Muscle Contraction Introduction .
[1]. The muscle contracts when it is stimulated. Contraction of the muscle is a physical or mechanical event. In addition, several other changes occur in the muscle.
[2]. Changes taking place during muscular contraction:
1. Electrical changes .
2. Physical changes .
3. Histological (molecular) changes .
4. Chemical changes
5. Thermal changes.
Electrical changes During Muscle Contraction .
[1]. Electrical events occur in the muscle during resting condition as well as active conditions.
[2]. Electrical potential in the muscle during resting condition is called resting membrane potential.
[3]. Electrical changes that occur in active conditions, i.e. when the muscle is stimulated are together called action potential.
[4]. Electrical potentials in a muscle (or any living tissue) are measured by using a cathode ray oscilloscope or computerized polygraph.
Resting membrane potential .
[1]. Resting membrane potential is defined as the electrical potential difference (voltage) across the cell membrane (between inside and outside of the cell) under resting condition.
[2]. It is also called membrane potential, transmembrane potential, transmembrane potential difference or transmembrane potential gradient.
[3]. When two electrodes are connected to a cathode ray oscilloscope through a suitable amplifier and placed over the surface of the muscle fiber, there is no potential difference, i.e. there is zero potential difference.
[4]. But, if one of the electrodes is inserted into the interior of muscle fiber, potential difference is observed across the sarcolemma (cell membrane).
[5]. There is negativity inside and positivity outside the muscle fiber. This potential difference is constant and is called resting membrane potential.
[6]. The condition of the muscle during resting membrane potential is called polarized state.
[7]. In human skeletal muscle, the resting membrane potential is –90 mV.
Ionic Basis of Resting Membrane Potential .
%20pump%20and%20diffusion%20of%20ions.jpg "Development of resting membrane potential by sodiumpotassium (Na+K+) pump and diffusion of ions") |
| Development of resting membrane potential by sodium-potassium (Na+K+) pump and diffusion of ions |
[1]. Development and maintenance of resting membrane potential in a muscle fiber or a neuron are carried out by movement of ions, which produce ionic imbalance across the cell membrane.
[2]. This results in the development of more positivity outside and more negativity inside the cell.
[3]. Ionic imbalance is produced by two factors:
1. Sodium-potassium pump
2. Selective permeability of cell membrane.
1. Sodium-potassium pump .
[1]. Sodium and potassium ions are actively transported in opposite directions across the cell membrane by means of an electrogenic pump called sodium-potassium pump.
[2]. It moves three sodium ions out of the cell and two potassium ions inside the cell by using energy from ATP.
[3]. Since more positive ions (cations) are pumped outside than inside, a net deficit of positive ions occurs inside the cell.
[4]. It leads to negativity inside and positivity outside the cell .
2. Selective permeability of cell membrane .
[1]. Permeability of cell membrane depends largely on the transport channels.
[2]. The transport channels are selective for the movement of some specific ions. Their permeability to these ions also varies.
[3]. Most of the channels are gated channels and the specific ions can move across the membrane only when these gated channels are opened.
[4]. Two types of channels are involved:
1 . Channels for major anions like proteins
2 . Leak channels.
1 . Channels for major anions (negatively charged substances) like proteins .
[1]. Channels for some of the negatively charged large substances such as proteins, organic phosphate and sulfate compounds are absent or closed.
[2]. Such substances remain inside the cell and play a major role in the development and maintenance of negativity inside the cell (resting membrane potential).
2. Leak channels .
[1]. Leak channels are the passive channels, which maintain the resting membrane potential by allowing movement of positive ions (Na+ and K+) across the cell membrane.
[2]. Three important ions, sodium, chloride and potassium are unequally distributed across the cell membrane. Na+ and Cl– are more outside and K+ is more inside.
[3]. Since, Cl– channels are mostly closed in resting conditions Cl– are retained outside the cell. Thus, only the positive ions, Na+ and K+ can move across the cell membrane.
[4]. Na+ is actively transported (against the concentration gradient) out of cell and K+ is actively transported (against the concentration gradient) into the cell. However, because of concentration gradient, Na+ diffuses back into the cell through Na+ leak channels and K+ diffuses out of the cell through K+ leak channels.
