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© 2012 Pearson Education, Inc. An Introduction to Muscle Tissue Muscle Tissue One of the four primary tissue types, divided into: Skeletal muscle tissue.

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Presentation on theme: "© 2012 Pearson Education, Inc. An Introduction to Muscle Tissue Muscle Tissue One of the four primary tissue types, divided into: Skeletal muscle tissue."— Presentation transcript:

1 © 2012 Pearson Education, Inc. An Introduction to Muscle Tissue Muscle Tissue One of the four primary tissue types, divided into: Skeletal muscle tissue Cardiac muscle tissue Smooth muscle tissue

2 © 2012 Pearson Education, Inc. 10-1 Functions of Skeletal Muscle Tissue Six Functions of Skeletal Muscle Tissue 1.Produce skeletal movement 2.Maintain posture and body position 3.Support soft tissues 4.Guard entrances and exits 5.Maintain body temperature 6.Store nutrient reserves

3 © 2012 Pearson Education, Inc. 10-2 Organization of Muscle Skeletal Muscles contain Muscle tissue (muscle cells or fibers) Connective tissues Nerves Blood vessels

4 © 2012 Pearson Education, Inc. Organization of Connective Tissues Muscles have three layers of connective tissues 1.Epimysium: exterior layer, separates muscle from surrounding tissue 2.Perimysium: surrounds each fascicle (bundles of muscle fibers). Contains blood vessel and nerve 3.Endomysium: Surrounds individual muscle cells (fibers). Contains capillaries, nerve fibers & myosatellite cells (stem cells)-involved in repair Endomysium, perimysium, and epimysium come together at ends of muscles to form a Tendon (bundle) or aponeurosis (sheet)-Attaches muscle to bone

5 © 2012 Pearson Education, Inc. Figure 10-1 The Organization of Skeletal Muscles Skeletal Muscle (organ) Muscle fascicle Muscle fibers Blood vessels EpimysiumPerimysium Endomysium Nerve Epimysium Blood vessels and nerves Endomysium Perimysium Tendon

6 © 2012 Pearson Education, Inc. Blood Vessels and Nerves Blood: each skeletal muscle receives blood from one artery and is drained by two veins Nerves: a single nerve supplies each skeletal muscle with information from the brain. Each nerve is composed of many motor neurons (cells). Motor neuron axons branch many times, each extending to a different skeletal muscle fiber

7 © 2012 Pearson Education, Inc. Skeletal Muscle Cell Development During development, groups of mesodermal cells (myoblasts) fuse to form multinucleate muscle fibers Unfused myoblasts are myosatellite cells; help repair muscle tissue

8 © 2012 Pearson Education, Inc. The Formation of a Multinucleate Skeletal Muscle Fiber Muscle fibers develop through the fusion of mesodermal cells called myoblasts. Myoblasts A muscle fiber forms by the fusion of myoblasts. A diagrammatic view and a micrograph of one muscle fiber. Up to 30 cm in length Myosatellite cell Nuclei Immature muscle fiber Myofibrils Mitochondria Myosatellite cell Mature muscle fiber Sarcolemma Nuclei Muscle fiber LM  612

9 © 2012 Pearson Education, Inc. 10-3 Characteristics of Skeletal Muscle Fibers Skeletal Muscle Cells: myofibers Are very long Multinucleate: Contain hundreds of nuclei Contain numerous mitochondria to provide ATP for contraction and relaxation Contain glycogen as glucose reserve for energy production Contain myoglobin as oxygen reserve

10 © 2012 Pearson Education, Inc. Muscle Fiber Sarcoplasm (cytoplasm of muscle fiber): Contains large amount of glycogen as a glucose source and myoglobin that stores oxygen Mitochondria: throughout the cell, near the contractile proteins. The fiber needs ATP to keep the cell prepared for contraction and for the contraction itself.

