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Muscles physiology
 

Muscles physiology

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  • Here is another diagram of a sarcomere. Note the A band. It is formed by both myosin and actin filaments. The part of the sarcomere with only actin filaments is called the I band. This is a sarcomere that is relaxed.
  • Titin is the largest polypeptide yet discovered (~3.5 MDa). Single moleules span from the Z- to M-line (yellow in the diagram). These have two main functions: In the thick (myosin) filament part of the myofibril we have proposed the titin molecule regulates exact myosin assembly by acting as a giant template or "protein-ruler". We are exploring this hypothesis by binding assays with myosin using the whole proteins and fragments prepared by proteolysis and cDNA expression. The remainder of the titin molecule forms an elastic connection between the end of the thick filaments and the Z-line. These connections give muscle its passive tension and they also keep thick filaments centered between Z-discs. (Without this there would be force imbalances in the opposite halves of thick filaments during active contraction). Nebulin aligns actin filaments
  • The string of green circles represents an actin filament. There are binding sites in the filament for the attachment of myosin heads. *In a relaxed muscle the binding sites are covered by tropomyosin. The tropomyosin has molecules of troponin attached to it. *Calcium, shown in yellow, will attach to troponin. *Calcium will change the position of the troponin, tropomyosin complex. *The troponin, tropomyosin complex has now moved so that the binding sites are longer covered by the troponin, tropomyosin complex.
  • The binding sites are now exposed and myosin heads are able to attach to form cross bridges.*  
  • A motor unit is all the muscle cells controlled by one nerve cell. This diagram represents two motor units. Motor unit one illustrates two muscle cells controlled by one nerve cell. When the nerve sends a message it will cause both muscle cells to contract. Motor unit two has three muscle cells innervated by one nerve cell.

Muscles physiology Muscles physiology Presentation Transcript

  •  
  • Muscular System Functions
    • Body movement
    • Maintenance of posture
    • Respiration
    • Production of body heat
    • Communication
    • Constriction of organs and vessels
    • Heart beat
    9-
  • Properties of Muscle
    • Responsiveness (excitability)
      • capable of response to chemical signals, stretch or other signals & responding with electrical changes across the plasma membrane
    • Conductivity
      • local electrical change triggers a wave of excitation that travels along the muscle fiber
    • Contractility -- shortens when stimulated
    • Extensibility -- capable of being stretched
    • Elasticity -- returns to its original resting length after being stretched
    9-
  • Muscle Tissue Types
    • Skeletal
      • Attached to bones
      • Nuclei multiple and peripherally located
      • Striated, Voluntary and involuntary (reflexes)
    • Smooth
      • Walls of hollow organs, blood vessels, eye, glands, skin
      • Single nucleus centrally located
      • Not striated, involuntary, gap junctions in visceral smooth
    • Cardiac
      • Heart
      • Single nucleus centrally located
      • Striations, involuntary, intercalated disks
    9-
    • Skeletal muscle:-
    • It has well developed cross striations.
    • Doesn’t contract in the absence of nervous stimulation.
    • Lacks anatomic & functional connections between individual muscle fibers.
    • It is under voluntary control.
    • Cardiac muscle also has cross-striations but it contracts rhythmically in the absence of external innervations owing to the presence of pace maker cells that discharge spontaneously.
    • Smooth m. lacks cross-striations . Found in most hollow viscera ,it contains pacemakers that discharge irregularly .
  • Skeletal muscle morphology:-
    • Sk.m is made up of muscle fibers that are the “ building blocks ” of muscular system . They begin & end in tendons ,arranged in parallel so that force of cont. is additive.
    • Each m. fiber is a single cell multinucleated , long cylindrical & surrounded by cell memb
    • ( sarcolemma ), there are no bridges between cells.
    • Muscle fibers are made up of myofibrils which are divided into filaments that made up of contractile proteins.
    • The contractile mechanism in sk.m. depends on the proteins: myosin II , actin , tropomyosin & troponin. Troponin made up of troponin I, troponinT& troponin C.
    • α – actinin binds actin to Z line .titin connects the Z line to the M line providing structural support & elasticity.