[5]. In resting conditions, almost all the K+ leak channels are opened but most of the Na+ leak channels are closed. Because of this, K+, which are transported actively into the cell, can diffuse back out of the cell in an attempt to maintain the concentration equilibrium.
[6]. But among the Na+, which are transported actively out of the cell, only a small amount can diffuse back into the cell. That means, in resting conditions, the passive K+ efflux is much greater than the passive Na+ influx.
[7]. It helps in establishing and maintaining the resting membrane potential. After establishment of the resting membrane potential (i.e. inside negativity and outside positivity), the efflux of K+ stops in spite of concentration gradient.
[8]. It is because of two reasons:
1. Positivity outside the cell repels positive K+ and prevents further efflux of these ions
2. Negativity inside the cell attracts positive K+ and prevents further leakage of these ions outside.
Importance of intracellular potassium ions .
[1]. Concentration of K+ inside the cell is about 140 mEq/L. It is almost equal to that of Na+ outside. The high concentration of K+ inside the cell is essential to check the negativity.
[2]. Normally, the negativity (resting membrane potential) inside the muscle fiber is –90 mV and in a nerve fiber, it is –70 mV.
[3]. It is because of the presence of negatively charged proteins, organic phosphates and sulfates, which cannot move out normally.
[4]. Suppose if the K+ is not present or decreased, the negativity increases beyond –120 mV, which is called hyperpolarization.
[5]. At this stage, the development of action potential is either delayed or does not occur.
Action potential .
[1]. Action potential is defined as a series of electrical changes that occur in the membrane potential when the muscle or nerve is stimulated.
[2]. Action potential occurs in two phases:
1. Depolarization
2. Repolarization.
Depolarization .
[1]. Depolarization is the initial phase of action potential in which inside of the muscle becomes positive and outside becomes negative.
[2]. That is, the polarized state (resting membrane potential) is abolished resulting in depolarization.
Repolarization .
[1]. Repolarization is the phase of action potential in which the muscle reverses back to the resting membrane potential.
[2]. That is, within a short time after depolarization the inside of muscle becomes negative and outside becomes positive. So, the polarized state of the muscle is reestablished.
Action potential curve.
.jpg "Action potential in a skeletal muscle") |
| Action potential in a skeletal muscle A = Opening of few Na+ channels B = Opening of many Na+ channels C = Closure of Na+ channels and opening |
[1]. Action potential curve is the graphical registration of electrical activity that occurs in an excitable tissue such as muscle after stimulation.
[2]. It shows three major parts:
1. Latent period
2. Depolarization
3. Repolarization.
Resting membrane potential in skeletal muscle is –90 mV and it is recorded as a straight baseline .
1. Latent Period .
[1]. Latent period is the period when no change occurs in the electrical potential immediately after applying the stimulus.
[2]. It is a very short period with duration of 0.5 to 1 millisecond.
[3]. When a stimulus is applied, there is a slight irregular deflection of baseline for a very short period. This is called stimulus artifact.
[4]. The artifact occurs because of the disturbance in the muscle due to leakage of current from stimulating electrode to the recording electrode. The stimulus artifact is followed by latent period.
2. Depolarization .
[1]. Depolarization starts after the latent period. Initially, it is very slow and the muscle is depolarized for about 15 mV.
[2]. After the initial slow depolarization for 15 mV (up to –75 mV), the rate of depolarization increases suddenly.
[3]. The point at which, the depolarization increases suddenly is called firing level.
[4]. From firing level, the curve reaches isoelectric potential (zero potential) rapidly and then shoots up (overshoots) beyond the zero potential (isoelectric base) up to +55 mV. It is called overshoot.
3. Repolarization .
[1]. When depolarization is completed (+55 mV), the repolarization starts.
[2]. Initially, the repolarization occurs rapidly and then it becomes slow.
[3]. Rapid rise in depolarization and the rapid fall in repolarization are together called spike potential. It lasts for 0.4 millisecond.
[4]. Rapid fall in repolarization is followed by a slow repolarization. It is called after depolarization or negative after potential. Its duration is 2 to 4 milliseconds.
[5]. After reaching the resting level (–90 mV), it becomes more negative beyond resting level.
