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MUSCLE PHYSIOLOGY INDIAN DENTAL ACADEMY Leader in continuing dental education


Muscles are broadly classified into 3 types – Skeletal muscle – Smooth muscle – Cardiac muscle

Muscle contains: – 75% water – 20% protein – 5% organic and inorganic compounds

40 % of the body is skeletal muscle 10 % is smooth and cardiac muscle. 40% of adult body weight 50% of child’s body weight

FASCIA Connective tissue that encases the muscles Functions of fascia – – Protect muscle fibers – Attach muscle to bone – Provide structure for network of nerves and blood/lymph vessels

Layers of fascia – – Epimysium • Surface of muscle • Tapers at ends to form tendon

– Perimysium • Divides muscle fibers into bundles or fascicles

– Endomysium • Surrounds single muscle fibers

SKELETAL MUSCLE All skeletal muscles are composed of numerous fibers ranging from 10 to 80 micrometers in diameter. In most skeletal muscles, each fiber extends the entire length of the muscle. Each fiber is usually innervated by only one nerve ending, located near the middle of the fiber, except for about 2 % of the fibers

Sarcolemma- it is the cell membrane of the muscle fiber. consists of • true cell membrane - plasma membrane, • outer coat made up of a thin layer of polysaccharide material that contains numerous thin collagen fibrils – At the end of the muscle fiber sarcolemma fuses with a tendon fiber

Sarcoplasm- The spaces between the myofibrils are filled with intracellular fluid called sarcoplasm, containing large quantities of potassium, magnesium, phosphate, and multiple protein enzymes Large numbers of mitochondria that lie parallel to the myofibrils are present that provide ATP

Sarcoplasmic Reticulum -

surrounding the myofibrils of each muscle fiber is an extensive reticulum called the sarcoplasmic reticulum. This reticulum has a special organization that is extremely important in controlling muscle contraction.

Myofibrils – Each muscle fiber contains several hundred to several thousand myofibrils Each myofibril is composed of about 1500 adjacent myosin filaments and 3000 actin filaments, which are large polymerized protein molecules that cause the actual muscle contraction.

The thick filaments are myosin and the thin filaments are actin. myosin and actin filaments partially interdigitate and thus cause the myofibrils to have alternate light and dark bands.

I bands-

isotropic to polarized light. light bands contain only actin filaments

A bands- anisotropic to polarized light. dark bands contain myosin and ends of the actin filaments

Z disc - composed of filamentous proteins, passes cross wise across the myofibril and also crosswise from myofibril to myofibril, attaching the myofibrils to one another across the muscle fiber giving them a striated appearance.

The ends of the actin filaments are attached to the Z disc. Filaments extend in both directions to interdigitate with the myosin filaments

Sarcomere – The portion of the myofibril that lies between two successive Z discs When the muscle fiber is contracted, the length of the sarcomere is about 2 micrometers. The actin filaments completely overlap the myosin filaments and the tips of the actin filaments begin to overlap

Steps In Muscle Contraction Excitation – Action potential – Neurotransmitter release – Muscle fiber depolarization - Ca++ release from sarcoplasmic reticulum

Coupling – Ca++ binds to troponin-tropomyosin complex

Contraction – Ca++ binding moves troponin-tropomyosin complex – Myosin heads attach to actin – Crossbridge cycling

Relaxation – Ca++ removed from troponin-tropomyosin complex – Cross bridge detachment – Ca++ pumped into SR – active transport

General Mechanism of Muscle Contraction Initiation and execution of muscle contraction occur in the following steps 1. An action potential travels along a motor nerve to its endings on muscle fibers. 2. At each ending, the nerve secretes a small amount of the neurotransmitter substance acetylcholine.

3. The acetylcholine acts on a local area of the muscle fiber membrane to open multiple acetylcholine gated channels through protein molecules floating in the membrane. 4. This allows large quantities of sodium ions to diffuse to the interior of the muscle fiber membrane. This initiates an action potential at the membrane. 5. The action potential travels along the muscle fiber membrane

6. The action potential depolarizes the muscle membrane, it causes the sarcoplasmic reticulum to release large quantities of calcium ions that have been stored within this reticulum. 7. The calcium ions initiate attractive forces between the actin and myosin filaments, causing them to slide alongside each other, which is the contractile process.

