Chapter 11 Lecture Outline 11 1 Copyright c

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Chapter 11 Lecture Outline 11 -1 Copyright (c) The Mc. Graw-Hill Companies, Inc. Permission

Chapter 11 Lecture Outline 11 -1 Copyright (c) The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display.

Muscle Cells Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or

Muscle Cells Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Muscle fiber Nucleus A band I band Z disc Openings into transverse tubules Mitochondria Sarcoplasmic reticulum Triad: Terminal cisternae Transverse tubule Figure 11. 2 Sarcolemma Sarcoplasm Myofibrils Myofilaments • • types and characteristics of muscular tissue microscopic anatomy of skeletal muscle nerve-muscle relationship behavior of skeletal muscle fibers behavior of whole muscles muscle metabolism cardiac and smooth muscle 11 -2

Introduction to Muscle • movement is a fundamental characteristic of all living things •

Introduction to Muscle • movement is a fundamental characteristic of all living things • muscle cells are capable of converting the chemical energy of ATP into mechanical energy • types of muscle – skeletal, cardiac and smooth • physiology of skeletal muscle – basis of warm-up, quickness, strength, endurance and fatigue 11 -3

Characteristics of Muscle • responsiveness (excitability) – to chemical signals, stretch and electrical changes

Characteristics of Muscle • responsiveness (excitability) – to chemical signals, stretch and 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 between contractions • elasticity – returns to its original resting length after being stretched 11 -4

Skeletal Muscle • skeletal muscle - voluntary, striated muscle attached to one or more

Skeletal Muscle • skeletal muscle - voluntary, striated muscle attached to one or more bones Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. • striations - alternating light and dark transverse bands Nucleus Muscle fiber – results from an overlapping of internal contractile proteins Endomysium • voluntary – usually subject to conscious control Striations © Ed Reschke • muscle cell, muscle fiber, (myofiber) as long as 30 cm Figure 11. 1 11 -5

Connective Tissue Elements • tendons are attachments between muscle and bone matrix – –

Connective Tissue Elements • tendons are attachments between muscle and bone matrix – – – endomysium – connective tissue around muscle cells perimysium – connective tissue around muscle fascicles epimysium – connective tissue surrounding entire muscle continuous with collagen fibers of tendons in turn, with connective tissue of bone matrix • collagen is somewhat extensible and elastic – stretches slightly under tension and recoils when released • resists excessive stretching and protects muscle from injury • returns muscle to its resting length • contribute to power output and muscle efficiency 11 -6

Structure of a Skeletal Muscle Fiber Copyright © The Mc. Graw-Hill Companies, Inc. Permission

Structure of a Skeletal Muscle Fiber Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Muscle fiber Nucleus A band I band Z disc Openings into transverse tubules Mitochondria Sarcoplasmic reticulum Triad: Terminal cisternae Transverse tubule Sarcolemma Myofibrils Sarcoplasm Myofilaments Figure 11. 2 11 -7

The Muscle Fiber • • • sarcolemma – plasma membrane of a muscle fiber

The Muscle Fiber • • • sarcolemma – plasma membrane of a muscle fiber sarcoplasm – cytoplasm of a muscle fiber myofibrils – long protein bundles that occupies the main portion of the sarcoplasm – glycogen – stored in abundance to provide energy with heightened exercise – myoglobin – red pigment – stores oxygen needed for muscle activity • multiple nuclei – flattened nuclei pressed against the inside of the sarcolemma – myoblasts – stem cells that fuse to form each muscle fiber – satellite cells – unspecialized myoblasts remaining between the muscle fiber and endomysium • may multiply and produce new muscle fibers to some degree • • • repair by fibrosis rather than regeneration of functional muscle mitochondria – packed in spaces between myofibrils sarcoplasmic reticulum (SR) - smooth ER that forms a network around each myofibril – calcium reservoir – calcium activates the muscle contraction process • • • terminal cisternae – dilated end-sacs of SR which cross muscle fiber from one side to the other T tubules – tubular infoldings of the sarcolemma which penetrate through the cell and emerge on the other side triad – a T tubule and two terminal cisterns 11 -8

Thick Myofilaments Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or

Thick Myofilaments Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Head Tail (a) Myosin molecule Myosin head (b) Thick filament Figure 11. 3 a-b • made of several hundred myosin molecules – shaped like a golf club • two chains intertwined to form a shaft-like tail • double globular head – heads directed outward in a helical array around the bundle • heads on one half of the thick filament angle to the left • heads on the other half angle to the right • bare zone with no heads in the middle 11 -9

Thin Myofilaments • fibrous (F) actin - two intertwined strands – string of globular

Thin Myofilaments • fibrous (F) actin - two intertwined strands – string of globular (G) actin subunits each with an active site that can bind to head of myosin molecule • tropomyosin molecules – each blocking 6 or 7 active sites on G actin subunits • troponin molecule - small, calcium-binding protein on each tropomyosin molecule Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Tropomyosin (c) Thin filament Troponin complex G actin Figure 11. 3 c 11 -10

Elastic Myofilaments • titin (connectin) – huge springy protein – flank each thick filament

Elastic Myofilaments • titin (connectin) – huge springy protein – flank each thick filament and anchor it to the Z disc – helps stabilize thick filament – center it between the thin filaments – prevents over stretching 11 -11

Regulatory and Contractile Proteins Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for

Regulatory and Contractile Proteins Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Myosin head (b) Thick filament Tropomyosin Troponin complex (c) Thin filament • contractile proteins - myosin and actin G actin Figure 11. 3 b-c – do the work • regulatory proteins - tropomyosin and troponin – like a switch that determine when the fiber can contract and when it cannot – contraction activated by release of calcium into sarcoplasm and its binding to troponin, – troponin changes shape and moves tropomyosin off the active 11 -12 sites on actin

Overlap of Thick and Thin Filaments Copyright © The Mc. Graw-Hill Companies, Inc. Permission

Overlap of Thick and Thin Filaments Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Thick filament Thin filament Bare zone (d) Portion of a sarcomere showing the overlap of thick and thin filaments Figure 11. 3 d 11 -13

Accessory Proteins • at least seven other accessory proteins in or associated with thick