[6]. This is called after hyperpolarization or positive after potential. This lasts for more than 50 milliseconds. After this, the normal resting membrane potential is restored slowly.
Ionic Basis of Action Potential .
[1]. Voltage gated Na+ channels and the voltage gated K+ channels play important role in the development of action potential.
[2]. During the onset of depolarization, voltage gated sodium channels open and there is slow influx of Na+.
[3]. When depolarization reaches 7 to 10 mV, the voltage gated Na+ channels start opening at a faster rate. It is called Na+ channel activation.
[4]. When the firing level is reached, the influx of Na+ is very great and it leads to overshoot. But the Na+ transport is short lived. It is because of rapid inactivation of Na+ channels.
[5]. Thus, the Na+ channels open and close quickly. At the same time, the K+ channels start opening. This leads to efflux of K+ out of the cell, causing repolarization.
[6]. Unlike the Na+ channels, the K+ channels remain open for longer duration.
[7]. These channels remain opened for few more milliseconds after completion of repolarization.
[8]. It causes efflux of more number of K+ producing more negativity inside. It is the cause for hyperpolarization.
Monophasic Action Potential .
[1]. Monophasic action potential is the series of electrical changes that occur in a stimulated muscle or nerve fiber, which is recorded by placing one electrode on its surface and the other inside.
[2]. It is characterized by a positive deflection.
Biphasic Action Potential .
 |
| Biphasic action potential in an axon recorded by placing both the electrodes outside the axonA = Resting state – zero potential B = Depolarization of membrane under first electrode C = Repolarization of membrane under first electrode |
[1]. Biphasic or diphasic action potential is the series of electrical changes in a stimulated muscle or nerve fiber, which is recorded by placing both the recording electrodes on the surface of the muscle or nerve fiber.
[2]. It is characterized by a positive deflection followed by an isoelectric pause and a negative deflection.
Recording of biphasic action potential .
Biphasic action potential is recorded by extracellular electrodes, i.e. by placing both the recording electrodes on the surface of a nerve fiber or muscle.
Sequence of events of biphasic action potential:
[1] . In resting state before stimulation, the potential difference between the two electrodes is zero. So the recording shows a baseline .
[2] . When the axon is stimulated at one end, the action potential (impulse) is generated and it travels towards the other end of an axon by passing through the recording electrodes.
When the impulse reaches first electrode, the membrane under this electrode becomes depolarized (outside negative) but the membrane under second electrode is still in polarized state (outside positive).
[3] . When the impulse crosses and travels away from the first electrode, the membrane under this electrode is repolarized.
Later when the impulse just travels in between the two electrodes (before reaching the second electrode) the potential difference between both the electrode falls to zero and the baseline is recorded .
[4] . When the impulse reaches the second electrode, the membrane under this electrode is depolarized (outside negative) and a negative deflection is recorded .
[5] . When the impulse travels away from second electrode, the membrane under this gets repolarized. Once again the potential difference between the two electrodes becomes zero and the graph shows the baseline .
Since this recording shows both positive and negative components it is called biphasic action potential.
Effect of crushing or local anesthetics .
When a small portion of axon between the two electrodes is affected by crushing or local anesthetics, the action potential cannot travel through this part of the axon. So, while recording the potential only a single deflection (monophasic) action potential is recorded .
Compound Action Potential .
[1]. Compound action potential (CAP) is the algebraic summation of all the action potentials produced by all the nerve fibers.
[2]. Each nerve is made up of thousands of axons. While stimulating the whole nerve, all the nerve fibers are activated and produce action potential.
[3]. The compound action potential is obtained by recording all the action potentials simultaneously.
Graded potential .
[1]. Graded potential is a mild local change in the membrane potential that develops in receptors, synapse or neuromuscular junction when stimulated.
[2]. It is also called graded membrane potential, graded depolarization or local potential.
[3]. It is non-propagative and characterized by mild depolarization or hyperpolarization.
[4]. In most of the cases, the graded potential is responsible for the generation of action potential.
[5]. However, in some cases the graded potential hyper polarizes the membrane potential (more negativity than resting membrane potential) and inhibits the generation of action potential (as in inhibitory synapses: .
Different Graded potentials .