8. After a fraction of a second, the calcium ions are pumped back into the sarcoplasmic reticulum by a Ca++ membrane pump, this removal of calcium ions from the myofibrils causes the muscle contraction to cease.

Muscle Action Potential Resting membrane potential: about -80 to -90 millivolts Duration of action potential: 1 to 5 milliseconds Velocity of conduction: 3 to 5 m/sec-

ACTION POTENTIAL –rapid changes in the membrane potential that spread rapidly along the fiber membrane.

Resting Stage- the membrane potential before the action potential begins. The membrane is polarized during this stage because of the -90 millivolts negative membrane potential that is present.

Depolarization Stage – membrane becomes very permeable to sodium ions, allowing diffusion of the ions.

Repolarization Stage.- after a few 10,000ths of a second the sodium channels begin to close and the potassium channels open more than normal. Rapid diffusion of potassium ions to the exterior reestablishes the normal negative resting membrane potential.

Voltage-Gated Sodium and Potassium Channels

At rest, virtually all of the voltage-gated channels are closed, potassium and sodium can only slowly move across the membrane, through the passive "leak" channels

The first thing that occurs when a depolarizing graded potential reaches the threshold is that the voltage gated Na+ channels begin to open and Na+ influx into the cell exceeds K+ efflux out of the cell

Two things happen next: As the membrane depolarizes further and the cell becomes positive inside and negative outside, the flow of Na+ will decrease.


Even more importantly, the voltage- gated Na+ channels close When the inactivation gates close, Na+ influx stops and the repolarizing phase takes place.


Next, the voltage gated K+ channels are activated at the time the action potential reaches its peak. At this time, both concentration and electrical gradients favour the movement of K+ out of the cell.

These channels are also inactivated with time but not until after the efflux of K+ has returned the membrane potential to, or below the resting level (after hyperpolarization /positive afterpotential).

The Neuromuscular Junction Each nerve ending makes a junction, called the neuromuscular junction, with the muscle fiber near its midpoint The action potential initiated in the muscle fiber by the nerve signal travels in both direction toward the muscle fiber ends. With the exception of about 2 % of the muscle fibers, there is only one such junction per muscle fiber.

Motor end plate Branching Nerve Terminals - nerve fibers invaginate into the surface of the muscle fiber but lie outside the plasma membrane. Covered by Schwann cells that insulate it from the surrounding fluids.

Subneural clefts – numerous small folds of the muscle membrane which increase the surface area at which the synaptic transmitter can act.

Synaptic trough - invaginated membrane

Synaptic cleft - space between the terminal and the fiber membrane (20 to 30 nanometers wide.)

Acetylcholine is stored in synaptic vesicles (300,000) which are in the terminals of a single end plate When a nerve impulse reaches the neuromuscular junction, about 125 vesicles of acetylcholine are released from the terminals into the synaptic space

During the action potential the calcium channels open and calcium ions to diffuse from the synaptic space to the interior of the nerve terminal. The calcium ions attract the acetylcholine vesicles, drawing them to the neural membrane The vesicles fuse with the neural membrane and empty their acetylcholine into the synaptic space by exocytosis.

Acetylcholine-gated ion channels, are located almost entirely near the mouths of the subneural clefts. Has 5 subunit proteins, two alpha and one each of beta, delta, and gamma proteins. After the Ach attaches a conformational change occurs that opens the channel

the principal effect of opening channels - allows sodium ions to pour to the inside of the fiber, carrying with them positive charges creating a local positive potential change inside the muscle fiber membrane, called the end plate potential. this end plate potential initiates an action potential that spreads along the muscle membrane and thus causes muscle contraction.

Destruction of the Released Acetylcholine Most is destroyed by the enzyme acetylcholinesterase, which is attached to the spongy layer of the connective tissue that fills the synaptic space between the presynaptic nerve terminal and the postsynaptic muscle membrane.

A small amount of acetylcholine diffuses out of the synaptic space and is then no longer available to act on the muscle fiber membrane.

Safety Factor of Transmission at the Neuromuscular Junction – Each impulse at the neuromuscular junction causes about 3 times as much end plate potential as that required to stimulate the muscle fiber. – Stimulation of the nerve fiber at rates greater than 100 times/sec for several minutes diminishes the number of acetylcholine vesicles so that impulse fail to pass into the muscle fiber- called fatigue

A new action potential cannot occur in an excitable fiber as long as the membrane is still depolarized from the preceding action potential. Shortly after the action potential the sodium channels (or calcium channels, or both) become inactivated, and any amount of excitatory signal applied to these channels at this point will not open the inactivation gates.