Accessory Proteins • at least seven other accessory proteins in or associated with thick or thin filaments – anchor the myofilaments, regulate length of myofilaments, alignment of myofilaments for maximum effectiveness Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Endomysium Linking proteins Basal lamina • dystrophin – most clinically important – links actin in outermost myofilaments to transmembrane proteins and eventually to fibrous endomysium surrounding the entire muscle cell – transfers forces of muscle contraction to connective tissue around muscle cell – genetic defects in dystrophin produce disabling disease muscular dystrophy Sarcolemma Dystrophin Thin filament Thick filament Figure 11. 4 11 -14

Striations • myosin and actin are proteins that occur in all cells – function

Striations • myosin and actin are proteins that occur in all cells – function in cellular motility, mitosis, transport of intracellular material • organized in a precise way in skeletal and cardiac muscle – A band – dark – A stands for anisotropic • part of A band where thick and thin filaments overlap is especially dark • H band in the middle of A band – just thick filaments • M line is in the middle of the H band – I band – alternating lighter band – I stands for isotropic • the way the bands reflect polarized light – z disc – provides anchorage for thin filaments and elastic filaments • bisects I band – sarcomere – the segment of the myofibril from one z disc to the next Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Sarcomere A band I band H band (b) Z disc Thick filament Thin filament Elastic filament M line Figure 11. 5 b Titin Z disc 11 -15

Striations and Sarcomeres Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction

Striations and Sarcomeres Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Nucleus M line Z disc H band A band I band 1 I band 2 3 4 Individual myofibrils 5 Sarcomere (a) Visuals Unlimited Figure 11. 5 a • sarcomere – functional contractile unit of the muscle fiber – muscle shortens because individual sarcomeres shorten – pulls z discs closer to each other 11 -16

Sarcomeres • sarcomere - segment from Z disc to Z disc – functional contractile

Sarcomeres • sarcomere - segment from Z disc to Z disc – functional contractile unit of muscle fiber • muscle cells shorten because their individual sarcomeres shorten – Z disc (Z lines) are pulled closer together as thick and thin filaments slide past each other • neither thick nor thin filaments change length during shortening – only the amount of overlap changes • during shortening dystrophin & linking proteins also pull on extracellular proteins – transfers pull to extracellular tissue 11 -17

The Nerve-Muscle Relationship • skeletal muscle never contracts unless stimulated by a nerve •

The Nerve-Muscle Relationship • skeletal muscle never contracts unless stimulated by a nerve • if nerve connections are severed or poisoned, a muscle is paralyzed • denervation atrophy – shrinkage of paralyzed muscle when connection not restored • somatic motor neurons – nerve cells whose cell bodies are in the brainstem and spinal cord that serve skeletal muscles • somatic motor fibers –their axons that lead to the skeletal muscle – each nerve fiber branches out to a number of muscle fibers – each muscle fiber is supplied by only one motor neuron 11 -18

Motor Units • motor unit – one nerve fiber and all the muscle fibers

Motor Units • motor unit – one nerve fiber and all the muscle fibers innervated by it • muscle fibers of one motor unit Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. – dispersed throughout the muscle Spinal cord – contract in unison – produce weak contraction over wide area – provides ability to sustain long-term contraction as motor units take turns contracting (postural control) Motor – effective contraction usually requires the neuron 1 contraction of several motor units at once Motor neuron 2 • • • average motor unit – 200 muscle fibers for each motor unit small motor units - fine degree of control – 3 -6 muscle fibers per neuron – eye and hand muscles large motor units – more strength than control – powerful contractions supplied by large motor units – gastrocnemius – 1000 muscle fibers per neuron – many muscle fibers per motor unit Neuromuscular junction Skeletal muscle fibers Figure 11. 6 11 -19

The Neuromuscular Junction • synapse – point where a nerve fiber meets its target

The Neuromuscular Junction • synapse – point where a nerve fiber meets its target cell • neuromuscular junction (NMJ) - when target cell is a muscle fiber • each terminal branch of the nerve fiber within the NMJ forms separate synapse with the muscle fiber • one nerve fiber stimulates the muscle fiber at several points within the NMJ 11 -20

Components of Neuromuscular Junction • synaptic knob - swollen end of nerve fiber –

Components of Neuromuscular Junction • synaptic knob - swollen end of nerve fiber – contains synaptic vesicles filled with acetylcholine (ACh) • synaptic cleft - tiny gap between synaptic knob and muscle sarcolemma • Schwann cell envelops & isolates all of the NMJ from surrounding tissue fluid • synaptic vesicles undergo exocytosis releasing ACh into synaptic cleft • 50 million ACh receptors – proteins incorporated into muscle cell plasma membrane – junctional folds of sarcolemma beneath synaptic knob • increases surface area holding ACh receptors – lack of receptors leads to paralysis in disease myasthenia gravis • basal lamina - thin layer of collagen and glycoprotein separates Schwann cell and entire muscle cell from surrounding tissues – contains acetylcholinesterase (ACh. E) that breaks down ACh after contraction causing relaxation 11 -21

Neuromuscular Junction Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or

Neuromuscular Junction Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Motor nerve fiber Myelin Synaptic knob Schwann cell Synaptic vesicles (containing ACh) Basal lamina Sarcolemma Synaptic cleft Nucleus ACh receptor Junctional folds Mitochondria Nucleus Sarcoplasm Myofilaments Figure 11. 7 b 11 -22 (b)

Neuromuscular Junction - LM Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for

Neuromuscular Junction - LM Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Motor nerve fibers Neuromuscular junction Muscle fibers Figure 11. 7 a (a) 100 µm Victor B. Eichler 11 -23

Neuromuscular Toxins • toxins that interfere with synaptic function can paralyze the muscles •

Neuromuscular Toxins • toxins that interfere with synaptic function can paralyze the muscles • some pesticides contain cholinesterase inhibitors – bind to acetylcholinesterase and prevent it from degrading ACh – spastic paralysis - a state of continual contraction of the muscles – possible suffocation • tetanus (lockjaw) is a form of spastic paralysis caused by toxin of Clostridium tetani – glycine in the spinal cord normally stops motor neurons from producing unwanted muscle contractions – tetanus toxin blocks glycine release in the spinal cord and causes overstimulation and spastic paralysis of the muscles • flaccid paralysis – a state in which the muscles are limp and cannot contract – curare – compete with ACh for receptor sites, but do not stimulate the muscles – plant poison used by South American natives to poison blowgun darts • botulism – type of food poisoning caused by a neuromuscular toxin secreted by the bacterium Clostridium botulinum – blocks release of ACh causing flaccid paralysis – Botox Cosmetic injections for wrinkle removal 11 -24

