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Chapter 10 Muscle Tissue • Alternating contraction and relaxation of cells • Chemical energy changed into mechanical energy Tortora & Grabowski 9/e 2000 JWS 10-1 3 Types of Muscle Tissue • Skeletal muscle – attaches to bone, skin or fascia – striated with light & dark bands visible with scope – voluntary control of contraction & relaxation Tortora & Grabowski 9/e 2000 JWS 10-2 3 Types of Muscle Tissue • Cardiac muscle – striated in appearance – involuntary control – autorhythmic because of built in pacemaker Tortora & Grabowski 9/e 2000 JWS 10-3 3 Types of Muscle Tissue • Smooth muscle – – – – attached to hair follicles in skin in walls of hollow organs -- blood vessels & GI nonstriated in appearance involuntary Tortora & Grabowski 9/e 2000 JWS 10-4 Functions of Muscle Tissue • Producing body movements • Stabilizing body positions • Regulating organ volumes – bands of smooth muscle called sphincters • Movement of substances within the body – blood, lymph, urine, air, food and fluids, sperm • Producing heat – involuntary contractions of skeletal muscle (shivering) Tortora & Grabowski 9/e 2000 JWS 10-5 Properties of Muscle Tissue • Excitability – respond to chemicals released from nerve cells • Conductivity – ability to propagate electrical signals over membrane • Contractility – ability to shorten and generate force • Extensibility – ability to be stretched without damaging the tissue • Elasticity – ability to return to original shape after being stretched Tortora & Grabowski 9/e 2000 JWS 10-6 Skeletal Muscle -- Connective Tissue • Superficial fascia is loose connective tissue & fat underlying the skin • Deep fascia = dense irregular connective tissue around muscle • Connective tissue components of the muscle include – epimysium = surrounds the whole muscle – perimysium = surrounds bundles (fascicles) of 10-100 muscle cells – endomysium = separates individual muscle cells • All these connective tissue layers extend beyond the muscle belly to form the tendon Tortora & Grabowski 9/e 2000 JWS 10-7 Connective Tissue Components Tortora & Grabowski 9/e 2000 JWS 10-8 Nerve and Blood Supply • Each skeletal muscle is supplied by a nerve, artery and two veins. • Each motor neuron supplies multiple muscle cells (neuromuscular junction) • Each muscle cell is supplied by one motor neuron terminal branch and is in contact with one or two capillaries. – nerve fibers & capillaries are found in the endomysium between individual cells Tortora & Grabowski 9/e 2000 JWS 10-9 Fusion of Myoblasts into Muscle Fibers • Every mature muscle cell developed from 100 myoblasts that fuse together in the fetus. (multinucleated) • Mature muscle cells can not divide • Muscle growth is a result of cellular enlargement & not cell division • Satellite cells retain the ability to regenerate new cells. Tortora & Grabowski 9/e 2000 JWS 10-10 Muscle Fiber or Myofibers • Muscle cells are long, cylindrical & multinucleated • Sarcolemma = muscle cell membrane • Sarcoplasm filled with tiny threads called myofibrils & myoglobin (red-colored, oxygen-binding protein) Tortora & Grabowski 9/e 2000 JWS 10-11 Transverse Tubules • T (transverse) tubules are invaginations of the sarcolemma into the center of the cell – filled with extracellular fluid – carry muscle action potentials down into cell • Mitochondria lie in rows throughout the cell –Tortora near the muscle proteins that use ATP during contraction10-12 & Grabowski 9/e 2000 JWS Myofibrils & Myofilaments • Muscle fibers are filled with threads called myofibrils separated by SR (sarcoplasmic reticulum) • Myofilaments (thick & thin filaments) are the contractile proteins of muscle Tortora & Grabowski 9/e 2000 JWS 10-13 Sarcoplasmic Reticulum (SR) • System of tubular sacs similar to smooth ER in nonmuscle cells • Stores Ca+2 in a relaxed muscle • Release of Ca+2 triggers muscle contraction Tortora & Grabowski 9/e 2000 JWS 10-14 Atrophy and Hypertrophy • Atrophy – wasting away of muscles – caused by disuse (disuse atrophy) or severing of the nerve supply (denervation atrophy) – the transition to connective tissue can not be reversed • Hypertrophy – increase in the diameter of muscle fibers – resulting from very forceful, repetitive muscular activity and an increase in myofibrils, SR & mitochondria