Absolute Refractory Period - period during which a second action potential cannot be elicited, even with a strong stimulus. Large myelinated nerve fibers 1/2500second.

Relative Refractory Period - lasts about Ÿ to ½ as long as the absolute period. During this time, stronger than normal stimuli can excite the fiber.

Cause of relative refractoriness : 1.

During this time, some of the sodium channels still have not been reversed from their inactivation state


the potassium channels are usually wide open at this time, causing greatly excess flow of positive potassium ion charges to the outside of the fiber opposing the stimulating signal

Excitation-Contraction Coupling Skeletal muscle fibers are so large that action potentials spreading along its surface membrane cause almost no current flow deep within the fiber. This is achieved by transmission of action potentials along transverse tubules (T tubules)

T tubules – – – – –

Very small transverse to the myofibrils. Penetrate muscle fibers from one side to the other They branch among themselves They are open to the exterior of the muscle fiber at their point of origination and so basically are internal extensions of the cell membrane. – The action potential spreads along the T tubules to the interior of the muscle fiber.

Sarcoplasmic reticulum– Terminal cisternae – Long longitudinal tubules The vesicular tubules have calcium ions in high concentration, and are released from each vesicle when an action potential occurs in the adjacent T tubule.

Molecular Mechanism of Muscle Contraction Sliding Filament Mechanism of Muscle Contraction.

Myosin Filament -The myosin filament is composed of multiple myosin molecules, each having a molecular weight of about 480,000.

myosin molecule - 6 polypeptide chains– 2 heavy chains- molecular weight 200,000 – 4 light chains - molecular weights 20,000 each.

heavy chains wrap spirally around each other to form a double helix, called the tail of the myosin molecule.

One end of each of these chains is folded bilaterally into a globular polypeptide structure called a myosin head. 4 light chains are also part of the myosin head. These light chains help control the function of the head during muscle contraction.

Myosin Filament - Made up of 200 or more individual myosin molecules. (Length -1.6 micrometers.) Tails of the myosin molecules bundle together to form the body of the filament, Heads of the molecules hang outward to the sides of the body.

Arm- part of the body of each myosin molecule along with the head,

Cross bridges- protruding arms and heads together. It is flexible at the hinges– where the arm leaves the body of the myosin filament, – where the head attaches to the arm.

The hinged arms allow the heads either to be extended far outward from the body of the myosin filament or to be brought close to the body. The hinged heads participate in the actual contraction process

There are no cross-bridge heads in the center of the myosin filament for a distance of 0.2 micrometer because the hinged arms extend away from the center.

The myosin filament itself is twisted so that each successive pair of crossbridges is axially displaced from the previous pair by 120 degrees. This ensures that the cross-bridges extend in all directions around the filament.

ATPase Activity of the Myosin Head -the myosin head functions as an ATPase enzyme. This allows the head to cleave ATP and to use the energy for the contraction process.

Actin Filament- composed of 3 protein components: actin, tropomyosin, and troponin.

Actin - double stranded F-actin protein molecule. – The two strands are wound in a helix. Each strand is composed of polymerized G-actin molecules, (molecular weight 42,000). – Attached to each one of the G-actin molecules is one molecule of ADP which are the active sites on the actin filaments with which the cross bridges of the myosin filaments interact to cause muscle contraction.

Actin filament - length -1 micrometer The bases of the actin filaments are inserted strongly into the Z discs; the ends of the filaments protrude in both directions

Troponin- Attached intermittently along the sides of the tropomyosin molecules complexes of three loosely bound protein subunits – troponin I - affinity for actin, – troponin T - for tropomyosin, – troponin C - for calcium ions

Tropomyosin Molecules-

molecular weight

70,000 length - 40 nanometers. These molecules are wrapped spirally around the sides of the F-actin helix In the resting state, the tropomyosin molecules lie on top of the active sites of the actin strands, so that attraction cannot occur between the actin and myosin filaments

Activation of the Actin filament The active sites on the normal actin filament of the relaxed muscle are inhibited or physically covered by the troponin tropomyosin complex.