  • Muscle fibre
  • General Organization of Skeletal Muscle Tissue
    • A muscle is anchored at each end by tough connective tissue (tendon) – attached to bone
    • Muscle comprised of long cylindrical, multinucleated cells called muscle fibers aligned in a parallel fashion
    • Each muscle fiber is composed of numerous parallel subunits called myofibrils which consist of longitudinally repeated units called sarcomeres (functional unit of striated muscle)
    • Each sacromere contains 2 kinds of long, thick proteins (called myofilaments ) arranged in precise geometric pattern with a Z-disk at each end
    • Extending from either end of Z-disk are thin filaments consisting largely of protein actin
    • Thin filaments interdigitate with thick filaments made primarily of protein myosin
  • Organization
  • Myofibrils = Contractile Organelles of Myofiber
    • Actin
    • Myosin
    • Tropomyosin
    • Troponin
    • Titin
    • Nebulin
    Contractile Regulatory Accessory Contain 6 types of protein:
  •  
  • Parts of a Muscle 9-
  • Striations
    • Dark A bands (regions) alternating with lighter I bands (regions)
      • anisotrophic (A) and isotropic (I) stand for the way these regions affect polarized light
    • A band is thick filament region
      • lighter, central H band area contains no thin filaments
    • I band is thin filament region
      • bisected by Z disc protein anchoring thick & thin
      • from one Z disc to the next is a sarcomere
  •  
  •  
    • The thick filaments are made up of myosin & thin filaments are made up of actin, tropomyosin, & troponin.
    • The thick fil. are lined up to form A bands whereas thin fil. Forms I bands.
    • Myosin II is made up of 2 heavy chains & 4 light chains.
    • The N-terminal portions of heavy chains & the light chains combine to form the globular heads which contain an actin binding site & a catalytic site that hydrolyzes ATP.
  • Thick Filaments
    • Made of 200 to 500 myosin molecules
      • 2 entwined golf clubs
    • Arranged in a bundle with heads directed outward in a spiral array around the bundled tails, heads found on each end with central area a bare zone with no heads
  •  
    • The thin filaments are made up of two chains of actin that form a long double helix.
    • Tropomyosin molecules are long filaments , located in the groove between the two chains in the actin.
    • Each thin filament contains 300-400 actin molecules & 40-60 tropomyosin molecules.
    • Troponin molecules are small globular units located at intervals along the tropomyosin molecules. Troponin T binds the other troponin components to tropomyosin. Troponin I inhibits the interaction of myosin with actin. Troponin C contains the binding sites for the Ca++ that initiates contraction.
  •  
  • Structure of Actin and Myosin 9-
  • Titin and Nebulin
    • Titin : biggest protein known (25,000 aa); elastic!
      • Stabilizes position of contractile filaments
      • Return to relaxed location
    • Nebulin : inelastic giant protein
      • Alignment of A & M
    Fig 12-6
    • Sarcotubular system:-
    • Made up of T-system & a sarcoplasmic reticulum. The T system are transverse tubules which are continuous with memb. of muscle fiber. The space between two layers of T-system is extension of ECS ( extra cellular space).
    • Sarcoplasmic reticulum has enlarged terminal cisterns. Central T sys. With a cistern of the sarcoplasmic retic.on either side called triads .
    • The function of T-sys. which is continuous with sarcolemma is rapid transmission of action potential from cell memb. to all fibrils in muscle. The sarcoplasmic retic. Is concerned with Ca++ movement & muscle metabolism .
  • More Anatomy
  •  
      • Electrical phenomena & ionic fluxes :-
    • Resting memb. potential of sk.m. is − 90 mv . a.p. lasts 2- 4 ms. It conducted along m. fibers at about 5 m /s. absolute refractory period is 1-3 ms.
    • Ionic distribution & fluxes:-
    • It is similar to nerve cell memb. depol. Is a manifestation of Na+ influx. repol. manifestation of K+ efflux .
    • Contractile responses:-
    • m. fiber memb. depol. Starts at motor end plate , the specialized structure under motor nerve ending . The a.p. transmitted along m.f. & initiates the contractile response.
    • Molecular basis of contraction:-
    • Sliding of thin filament over thick fil. Will lead to shortening & cont. of muscle. A band is constant but Z-lines move closer together until overlap.
    • The sliding occurs when myosin heads bond to actin, bend on rest of myosin molecule then detach . this cycle is repeated many times . Each myosin head has an actin-binding site & an ATP –binding site( an open cleft , when ATP enters it ,it hydrolyzed & cleft will close.). this will produce power stroke that moves actin on myosin .