[1] . End plate potential in neuromuscular junction
[2] . Electronic potential in nerve fibers
[3] . Receptor potential
[4] . Excitatory postsynaptic potential
[5] . Inhibitory postsynaptic potential .
Patch-clamp technique .
[1]. Patch-clamp technique or patch clamping is the method to measure the ion currents across the biological membranes. This advanced technique in modern electro physiology was established by Erwin Neher in 1992.
[2]. Patch clamp is modified as voltage clamp to study the ion currents across the membrane of neuron.
Procedure .
[1]. Patch-clamp experiments use mostly the cultured cells.
[2]. The cells isolated from the body are placed in dishes containing culture media and kept in an incubator.
Probing a single cell .
[1]. The dish with tissue culture cells is mounted on a microscope.
[2]. A micropipette with an opening of about 0.5 µ is also mounted by means of a pipette holder. The pipette is filled with saline solution.
[3]. An electrode is fitted to the pipette and connected to a recording device called patch-clamp amplifier.
[4]. The micropipette is pressed firmly against the membrane of an intact cell.
[5]. A gentle suction applied to the inside of the pipette forms a tight seal of giga ohms (GΩ) resistance between the membrane and the pipette.
[6]. This patch (minute part) of the cell membrane under the pipette is studied by means of various approaches called patch-clamp configurations .
Patch-clamp Configurations .
1. Cell-attached patch .
The cell is left intact with its membrane. This allows measurement of current flow through ion channel or channels under the micropipette .
2. Inside-out patch .
[1]. From the cell-attached configuration, the pipette is gently pulled away from the cell. It causes the detachment of a small portion of membrane from the cell.
[2]. The external surface of the membrane patch faces pipette solution. But internal surface of the membrane patch is exposed out hence the name inside out patch .
[3]. Pipette with membrane patch is inserted into a container with free solution. Concentration of ions can be altered in the free solution.
[4]. It is used to study the effect of alterations in the ion concentrations on the ion channels.
3. Whole-cell patch .
[1]. From the cell-attached configuration, further suction is applied to the inside of the pipette.
[2]. It causes rupture of the membrane and the pipette solution starts mixing with intracellular fluid.
[3]. When the mixing is complete, the equilibrium is obtained between the pipette solution and the intracellular fluid .
[4]. Whole-cell patch is used to record the current flow through all the ion channels in the cell. The cellular activity also can be studied directly.
4. Outside-out patch .
[1]. From the whole-cell configuration the pipette is gently pulled away from the cell. A portion of membrane is torn away from the cell.
[2]. Immediately, the free ends of the torn membrane fuse and reseal forming a membrane vesicle at tip of the pipette.
[3]. The pipette solution enters the membrane vesicle and forms the intracellular fluid. The vesicle is placed inside a bath solution, which forms the extracellular environment .
[4]. This patch is used to study the effect of changes in the extracellular environment on the ion channels.
[5]. It also helps to study the effects of neurotransmitters and compounds like ozone, G-protein regulators, etc. on the ion channels.
Physical Changes During Muscular Contraction .
[1]. Physical change, which takes place during muscular contraction, is the change in length of the muscle fibers or change in tension developed in the muscle.
[2]. Depending upon this, the muscular contraction is classified into two types namely isotonic contraction and isometric contraction .
Histological Changes During Muscular Contraction .
Actomyosin Complex .
[1]. In relaxed state of the muscle, the thin actin filaments from opposite ends of sarcomere are away from each other leaving a broad ‘H’ zone.
[2]. During contraction of the muscle, actin (thin) filaments glide over myosin (thick) filaments and form actomyosin complex.
Molecular Basis of Muscular contraction .
Molecular mechanism is responsible for formation of actomyosin complex that results in muscular contraction. It includes three stages:
1. Excitation-contraction coupling.
2. Role of troponin and tropomyosin.
3. Sliding mechanism.
1. Excitation-contraction Coupling .
 |
| Excitation-contraction coupling . |
[1]. Excitation-contraction coupling is the process that occurs in between the excitation and contraction of the muscle.
[2]. This process involves series of activities, which are responsible for the contraction of excited muscle.
Stages of excitation-contraction coupling .
[1]. When a muscle is excited (stimulated) by the impulses passing through motor nerve and neuromuscular junction, action potential is generated in the muscle fiber.
