Y khoa, y dược - Muscles and muscle tissue: Part C

9Muscles and Muscle Tissue: Part CForce of Muscle ContractionThe force of contraction is affected by:Number of muscle fibers stimulated (recruitment)Relative size of the fibers - hypertrophy of cells increases strengthForce of Muscle ContractionThe force of contraction is affected by:Frequency of stimulation - frequency allows time for more effective transfer of tension to noncontractile componentsLength-tension relationship - muscles contract most strongly when muscle fibers are 80–120% of their normal resting lengthFigure 9.21Largenumber ofmusclefibersactivatedContractile forceHighfrequency ofstimulationLargemusclefibersMuscle andsarcomerestretched to slightly over 100%of resting lengthFigure 9.22SarcomeresgreatlyshortenedSarcomeres atresting lengthSarcomeres excessivelystretched170%Optimal sarcomereoperating length(80%–120% ofresting length)100%75%Velocity and Duration of ContractionInfluenced by:Muscle fiber typeLoadRecruitmentMuscle Fiber TypeClassified according to two characteristics:Speed of contraction: slow or fast, according to:Speed at which myosin ATPases split ATPPattern of electrical activity of the motor neuronsMuscle Fiber TypeMetabolic pathways for ATP synthesis:Oxidative fibers—use aerobic pathwaysGlycolytic fibers—use anaerobic glycolysisMuscle Fiber TypeThree types: Slow oxidative fibersFast oxidative fibersFast glycolytic fibersTable 9.2Figure 9.23Predominanceof fast glycolytic(fatigable) fibersPredominanceof slow oxidative(fatigue-resistant)fibersSmall loadContractilevelocityContractiledurationEffects of ExerciseAerobic (endurance) exercise:Leads to increased:Muscle capillariesNumber of mitochondriaMyoglobin synthesisResults in greater endurance, strength, and resistance to fatigue May convert fast glycolytic fibers into fast oxidative fibersEffects of Resistance ExerciseResistance exercise (typically anaerobic) results in:Muscle hypertrophy (due to increase in fiber size)Increased mitochondria, myofilaments, glycogen stores, and connective tissueThe Overload PrincipleForcing a muscle to work hard promotes increased muscle strength and enduranceMuscles adapt to increased demandsMuscles must be overloaded to produce further gainsSmooth MuscleFound in walls of most hollow organs(except heart)Usually in two layers (longitudinal and circular)Figure 9.26Smallintestine(a)(b) Cross section of theintestine showing thesmooth muscle layers(one circular and theother longitudinal)running at rightangles to each other.MucosaLongitudinal layerof smooth muscle (shows smooth muscle fibers in cross section)Circular layer ofsmooth muscle (shows longitudinalviews of smooth muscle fibers) PeristalsisAlternating contractions and relaxations of smooth muscle layers that mix and squeeze substances through the lumen of hollow organsLongitudinal layer contracts; organ dilates and shortens Circular layer contracts; organ constricts and elongatesMicroscopic StructureSpindle-shaped fibers: thin and short compared with skeletal muscle fibersConnective tissue: endomysium onlySR: less developed than in skeletal muscle Pouchlike infoldings (caveolae) of sarcolemma sequester Ca2+No sarcomeres, myofibrils, or T tubules Table 9.3Table 9.3Innervation of Smooth MuscleAutonomic nerve fibers innervate smooth muscle at diffuse junctionsVaricosities (bulbous swellings) of nerve fibers store and release neurotransmittersFigure 9.27SmoothmusclecellVaricosities releasetheir neurotransmittersinto a wide synaptic cleft (a diffuse junction).SynapticvesiclesMitochondrionAutonomicnerve fibersinnervatemost smoothmuscle fibers.VaricositiesMyofilaments in Smooth MuscleRatio of thick to thin filaments (1:13) is much lower than in skeletal muscle (1:2)Thick filaments have heads along their entire lengthNo troponin complex; protein calmodulin binds Ca2+Myofilaments in Smooth MuscleMyofilaments are spirally arranged, causing smooth muscle to contract in a corkscrew mannerDense bodies: proteins that anchor noncontractile intermediate filaments to sarcolemma at regular intervalsFigure 9.28aFigure 9.28bContraction of Smooth MuscleSlow, synchronized contractions Cells are electrically coupled by gap junctionsSome cells are self-excitatory (depolarize without external stimuli); act as pacemakers for sheets of muscle Rate and intensity of contraction may be