11 © 2012 Pearson Education, Inc. Muscle Fiber Sarcolemma and Transverse Tubules Sarcolemma is the cell (plasma) membrane of a muscle fiber Important for transmission of an action potential in the muscle fiber Transverse tubules (T tubules)  Narrow tubes that are continuous with sarcolemma  These infoldings of the sarcolemma are important for transmission of action potential from the sarcolemma through the interior of the cell Allow entire muscle fiber to contract simultaneously

12 © 2012 Pearson Education, Inc. Figure 10-3 The Structure of a Skeletal Muscle Fiber Myofibril Sarcolemma Sarcoplasm Nuclei MUSCLE FIBER Mitochondria Sarcolemma Myofibril Thin filament Thick filament Sarcoplasmic reticulum T tubules Myofibrils Sarcoplasm Sarcolemma

13 © 2012 Pearson Education, Inc. Muscle Fiber Sarcoplasmic Reticulum (SR) Surrounds each myofibril Similar in structure to smooth endoplasmic reticulum Stores Calcium ions- Ca 2+ when muscle is relaxed Encircled by T tubules Terminal cisternae Expanded chambers of the SR on either side of the T tubule Concentrate Ca 2+ (via ion pumps) A muscle contraction begins when Ca 2+ is released from the terminal cisternae Two terminal cisterns and a T-tubule are a triad.

14 © 2012 Pearson Education, Inc. The combination of one T tubule and two terminal cisternae is called a Triad

15 © 2012 Pearson Education, Inc. Myofibrils and Myofilaments Lengthwise subdivisions within muscle fiber As long as muscle cell but much shorter in diameter; 100s- 1000s per cell Made up of bundles of protein filaments called myofilaments responsible for muscle contraction have repeating functional units called sarcomeres Consist of thin & thick filaments Muscle Fiber

16 © 2012 Pearson Education, Inc. Figure 10-3 The Structure of a Skeletal Muscle Fiber Myofibril Sarcolemma Sarcoplasm Nuclei MUSCLE FIBER Mitochondria Sarcolemma Myofibril Thin filament Thick filament Sarcoplasmic reticulum T tubules Myofibrils Sarcoplasm Sarcolemma

17 © 2012 Pearson Education, Inc. Sarcomeres Filaments are arranged in repeating units called sarcomeres, separated by Z discs (lines). The sarcomere is the structural and functional unit of skeletal muscle. Thick and thin filaments overlap each other in a pattern that creates striations  Consist of dark A bands and light I bands Muscle Fiber

18 © 2012 Pearson Education, Inc. A longitudinal section of a sarcomere, showing bands I band A band H band Z line Titin Zone of overlap M line Sarcomere Thin filament Thick filament Sarcomere: The I Band Contains thin filaments but no thick filaments Has Z lines: The centers of the I bands; Also mark the boundary between adjacent sarcomeres-Composed of proteins to anchor thin filaments

19 © 2012 Pearson Education, Inc. A longitudinal section of a sarcomere, showing bands I band A band H band Z line Titin Zone of overlap M line Sarcomere Thin filament Thick filament Sarcomere: The A Band Dense region of the sarcomere that contains thick or thick & thin filaments. Consists of: M line, H band : Thick filaments only Zone of overlap: Thick and Thin filaments

20 © 2012 Pearson Education, Inc. Thin Filaments-Contains four proteins 1.Actin : Two twisted rows of filamentous actin (F-actin) containing globular actn (G-actin) subunits The active sites on actin strands bind to myosin during muscle contraction 2.Nebulin: Holds the F-actin strands together 3.Tropomyosin: A double stranded chain that wraps around the actin chain Covers the active sites of G-actin; hence prevents actin–myosin interaction 4.Troponin: A globular protein with three subunits One subunit binds tropomyosin: forms a troponin/tropomyosin complex One subunit binds to actin; holding the troponin-tropomyosin in place One subunit binds Ca 2+; Resting cell Ca 2+ concentration is low so binding site is empty Contraction controlled by calcium binding to troponin

21 © 2012 Pearson Education, Inc. Figure 10-7ab Thick and Thin Filaments Z line M line Myofibril H band Sarcomere Troponin Active site TropomyosinG-actin molecules F-actin strand ActininZ lineTitin The gross structure of a thin filament, showing the attachment at the Z line The organization of G-actin subunits in an F-actin strand, and the position of the troponin–tropomyosin complex

22 © 2012 Pearson Education, Inc. Titin Myosin head Myosin tail The structure of a myosin molecule M line The structure of thick filaments, showing the orientation of the myosin molecules Thick Filaments: Myosin Myosin Head region: Made of two globular protein subunits  Binding site for actin  Binding and catalytic site for ATP: Split into ADP and Pi by ATPase enzyme activity  Causes head to be “cocked” and “energized”  In resting sarcomere, each myosin head is in the “energized” form During contraction, myosin interacts with the thin filament, forming cross- bridges with actin Myosin Tail region: Binds to other myosin molecules: Points towards M line