[2]. Action potential spreads over sarcolemma and also into the muscle fiber through the ‘T’ tubules. [3]. The ‘T’ tubules are responsible for the rapid spread of action potential into the muscle fiber. When the action potential reaches the cisternae of ‘L’ tubules, these cisternae are excited.
[4]. Now, the calcium ions stored in the cisternae are released into the sarcoplasm .
[5]. The calcium ions from the sarcoplasm move towards the actin filaments to produce the contraction. [6]. Thus, the calcium ion forms the link or coupling material between the excitation and the contraction of muscle. Hence, the calcium ions are said to form the basis of excitation-contraction coupling.
2. Role of Troponin and Tropomyosin .
[1]. Normally, the head of myosin molecules has a strong tendency to get attached with active site of F actin.
[2]. However, in relaxed condition, the active site of F actin is covered by the tropomyosin. Therefore, the myosin head cannot combine with actin molecule.
[3]. Large number of calcium ions, which are released from ‘L’ tubules during the excitation of the muscle, bind with troponin C.
[4]. The loading of troponin C with calcium ions produces some change in the position of troponin molecule.
[5]. It in turn, pulls tropomyosin molecule away from F actin.
[6]. Due to the movement of tropomyosin, the active site of F actin is uncovered and exposed. Immediately the head of myosin gets attached to the actin.
3. Sliding Mechanism and Formation of Actomyosin Complex – Sliding Theory .
 |
| Sliding mechanism . |
[1]. Sliding theory explains how the actin filaments slide over myosin filaments and form the actomyosin complex during muscular contraction. It is also called ratchet theory or walk along theory. [2]. Each cross bridge from the myosin filaments has got three components namely, a hinge, an arm and a head.
[3]. After binding with active site of F actin, the myosin head is tilted towards the arm so that the actin filament is dragged along with it . This tilting of head is called power stroke.
[4]. After tilting, the head immediately breaks away from the active site and returns to the original position. Now, it combines with a new active site on the actin molecule.
[5]. And, tilting movement occurs again. Thus, the head of cross bridge bends back and forth and pulls the actin filament towards the center of sarcomere.
[6]. In this way, all the actin filaments of both the ends of sarcomere are pulled. So, the actin filaments of opposite sides overlap and form actomyosin complex.
[7]. Formation of actomyosin complex results in contraction of the muscle. When the muscle shortens further, the actin filaments from opposite ends of the sarcomere approach each other. So, the ‘H’ zone becomes narrow.
[8]. And, the two ‘Z’ lines come closer with reduction in length of the sarcomere. However, the length of ‘A’ band is not altered. But, the length of ‘I’ band decreases.
[9]. When the muscular contraction becomes severe, the actin filaments from opposite ends overlap and the ‘H’ zone disappears.
Changes in sarcomere during muscular contraction .
Thus, changes that take place in sarcomere during muscular contraction are:
1. Length of all the sarcomeres decreases as the ‘Z’ lines come close to each other .
2. Length of the ‘I’ band decreases since the actin filaments from opposite side overlap .
3. ‘H’ zone either decreases or disappears .
4. Length of ‘A’ band remains the same.
Energy for Muscular Contraction .
[1]. Energy for movement of myosin head (power stroke) is obtained by breakdown of adenosine triphosphate (ATP) into adenosine diphosphate (ADP) and inorganic phosphate (Pi).
[2]. Head of myosin has a site for ATP. Actually the head itself can act as the enzyme ATPase and catalyze the breakdown of ATP.
[3]. Even before the onset of contraction, an ATP molecule binds with myosin head.
[4]. When tropomyosin moves to expose the active sites, the head is attached to the active site. Now ATPase cleaves ATP into ADP and Pi, which remains in head itself.
[5]. The energy released during this process is utilized for contraction.
[6]. When head is tilted, the ADP and Pi are released and a new ATP molecule binds with head. This process is repeated until the muscular contraction is completed.
Relaxation of the Muscle .
[1]. Relaxation of the muscle occurs when the calcium ions are pumped back into the L tubules. When calcium ions enter the L tubules, calcium content in sarcoplasm decreases leading to the release of calcium ions from the troponin.