Tortora & Grabowski 9/e 2000 JWS 10-15 Filaments and the Sarcomere • Thick and thin filaments overlap each other in a pattern that creates striations (light I bands and dark A bands) • The I band region contains only thin filaments. • They are arranged in compartments called sarcomeres, separated by Z discs. • In the overlap region, six thin filaments surround each thick filament Tortora & Grabowski 9/e 2000 JWS 10-16 Thick & Thin Myofilaments • Supporting proteins (M line, titin and Z disc help anchor the thick and thin filaments in place) Tortora & Grabowski 9/e 2000 JWS 10-17 Overlap of Thick & Thin Myofilaments within a Myofibril Dark(A) & light(I) bands visible with an electron microscope Tortora & Grabowski 9/e 2000 JWS 10-18 Exercise-Induced Muscle Damage • Intense exercise can cause muscle damage – electron micrographs reveal torn sarcolemmas, damaged myofibrils an disrupted Z discs – increased blood levels of myoglobin & creatine phosphate found only inside muscle cells • Delayed onset muscle soreness – 12 to 48 Hours after strenuous exercise – stiffness, tenderness and swelling due to microscopic cell damage Tortora & Grabowski 9/e 2000 JWS 10-19 The Proteins of Muscle • Myofibrils are built of 3 kinds of protein – contractile proteins • myosin and actin – regulatory proteins which turn contraction on & off • troponin and tropomyosin – structural proteins which provide proper alignment, elasticity and extensibility • titin, myomesin, nebulin and dystrophin Tortora & Grabowski 9/e 2000 JWS 10-20 The Proteins of Muscle -- Myosin • Thick filaments are composed of myosin – each molecule resembles two golf clubs twisted together – myosin heads (cross bridges) extend toward the thin filaments • Held in place by the M line proteins. Tortora & Grabowski 9/e 2000 JWS 10-21 The Proteins of Muscle -- Actin • Thin filaments are made of actin, troponin, & tropomyosin • The myosin-binding site on each actin molecule is covered by tropomyosin in relaxed muscle • The thin filaments are held in place by Z lines. From one Z line to the next is a sarcomere. Tortora & Grabowski 9/e 2000 JWS 10-22 The Proteins of Muscle -- Titin • Titan anchors thick filament to the M line and the Z disc. • The portion of the molecule between the Z disc and the end of the thick filament can stretch to 4 times its resting length and spring back unharmed. • Role in recovery of the muscle from being stretched. Tortora & Grabowski 9/e 2000 JWS 10-23 Other Structural Proteins • The M line (myomesin) connects to titin and adjacent thick filaments. • Nebulin, an inelastic protein helps align the thin filaments. • Dystrophin links thin filaments to sarcolemma and transmits the tension generated to the tendon. Tortora & Grabowski 9/e 2000 JWS 10-24 Sliding Filament Mechanism Of Contraction • Myosin cross bridges pull on thin filaments • Thin filaments slide inward • Z Discs come toward each other • Sarcomeres shorten.The muscle fiber shortens. The muscle shortens • Notice :Thick & thin filaments do not change in length Tortora & Grabowski 9/e 2000 JWS 10-25 How Does Contraction Begin? • Nerve impulse reaches an axon terminal & synaptic vesicles release acetylcholine (ACh) • ACh diffuses to receptors on the sarcolemma & Na+ channels open and Na+ rushes into the cell • A muscle action potential spreads over sarcolemma and down into the transverse tubules • SR releases Ca+2 into the sarcoplasm • Ca+2 binds to troponin & causes troponintropomyosin complex to move & reveal myosin binding sites on actin--the contraction cycle begins Tortora & Grabowski 9/e 2000 JWS 10-26 Excitation - Contraction Coupling • All the steps that occur from the muscle action potential reaching the T tubule to contraction of the muscle fiber. Tortora & Grabowski 9/e 2000 JWS 10-27 Contraction Cycle • Repeating sequence of events that cause the thick & thin filaments to move past each other. • 4 steps to contraction cycle – – – – ATP hydrolysis attachment of myosin to actin to form crossbridges power stroke detachment of myosin from actin • Cycle keeps repeating as long as there is ATP available & high Ca+2 level near thin filament Tortora & Grabowski 9/e 2000 JWS 10-28 Steps in the Contraction Cycle • Notice how the myosin head attaches and pulls on the thin filament with the energy released from ATP Tortora & Grabowski 9/e 2000 JWS 10-29 ATP and Myosin • • • • • • Myosin heads are activated by ATP Activated heads attach to actin & pull (power stroke) ADP is released. (ATP released P & ADP & energy) Thin filaments slide past the thick filaments ATP binds to myosin head & detaches it from actin All of these steps repeat over and over – if ATP is available & – Ca+ level near the troponin-tropomyosin complex is high Tortora & Grabowski 9/e 2000 JWS 10-30 Overview: From Start to Finish • • • • • • Tortora & Grabowski 9/e 2000 JWS Nerve ending Neurotransmittor Muscle membrane Stored Ca+2 ATP Muscle proteins 10-31 Relaxation • Acetylcholinesterase (AChE) breaks down ACh within the synaptic cleft • Muscle action potential ceases • Ca+2 release channels close • Active transport pumps Ca2+ back into storage in the sarcoplasmic reticulum • Calcium-binding protein (calsequestrin) helps hold Ca+2 in SR (Ca+2 concentration 10,000 times higher than in cytosol) • Tropomyosin-troponin complex recovers binding Tortora on & Grabowski 2000 JWS 10-32 site the 9/eactin Rigor Mortis • Rigor mortis is a state of muscular rigidity that begins 3-4 hours after death and lasts about 24 hours • After death, Ca+2 ions leak out of the SR and allow myosin heads to bind to actin • Since ATP synthesis has ceased, crossbridges cannot detach from actin until proteolytic enzymes begin to digest the decomposing cells. Tortora & Grabowski 9/e 2000 JWS 10-33 Length of Muscle Fibers • Optimal overlap of thick & thin filaments – produces greatest number of crossbridges and the greatest amount of tension • As stretch muscle (past optimal length) – fewer cross bridges exist & less force is produced • If muscle is overly shortened (less than optimal) – fewer cross bridges exist & less force is produced – thick filaments crumpled by Z discs • Normally – resting muscle length remains between 70 to 130% of the optimum Tortora & Grabowski 9/e 2000 JWS 10-34 Length Tension Curve • Graph of Force of contraction (Tension) versus Length of sarcomere • Optimal overlap at the top of the graph • When the cell is too stretched and little force is produced • When the cell is too short, again little force is produced Tortora & Grabowski 9/e 2000 JWS 10-35 Neuromuscular Junction (NMJ) or Synapse • NMJ = myoneural junction – end of axon nears the surface of a muscle fiber at its motor end& plate separated by synaptic cleft or gap) Tortora Grabowskiregion 9/e 2000 (remain JWS 10-36 Structures of NMJ Region • Synaptic end bulbs are swellings of axon terminals • End bulbs contain synaptic vesicles filled with acetylcholine (ACh) • Motor end plate membrane contains 30 million ACh receptors. Tortora & Grabowski 9/e 2000 JWS 10-37 Events Occurring After a Nerve Signal • Arrival of nerve impulse at nerve terminal causes release of ACh from synaptic vesicles • ACh binds to receptors on muscle motor end plate opening the gated ion channels so that Na+ can rush into the muscle cell • Inside of muscle cell becomes more positive, triggering a muscle action potential that travels over the cell and down the T tubules • The release of Ca+2 from the SR is triggered and the muscle cell will shorten & generate force • Acetylcholinesterase breaks down the ACh attached to the receptors on the motor end plate so the muscle action Tortora & Grabowski 9/e 2000 JWSand the muscle cell will relax. 10-38 potential will cease Pharmacology of the NMJ • Botulinum toxin blocks release of neurotransmitter at the NMJ so muscle contraction can not occur – bacteria found in improperly canned food – death occurs from paralysis of the diaphragm • Curare (plant poison from poison arrows) – causes muscle paralysis by blocking the ACh receptors – used to relax muscle during surgery • Neostigmine (anticholinesterase agent) – blocks removal of ACh from receptors so strengthens weak muscle contractions of myasthenia gravis – also an antidote for curare after surgery is finished Tortora & Grabowski 9/e 2000 JWS 10-39 Muscle Metabolism Production of ATP in Muscle Fibers • Muscle uses ATP at a great rate when active • Sarcoplasmic ATP only lasts for few seconds • 3 sources of ATP production within muscle – creatine phosphate – anaerobic cellular respiration – anaerobic cellular respiration Tortora & Grabowski 9/e 2000 JWS 10-40 Creatine Phosphate • Excess