23 © 2012 Pearson Education, Inc. Sarcomere Structure A longitudinal section of a sarcomere, showing bands I band A band H band Z line Titin Zone of overlap M line Sarcomere Thin filament Thick filament Titin a re strands of elastic protein that reach from tips of thick filaments to the Z line Keeps thick and thin filaments in alignment Recoil after stretching; Aids in restoring sarcomere to proper length after contraction

24 © 2012 Pearson Education, Inc. Sarcomere Structure A corresponding view of a sarcomere in a myofibril from a muscle fiber in the gastrocnemius muscle of the calf I bandA band H band Z line Zone of overlap M line Sarcomere Z line Myofibril TEM  64,000

25 © 2012 Pearson Education, Inc. 10-4 Components of the Neuromuscular Junction  Skeletal muscle fibers begin contraction when signals from nervous system cause them to release their internal calcium stores.  Communication of nervous and muscle fibers occurs at special intercellular connections called the neuromuscular junction (NMJ)

26 © 2012 Pearson Education, Inc. 10-4 Components of the Neuromuscular Junction Neuromuscular junction (NMJ) has three parts : 1.Synaptic terminal (synaptic end knobs) of axon of motor neuron 2.Synaptic cleft 3.Motor end plate of muscle fiber

27 © 2012 Pearson Education, Inc. A&P FLIX Events at the Neuromuscular Junction © 2015 Pearson Education, Inc.

28 © 2012 Pearson Education, Inc. Figure 10-9 Events at the Neuromuscular Junction (Part 3 of 9). Axon Motor end plate Myofibril Motor end plate Axon terminal Path of electrical impulse (action potential) Motor neuron Neuromuscular junction SEE BELOW Sarcoplasmic reticulum A single axon may branch to control more than one skeletal muscle fiber, but each muscle fiber has only one neuromuscular junction (NMJ). At the NMJ, the axon terminal of the neuron lies near the motor end plate of the muscle fiber.

29 © 2012 Pearson Education, Inc. Figure 10-11 Skeletal Muscle Innervation The synaptic cleft, a narrow space, separates the synaptic terminal of the neuron from the opposing motor end plate. Junctional fold of motor end plate AChE Vesicles ACh The cytoplasm of the synaptic terminal contains vesicles filled with molecules of acetylcholine, or ACh. Acetylcholine is a neurotransmitter, a chemical released by a neuron to change the permeability or other properties of another cell’s plasma membrane. The synaptic cleft and the motor end plate contain molecules of the enzyme acetylcholinesterase (AChE), which breaks down ACh.

30 © 2012 Pearson Education, Inc. Figure 10-11 Skeletal Muscle Innervation Arriving action potential The stimulus for ACh release is the arrival of an electrical impulse, or action potential, at the synaptic terminal.

31 © 2012 Pearson Education, Inc. Figure 10-11 Skeletal Muscle Innervation When the action potential reaches the neuron’s synaptic terminal, permeability changes in the membrane trigger the exocytosis of ACh into the synaptic cleft. Exocytosis occurs as vesicles fuse with the neuron’s plasma membrane. Motor end plate

32 © 2012 Pearson Education, Inc. Figure 10-11 Skeletal Muscle Innervation ACh receptor site ACh molecules diffuse across the synatpic cleft and bind to ACh receptors on the surface of the motor end plate. ACh binding triggers the generation of an action potential in the myofiber that spreads along the sarcolemma. Myofiber is excited.

33 © 2012 Pearson Education, Inc. Figure 10-11 Skeletal Muscle Innervation AChE quickly breaks down the ACh on the motor end plate and in the synaptic cleft, thus inactivating the ACh receptor sites. Action potential AChE

34 © 2012 Pearson Education, Inc. A&P FLIX Excitation-Contraction Coupling © 2015 Pearson Education, Inc.

35 © 2012 Pearson Education, Inc. Figure 10-10 Excitation-Contraction Coupling.

36 © 2012 Pearson Education, Inc. 10-4 Skeletal Muscle Contraction The Contraction Cycle 1.Contraction Cycle Begins 2.Active-Site Exposure 3.Cross-Bridge Formation 4.Myosin Head Pivoting 5.Cross-Bridge Detachment 6.Myosin Reactivation © 2015 Pearson Education, Inc.

