This is called the safety factor for propagation.