  •  
    • Each thick fil. has 500 myosin head , each cycle about 5 times / s. during rapid cont.
    • ATP is catalyzed by ATPase activity in heads of myosin, in contact with actin.
    • Depol. Of m.f. which initiates cont. is called excitation –cont. coupling.
    • The a.p transmitted to all fibrils via T- system. releasing of Ca++ from terminal cisterns of sarcoplasmic retic. will initiate cont by binding to troponin C.
  • Cross-Bridge Movement 9-
    • In resting muscle , troponin I is tightly bound to actin & tropomyosin covers the sites where myosin heads bind to actin. Thus the troponin-tropomyosin complex constitutes a relaxing protein that inhibits the interaction between actin & myosin .
    • When Ca++ released by a.p , binds to troponin C, the binding of troponin I to actin is weakened , tropomyosin moves laterally, uncovers binding sites for myosin heads. ATP then split & contraction occur.
    • 7 myosin binding sites are uncovered for each molecule of troponin that binds a Ca++ ion.
    • After releasing Ca++ , the sarcoplasmic retic. reaccumulate it by actively transporting it into longitudinal portion of reticulum by Ca++-Mg++ ATPase pump, then Ca++ diffuses to terminal cisterns ,where it is stored for next a.p.
    • Once Ca++ conc. has been lowered , muscle relaxes .ATP provides energy for both cont.& relax. if transport of Ca++ into retic. is inhibited ,relax. not occur , even though there are no a.p. leading to sustained cont. called a contracture .
    • .
  • Binding Site Tropomyosin Troponin
  • Myosin
  • Motor Units
    • Skeletal muscle must be stimulated by a nerve or it will not contract (paralyzed)
    • Cell bodies of somatic motor neurons are in brainstem or spinal cord
    • Axons of somatic motor neurons are called somatic motor fibers
      • each branches, on average, into 200 terminal branches that supply one muscle fiber each
    • Each motor neuron and all the muscle fibers it innervates are called a motor unit
  •  
  • Motor Units
    • Fine control
      • small motor units contain as few as 20 muscle fibers per nerve fiber
      • eye muscles
    • Strength control
      • gastrocnemius muscle has 1000 fibers per nerve fiber
  • Neuromuscular Junctions
    • Synapse is region where nerve fiber makes a functional contact with its target cell (NMJ)
    • Neurotransmitter released from nerve fiber causes stimulation of muscle cell (acetylcholine)
    • Components of synapse
      • synaptic knob is swollen end of nerve fiber
        • contains vesicles filled with ACh
      • motor end plate is region of muscle cell surface
        • has ACh receptors which bind ACh released from nerve
        • acetylcholinesterase is enzyme that breaks down ACh & causes relaxation
      • schwann cell envelopes & isolates NMJ
  •  
  • Muscle Contraction & Relaxation
    • Four phases involved in this process
      • excitation where action potentials in the nerve lead to formation of action potentials in muscle fiber
      • excitation-contraction coupling refers to action potentials on the sarcolemma activate myofilaments
      • contraction is shortening of muscle fiber or at least formation of tension
      • relaxation is return of fiber to its resting length
  • Excitation (steps 1 & 2)
    • Nerve signal stimulates voltage-gated calcium channels that result in exocytosis of synaptic vesicles containing ACh
  • Excitation (steps 3 & 4)
    • Binding of ACh opens Na+ and K+ channels resulting in an end-plate potential (EPP)
  • Excitation (step 5)
    • Voltage change in end-plate region (EPP) opens nearby voltage-gated channels in plasma membrane producing an action potential
  • Excitation-Contraction Coupling(steps 6&7)
    • Action potential spreading over sarcolemma reaches T tubules -- voltage-gated channels open in T tubules causing calcium gates to open in SR
  • Excitation-Contraction Coupling (steps 8&9)
    • Calcium release causes binding of myosin to active sites on actin
  • Contraction (steps 10 & 11)
    • Myosin head with an ATP molecule bound to it can form a cross-bridge (myosin ATPase releases the energy allowing the head to move into position)
  • Contraction (steps 12 & 13)
    • Power stroke shows myosin head releasing the ADP & phosphate and flexing as it pulls thin filament along -- binding of more ATP releases head from the thin filament
  • Relaxation (steps 14 & 15)
    • Stimulation ceases and acetylcholinesterase removes ACh from receptors so stimulation of the muscle cell ceases