modified by neural and chemical stimuliContraction of Smooth MuscleSliding filament mechanismFinal trigger is  intracellular Ca2+Ca2+ is obtained from the SR and extracellular spaceRole of Calcium IonsCa2+ binds to and activates calmodulin Activated calmodulin activates myosin (light chain) kinaseActivated kinase phosphorylates and activates myosin Cross bridges interact with actin Table 9.3Table 9.3Figure 9.29 Calcium ions (Ca2+)enter the cytosol fromthe ECF via voltage-dependent or voltage-independent Ca2+channels, or fromthe scant SR.ATPPiPiExtracellular fluid (ECF)ADPCa2+Ca2+Ca2+Plasma membraneSarcoplasmicreticulumInactive calmodulinInactive kinaseInactivemyosin moleculeActivated (phosphorylated)myosin moleculeActivated kinaseActivated calmodulinCytoplasm Ca2+ binds to andactivates calmodulin. Activated calmodulinactivates the myosinlight chain kinaseenzymes. The activated kinase enzymescatalyze transfer of phosphateto myosin, activating the myosinATPases. Activated myosin forms crossbridges with actin of the thinfilaments and shortening begins.ThinfilamentThickfilament12345Figure 9.29, step 1 Calcium ions (Ca2+)enter the cytosol fromthe ECF via voltage-dependent or voltage-independent Ca2+channels, or fromthe scant SR.Extracellular fluid (ECF)Ca2+Ca2+Plasma membraneSarcoplasmicreticulumCytoplasm1Figure 9.29, step 2Ca2+Inactive calmodulinActivated calmodulinCa2+ binds to andactivates calmodulin.2Figure 9.29, step 3Inactive kinaseActivated kinase Activated calmodulinactivates the myosinlight chain kinaseenzymes.3Figure 9.29, step 4ATPPiPiADPInactivemyosin moleculeActivated (phosphorylated)myosin molecule The activated kinase enzymescatalyze transfer of phosphateto myosin, activating the myosinATPases.4Figure 9.29, step 5 Activated myosin forms crossbridges with actin of the thinfilaments and shortening begins.ThinfilamentThickfilament5Figure 9.29 Calcium ions (Ca2+)enter the cytosol fromthe ECF via voltage-dependent or voltage-independent Ca2+channels, or fromthe scant SR.ATPPiPiExtracellular fluid (ECF)ADPCa2+Ca2+Ca2+Plasma membraneSarcoplasmicreticulumInactive calmodulinInactive kinaseInactivemyosin moleculeActivated (phosphorylated)myosin moleculeActivated kinaseActivated calmodulinCytoplasm Ca2+ binds to andactivates calmodulin. Activated calmodulinactivates the myosinlight chain kinaseenzymes. The activated kinase enzymescatalyze transfer of phosphateto myosin, activating the myosinATPases. Activated myosin forms crossbridges with actin of the thinfilaments and shortening begins.ThinfilamentThickfilament12345Contraction of Smooth MuscleVery energy efficient (slow ATPases)Myofilaments may maintain a latch state for prolonged contractionsRelaxation requires:Ca2+ detachment from calmodulinActive transport of Ca2+ into SR and ECFDephosphorylation of myosin to reduce myosin ATPase activityRegulation of ContractionNeural regulation:Neurotransmitter binding   [Ca2+] in sarcoplasm; either graded (local) potential or action potentialResponse depends on neurotransmitter released and type of receptor moleculesRegulation of ContractionHormones and local chemicals:May bind to G protein–linked receptorsMay either enhance or inhibit Ca2+ entrySpecial Features of Smooth Muscle Contraction Hyperplasia:Smooth muscle cells can divide and increase their numbersExample:estrogen effects on uterus at puberty and during pregnancyTable 9.3Types of Smooth MuscleSingle-unit (visceral) smooth muscle: Sheets contract rhythmically as a unit (gap junctions)Often exhibit spontaneous action potentialsArranged in opposing sheets and exhibit stress-relaxation responseTypes of Smooth Muscle: MultiunitMultiunit smooth muscle:Located in large airways, large arteries, arrector pili muscles, and iris of eyeGap junctions are rareArranged in motor unitsGraded contractions occur in response to neural stimuliMuscular DystrophyGroup of inherited muscle-destroying diseasesMuscles enlarge due to fat and connective tissue depositsMuscle fibers atrophyMuscular DystrophyDuchenne muscular dystrophy (DMD):Most common and severe typeInherited, sex-linked, carried by females and expressed in males (1/3500) as lack of dystrophinVictims become clumsy and fall frequently; usually die of respiratory failure in their 20sNo cure, but viral gene therapy or infusion of stem cells with correct dystrophin genes show promise