[2]. It causes detachment of myosin from actin followed by relaxation of the muscle .
[3]. The detachment of myosin from actin obtains energy from breakdown of ATP. Thus, the chemical process of muscular relaxation is an active process although the physical process is said to be passive.
Molecular Motors .
Along with other proteins and some enzymes, actin and myosin form the molecular motors, which are involved in movements.
Chemical Changes During Muscular Contraction .
Liberation of Energy .
Energy necessary for muscular contraction is liberated during the processes of breakdown and resynthesis of ATP.
Breakdown of ATP .
[1]. During muscular contraction, the supply of energy is from the breakdown of ATP.
[2]. This is broken into ADP and inorganic phosphate (Pi) and energy is liberated.
[3]. ATP → ADP + Pi ↓ Energy
[4]. Energy liberated by breakdown of ATP is responsible for the following activities during muscular contraction:
1. Spread of action potential into the muscle .
2. Liberation of calcium ions from cisternae of ‘L’ tubules into the sarcoplasm .
3. Movements of myosin head .
4. Sliding mechanism.
Energy liberated during ATP breakdown is sufficient for maintaining full contraction of the muscle for a short duration of less than one second.
Resynthesis of ATP .
[1]. Adenosine diphosphate, which is formed during ATP breakdown, is immediately utilized for the resynthesis of ATP. But, for the resynthesis of ATP, the ADP cannot combine with Pi.
[2]. It should combine with a high energy phosphate radical.
[3]. There are two sources from which the high energy phosphate is obtained namely, creatine phosphate and carbohydrate metabolism.
Resynthesis of ATP from creatine phosphate .
[1]. Immediate supply of high-energy phosphate radical is from the creatine phosphate (CP). Plenty of CP is available in resting muscle.
[2]. In the presence of the enzyme creatine phosphotransferase, high energy phosphate is released from creatine phosphate. The reaction is called Lohmann’s reaction.
[3]. ADP + CP → ATP + Creatine .
[4]. Energy produced in this reaction is sufficient to maintain muscular contraction only for few seconds.
[5]. Creatine should be resynthesized into creatine phosphate and this requires the presence of high energy phosphate. So, the required amount of high energy phosphate radicals is provided by the carbohydrate metabolism in the muscle.
Resynthesis of ATP by carbohydrate metabolism .
[1]. Carbohydrate metabolism starts with catabolic reactions of glycogen in the muscle. In resting muscle, an adequate amount of glycogen is stored in sarcoplasm.
[2]. Each molecule of glycogen undergoes catabolism, to produce ATP.
[3]. The energy liberated during the catabolism of glycogen can cause muscular contraction for a longer period.
[4]. The first stage of catabolism of glycogen is via glycolysis. It is called glycolytic pathway or Embden-Meyerhof pathway .
Glycolysis .
[1]. Each glycogen molecule is converted into 2 pyruvic acid molecules.
[2]. Only small amount of ATP (2 molecules) is synthesized in this pathway. This pathway has 10 steps. [3]. Each step is catalyzed by one or two enzymes .
[4]. During glycolysis, 4 hydrogen atoms are released which are also utilized for formation of additional molecules of ATP.
[5]. Formation of ATP by the utilization of hydrogen . Further changes in pyruvic acid depend upon the availability of oxygen.
[6]. In the absence of oxygen, the pyruvic acid is converted into lactic acid that enters the Cori cycle. It is known as anaerobic glycolysis.
[7]. If oxygen is available, the pyruvic acid enters into Krebs cycle. It is known as aerobic glycolysis.
Cori cycle .
[1]. Lactic acid is transported to liver where it is converted into glycogen and stored there.
[2]. If necessary, glycogen breaks into glucose, which is carried by blood to muscle. Here, the glucose is converted into glycogen, which enters the Embden-Meyerhof pathway .
Krebs cycle .
[1]. Krebs cycle is otherwise known as tricarboxylic acid cycle (TCA cycle) or citric acid cycle. A greater amount of energy is liberated through this cycle.
[2]. The pyruvic acid derived from glycolysis is taken into mitochondria where it is converted into acetyl coenzyme A with release of 4 hydrogen atoms.