37 © 2012 Pearson Education, Inc. A&P FLIX The Cross Bridge Cycle © 2015 Pearson Education, Inc.

38 © 2012 Pearson Education, Inc. Figure 10-12 The Contraction Cycle Myosin head Troponin Tropomyosin Actin Release of calcium from SR at the zone of overlap. Contraction Cycle Begins

39 © 2012 Pearson Education, Inc. Figure 10-12 The Contraction Cycle Calcium ions bind to troponin, weakening the bond between actin and the troponin– tropomyosin complex. The troponin molecule then changes position, rolling the tropomyosin molecule away from the active sites on actin and allowing interaction with the energized myosin heads. Active-Site Exposure Sarcoplasm Active site

40 © 2012 Pearson Education, Inc. Figure 10-12 The Contraction Cycle Once the active sites are exposed, the energized myosin heads bind to them, forming cross-bridges. Cross-Bridge Formation

41 © 2012 Pearson Education, Inc. Figure 10-12 The Contraction Cycle After cross-bridge formation, the energy that was stored in the resting state is released as the myosin head pivots toward the M line. This action is called the power stroke; when it occurs, the bound ADP and phosphate group are released. Myosin Head Pivoting

42 © 2012 Pearson Education, Inc. Figure 10-12 The Contraction Cycle When another ATP binds to the myosin head, the link between the myosin head and the active site on the actin molecule is broken. The active site is now exposed and able to form another cross-bridge. Cross-Bridge Detachment

43 © 2012 Pearson Education, Inc. Figure 10-12 The Contraction Cycle Myosin reactivation occurs when the free myosin head splits ATP into ADP and P. The energy released is used to recock the myosin head. Myosin Reactivation

44 © 2012 Pearson Education, Inc. Sliding Filaments and Muscle Contraction What happens when a skeletal muscle fiber contracts? Sliding filament theory: Observations The H and I bands of the sarcomere get smaller The zones of overlap get larger Z lines move closer together The width of A zone stays the same

45 © 2012 Pearson Education, Inc. Sliding Filaments and Muscle Contraction What happens when a skeletal muscle fiber contracts? Sliding filament theory: Explanation Thin filaments of sarcomere slide toward center (M line) of each sarcomere, alongside thick filaments

46 © 2012 Pearson Education, Inc. Figure 10-8a Changes in the Appearance of a Sarcomere during the Contraction of a Skeletal Muscle Fiber A band I band Z line H band Z line A relaxed sarcomere

47 © 2012 Pearson Education, Inc. Figure 10-8b Changes in the Appearance of a Sarcomere during the Contraction of a Skeletal Muscle Fiber Z line A band I band H band A contracted sarcomere  A band stays the same width  Z lines move closer together  Zones of overlap get bigger  H & I band gets smaller

48 © 2012 Pearson Education, Inc. Sliding Filaments and Muscle Contraction During a contraction, thick and thin filaments slide past each other, pulling the Z lines behind them Sliding occurs in every sarcomere along the myofibril - Myofibril gets shorter Myofibrils attached to sarcolemma at each Z line - Muscle fiber also gets shorter

49 © 2012 Pearson Education, Inc. Figure 10-13 Steps Involved in Skeletal Muscle Contraction and Relaxation (Part 1 of 2). Ca 2+ Actin Myosin Cytosol T tubule Sarcoplasmic reticulum Sarcolemma Axon terminal ACh released Action potential reaches T tubule Steps That Initiate a Muscle Contraction 1 2 3 ACh is released at the neuromuscular junction and binds to ACh receptors on the sarcolemma. An action potential is generated and spreads across the membrane surface of the muscle fiber and along the T tubules. The sarcoplasmic reticulum releases stored calcium ions. Sarcoplasmic reticulum releases Ca 2+ 4 5 Active site exposure and cross-bridge formation Calcium ions bind to troponin, exposing the active sites on the thin filaments. Cross-bridges form when myosin heads bind to those active sites. Contraction cycle begins The contraction cycle begins as repeated cycles of cross-bridge binding, pivoting, and detachment occur—all powered by ATP.