Electrically Excitable Cells • muscle fibers and neurons are electrically excitable cells – their

Electrically Excitable Cells • muscle fibers and neurons are electrically excitable cells – their plasma membrane exhibits voltage changes in response to stimulation • electrophysiology - the study of the electrical activity of cells • in an unstimulated (resting) cell – there are more anions (negative ions) on the inside of the plasma membrane than on the outside – the plasma membrane is electrically polarized (charged) – there are excess sodium ions (Na+) in the extracellular fluid (ECF) – there are excess potassium ions (K+) in the intracellular fluid (ICF) – also in the ICF, there anions such as proteins, nucleic acids, and phosphates that cannot penetrate the plasma membrane – these anions make the inside of the plasma membrane negatively charged by comparison to its outer surface • voltage (electrical potential) – a difference in electrical charge from one point to another • resting membrane potential – about -90 m. V – maintained by sodium-potassium pump 11 -25

Electrically Excitable Cells • stimulated (active) muscle fiber or nerve cell – – –

Electrically Excitable Cells • stimulated (active) muscle fiber or nerve cell – – – ion gates open in the plasma membrane Na+ instantly diffuses down its concentration gradient into the cell these cations override the negative charges in the ICF depolarization - inside of the plasma membrane becomes briefly positive immediately, Na+ gates close and K+ gates open K+ rushes out of cell repelled by the positive sodium charge and partly because of its concentration gradient loss of positive potassium ions turns the membrane negative again (repolarization) action potential – quick up-and-down voltage shift from the negative RMP to a positive value, and back to the negative value again. RMP is a stable voltage seen in a waiting muscle or nerve cell action potential is a quickly fluctuating voltage seen in an active stimulated cell an action potential at one point on a plasma membrane causes another one to happen immediately in front of it, which triggers another one a 11 -26 little farther along and so forth

Muscle Contraction & Relaxation • four major phases of contraction and relaxation – excitation

Muscle Contraction & Relaxation • four major phases of contraction and relaxation – excitation • the process in which nerve action potentials lead to muscle action potentials – excitation-contraction coupling • events that link the action potentials on the sarcolemma to activation of the myofilaments, thereby preparing them to contract – contraction • step in which the muscle fiber develops tension and may shorten – relaxation • when its work is done, a muscle fiber relaxes and returns to its 11 -27 resting length

Excitation of a Muscle Fiber Copyright © The Mc. Graw-Hill Companies, Inc. Permission required

Excitation of a Muscle Fiber Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Nerve signal Ca 2+ enters synaptic knob Motor nerve fiber Sarcolemma Synaptic vesicles Synaptic knob ACh Synaptic cleft ACh receptors 1 Arrival of nerve signal ACh 2 Acetylcholine (ACh) release ACh K+ ACh receptor Sarcolemma Na+ 4 Opening of ligand-regulated ion gate; creation of end–plate potential 3 Binding of ACh to receptor K+ Plasma membrane of synaptic knob Na+ Voltage-regulated ion gates Sarcolemma 5 Opening of voltage-regulated ion gates; creation of action potentials Figure 11. 8 11 -28

Excitation (steps 1 and 2) Copyright © The Mc. Graw-Hill Companies, Inc. Permission required

Excitation (steps 1 and 2) Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Nerve signal Motor nerve fiber Ca 2+ enters synaptic knob Sarcolemma Synaptic vesicles ACh receptors 1 Arrival of nerve signal Synaptic cleft 2 Acetylcholine (ACh) release Figure 11. 8 (1 -2) • nerve signal opens voltage-gated calcium channels in synaptic knob • calcium stimulates exocytosis of ACh from synaptic vesicles 11 -29 • ACh released into synaptic cleft

Excitation (steps 3 and 4) Copyright © The Mc. Graw-Hill Companies, Inc. Permission required

Excitation (steps 3 and 4) Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. ACh Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. ACh K+ ACh receptor Sarcolemma Na+ 4 Opening of ligand-regulated ion gate; creation of end–plate potential 3 Binding of ACh to receptor Figure 11. 8 (3 -4) • two ACh molecules bind to each receptor protein, opening Na+ and K+ channels. • Na+ enters shifting RMP goes from -90 m. V to +75 m. V, then K+ exits and RMP returns to -90 m. V - quick voltage shift is called an end-plate potential (EPP). 11 -30

Excitation (step 5) Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction

Excitation (step 5) Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. K+ Plasma membrane of synaptic knob Na+ Voltage-regulated ion gates Sarcolemma 5 Opening of voltage-regulated ion gates; creation of action potentials Figure 11. 8 (5) • voltage change (EPP) in end-plate region opens nearby voltage-gated channels producing an action potential that spreads over muscle 11 -31 surface.

Excitation-Contraction Coupling in Skeletal Muscle Copyright © The Mc. Graw-Hill Companies, Inc. Permission required

Excitation-Contraction Coupling in Skeletal Muscle Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Terminal cisterna of SR T tubule Sarcoplasmic reticulum Ca 2+ 6 Action potentials propagated down T tubules 7 Calcium released from terminal cisternae Figure 11. 9 (6 -9) Active sites Ca 2+ Troponin Tropomyosin Actin Thin filament Ca 2+ 8 Binding of calcium to troponin Myosin 9 Shifting of tropomyosin; exposure of active sites on actin 11 -32

Excitation-Contraction Coupling (steps 6 and 7) Copyright © The Mc. Graw-Hill Companies, Inc. Permission

Excitation-Contraction Coupling (steps 6 and 7) Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Terminal cisterna of SR T tubule Sarcoplasmic reticulum Ca 2+ 6 Action potentials propagated down T tubules 7 Calcium released from terminal cisternae Figure 11. 9 (6 -7) • action potential spreads down into T tubules • opens voltage-gated ion channels in T tubules and Ca+2 channels in SR 11 -33 +2 • Ca enters the cytosol

Excitation-Contraction Coupling (steps 8 and 9) Copyright © The Mc. Graw-Hill Companies, Inc. Permission