  • Relaxation (step 16)
    • Active transport pumps calcium back into SR where it binds to calsequestrin
    • ATP is needed for muscle relaxation as well as muscle contraction
  • Relaxation (steps 17 & 18)
    • Loss of calcium from sarcoplasm results in hiding of active sites and cessation of the production or maintenance of tension
  • Role of Calcium
    • Myosin cross-bridges can bind to actin only when binding sites are available – in resting muscle, myosin binding sites on actin thin filaments are covered by tropomyosin
    • Tropomyosin moves away from myosin binding sites when Ca2+ binds to troponin
  • Muscle Contraction Summary
    • Nerve impulse reaches myoneural junction
    • Acetylcholine is released from motor neuron
    • Ach binds with receptors in the muscle membrane to allow sodium to enter
    • Sodium influx will generate an action potential in the sarcolemma
  • Muscle Contraction Continued
    • Action potential travels down T tubule
    • Sarcoplamic reticulum releases calcium
    • Calcium binds with troponin to move the troponin, tropomyosin complex
    • Binding sites in the actin filament are exposed
  • Muscle Contraction Continued
    • Myosin head attach to binding sites and create a power stroke
    • ATP detaches myosin heads and energizes them for another contaction
    • When action potentials cease the muscle stop contracting
    • The muscle twitch:-
    • A simple a.p. causes a brief cont. followed by relaxation. this process called muscle twitch. Twitch starts 2 ms after a depol. Of memb. the duration varies with type of muscle. Fast m.f. ( those concerned with fine rapid movement) have short twitch duration as 7.5 ms. Slow m.f ( those involved in strong , sustained movements) have twitch durations up to 100 ms.
  •  
  • Muscle Twitch
    • Threshold is minimum voltage necessary to produce contraction
      • a single brief stimulus at that voltage produces a quick cycle of contraction & relaxation called a twitch
    • Phases of a twitch contraction
      • latent period (2 msec) is delay between stimulus & onset of twitch
      • contraction phase is period during which tension develops and shortens
      • relaxation phase shows a loss of tension & return to resting length
      • refractory period is period when muscle will not respond to new stimulus
    • Summation of contractions:-
    • The fiber is electrically refractory only during rising & part of the falling phase of spike potential. at this time cont beginning by first stimulus, repeated stimulation before relaxation has occurred will produce additional cont. added to already present cont. this phenomena known as summation of contractions . The tension here is greater than single muscle twitch.
    • With repeated stimulation , continuous cont. occur called complete tetanus , when there is no relaxation .
  •  
    • Incomplete tetanus occur when there are periods of incomplete relaxation . The tension developed during complete tetanus is 4 times that of single muscle twitch.
    • Treppe :-
    • When a series stimuli delivered to sk.m , at frequency just below tetanizing frequency , so there is an increase in tension until after several cont. a uniform tension / cont. will developed . this phenomenon known as treppe ( staircase).
  • Treppe
    • Graded response
    • Occurs in muscle rested for prolonged period
    • Each subsequent contraction is stronger than previous until all equal after few stimuli
    9-
  • Multiple-Wave Summation
    • As frequency of action potentials increase, frequency of contraction increases
      • Incomplete tetanus
        • Muscle fibers partially relax between contraction
      • Complete tetanus
        • No relaxation between contractions
      • Multiple-wave summation
        • Muscle tension increases as contraction frequencies increase
    9-
    • Relation between muscle length, tension & velocity of cont:
    • Passive tension is measured at a given distance ,then the muscle is stimulated electrically then total tension is measured. The difference between both is active tension .
    • The length of muscle which the active tension is max, is called resting length.
    • The reaction between length- tension in sk.m. is due to sliding filament ,and cross –linkage between actin & myosin molecules.
    • When muscle is stretched the overlap is reduced . when muscle is shorter than resting length , the thin filaments overlap & cross-linkage also reduces.