When calcium ions combine with troponin C, the troponin complex undergoes a conformational change that moves it deeper into the groove between the two actin strands. This uncovers the active sites of the actin

What Keeps the Myosin and Actin Filaments in Place? The side-by-side relationship between the myosin and actin filaments is achieved by a large number of filamentous molecules of a protein called titin. (molecular weight- 3 million)

It is filamentous, and very springy. These molecules act as a framework that hold the myosin and actin filaments in place The titin molecule itself acts as template for initial formation of portions of the contractile filaments of the sarcomere, especially the myosin filaments.

The Walk-Along Theory of Contraction

When a head attaches to an active site, changes in the intramolecular forces between the head and arm of its cross-bridge occur. The head tilts toward the arm and drags the actin filament along with it (power stroke) Immediately after tilting, the head automatically breaks away from the active site.

The head returns to its extended direction, it combines with a new active site farther down along the actin filament.

Chemical Events In the Motion of the Myosin Head 1. Before contraction -the heads of the crossbridges bind with ATP. The ATPase activity of the myosin head immediately cleaves the ATP but leaves the cleavage products, ADP plus phosphate ion, bound to the head. In this state, the head extends perpendicularly toward the actin filament but is not yet attached to the actin

2. When the troponin - tropomyosin complex binds with calcium ions, active sites on the actin filament are uncovered, and the myosin heads then bind with these.

3.For the power stroke the energy that activates it already stored, like a "cocked" spring, by the conformational change that occurred in the head when the ATP molecule was cleaved earlier.

4. Once the head of the cross-bridge tilts, it allows release of the ADP and phosphate ion. At the site of release of the ADP, a new molecule of ATP binds. This binding of new ATP causes detachment of the head from the actin. 5. After the head has detached from the actin, the new molecule of ATP is cleaved to begin the next cycle, leading to a new power stroke.

The process proceeds again and again until the actin filaments pull the Z membrane up against the ends of the myosin filaments or until the load on the muscle becomes too great for further pulling to occur.

RELAXATION –muscle contraction continues as long as the calcium ions remain in high concentration and thus A continually active calcium pump located in the walls of the sarcoplasmic reticulum pumps calcium ions away from the myofibrils back into the sarcoplasmic tubules. This pump can concentrate the calcium ions about 1O,OOO-fold inside the tubules. Inside the reticulum is a protein called calsequestrin that can bind up to 40 times more calcium.

Effect of Amount of Actin and Myosin Filament Overlap on Tension Developed by the Contracting Muscle

Point D- no actin-myosin overlap. Tension developed by the muscle - 0.

Point C- actin filament has overlapped all the

cross-bridges of the myosin filament but not reached the center. Length -2.2 micrometers.

Point B- two actin filaments begin to overlap each other. Length -2 micrometers.

Point A-

the two Z discs of the sarcomere abut the ends of the myosin filaments. Length - 1.65 micrometers

Effect of Muscle Length on Force of Contraction in the Whole Intact Muscle. Other factors to be considered – – connective tissue – different parts of the muscle do not contract the same amount.

Active tension decreases as the muscle is stretched beyond its normal length

Relation of Velocity of Contraction to Load Against no load-skeletal muscle contracts in about 0.1 second When loads are applied, the velocity of contraction becomes progressively less When load is equal to the maximum force of the muscle, the velocity of contraction is zero and no contraction results

Work Output During Muscle Contraction Sources of energy for muscle contraction – Phosphocreatine – Glycolysis of glycogen – Oxidative metabolism.

The percentage of the input energy to muscle is less than 25 % with the remainder becoming heat.

Types Of Contraction Isometric Contraction- when the muscle does not shorten during contraction

Isotonic Contraction- when muscle shortens but the tension on the muscle remains constant throughout the contraction.

Fast And Slow Muscle Fibers. Muscles that react rapidly are composed mainly of fast fibers with small numbers of slow fibers. Muscles that respond slowly but with prolonged contraction are composed mainly of slow fibers

Fast Fibers Large fibers

Slow Fibers Smaller fibers.

Less extensive blood supply

Extensive blood vessel Supply

Fewer mitochondria,

Increased numbers of mitochondria,

No myoglobin present in fibers

Large amounts of myoglobin

Large amounts of glycolytic enzymes

Less amounts of glycolytic enzymes

Extensive sarcoplasmic Less extensive sarcoplasmic reticulum reticulum

Motor neurons Small muscles that react rapidly and whose control must be exact have more nerve fibers for fewer muscle fiber Large muscles that do not require fine control may have several hundred muscle fibers in a motor unit.