[3]. The acetyl coenzyme A enters the Krebs cycle.
[4]. Krebs cycle is a series of reactions by which acetyl coenzyme A is degraded in various steps to form carbon dioxide and hydrogen atoms.
[5]. All these reactions occur in the matrix of mitochondrion.
[6]. During Krebs cycle, 2 molecules of ATP and 16 atoms of hydrogen are released. Hydrogen atoms are also utilized for the formation of ATP .
Significance of Hydrogen Atoms Released during Carbohydrate Metabolism .
Altogether 24 hydrogen atoms are released during glycolysis and Krebs cycle:
4H : During breakdown of glycogen into pyruvic acid
4H : During formation of acetyl coenzyme A from pyruvic acid
16H : During degradation of acetyl coenzyme A in Krebs cycle.
[1]. Hydrogen atoms are released in the form of two pockets into intracellular fluid and it is catalyzed by the enzyme dehydrogenase.
[2]. Once released, 20 hydrogen atoms combine with nicotinamide adenine dinucleotide (NAD), which acts as hydrogen carrier. NAD transfers the hydrogen atoms to the cytochrome system where oxidative phosphorylation takes place.
[3]. Oxidative phosphorylation is the process during which the ATP molecules are formed by utilizing hydrogen atoms.
[4]. For every 2 hydrogen atoms 3 molecules of ATP are formed. So, from 20 hydrogen atoms 30 molecules of ATP are formed.
[5]. Remaining 4 hydrogen atoms enter the oxidative phosphorylation processes directly without combining with NAD.
[6]. Only 2 ATP molecules are formed for every 2 hydrogen atoms. So, 4 hydrogen atoms give rise to 4 ATP molecules.
[7]. Thus, 34 ATP molecules are formed from the hydrogen atoms released during glycolysis and Krebs cycle.
Summary of Resynthesis of ATP during Carbohydrate Metabolism .
A total of 38 ATP molecules are formed during breakdown of each glycogen molecule in the muscle as summarized below:
During glycolysis : 2 molecules of ATP
During Krebs cycle : 2 molecules of ATP
By utilization of hydrogen : 34 molecules of ATP
Total : 38 molecules of ATP
Changes in pH During Muscular Contraction .
Reaction and the pH of muscle are altered in different stages of muscular contraction.
In Resting Condition .
During resting condition, the reaction of muscle is alkaline with a pH of 7.3.
During Onset of Contraction .
At the beginning of the muscular contraction, the reaction becomes acidic. The acidity is due to dephosphorylation of ATP into ADP and Pi.
During Later Part of Contraction .
During the later part of contraction, the muscle becomes alkaline. It is due to the resynthesis of ATP from CP.
At the End of Contraction .
At the end of contraction, the muscle becomes once again acidic. This acidity is due to the formation of pyruvic acid and/or lactic acid.
Thermal Changes During Muscular Contraction .
During muscular contraction, heat is produced. Not all the heat is liberated at a time. It is released in different stages:
1. Resting heat
2. Initial heat
3. Recovery heat.
Resting Heat .
Heat produced in the muscle at rest is called the resting heat. It is due to the basal metabolic process in the muscle.
Initial Heat .
During muscular activity, heat production occurs in three stages:
1. Heat of activation
2. Heat of shortening
3. Heat of relaxation.
1. Heat of Activation .
[1]. Heat of activation is the heat produced before the actual shortening of the muscle fibers.
[2]. Most of this heat is produced during the release of calcium ions from ‘L’ tubules. It is also called maintenance heat.
2. Heat of Shortening .
[1]. Heat of shortening is the heat produced during contraction of muscle.
[2]. The heat is produced due to various structural changes in the muscle fiber like movements of cross bridges and myosin heads and breakdown of glycogen.
3. Heat of Relaxation .
[1]. Heat released during relaxation of the muscle is known as the heat of relaxation.
[2]. In fact, it is the heat produced during the contraction of muscle due to breakdown of ATP molecule. It is released when the muscle lengthens during relaxation.
Recovery heat .
[1]. Recovery heat is the heat produced in the muscle after the end of activities.
[2]. After the end of muscular activities, some amount of heat is produced due to the chemical processes involved in resynthesis of chemical substances broken down during contraction .
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