ATP within resting muscle used to form creatine phosphate • Creatine phosphate 3-6 times more plentiful than ATP within muscle • Its quick breakdown provides energy for creation of ATP • Sustains maximal contraction for 15 sec (used for 100 meter dash). • Athletes tried creatine supplementation – gain muscle mass but shut down bodies own synthesis (safety?) Tortora & Grabowski 9/e 2000 JWS 10-41 Anaerobic Cellular Respiration • ATP produced from glucose breakdown into pyruvic acid during glycolysis – if no O2 present • pyruvic converted to lactic acid which diffuses into the blood • Glycolysis can continue anaerobically to provide ATP for 30 to 40 seconds of maximal activity (200 meter race) Tortora & Grabowski 9/e 2000 JWS 10-42 Aerobic Cellular Respiration • ATP for any activity lasting over 30 seconds – if sufficient oxygen is available, pyruvic acid enters the mitochondria to generate ATP, water and heat – fatty acids and amino acids can also be used by the mitochondria • Provides 90% of ATP energy if activity lasts more than 10 minutes Tortora & Grabowski 9/e 2000 JWS 10-43 Muscle Fatigue • Inability to contract after prolonged activity – central fatigue is feeling of tiredness and a desire to stop (protective mechanism) – depletion of creatine phosphate – decline of Ca+2 within the sarcoplasm • Factors that contribute to muscle fatigue – insufficient oxygen or glycogen – buildup of lactic acid and ADP – insufficient release of acetylcholine from motor neurons Tortora & Grabowski 9/e 2000 JWS 10-44 Oxygen Consumption after Exercise • Muscle tissue has two sources of oxygen. – diffuses in from the blood – released by myoglobin inside muscle fibers • Aerobic system requires O2 to produce ATP needed for prolonged activity – increased breathing effort during exercise • Recovery oxygen uptake – elevated oxygen use after exercise (oxygen debt) – lactic acid is converted back to pyruvic acid – elevated body temperature means all reactions faster Tortora & Grabowski 9/e 2000 JWS 10-45 The Motor Unit • Motor unit = one somatic motor neuron & all the skeletal muscle cells (fibers) it stimulates – muscle fibers normally scattered throughout belly of muscle – One nerve cell supplies on average 150 muscle cells that all contract in unison. • Total strength of a contraction depends on how many motor units are activated & how large the motor units are Tortora & Grabowski 9/e 2000 JWS 10-46 Twitch Contraction • Brief contraction of all fibers in a motor unit in response to – single action potential in its motor neuron – electrical stimulation of the neuron or muscle fibers • Myogram = graph of a twitch contraction – the action potential lasts 1-2 msec & Grabowski 9/e 2000 JWS lasts from 20 to 200 msec – Tortora the twitch contraction 10-47 Myogram of a Twitch Contraction Tortora & Grabowski 9/e 2000 JWS 10-48 Parts of a Twitch Contraction • Latent Period--2msec – Ca+2 is being released from SR – slack is being removed from elastic components • Contraction Period – 10 to 100 msec – filaments slide past each other • Relaxation Period – 10 to 100 msec – active transport of Ca+2 into SR • Refractory Period – muscle can not respond and has lost its excitability – Tortora 5 msec for skeletal & 300 msec for cardiac muscle & Grabowski 9/e 2000 JWS 10-49 Wave Summation • If second stimulation applied after the refractory period but before complete muscle relaxation---second contraction is stronger than first Tortora & Grabowski 9/e 2000 JWS 10-50 Complete and Incomplete Tetanus • Unfused tetanus – if stimulate at 20-30 times/second, there will be only partial relaxation between stimuli • Fused tetanus – if stimulate at 80-100 times/second, a sustained contraction Tortora & Grabowski 9/e 2000 JWS 10-51 with no relaxation between stimuli will result Explanation of Summation & Tetanus • Wave summation & both types of tetanus result from Ca+2 remaining in the sarcoplasm • Force of 2nd contraction is easily added to the first, because the elastic elements remain partially contracted and do not delay the beginning of the next contraction Tortora & Grabowski 9/e 2000 JWS 10-52 Motor Unit Recruitment • Motor units in a whole muscle fire asynchronously – some fibers are active others are relaxed – delays muscle fatigue so contraction can be sustained • Produces smooth muscular