Force Summation. Summation - adding together of individual twitch contractions to increase the intensity of overall muscle contraction. – Types • Multiple fiber summation • Frequency summation

Multiple Fiber Summation- When the CNS sends a weak signal to contract a muscle, the smaller motor units of the muscle are stimulated in preference to the larger motor units. As the strength of the signal increases, larger motor units begin to be excited (size principle.) Cause -smaller motor units are driven by small motor nerve fibers, and are more excitable than the larger ones

Frequency Summation and Tetanization As frequency increases, a new contraction occurs before the preceding one is over. As a result, the 2nd contraction is added partially to the 1st , so that the total strength of contraction rises with increasing frequency.

Tetanization - When the frequency reaches a critical level, the successive contractions fuse together, and the whole muscle contraction appears to be smooth and continuous

The Staircase Effect (Treppe) When a muscle begins to contract after a long period of rest, its initial strength of contraction is as little as ½ its strength 10 to 50 muscle twitches later. Cause – increase in calcium ions in the cytosol because of the release of more and more ions from the sarcoplasmic reticulum with each successive muscle action potential and failure of the sarcoplasm to recapture the ions immediately.

Skeletal Muscle Tone. Muscle tone- Even when muscles are at rest, a certain amount of tautness remains. It results entirely from a low rate of nerve impulses coming from the spinal cord.

Muscle Fatigue. Prolonged and strong contraction of a muscle leads to the state of muscle fatigue. It results mainly from inability of the contractile and metabolic processes of the muscle fibers to continue supplying the same work output.

Muscle Hypertrophy – When the total mass of a muscle increases – When muscles are stretched to greater than normal length causing new sarcomeres to be added at the ends of the muscle fibers – Results from an increase in the number of actin and myosin filaments – Rate of synthesis of muscle contractile proteins is far greater

When a muscle loses its nerve supply, it no longer receives the contractile signals that are required to maintain normal muscle size and atrophy begins If the nerve supply grows back rapidly, return of function can occur in 3 months. Beyond that the capability of functional return becomes less, with no further return of function after 1 to 2 years.

Rigor Mortis Several hours after death, the muscles contract and become rigid, even without action potentials. This rigidity results from loss of all the ATP, which is required to cause separation of the crossbridges from the actin filaments during the relaxation process.

SMOOTH MUSCLE Smooth Muscle -1 to 5 micrometers – diameter 20 - 500 micrometers in length

Two major types– Multi-unit smooth muscle – Unitary smooth muscle.

Multi-Unit Smooth Muscle– Composed of discrete, separate smooth muscle fibers. – Each fiber operates independently – Innervated by a single nerve ending – Outer surfaces are covered by a thin layer of basement membrane – Each fiber can contract independently of the others, and their control is exerted mainly by nerve signals.

Unitary Smooth Muscle– smooth muscle fibers that contract together as a single unit. – fibers are arranged in sheets or bundles, and their cell membranes are adherent to one another – cell membranes are joined by gap junctions through which ions can flow freely – Syncytial interconnections among fibers.

Smooth muscle have actin and myosin filaments having chemical characteristics similar and interact with each other in much the same way to those of the skeletal muscle They do not not contain the normal troponin complex

Actin filaments are attached to dense bodies. Some dense bodies of adjacent cells are bonded together by intercellular bridges which transmit the force of contraction from one cell to the next. Ends of actin filaments overlap a myosin filament located midway between the dense bodies. Myosin filaments have sidepolar crossbridges - bridges on both sides hinge in the opposite

The rapidity of cycling of the myosin cross-bridges in smooth muscle cycle is much, much slower than in skeletal muscle (1/10 to 1/300) Reason- The cross-bridge heads have far less ATPase activity than in skeletal muscle.

But the fraction of time that the cross-bridges remain attached to the actin filaments, which determines the force of contraction, is increased in smooth muscle - 4 to 6 kg/cm2

Only 1/10 to 1/300 as much energy is required to sustain the same tension of contraction in smooth muscle as in skeletal muscle. smooth muscles – begin to contract 50 - 100 milliseconds after excitation – reach full contraction - 0.5 second later, – decline in contractile force -another 1 to 2 sec – total contraction time - 1 to 3 sec.