  • Muscle Length and Tension 9-
  • Types of Muscle Contractions
    • Isometric : No change in length but tension increases
      • Postural muscles of body
    • Isotonic : Change in length but tension constant
      • Concentric : Overcomes opposing resistance and muscle shortens
      • Eccentric : Tension maintained but muscle lengthens
    • Muscle tone : Constant tension by muscles for long periods of time
    9-
  • Isometric & Isotonic Contractions
  • Slow and Fast Fibers
    • Slow-twitch or high-oxidative
      • Contract more slowly, smaller in diameter, better blood supply, more mitochondria, more fatigue-resistant than fast-twitch
    • Fast-twitch or low-oxidative
      • Respond rapidly to nervous stimulation, contain myosin to break down ATP more rapidly, less blood supply, fewer and smaller mitochondria than slow-twitch
    • Distribution of fast-twitch and slow twitch
      • Most muscles have both but varies for each muscle
    9-
  • Muscle Fiber Classification Oxidative only Oxidative or glycolytic
    • Energy sources & metabolism:-
    • m. cont requires energy & muscle is called a “ machine” converting chemical energy into mechanical work . source of energy is energy – rich organic phosphate derivatives in muscle.
    • Phosphorylcreatine:-
    • ATP is resynthesized from ADP by addition of a phosphate group . this reaction requires energy which supplied by break down of glucose to CO2 & H2O . but there is another compound called Phosphorylcreatine which is the source of energy of muscle cont .
    • Carbohydrate & lipid breakdown:-
    • At rest & light exercise muscle utilize free fatty acids for energy source but if intensity of exercise increases lipids alone cannot supply energy , so utilization of CHO will be predominant source for energy.
    • Glucose in bd stream enters cells, when after several chemical reactions become pyruvate . another source is glycogen which is present in liver & sk.m. when O2 present pyruvate enters citric acid cycle & end product is sufficient energy to form large quantities of ATP from ADP this process called aerobic glycolysis .
    • If O2 is insufficient pyruvate doesn’t enter citric acid cycle but reduced to lactate with net result of much small amount of ATP this process is called anaerobic glycolysis.
    • The oxygen debt mechanism:-
    • During m. exercise , the m. bd. Vessels dilate , blood flow is ↑ & O2 supply ↑ up to a point the ↑ in O2 consumption is proportionate to energy expended until it reaches a stage that aerobic pathway for production of ATP is not enough , so that anaerobic pathway will start by breakdown of glucose to lactate.
    • Use of anaerobic pathway is self-limiting because lactate accumulate in muscle leading to decline in PH.
    • After a period of exertion is over, extra O2 is consumed to remove lactate ,replenish ATP , Phosphorylcreatine stores & small amount of O2 that come from myoglobin. This extra O2 consumption called oxygen debt
  • Fatigue
    • Fatigue is progressive weakness & loss of contractility from prolonged use
    • Causes
      • ATP synthesis declines as glycogen is consumed
      • ATP shortage causes sodium-potassium pumps to fail to maintain membrane potential & excitability
      • lactic acid lowers pH of sarcoplasm inhibiting enzyme function
      • accumulation of extracellular K+ lowers the membrane potential & excitability
      • motor nerve fibers use up their acetylcholine
    • Cardiac muscle
    • Morphology :-
    • The striations in cardiac m. are similar to those in sk.m there are large no. of mitochondria .Z-lines are present .m.fibers branch & interdigitate , the end of one m.fiber abuts on another through an extensive series of folds. these areas occur at Z- line called intercalated disks . They provide a strong union between fibers ,that contractile unit can be transmitted along its axis to the next.
    • The cell membs of adjacent fibers fuse forming gap junctions . These junctions provide low-resistance bridges for:-
    • 1) spread of excitation from one fiber to another .
    • 2) they permit cardiac m. to function as if were a syncytium.
    • The T-system in cardiac m. is located at the Z-lines . like sk.m cardiac m. contains myosin, actin, tropomyosin & troponin. It also contains Dystrophin.
  •  
  •  
    • Electrical properties:-
    • Resting memb. & action potentials:-
    • Resting memb. of cardiac.m. is about – 90mv. Stimulation produces a propagated a.p., then depol. Proceeds rapidly , an overshoot is present, but it is followed by a plateau before the memb. potential returns to the baseline. Depol. Lasts 2ms . But plateau & repol lasts 200ms . The extracellular recording include a spike & a later wave that resemble QRS complex & T wave of ECG.
    • Changes in external K+ conc. affect the resting memb. potential, whereas changes in external Na+ conc. affect the magnitude of a.p.