contraction – not series of jerky movements • Precise movements require smaller contractions – motor units must be smaller (less fibers/nerve) • Large motor units are active when large tension is needed Tortora & Grabowski 9/e 2000 JWS 10-53 Muscle Tone • Involuntary contraction of a small number of motor units (alternately active and inactive in a constantly shifting pattern) – keeps muscles firm even though relaxed – does not produce movement • Essential for maintaining posture (head upright) • Important in maintaining blood pressure – tone of smooth muscles in walls of blood vessels Tortora & Grabowski 9/e 2000 JWS 10-54 Isotonic and Isometric Contraction • Isotonic contractions = a load is moved – concentric contraction = a muscle shortens to produce force and movement – eccentric contractions = a muscle lengthens while maintaining force and movement • Isometric contraction = no movement occurs – tension is generated without muscle shortening – maintaining & supports objects in a fixed position 10-55 Tortora & Grabowskiposture 9/e 2000 JWS Variations in Skeletal Muscle Fibers • Myoglobin, mitochondria and capillaries – red muscle fibers • more myoglobin, an oxygen-storing reddish pigment • more capillaries and mitochondria – white muscle fibers • less myoglobin and less capillaries give fibers their pale color • Contraction and relaxation speeds vary – how fast myosin ATPase hydrolyzes ATP • Resistance to fatigue – different metabolic reactions used to generate ATP Tortora & Grabowski 9/e 2000 JWS 10-56 Classification of Muscle Fibers • Slow oxidative (slow-twitch) – red in color (lots of mitochondria, myoglobin & blood vessels) – prolonged, sustained contractions for maintaining posture • Fast oxidative-glycolytic (fast-twitch A) – red in color (lots of mitochondria, myoglobin & blood vessels) – split ATP at very fast rate; used for walking and sprinting • Fast glycolytic (fast-twitch B) – white in color (few mitochondria & BV, low myoglobin) & Grabowskimovements 9/e 2000 JWS for short duration; used for weight-lifting 10-57 –Tortora anaerobic Fiber Types within a Whole Muscle • Most muscles contain a mixture of all three fiber types • Proportions vary with the usual action of the muscle – neck, back and leg muscles have a higher proportion of postural, slow oxidative fibers – shoulder and arm muscles have a higher proportion of fast glycolytic fibers • All fibers of any one motor unit are same. • Different fibers are recruited as needed. Tortora & Grabowski 9/e 2000 JWS 10-58 Anabolic Steroids • Similar to testosterone • Increases muscle size, strength, and endurance • Many very serious side effects – – – – – – liver cancer kidney damage heart disease mood swings facial hair & voice deepening in females atrophy of testicles & baldness in males Tortora & Grabowski 9/e 2000 JWS 10-59 Anatomy of Cardiac Muscle • • • • Striated , short, quadrangular-shaped, branching fibers Single centrally located nucleus Cells connected by intercalated discs with gap junctions Same arrangement of thick & thin filaments as skeletal Tortora & Grabowski 9/e 2000 JWS 10-60 Cardiac versus Skeletal Muscle • More sarcoplasm and mitochondria • Larger transverse tubules located at Z discs, rather than at A-l band junctions • Less well-developed SR • Limited intracellular Ca+2 reserves – more Ca+2 enters cell from extracellular fluid during contraction • Prolonged delivery of Ca+2 to sarcoplasm, produces a contraction that last 10 -15 times longer than in skeletal muscle Tortora & Grabowski 9/e 2000 JWS 10-61 Appearance of Cardiac Muscle • Striated muscle containing thick & thin filaments • T tubules located at Z discs & less SR Tortora & Grabowski 9/e 2000 JWS 10-62 Physiology of Cardiac Muscle • Autorhythmic cells – contract without stimulation • Contracts 75 times per min & needs lots O2 • Larger mitochondria generate ATP aerobically • Sustained contraction possible due to slow Ca+2 delivery – Ca+2 channels to the extracellular fluid stay open Tortora & Grabowski 9/e 2000 JWS 10-63 Two Types of Smooth Muscle • Visceral (single-unit) – in the walls of hollow viscera & small BV – autorhythmic – gap junctions cause fibers to contract in unison • Multiunit – individual fibers with own motor neuron ending – found in large arteries, large airways, arrector pili muscles,iris & ciliary body Tortora & Grabowski 9/e 2000 JWS 10-64 Microscopic Anatomy of Smooth Muscle • Small, involuntary muscle cell -- tapering at ends • Single, oval, centrally located nucleus • Lack T tubules & have little SR for Ca+2 storage Tortora & Grabowski 9/e 2000 JWS 10-65 Microscopic Anatomy of Smooth Muscle • Thick & thin myofilaments not orderly arranged so lacks sarcomeres • Sliding of thick & thin filaments generates tension • Transferred to intermediate filaments & dense bodies attached to sarcolemma • Muscle fiber contracts and twists into a helix as it shortens -- relaxes by untwisting Tortora & Grabowski 9/e 2000 JWS 10-66 Physiology of Smooth Muscle • Contraction starts slowly & lasts longer – no transverse tubules & very little SR – Ca+2 must flows in from outside • Calmodulin replaces troponin – Ca+2 binds to calmodulin turning on an enzyme (myosin light chain kinase) that phosphorylates the myosin head so that contraction can occur – enzyme works slowly, slowing contraction Tortora & Grabowski 9/e 2000 JWS 10-67 Smooth Muscle Tone • Ca+2 moves slowly out of the cell – delaying relaxation and providing for state of continued partial contraction – sustained long-term • Useful for maintaining blood pressure or a steady pressure on the contents of GI tract Tortora & Grabowski 9/e 2000 JWS 10-68 Regulation of Contraction • Regulation of contraction due to – nerve signals from autonomic nervous system – changes in local conditions (pH, O2, CO2, temperature & ionic concentrations) – hormones (epinephrine -- relaxes muscle in airways & some blood vessels) • Stress-relaxation response – when stretched, initially contracts & then tension decreases to what is needed – stretch hollow organs as they fill & yet pressure remains fairly constant –Tortora when empties, rebounds & walls firm up10-69 & Grabowski 9/e 2000muscle JWS Regeneration of Muscle • Skeletal muscle fibers cannot divide after 1st year – growth is enlargement of existing cells – repair • satellite cells & bone marrow produce some new cells • if not enough numbers---fibrosis occurs most often • Cardiac muscle fibers cannot divide or regenerate – all healing is done by fibrosis (scar formation) • Smooth muscle fibers (regeneration is possible) – cells can grow in size (hypertrophy) – some cells (uterus) can divide (hyperplasia) – new fibers form from stem cells in BV walls10-70 Tortora & Grabowski 9/e can 2000 JWS Developmental Anatomy of the Muscular System • Develops from mesoderm • Somite formation – blocks of mesoderm give rise to vertebrae and skeletal muscles of the back • Muscles of head & limbs develop from general mesoderm Tortora & Grabowski 9/e 2000 JWS 10-71 Aging and Muscle Tissue • Skeletal muscle starts to be replaced by fat beginning at 30 – “use it or lose it” • Slowing of reflexes & decrease in maximal strength • Change in fiber type to slow oxidative fibers may be due to lack of use or may be result of aging Tortora & Grabowski 9/e 2000 JWS 10-72 Myasthenia Gravis • Progressive autoimmune disorder that blocks the ACh receptors at the neuromuscular junction • The more receptors are damaged the weaker the muscle. • More common in women 20 to 40 with possible line to thymus gland tumors • Begins with double vision & swallowing difficulties & progresses to paralysis of respiratory muscles • Treatment includes steroids that reduce antibodies that bind to ACh receptors and inhibitors of acetylcholinesterase Tortora & Grabowski 9/e 2000 JWS 10-73 Muscular Dystrophies • Inherited, muscle-destroying diseases • Sarcolemma tears during muscle contraction • Mutated gene is on X chromosome so problem is with males almost exclusively • Appears by age 5 in males and by 12 may be unable to walk • Degeneration of individual muscle fibers produces atrophy of the skeletal muscle • Gene therapy is hoped for with the most common form = Duchenne muscular dystrophy Tortora & Grabowski 9/e 2000 JWS 10-74 Abnormal Contractions • Spasm = involuntary contraction of single muscle • Cramp = a painful spasm • Tic = involuntary twitching of muscles normally under voluntary control--eyelid or facial muscles • Tremor = rhythmic, involuntary contraction of opposing muscle groups • Fasciculation = involuntary, brief twitch of a motor unit visible under the skin Tortora & Grabowski 9/e 2000 JWS 10-75