Visceral unitary type of smooth muscle of many hollow organs, have the ability to return to nearly its original force of contraction seconds or minutes after it has been elongated or shortened.

Regulation of Contraction by Calcium Ions– the initiating stimulus for most smooth muscle contraction is an increase in intracellular calcium ions. – Caused by – • nerve stimulation • hormonal stimulation, • stretch of the fiber • change in the chemical environment of the fiber.


The calcium ions bind with calmodulin.


The calmodulin-calcium combination joins with and activates myosin kinase, a phosphorylating enzyme.


In response the regulatory chain of the myosin head becomes phosphorylated and the head now binds with the actin filament and proceeds through the entire cycling process causing muscle contraction.

Cessation of ContractionWhen the calcium ion concentration falls below a critical level, the contraction processes automatically except for the phosphorylation of the myosin head. Reversal of this requires enzyme myosin phosphatase, which splits the phosphate from the regulatory light chain. Then the cycling stops and contraction ceases.

Latch Mechanism Once smooth muscle has developed full contraction, the amount of continuing excitation usually can be reduced to far less than the initial level, yet the muscle maintains its full force of contraction. Importance - can maintain prolonged tonic contraction in smooth muscle for hours with little use of energy.

When the myosin kinase and myosin phosphatase enzymes are activated, the cycling frequency of the myosin heads and the velocity of contraction are great. As the activation of the enzymes decreases, the cycling frequency decreases But the deactivation of these enzymes allows the myosin heads to remain attached to the actin filament for a longer proportion of the cycling period.

Therefore, the number of heads attached to the actin filament at any given time remains large. Because the number of heads attached to the actin determines the force of contraction, tension is maintained, yet little energy is used by the muscle, because ATP is not degraded to ADP.

Neuromuscular Junctions of Smooth Muscle The autonomic nerve fibers that innervate smooth muscle generally branch diffusely on top of a sheet of muscle fibers, These fibers do not make direct contact with the smooth muscle fiber cell membranes but instead form diffuse junctions that secrete their transmitter substance into the matrix a few nanometers to a few micrometers away

The fine terminal axons have multiple varicosities distributed along their axes. At these points the schwann cells are interrupted so that transmitter substance can be secreted through the walls of the varicosities. These are called as contact junctions In the varicosities are vesicles which contain acetylcholine and norepinephrine

When acetylcholine excites a muscle fiber, norepinephrine ordinarily inhibits it. Conversely, when acetylcholine inhibits a fiber, norepinephrine usually excites it Reason -the type of receptor determines whether the smooth muscle is inhibited or excited and also determines which of the two transmitters, acetylcholine or norepinephrine, is effective in causing the excitation or inhibition.

Action Potentials in Smooth Muscle The normal resting membrane potential is usually about -50 to -60 millivolts

The action potentials of visceral smooth muscle occur in one of two forms: – Spike potentials – Action potentials with plateaus.

Spike Potentials similar to the skeletal muscles occur in most types of unitary smooth muscle duration -10 to 50 milliseconds

Action Potentials with PlateausThe repolarization is delayed for several hundred to as much as 1000 milliseconds (1 second). Importance - can account for the prolonged contraction that occurs in the ureter, the uterus etc

Smooth muscle cell membrane have more voltagegated calcium channels than does skeletal muscle but few voltage gated sodium channels. Thus calcium ions are mainly responsible for the action potential. They open more slowly than sodium channels, and remain open much longer accounting for the prolonged plateau action potentials Calcium ions act directly on the smooth muscle contractile mechanism to cause contraction.

Slow Wave Potentials Some smooth muscle are self-excitatory. ie: action potential arises within the smooth muscle cell without an extrinsic stimulus. Often associated with a basic slow wave rhythm of the membrane potential. It is not a self regenerative process that spreads progressively over the membranes of the muscle fibers

Cause – The membrane potential becomes more negative when sodium is pumped rapidly and less negative when the sodium pump becomes less active. – Or - the conductance of the ion channels increase and decrease rhythmically.

When they are strong enough, they can initiate action potentials.