    • The initial rapid depol. & overshoot ( phase 0 ) are due to opening of voltage – gated Na+ channels.
    • The initial rapid repol. ( phase 1 ) is due to closure of Na+ channels .the prolonged plateau ( phase 2 ) is due to slower but prolonged opening of voltage – gated Ca++ channels. Final repol.( phase 3 ) is due to closure of Ca++ channels & K+ efflux. This restores the resting potential ( phase 4 ).
    • The fast Na+ channel in cardiac m. has two gates, an outer gate that opens at the start of depol. at a memb. potential of –70 to-80 mv .and an inner gate that then closes and precludes further influx until a.p is over(Na+ inactivation)
    • The the slow Ca++ channel is activated at a memb. potential of -30 to -40 mv . there are at least 8 kinds of K+ channel in the heart. in cardiac m. the repol. time decreases at rate of 75 b/mi.( a.p. is 0.25 sec), but at rate of 200 b/min. ( 0.15sec.)
    • Mechanical properties:-
    • contractile response:-
    • It begins just after start of depol.& lasts 1.5 times as long as a.p.
    • The role of Ca++ is similar to sk.m. however it is the influx of extracellular Ca++ that is triggered by activation of dihydropyridine channels in the T-sys rather than depol by stored Ca++ from the sarcoplasmic reticulum.
    • During phase 0-2 and about half phase 3 until a.p. reaches approximately -50 mv during repol , cardiac m. cannot be excited again i.e. it is in its absolute refractory period .it remains refractory until phase 4. therefore , tetanus of sk.m cannot occur. Tetanization of cardiac m. is lethal
  •  
    • Isoforms:-
    • Cardiac muscle is slow and has low ATPase activity. Its fibers dependent on oxidative metabolism, needs continuous O2 supply.
    • The human heart contains α and β MHC both in atria, but α is more. Whereas only β isoforms is found in ventricles.
    • Correlation between m. fiber length & tension :-
    • It is similar to Sk.m. there is a resting length at which the tension developed is maximal.
    • In the body the initial length of the fibers is determined by degree of diastolic filling of heart & pressure in ventricle is proportionate to total tension develop
    • ( starlings law of the heart ).
    • .
  •  
    • Force of cont. of cardiac m. are ↑ by catecholamines without ↑ in length and it is mediated through β1 adrenergic receptors & c- AMP . it is called positively inotropic effect of catecholamines
    • heart also contains β2 –adrenergic receptors which act through c- AMP and it is more in atria.
    • Digitalis glycosides ↑ cardiac cont. by inhibiting Na+ -K+ ATPase in cell memb. of m.fibers . the resultant ↑ in intracellular Na+ & ↓ Na+ gradient across cell memb.↓ Na+ influx & Ca++ efflux through Na+ -Ca++ exchange antiport in the cell memb. so ↑ intracellular Ca++ which ↑ strength of cont. of cardiac m.
    • Metabolism:-
    • Under basal conditions 35% of caloric needs of human heart are provided by CHO, 5% ketones & a.a & 60 % by fat.
    • Pace maker tissue:-
    • The heart continues to beat after all nerves to it are sectioned. It is due to presence of specialized pacemaker tissue that can initiate repetitive a.p. the pace maker tissue makes up the conduction system that spread impulses through out heart. They have unstable memb. potential that slowly decreases after each impulse until reaches firing level.
  •  
    • Smooth muscle
    • morphology:- Fusiform cells with one nucleus
      • 30 to 200 microns long & 5 to 10 microns wide
    • 1) S.m lacks cross striations.
    • 2) Actin & myosin II are present & slide on
    • each other but not arranged in regular arrays.
    • 3) Instead of Z- lines there are dense bodies in
    • cytoplasm & attached to cell memb. bound by
    • α- actinin to actin filaments.
    • 4) Troponin is absent.
    • 5) Sarcoplasmic reticulum is poorly developed.
    • 6) Contain few mitochondria and depends on glycolysis for their metabolic needs.
  •  
    • Types
    • Divided into :-
    • 1- visceral s.m (single unit) :-
    • as in intestine , uterus , ureters .they has low –resistance bridges & functions in a syncytial fashion. The bridges like in cardiac m. form gap-junction.
    • 2 - multi –unit s.m :-
    • made up of individual units without interconnecting bridges. It is found in iris of the eye , in which fine graded cont. occur. It is not under voluntary control, but has many functional similarities to sk. M.