Excitation-Contraction Coupling (steps 8 and 9) Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Ca 2+ Troponin Tropomyosin Active sites Actin Thin filament Myosin Ca 2+ 8 Binding of calcium 9 Shifting of tropomyosin; to troponin exposure of active sites on actin Figure 11. 9 (8 -9) • calcium binds to troponin in thin filaments • troponin-tropomyosin complex changes shape and exposes active sites 11 -34 on actin

Contraction (steps 10 and 11) Copyright © The Mc. Graw-Hill Companies, Inc. Permission required

Contraction (steps 10 and 11) Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Troponin Tropomyosin • myosin ATPase enzyme in myosin head hydrolyzes an ATP molecule • activates the head “cocking” it in an extended position ADP Pi Myosin 10 Hydrolysis of ATP to ADP + Pi; activation and cocking of myosin head – ADP + Pi remain attached Cross-bridge: Actin Myosin 11 Formation of myosin–actin cross-bridge Figure 11. 10 (10 -11) • head binds to actin active site forming a myosin - actin cross-bridge 11 -35

Contraction (steps 12 and 13) Copyright © The Mc. Graw-Hill Companies, Inc. Permission required

Contraction (steps 12 and 13) Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. • myosin head releases ADP and Pi, flexes pulling thin filament past thick power stroke • upon binding more ATP, myosin releases actin and process is repeated – each head performs 5 power strokes per second – each stroke utilizes one molecule of ATP 13 Binding of new ATP; breaking of cross-bridge ADP PPii 12 Power stroke; sliding of thin filament over thick filament Figure 11. 10 (12 -13) 11 -36

Relaxation (steps 14 and 15) Copyright © The Mc. Graw-Hill Companies, Inc. Permission required

Relaxation (steps 14 and 15) Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. ACh. E ACh 14 Cessation of nervous stimulation and ACh release 15 ACh breakdown by acetylcholinesterase (ACh. E) Figure 11. 11 (14 -15) • nerve stimulation & ACh release stop • ACh. E breaks down ACh & fragments reabsorbed into synaptic knob 11 -37 • stimulation by ACh stops

Relaxation (step 16) Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction

Relaxation (step 16) Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Terminal cisterna of SR Ca 2+ 16 Reabsorption of calcium ions by sarcoplasmic reticulum Figure 11. 11 (16) • Ca+2 pumped back into SR by active transport. Ca+2 binds to calsequestrin while in storage in SR • ATP is needed for muscle relaxation as well as muscle contraction. 11 -38

Relaxation (steps 17 and 18) • Ca+2 removed from troponin is pumped back into

Relaxation (steps 17 and 18) • Ca+2 removed from troponin is pumped back into SR Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Ca 2+ • tropomyosin reblocks the active sites ADP Pi 17 • muscle fiber ceases to produce or maintain tension Loss of calcium ions from troponin Tropomyosin • muscle fiber returns to its resting length – due to recoil of elastic components & contraction of antagonistic muscles Ca 2+ ATP 18 Return of tropomyosin to position blocking active sites of actin Figure 11. 11 (17 -18) 11 -39

Rigor Mortis • rigor mortis - hardening of muscles and stiffening of body beginning

Rigor Mortis • rigor mortis - hardening of muscles and stiffening of body beginning 3 to 4 hours after death – – deteriorating sarcoplasmic reticulum releases Ca+2 deteriorating sarcolemma allows Ca+2 to enter cytosol Ca+2 activates myosin-actin cross-bridging muscle contracts, but can not relax. • muscle relaxation requires ATP, and ATP production is no longer produced after death – fibers remain contracted until myofilaments begins to decay • rigor mortis peaks about 12 hours after death, then diminishes over the next 48 to 60 hours 11 -40

Length-Tension Relationship • Length – Tension Relationship - the amount of tension generated by

Length-Tension Relationship • Length – Tension Relationship - the amount of tension generated by a muscle and the force of contraction depends on how stretched or contracted it was before it was stimulated • if overly contracted at rest, a weak contraction results – thick filaments too close to Z discs and can’t slide • if too stretched before stimulated, a weak contraction results – little overlap of thin and thick does not allow for very many cross bridges to form • optimum resting length produces greatest force when muscle contracts – muscle tone – central nervous system continually monitors and adjusts the length of the resting muscle, and maintains a state of partial contraction called muscle tone – maintains optimum length and makes the muscles ideally ready for 11 -41 action

Length-Tension Relationship Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or

Length-Tension Relationship Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Optimum resting length (2. 0– 2. 25µm) z z Overly contracted z z z Overly stretched z Tension (g) generated upon stimulation 1. 0 0. 5 0. 0 1. 0 2. 0 3. 0 Sarcomere length (µm) before stimulation Figure 11. 12 4. 0 11 -42

Behavior of Whole Muscles • myogram – a chart of the timing and strength

Behavior of Whole Muscles • myogram – a chart of the timing and strength of a muscle’s contraction • weak, subthreshold electrical stimulus causes no contraction • threshold - the minimum voltage necessary to generate an action potential in the muscle fiber and produce a contraction – twitch – a quick cycle of contraction when stimulus is at threshold or higher Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Relaxation phase Contraction phase Muscle tension • the response of a muscle to weak electrical stimulus seen in frog gastrocnemius - sciatic nerve preparation Latent period Time of stimulation Time Figure 11. 13 11 -43

Phases of a Twitch Contraction • latent period - 2 msec delay between the

Phases of a Twitch Contraction • latent period - 2 msec delay between the onset of stimulus and onset of twitch response – time required for excitation, excitation-contraction coupling and tensing of elastic components of the muscle – internal tension – force generated during latent period and no shortening of the muscle occurs • contraction phase – phase in which filaments slide and the muscle shortens – once elastic components are taut, muscle begins to produce external tension – in muscle that moves a load – short-lived phase • relaxation phase - SR quickly reabsorbs Ca+2, myosin releases the thin filaments and tension declines – muscle returns to resting length – entire twitch lasts from 7 to 100 msec 11 -44

Contraction Strength of Twitches • at subthreshold stimulus – no contraction at all •