50 © 2012 Pearson Education, Inc. Figure 10-13 Steps Involved in Skeletal Muscle Contraction and Relaxation (Part 2 of 2). Ca 2+ Actin Myosin Cytosol T tubule Sarcoplasmic reticulum Sarcolemma Axon terminal ACh is broken down Sarcoplasmic reticulum reabsorbs Ca 2+ Steps That End a Muscle Contraction 6 7 8 ACh is broken down by acetylcholinesterase (AChE), ending action potential generation As the calcium ions are reabsorbed, their concentration in the cytosol decreases. Without calcium ions, the tropomyosin returns to its normal position and the active sites are covered again. Active sites covered, and cross-bridge formation ends 9 10 Contraction ends Without cross-bridge formation, contraction ends. Muscle relaxation occurs The muscle returns passively to its resting length.

51 © 2012 Pearson Education, Inc. 10-5 Tension Production and Contraction Types Tension Production by Muscles Fibers Force (tension) produced by muscle contraction depends on the frequency of stimulation and number of neurons sending stimulation The Frequency of Stimulation A single neural stimulation produces a single contraction or twitch which lasts about 7–100 msec. Sustained muscular contractions require many repeated stimuli

52 © 2012 Pearson Education, Inc. Figure 10-15b Myogram: The Development of Tension in a Twitch Tension Myogram for a single twitch in the gastrocnemius muscle. Stimulus Maximum tension development Resting phase Latent period Contraction phase Relaxation phase

53 © 2012 Pearson Education, Inc. Figure 10-15a The Development of Tension in a Twitch Eye muscle Soleus Gastrocnemius Tension Time (msec) Stimulus A myogram showing differences in tension over time for a twitch in different skeletal muscles.

54 © 2012 Pearson Education, Inc. Tension Production by Muscles Fibers Depends on the frequency of stimulation and the number of muscle fibers stimulated. Levels of muscle tension Treppe Wave Summation Incomplete Tetanus Complete Tetanus

55 © 2012 Pearson Education, Inc. Effects of Changing Frequency of Stimulation Treppe: Stair-step increase in twitch tension. Repeated stimulations immediately after relaxation phase: Stimulus frequency <50/second (not enough time for all the Ca 2+ to be pumped back into SR in between stimulations) Wave summation: Repeated stimulations before the end of relaxation phase. Causes increasing tension or summation of twitches-contractions are stronger. Stimulus frequency >50/second Incomplete tetanus: Incomplete tetanus occurs if the stimulus frequency increases further. Tension production rises to a peak, and the periods of relaxation are very brief. Stimulus rate 20-30/sec Complete tetanus: sustained contraction that has no relaxation between stimuli. Stimulus rate 80-100 times/sec

56 © 2012 Pearson Education, Inc.

57 The Motor Unit Motor unit: One motor neuron and all the skeletal myofibers it innervates (stimulates) Motor neuron may control a few to to 2,000 fibers/motor unit. Small motor units found in muscles needed to perform fine skills; Largest motor units found in postural muscles Causes a simultaneous contraction of all the muscle fibers that are connected to that motor neuron Total strength of contraction in a muscle depends on how many motor units are activated and the size of the motor units

58 © 2012 Pearson Education, Inc. Recruitment Recruitment: motor units in a whole muscle are stimulated asynchronously: some fibers active while others are relaxed. Delays muscle fatigue during sustained contraction Produces smooth contraction

59 © 2012 Pearson Education, Inc. Muscle tone The resting sustained tension in a skeletal muscle is called muscle tone Muscle with muscle tone: firm and solid Muscle without muscle tone: limp and flaccid Unconscious nerve impulses maintain the muscles in a partially contracted state; but not enough tension to produce movement Muscle tone helps stabilize the position of the bones and joints Increasing muscle tone increases metabolic energy used, even at rest

60 © 2012 Pearson Education, Inc. Muscle contractions may be Isotonic or Isometric Isotonic contraction: Muscle tension greater than the load. Myofilaments are able to slide past each other during contractions. The muscle shortens and movement occurs Example: walking, lifting a book off your desk Isometric contraction: muscle produces force, but no movement occurs Muscle does not shorten Example: maintaining posture, supports object in a fixed position, or in attempting to lift an object that is too heavy

61 © 2012 Pearson Education, Inc. Source for Glucose and Oxygen in Aerobic respiration Glucose Stored as glycogen in liver and skeletal muscles Oxygen Bound to myoglobin and hemoglobin

62 © 2012 Pearson Education, Inc. 10-6 Energy to Power Contractions Energy Use and the Level of Muscular Activity At rest: Skeletal muscles at rest metabolize fatty acids and store glycogen During light activity, muscles generate ATP through aerobic breakdown of carbohydrates, lipids, or amino acids At peak activity, energy is provided by anaerobic reactions that generate lactic acid as a by-product © 2015 Pearson Education, Inc.