  • Types of Smooth Muscle
    • Multiunit smooth muscle
      • in largest arteries, iris, pulmonary air passages, arrector pili muscles
      • terminal nerve branches synapse on individual myocytes in a motor unit
      • independent contraction
    • Single-unit smooth muscle
      • in most blood vessels & viscera as circular & longitudinal muscle layers
      • electrically coupled by gap junctions
      • large number of cells contract as a unit
  • Stimulation of Smooth Muscle
    • Involuntary & contracts without nerve stimulation
      • hormones, CO2, low pH, stretch, O2 deficiency
      • pacemaker cells in GI tract are autorhythmic
    • Autonomic nerve fibers have beadlike swellings called varicosities containing synaptic vesicles
      • stimulates multiple myocytes at diffuse junctions
  •  
    • Visceral s.m :-
    • electrical & mechanical activity:-
    • Visceral s.m has unstable memb. potential. it shows continuous irregular cont. independent of nerve supply. This maintains partial cont. called tonus or tone . The memb. potential is about -50 mv .
    • There are sin- wave like fluctuations, spikes duration 50 ms . the spikes may occur on rising or falling phases of the sine wave.
    • There are pacemaker potentials but generated in multiple foci .the excitation –cont. coupling is very slow the.m. starts to cont. about 200ms after start of spike & 150 ms after spike is over. Peak cont. reaches 500 ms after spike.
  •  
      • Molecular basis for cont.:-
    • Ca++ involved in initiation of cont. of s.m. like in sk.m but visceral s.m. has poorly developed sarcoplasmic reticulum, so intracellular Ca++ is due to Ca++ influx from ECF via voltage gated Ca++ channels.
    • Myosin must be phosphorylated for activation of myosin ATPase which is not necessary in sk.m.
    • In s.m Ca++ binds to calmodulin & resulting complex activates calmodulin- dependent myosin light chain kinase. this enzyme catalyzes phosphorylation of light chain & myosin ATPase will activate , actin slides on myosin & cont. occur, but in sk.m & cardiac m cont. is triggered by binding of Ca++ to troponin C.
    • Myosin dephosphorylated by phosphatase in the cell, but this will not lead to relaxation of s.m. instead s.m. has a latch bridge mechanism by which dephosphorylated myosin cross-bridges remain attached to actin for some time after the cytoplasmic Ca++ conc. falls .this produces sustained cont. which is important in vascular s.m. relaxation of s.m. occur when there is final dissociation of Ca++ -calmodulin complex.
  •  
  •  
  •  
  •  
      • Stimulation
    • Visceral s.m. contracts when stretched in the absence of extrinsic innervation, Stretch will lead to ↓ in memb. p , ↑ in frequencies of spikes & ↑ in tone.
    • Adding of E or NE to preparation of intestinal s.m . memb. p become larger, spike ↓ in frequency& muscle relaxes. NE exerts both β & α action on s.m. β action ↓ m. tension through c-AMP ( binding intracellular Ca++) . The α action is inhibition of cont. by ↑ Ca++ efflux from muscle cell.
    • Ach has opposite effect of E. Ach ↓ memb. p. , spikes become more frequent. Muscles become more active. The effect of Ach through phospholipase C& IP3 which ↑ intracellular Ca++ conc.
  •  
    • Function of the nerve supply to s.m
    • Mammals visceral m. has dual nerve supply from two divisions of autonomic nervous system.
    • Estrogen ↓the memb. p. of uterine s.m. progesterone ↑ memb. p. & inhibits the electrical & contractile activity of uterine m.
    • Relation of length to tension:-
    • Plasticity:-
    • If a piece of visceral s.m is stretched , first it ↑ tension however if s.m continue in stretching tension gradually ↓ .this is called plasticity of s.m .
    • Multi- unit s.m :-
    • Unlike visceral s.m multi unit s.m is
    • 1) nonsyncytial & cont do not spread widely through it. because of this cont. multi- unit is more fine & localized than those of visceral s.m.
    • 2) Like visceral multi-unit s.m is very sensitive to chemical mediators:- NE causes repeated firing of muscle after a single stimulus leading to an irregular tetanus rather than a single twitch.
    • The twitch cont of muscle-unit is like sk.m. except that its duration is 10 times as long.