Contraction Strength of Twitches • at subthreshold stimulus – no contraction at all • at threshold intensity and above - a twitch is produced – twitches caused by increased voltage are no stronger than those at threshold • not exactly true that muscle fiber obeys an all-or-none law contracting to its maximum or not at all – electrical excitation of a muscle follows all-or-none law – not true that muscle fibers follow the all or none law – twitches vary in strength depending upon: • stimulus frequency - stimuli arriving closer together produce stronger twitches • concentration of Ca+2 in sarcoplasm can vary the frequency • how stretched muscle was before it was stimulated • temperature of the muscles – warmed-up muscle contracts more strongly – enzymes work more quickly • lower than normal p. H of sarcoplasm weakens the contraction - fatigue • state of hydration of muscle affects overlap of thick & thin filaments • muscles need to be able to contract with variable strengths for different tasks 11 -45

Recruitment and Stimulus Intensity Stimulus voltage Copyright © The Mc. Graw-Hill Companies, Inc. Permission

Recruitment and Stimulus Intensity Stimulus voltage Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Threshold 1 2 3 Stimuli to nerve 4 5 6 7 8 9 Proportion of nerve fibers excited Tension Maximum contraction Figure 11. 14 1 2 3 4 5 6 7 8 9 Responses of muscle • stimulating the nerve with higher and higher voltages produces stronger contractions – higher voltages excite more and more nerve fibers in the motor nerve which stimulates more and more motor units to contract • recruitment or multiple motor unit (MMU) summation – the process of bringing more motor units into play 11 -46

Twitch Strength & Stimulus Frequency Copyright © The Mc. Graw-Hill Companies, Inc. Permission required

Twitch Strength & Stimulus Frequency Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Treppe Twitch Muscle twitches Stimuli Figure 11. 15 a, b • when stimulus intensity (voltage) remains constant twitch strength can vary with the stimulus frequency • up to 10 stimuli per second (a) (b) – each stimulus produces identical twitches and full recovery between twitches • 10 -20 stimuli per second produces treppe (staircase) phenomenon – muscle still recovers fully between twitches, but each twitch develops more tension than the one before – stimuli arrive so rapidly that the SR does not have time between stimuli to completely reabsorb all of the Ca+2 it released – Ca+2 concentration in the cytosol rises higher and higher with each stimulus causing subsequent twitches to be stronger – heat released by each twitch cause muscle enzymes such as myosin ATPase to 11 -47 work more efficiently and produce stronger twitches as muscle warms up

Incomplete and Complete Tetanus Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for

Incomplete and Complete Tetanus Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Incomplete tetanus Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Complete tetanus Fatigue (d) Figure 11. 15 c, d • 20 -40 stimuli per second produces incomplete tetanus (c) – – – – each new stimulus arrives before the previous twitch is over new twitch “rides piggy-back” on the previous one generating higher tension temporal summation – results from two stimuli arriving close together wave summation – results from one wave of contraction added to another each twitch reaches a higher level of tension than the one before muscle relaxes only partially between stimuli produces a state of sustained fluttering contraction called incomplete 11 -48 tetanus

Incomplete and Complete Tetanus Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for

Incomplete and Complete Tetanus Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Incomplete tetanus Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Complete tetanus Fatigue (d) Figure 11. 15 c, d • 40 -50 stimuli per second produces complete tetanus (c) – muscle has no time to relax at all between stimuli – twitches fuse to a smooth, prolonged contraction called complete tetanus – a muscle in complete tetanus produces about four times the tension as a single twitch – rarely occurs in the body, which rarely exceeds 25 stimuli per second – smoothness of muscle contractions is because motor units function asynchronously • when one motor unit relaxes, another contracts and takes over so the muscle does not lose tension 11 -49

Isometric and Isotonic Contractions Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for

Isometric and Isotonic Contractions Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Muscle develops tension but does not shorten Muscle shortens, tension remains constant Muscle lengthens while maintaining tension Movement No movement (a) Isometric contraction • • (b) Isotonic concentric contraction (c) Isotonic eccentric contraction Figure 11. 16 isometric muscle contraction – muscle is producing internal tension while an external resistance causes it to stay the same length or become longer – can be a prelude to movement when tension is absorbed by elastic component of muscle – important in postural muscle function and antagonistic muscle joint stabilization isotonic muscle contraction – muscle changes in length with no change in tension – concentric contraction – muscle shortens while maintains tension 11 -50 – eccentric contraction – muscle lengthens as it maintains tension

Isometric and Isotonic Phases of Contraction Length or Tension Copyright © The Mc. Graw-Hill

Isometric and Isotonic Phases of Contraction Length or Tension Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Muscle tension Muscle length Isometric phase Isotonic phase Figure 11. 17 Time • at the beginning of contraction – isometric phase – muscle tension rises but muscle does not shorten • when tension overcomes resistance of the load – tension levels off • muscle begins to shorten and move the load – isotonic phase 11 -51

Muscle Metabolism • all muscle contraction depends on ATP • ATP supply depends on

Muscle Metabolism • all muscle contraction depends on ATP • ATP supply depends on availability of: – oxygen – organic energy sources such as glucose and fatty acids • two main pathways of ATP synthesis – anaerobic fermentation • enables cells to produce ATP in the absence of oxygen • yields little ATP and toxic lactic acid, a major factor in muscle fatigue – aerobic respiration • produces far more ATP • less toxic end products (CO 2 and water) • requires a continual supply of oxygen 11 -52

Modes of ATP Synthesis During Exercise Copyright © The Mc. Graw-Hill Companies, Inc. Permission

Modes of ATP Synthesis During Exercise Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. 0 10 seconds 40 seconds Duration of exercise Repayment of oxygen debt Mode of ATP synthesis Aerobic respiration using oxygen from myoglobin Phosphagen system Glycogen– lactic acid system (anaerobic fermentation) Aerobic respiration supported by cardiopulmonary function Figure 11. 18 11 -53

Immediate Energy Needs • short, intense exercise (100 m dash) – oxygen need is

Immediate Energy Needs • short, intense exercise (100 m dash) – oxygen need is briefly supplied by myoglobin for a limited amount of aerobic respiration at onset – rapidly depleted – muscles meet most of ATP demand by borrowing phosphate groups (Pi) from other molecules and transferring them to ADP • two enzyme systems control these phosphate transfers – myokinase – transfers Pi from one ADP to another converting the latter to ATP – creatine kinase – obtains Pi from a phosphate-storage molecule creatine phosphate (CP) • fast-acting system that helps maintain the ATP level while other ATP-generating mechanisms are being activated • phosphagen system – ATP and CP collectively – provides nearly all energy used for short bursts of intense activity • one minute of brisk walking • 6 seconds of sprinting or fast swimming • important in activities requiring brief but maximum effort – football, baseball, and weight lifting 11 -54