Source of Calcium Ions Almost all the calcium ions that cause contraction enter the muscle cell from the extracellular fluid at the time of the action potential. There is a rapid diffusion of the calcium ions into the cell from the extracellular fluid when the calcium pores open. Time required - 200 to 300 milliseconds and is called - latent period This latent period is about 50 times as great for smooth muscle as for skeletal muscle contraction.

When the extracellular fluid calcium ion concentration falls to 1/3 to 1/10 normal, smooth muscle contraction usually ceases. Calcium ions are removed by a calcium pump that pumps calcium ions out into the extracellular fluid, or into a sarcoplasmic reticulum

Smooth Muscle Sarcoplasmic Reticulumcaveolae – analog of the transverse tubule system of skeletal muscle. They excite calcium ion release from the abutting sarcoplasmic tubules

MUSCLE RECEPTORS Receptors provide information regarding: – Chemical changes (i.e., O2, CO2, H+) – Tension development: Golgi Tendon Organs – Muscle length: Muscle spindles Information from these receptors provides information about the energetic requirements of exercising muscle and about movement patterns

Muscle spindle – – Detect dynamic and static changes in muscle length– Stretch reflex – Stretch on muscle causes reflex contraction

Golgi tendon organ (GTO) – – Monitor tension developed in muscle – Prevents damage during excessive force generation – Stimulation results in reflex relaxation of muscle

Muscle spindles respond to muscle stretch Gamma motor neurons are co activated during contraction – Cause contraction of fibers within muscle spindle – Deviations in consistency signal excessive stretch

Golgi Tendon Organ Located in tendon Monitor muscle tension Activation causes inhibition of alphamotor neuron Is a safety mechanism against excessive force during contraction


Causes contraction of stretched muscle

Receptor – proprioceptive nerve endings called muscle spindles

Impulses are conducted by group 1A sensory nerve endings Impulse carried by motoneurons / alpha efferent

Functional significance – serves as a mechanism for upright posture In mandible it acts to maintain the postural rest position in reln to the maxilla


Resistance is encountered as soon as the muscle is stretched throughout the initial part of the bending. This resistance is due to the hyperactive reflex contraction of the muscle in response to the myotactic reflex If flexion is forcibly carried further, a point is reached at which all resistance stops, and the previously rigid limb collapses readily "clasp-knife" reaction

functional significance - to protect the overload by preventing damaging contraction against strong stretching forces. The stimulus to elicit the clasp-knife reflex is excessive stretch and, when elicited, inhibits muscular contraction, thus causing the muscle to relax.

Receptors - Golgi tendon organs impulses are conducted by the Group 1B sensory nerve fiber Impulses act on the motor neuron, or alpha efferent.

NEURO TROPHISM Definition - interaction between nerves and other cells which initiate or control molecular modifications in other cells (Guth 1969) Or is a non impulse transmitting neural function that involves axoplasmic transport and provides from long term interactions between the nervous and innervated tissue that homeostatically regulate the morphological, compositional and functional integrity of those tissues.

Three types Neuro epithelial trophism Neuro visceral trophism Neuro muscular trophism

NEURO-MUSCULAR TROPHISM: Skeletal muscle ontogenesis normally requires motor neuron innervation to proceed past the stage of myotubes Embryonic myogenesis is independent of neural innervation and trophic control.

Approximately at the myoblast stage of differentiation, neural innervation is established without which further myogenesis cannot continue. Neurotrophic influences are involved rather than conductive influences

Cross-innervation experiments show that many significant morphologic, biochemical and functional parameters of the re-innervated muscle come to resemble those of the muscle formerly innervated by the now ectopically implanted nerve. Therefore, these parameters of skeletal muscle are nervespecific, not muscle specific

Conformational features of myosin are determined by the nature of the innervation and that the complex chain of events leading to particular expression of the genetic – embryonic potential is not wholly within the cell, but also includes informational elements contributed by the nerve

Research shows that a qualitatively different myosin that resembles that of the muscle, formerly innervated by the nerve, is synthesized in crossinnvervated muscle, which indicates that a new species of protein has been synthesized, and it is therefore, suggested that the nerve influences gene expression in the cell.

Implication of these data: Since periosteal functional matrices regulate the size and shape of specifically related skeletal units, it is apparent that the genetic control of the structural, chemical and functional attributed of these same matrices cannot reside solely in the matrices themselves, but rather reflect constant neurotrophically regulated homeostatic control of genome.

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