63 © 2012 Pearson Education, Inc. Figure 10-20 Muscle Metabolism (Part 1 of 3). Fatty acids O 2 G Blood vessels Glycogen CP ATP Glucose ADP Creatine ADP Mitochondria CO 2 Muscle Metabolism in a Resting Muscle Fiber In a resting skeletal muscle, the demand for ATP is low, and there is more than enough oxygen available for mitochondria to meet that demand. Resting muscle fibers absorb fatty acids, which are broken down in the mitochondria creating a surplus of ATP. Some mitochondrial ATP is used to convert absorbed glucose to glycogen. Mitochondrial ATP is also used to convert creatine to creatine phosphate (CP). This results in the buildup of energy reserves (glycogen and CP) in the muscle.

64 © 2012 Pearson Education, Inc. Figure 10-20 Muscle Metabolism (Part 2 of 3). Muscle Metabolism during Moderate Activity During moderate levels of activity, the demand for ATP increases. There is still enough oxygen for the mitochondria to meet that demand, but no excess ATP is produced. The muscle fiber now relies primarily on the aerobic metabolism of glucose (cellular respiration) from stored glycogen to generate ATP. If the glycogen reserves are low, the muscle fiber can also break down other substrates, such as fatty acids. All of the ATP now produced is used to power muscle contraction. Fatty acids O2O2 Glucose Glycogen ADP ATP 2 2 34 ATP 34 To myofibrils to support muscle contraction CO 2 Pyruvate

65 © 2012 Pearson Education, Inc. Figure 10-20 Muscle Metabolism (Part 3 of 3). Muscle Metabolism during Peak Activity During peak levels of activity, the demand for ATP is enormous. Oxygen cannot diffuse into the fiber fast enough for the mitochondria to meet that demand. Only a third of the cell’s ATP needs can be met by the mitochondria (not shown). Lactate Glucose Lactate H+H+ Glycogen Creatine Pyruvate 2 2 ADP ATP CP To myofibrils to support muscle contraction The rest of the ATP comes from glycolysis, and when this produces pyruvate faster than the mitochondria can utilize it, the pyruvate builds up in the cytosol. This process is called anaerobic metabolism because no oxygen is used. Under these conditions, pyruvate is converted to lactic acid, which dissociates into a lactate ion and a hydrogen ion. The buildup of hydrogen ions increases fiber acidity, which inhibits muscle contraction, leading to rapid fatigue. ATP

66 © 2012 Pearson Education, Inc. The Oxygen Debt After exercise or other exertion: The body needs more oxygen than usual to normalize metabolic activities: to restore ATP, CP and glycogen reserves to former levels (recovery period) Resulting in heavy breathing Also called excess postexercise oxygen consumption (EPOC)

67 © 2012 Pearson Education, Inc. Heat Production by Active Muscles During catabolic reactions such as anaerobic and aerobic respiration, only some of the released energy is captured by the cell the rest is lost as heat energy Active muscles produce heat Up to 70% of muscle energy can be lost as heat, raising body temperature

68 © 2012 Pearson Education, Inc. Hormones and Muscle Metabolism Growth hormone, testosterone: stimulate contractile protein synthesis and muscle enlargement Anabolic steroids similar to testosterone but numerous side effects Thyroid hormone elevate the rate of energy consumption in resting and active muscles Epinephrine (adrenaline): During crisis, increase duration of stimulation and force of contraction

69 © 2012 Pearson Education, Inc. 10-7 Types of Muscles Fibers and Endurance Force is the maximum amount of tension produced by a muscle or muscle group Endurance is the amount of time an activity can be sustained by an individual Force and endurance depend on: The types of muscle fibers (fast, slow, intermediate) Physical conditioning

70 © 2012 Pearson Education, Inc. Marathoners versus Sprinters Runners do not usually compete at short and long distances. Natural differences in the muscles of these athletes favor sprinting or long-distance running. Leg muscles contain two main types of muscle fibers: slow fibers and fast fibers

71 © 2012 Pearson Education, Inc. Figure 6.0

72 © 2012 Pearson Education, Inc. 10-7 Types of Muscle Fibers and Endurance Three Major Types of Skeletal Muscle Fibers 1. Fast fibers 2. Slow fibers 3. Intermediate fibers © 2015 Pearson Education, Inc.