Immediate Energy Needs Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction

Immediate Energy Needs Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. ADP Pi Myokinase ATP AMP ADP Creatine phosphate Pi Figure 11. 19 Creatine kinase ATP 11 -55

Short-Term Energy Needs • as the phosphagen system is exhausted • muscles shift to

Short-Term Energy Needs • as the phosphagen system is exhausted • muscles shift to anaerobic fermentation – muscles obtain glucose from blood and their own stored glycogen – in the absence of oxygen, glycolysis can generate a net gain of 2 ATP for every glucose molecule consumed – converts glucose to lactic acid • glycogen-lactic acid system – the pathway from glycogen to lactic acid • produces enough ATP for 30 – 40 seconds of maximum 11 -56 activity

Long-Term Energy Needs • after 40 seconds or so, the respiratory and cardiovascular systems

Long-Term Energy Needs • after 40 seconds or so, the respiratory and cardiovascular systems “catch up” and deliver oxygen to the muscles fast enough for aerobic respiration to meet most of the ATP demands • aerobic respiration produces 36 ATP per glucose – efficient means of meeting the ATP demands of prolonged exercise – one’s rate of oxygen consumption rises for 3 to 4 minutes and levels off to a steady state in which aerobic ATP production keeps pace with demand – little lactic acid accumulates under steady state conditions – depletion of glycogen and blood glucose, together with the loss of fluid and electrolytes through sweating, set limits on endurance and performance even when lactic acid does not 11 -57

Fatigue • muscle fatigue - progressive weakness and loss of contractility from prolonged use

Fatigue • muscle fatigue - progressive weakness and loss of contractility from prolonged use of the muscles – repeated squeezing of rubber ball – holding text book out level to the floor • causes of muscle fatigue – ATP synthesis declines as glycogen is consumed – ATP shortage slows down the Na+ - K+ pumps • compromises their ability to maintain the resting membrane potential and excitability of the muscle fibers – lactic acid lowers p. H of sarcoplasm • inhibits enzymes involved in contraction, ATP synthesis, and other aspects of muscle function – release of K+ with each action potential causes the accumulation of extracellular K+ • hyperpolarizes the cell and makes the muscle fiber less excitable – motor nerve fibers use up their ACh • less capable of stimulating muscle fibers – junctional fatigue – central nervous system, where all motor commands originate, fatigues by unknown processes, so there is less signal output to the skeletal muscles 11 -58

Endurance • endurance – the ability to maintain high-intensity exercise for more than 4

Endurance • endurance – the ability to maintain high-intensity exercise for more than 4 to 5 minutes – determined in large part by one’s maximum oxygen uptake (VO 2 max) – maximum oxygen uptake – the point at which the rate of oxygen consumption reaches a plateau and does not increase further with an added workload • • proportional to body size peaks at around age 20 usually greater in males than females can be twice as great in trained endurance athletes as in untrained person – results in twice the ATP production 11 -59

Oxygen Debt • heavy breathing continues after strenuous exercise – excess post-exercise oxygen consumption

Oxygen Debt • heavy breathing continues after strenuous exercise – excess post-exercise oxygen consumption (EPOC) – the difference between the resting rate of oxygen consumption and the elevated rate following exercise. – typically about 11 liters extra is needed after strenuous exercise – repaying the oxygen debt • needed for the following purposes: – replace oxygen reserves depleted in the first minute of exercise • oxygen bound to myoglobin and blood hemoglobin, oxygen dissolved in blood plasma and other extracellular fluid, and oxygen in the air in the lungs – replenishing the phosphagen system • synthesizing ATP and using some of it to donate the phosphate groups back to creatine until resting levels of ATP and CP are restored – oxidizing lactic acid • 80% of lactic acid produced by muscles enter bloodstream • reconverted to pyruvic acid in the kidneys, cardiac muscle, and especially the liver • liver converts most of the pyruvic acid back to glucose to replenish the glycogen stores of the muscle. – serving the elevated metabolic rate • occurs while the body temperature remains elevated by exercise and consumes more 11 -60 oxygen

Beating Muscle Fatigue • Taking oral creatine increases level of creatine phosphate in muscle

Beating Muscle Fatigue • Taking oral creatine increases level of creatine phosphate in muscle tissue and increases speed of ATP regeneration – useful in burst type exercises – weight-lifting – risks are not well known • muscle cramping, electrolyte imbalances, dehydration, water retention, stroke • kidney disease from overloading kidney with metabolite creatinine • carbohydrate loading – dietary regimen – packs extra glycogen into muscle cells – extra glycogen is hydrophilic and adds 2. 7 g water/ g glycogen • athletes feel sense of heaviness outweighs benefits of extra available glycogen 11 -61

Physiological Classes of Muscle Fibers • slow oxidative (SO), slow-twitch, red, or type I

Physiological Classes of Muscle Fibers • slow oxidative (SO), slow-twitch, red, or type I fibers – abundant mitochondria, myoglobin and capillaries - deep red color • adapted for aerobic respiration and fatigue resistance – relative long twitch lasting about 100 msec – soleus of calf and postural muscles of the back • fast glycolytic (FG), fast-twitch, white, or type II fibers – fibers are well adapted for quick responses, but not for fatigue resistance – rich in enzymes of phosphagen and glycogen-lactic acid systems generate lactic acid causing fatigue – poor in mitochondria, myoglobin, and blood capillaries which gives pale appearance • SR releases & reabsorbs Ca+2 quickly so contractions are quicker (7. 5 msec/twitch) – extrinsic eye muscles, gastrocnemius and biceps brachii • ratio of different fiber types have genetic predisposition – born sprinter – muscles differ in fiber types - gastrocnemius is predominantly FG for quick movements (jumping) 11 -62 – soleus is predominantly SO used for endurance (jogging)

FG and SO Muscle Fibers Copyright © The Mc. Graw-Hill Companies, Inc. Permission required

FG and SO Muscle Fibers Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. FG SO Figure 11. 20 11 -63

Strength and Conditioning • muscles can generate more tension than the bones and tendons

Strength and Conditioning • muscles can generate more tension than the bones and tendons can withstand • muscular strength depends on: – primarily on muscle size • a muscle can exert a tension of 3 or 4 kg / cm 2 of cross-sectional area – fascicle arrangement • pennate are stronger than parallel, and parallel stronger than circular – size of motor units • larger the motor unit the stronger the contraction – multiple motor unit summation – recruitment • when stronger contraction is required, the nervous system activates more motor units – temporal summation • nerve impulses usually arrive at a muscle in a series of closely spaced action potentials • the greater the frequency of stimulation, the more strongly a muscle contracts – length – tension relationship • a muscle resting at optimal length is prepared to contract more forcefully than a muscle that is excessively contracted or stretched – fatigue • fatigued muscles contract more weakly than rested muscles 11 -64

Strength and Conditioning • resistance training (weight lifting) – contraction of a muscles against

Strength and Conditioning • resistance training (weight lifting) – contraction of a muscles against a load that resist movement – a few minutes of resistance exercise a few times a week is enough to stimulate muscle growth – growth is from cellular enlargement – muscle fibers synthesize more myofilaments and myofibrils and grow thicker • endurance training (aerobic exercise) – improves fatigue resistant muscles – slow twitch fibers produce more mitochondria, glycogen, and acquire a greater density of blood capillaries – improves skeletal strength – increases the red blood cell count and oxygen transport capacity of the blood – enhances the function of the cardiovascular, respiratory, and nervous systems 11 -65

Cardiac Muscle • limited to the heart where it functions to pump blood •

Cardiac Muscle • limited to the heart where it functions to pump blood • required properties of cardiac muscle – contraction with regular rhythm – muscle cells of each chamber must contract in unison – contractions must last long enough to expel blood – must work in sleep or wakefulness, with out fail, and without conscious attention – must be highly resistant to fatigue 11 -66

Cardiac Muscle • characteristics of cardiac muscle cells – striated like skeletal muscle, but

Cardiac Muscle • characteristics of cardiac muscle cells – striated like skeletal muscle, but myocytes (cardiocytes) are shorter and thicker – each myocyte is joined to several others at the uneven, notched linkages – intercalated discs • appear as thick dark lines in stained tissue sections • electrical gap junctions allow each myocyte to directly stimulate its neighbors • mechanical junctions that keep the myocytes from pulling apart – sarcoplasmic reticulum less developed, but T tubules are larger and admit supplemental Ca 2+ from the extracellular fluid – damaged cardiac muscle cells repair by fibrosis • a little mitosis observed following heart attacks • not in significant amounts to regenerate functional muscle 11 -67

Cardiac Muscle – can contract without need for nervous stimulation • contains a built-in

Cardiac Muscle – can contract without need for nervous stimulation • contains a built-in pacemaker that rhythmically sets off a wave of electrical excitation • wave travels through the muscle and triggers contraction of heart chambers • autorhythmic – because of its ability to contract rhythmically and independently – autonomic nervous system does send nerve fibers to the heart • can increase or decrease heart rate and contraction strength – very slow twitches - does not exhibit quick twitches like skeletal muscle • maintains tension for about 200 to 250 msec • gives the heart time to expel blood – uses aerobic respiration almost exclusively • rich in myoglobin and glycogen • has especially large mitochondria – 25% of volume of cardiac muscle cell – 2% of skeletal muscle cell with smaller mitochondria – very adaptable with respect to fuel used – very vulnerable to interruptions of oxygen supply – highly fatigue resistant 11 -68

Smooth Muscle • composed of myocytes that have a fusiform shape • there is

Smooth Muscle • composed of myocytes that have a fusiform shape • there is only one nucleus, located near the middle of the cell • no visible striations – reason for the name ‘smooth muscle’ – thick and thin filaments are present, but not aligned with each other • z discs are absent and replaced by dense bodies – well ordered array of protein masses in cytoplasm – protein plaques on the inner face of the plasma membrane • cytoplasm contains extensive cytoskeleton of intermediate filament – attach to the membrane plaques and dense bodies – provide mechanical linkages between the thin myofilaments and the plasma membrane • sarcoplasmic reticulum is scanty and there are no T tubules • Ca 2+ needed for muscle contraction comes from the ECF by way of Ca 2+ channels in the sarcolemma • some smooth muscles lack nerve supply, while others receive autonomic fibers, not somatic motor fibers as in skeletal muscle • capable of mitosis and hyperplasia • injured smooth muscle regenerates well 11 -69

2 Types of Smooth Muscle Copyright © The Mc. Graw-Hill Companies, Inc. Permission required

2 Types of Smooth Muscle Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. • multiunit smooth muscle – occurs in some of the largest arteries and pulmonary air passages, in piloerector muscles of hair follicle, and in the iris of the eye Autonomic nerve fibers Synapses – autonomic innervation similar to skeletal muscle • terminal branches of a nerve fiber synapse with individual myocytes and form a motor unit • each motor unit contracts independently of the others (a) Multiunit smooth muscle Figure 11. 21 a 11 -70

2 Types of Smooth Muscle Copyright © The Mc. Graw-Hill Companies, Inc. Permission required

2 Types of Smooth Muscle Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. • single-unit smooth muscle Autonomic nerve fibers – more widespread – occurs in most blood vessels, in the digestive, respiratory, urinary, and reproductive tracts – also called visceral muscle Varicosities • often in two layers – inner circular – outer longitudinal – myocytes of this cell type are electrically coupled to each other by gap junctions – they directly stimulate each other and a large number of cells contract as a single unit Gap junctions (b) Single-unit smooth muscle Figure 11. 21 b 11 -71

Layers of Visceral Muscle Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for

Layers of Visceral Muscle Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Mucosa: Epithelium Lamina propria Muscularis mucosae Muscularis externa: Circular layer Longitudinal layer Figure 11. 22 11 -72

Stimulation of Smooth Muscle • smooth muscle is involuntary and can contract without nervous

Stimulation of Smooth Muscle • smooth muscle is involuntary and can contract without nervous stimulation – can contract in response to chemical stimuli • hormones, carbon dioxide, low p. H, and oxygen deficiency • in response to stretch • single unit smooth muscle in stomach and intestines has pacemaker cells that set off waves of contraction throughout the entire layer of muscle • most smooth muscle is innervated by autonomic nerve fibers – can trigger and modify contractions – stimulate smooth muscle with either acetylcholine or norepinephrine – can have contrasting effects • relax the smooth muscle of arteries • contract smooth muscles of the bronchioles • in single unit smooth, each autonomic nerve fibers has up to 20, 000 beadlike swelling called varicosities – each contains synaptic vesicles and a few mitochondria – nerve fiber passes amid several myocytes and stimulates all of them at once when it releases its neurotransmitter • no motor end plates, but receptors scattered throughout the surface – diffuse 11 -73 junctions – no one-to-one relationship between nerve fiber and myocyte

Stimulation of Smooth Muscle Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for

Stimulation of Smooth Muscle Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Autonomic nerve fiber Varicosities Mitochondrion Synaptic vesicle Single-unit smooth muscle Figure 11. 23 11 -74

Contraction and Relaxation • contraction is triggered by Ca+2, energized by ATP, and achieved

Contraction and Relaxation • contraction is triggered by Ca+2, energized by ATP, and achieved by sliding thin past thick filaments • contraction begins in response to Ca+2 that enters the cell from ECF, a little internally from sarcoplasmic reticulum – voltage, ligand, and mechanically-gated (stretching) Ca+2 channels open to allow Ca+2 to enter cell • calcium binds to calmodulin on thick filaments – activates myosin light-chain kinase – adds phosphate to regulatory protein on myosin head – and myosin ATPase, hydrolyzing ATP • enables myosin similar power and recovery strokes like skeletal muscle – thick filaments pull on thin ones, thin ones pull on dense bodies and membrane plaques – force is transferred to plasma membrane and entire cell shortens 11 -75 – puckers and twists like someone wringing out a wet towel

Contraction and Relaxation • contraction and relaxation very slow in comparison to skeletal muscle

Contraction and Relaxation • contraction and relaxation very slow in comparison to skeletal muscle – – – latent period in skeletal 2 msec, smooth muscle 50 - 100 msec tension peaks at about 500 msec (0. 5 sec) declines over a period of 1 – 2 seconds slows myosin ATPase enzyme and slow pumps that remove Ca+2 binds to calmodulin instead of troponin • activates kinases and ATPases that hydrolyze ATP • latch-bridge mechanism is resistant to fatigue – heads of myosin molecules do not detach from actin immediately – do not consume any more ATP – maintains tetanus tonic contraction (smooth muscle tone) • arteries – vasomotor tone intestinal tone – makes most of its ATP aerobically 11 -76

Contraction of Smooth Muscle Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for

Contraction of Smooth Muscle Copyright © The Mc. Graw-Hill Companies, Inc. Permission required for reproduction or display. Plaque Intermediate filaments of cytoskeleton Actin filaments Dense body Myosin (b) Contracted smooth muscle cells Figure 11. 24 (a) Relaxed smooth muscle cells 11 -77

Stretching Smooth Muscle • stretch can open mechanically-gated calcium channels in the sarcolemma causing

Stretching Smooth Muscle • stretch can open mechanically-gated calcium channels in the sarcolemma causing contraction – peristalsis – waves of contraction brought about by food distending the esophagus or feces distending the colon • propels contents along the organ • stress-relaxation response (receptive relaxation) helps hollow organs gradually fill (urinary bladder) – when stretched, tissue briefly contracts then relaxes – helps prevent emptying while filling 11 -78

Contraction and Stretching • skeletal muscle cannot contract forcefully if overstretched • smooth muscle

Contraction and Stretching • skeletal muscle cannot contract forcefully if overstretched • smooth muscle contracts forcefully even when greatly stretched – allows hollow organs such as the stomach and bladder to fill and then expel their contents efficiently • smooth muscle can be anywhere from half to twice its resting length and still contract powerfully • three reasons: – there are no z discs, so thick filaments cannot butt against them and stop contraction – since thick and thin filaments are not arranged in orderly sarcomeres, stretching does not cause a situation where there is too little overlap for crossbridges to form – the thick filaments of smooth muscle have myosin heads along their entire length, so cross-bridges can form anywhere • plasticity – the ability to adjust its tension to the degree of stretch – a hollow organ such as the bladder can be greatly stretched yet not become flabby when it is empty 11 -79

Muscular Dystrophy • muscular dystrophy - group of hereditary diseases in which skeletal muscles

Muscular Dystrophy • muscular dystrophy - group of hereditary diseases in which skeletal muscles degenerate and weaken, and are replaced with fat and fibrous scar tissue • Duchenne muscular dystrophy is caused by a sex-linked recessive trait (1 of 3500 live-born boys) – most common form – disease of males – diagnosed between 2 and 10 years of age – mutation in gene for muscle protein dystrophin • actin not linked to sarcolemma and cell membranes damaged during contraction, necrosis and scar tissue results – rarely live past 20 years of age due to affects on respiratory and cardiac muscle – incurable • facioscapulohumeral MD - autosomal dominant trait affecting both sexes equally – facial and shoulder muscles more than pelvic muscles • limb-girdle dystrophy – combination of several diseases of intermediate severity – affects shoulder, arm, and pelvic muscles 11 -80

Myasthenia Gravis • autoimmune disease in which antibodies attack neuromuscular junctions and bind ACh

Myasthenia Gravis • autoimmune disease in which antibodies attack neuromuscular junctions and bind ACh receptors together in clusters – disease of women between 20 and 40 – muscle fibers then removes the clusters of receptors from the sarcolemma by endocytosis – fiber becomes less and less sensitive to ACh – effects usually first appear in facial muscles • drooping eyelids and double vision, difficulty swallowing, and weakness of the limbs – strabismus – inability to fixate on the same point with both eyes • treatments – cholinesterase inhibitors retard breakdown of ACh allowing it to stimulate the muscle longer – immunosuppressive agents suppress the production of antibodies that destroy ACh receptors – thymus removal (thymectomy) – helps to dampen the overactive immune response that causes myasthenia gravis – plasmapheresis –technique to remove harmful antibodies from blood plasma 11 -81

Myasthenia Gravis drooping eyelids and weakness of muscles of eye movement 11 -82

Myasthenia Gravis drooping eyelids and weakness of muscles of eye movement 11 -82