73 © 2012 Pearson Education, Inc. Marathoners versus Sprinters Slow fibers (Red muscle) Slow to contract, slow to fatigue Thin fibers High oxygen supply-More blood supply, more myoglobin (red pigment, binds oxygen), more mitochondria Aerobic: Generate ATP using oxygen Fast fibers (White muscles) Quick to contract, but fatigue much more quickly Thick fibers, strong contraction, generate more power Less blood supply, less myoglobin, less mitochondria Can generate ATP anaerobically Intermediate fibers More closely resemble fast fibers but more blood supply more resistant to fatigue

74 © 2012 Pearson Education, Inc. Figure 10-21 Fast versus Slow Fibers. Capillary Smaller diameter, darker color due to myoglobin; fatigue resistant Larger diameter, paler color; easily fatigued Fast fibers Slow fibers LM × 170 LM × 783 LM × 170

75 © 2012 Pearson Education, Inc. Hypertrophy Muscle growth from heavy training Increases diameter of muscle fibers but not number of muscle fibers Increases number of myofibrils, mitochondria, glycogen reserves Atrophy Muscle shrinkage due to lack of muscle activity Reduces muscle size, tone, and power Caused by disuse, muscle or nerve injury or nervous system disorders Initially irreversible-physical therapy- but will be irreversible with continued loss of stimulation Muscle Atrophy and Hypertrophy

76 © 2012 Pearson Education, Inc. Importance of Exercise What you don’t use, you lose! Muscles become flaccid when inactive for days or weeks Muscle fibers break down proteins, become smaller and weaker With prolonged inactivity, fibrous tissue may replace muscle fibers

77 © 2012 Pearson Education, Inc. Physical Conditioning improves both power and endurance Anaerobic Training Use fast fibers Fatigue quickly with strenuous activity Improved by: frequent, brief, intensive workouts that causes muscle hypertrophy Aerobic Training Supported by mitochondria Require oxygen and nutrients Improved by: endurance by training fast fibers to be more like intermediate fibers Cardiovascular performance Interval Training Incorporates aerobic and anaerobic activities

78 © 2012 Pearson Education, Inc. Exercise-Induced Muscle Damage Intense exercise can cause muscle damage Delayed onset muscle soreness (DOMS) Occurs12 to 48 hours after strenuous exercise Stiffness, tenderness, and swelling due to microscopic cell damage Electron micrographs reveal torn sarcolemmas, damaged myofibrils and disrupted Z discs Increased blood levels of myoglobin and creatine phosphate

79 © 2012 Pearson Education, Inc. Cardiac Muscle Tissue Found in the heart wall Striated, short branching fibers Single, centrally-located nucleus Cells connected by intercalated discs with gap junctions and desmosomes Same arrangement of thick and thin filaments as skeletal muscle Fibers contract when stimulated by their own autorhythmic fibers

80 © 2012 Pearson Education, Inc. Cardiac vs. Skeletal Muscle Cardiac muscle Relatively more sarcoplasm and mitochondria Less well-developed SR Limited Ca +2 reserves. Calcium enters the cell from extracellular fluid during contraction Prolonged delivery of Ca +2 to sarcoplasm produces a contraction that lasts 10-15 times longer than in skeletal muscle

81 © 2012 Pearson Education, Inc. Smooth Muscle Non-striated, single centrally located nucleus,involuntary Lack T-tubules; have very little SR for Ca +2 storage-- Ca +2 must flow in from outside Protein that binds calcium ions in the sarcoplasm is calmodulin (as opposed to troponin in skeletal muscle) This facilitates myosin-actin binding and allows contraction to occur at a relatively slow rate

82 © 2012 Pearson Education, Inc. Table 10-4 A Comparison of Skeletal, Cardiac, and Smooth Muscle Tissues

83 © 2012 Pearson Education, Inc. Regeneration of muscle tissue Skeletal muscle fibers: cannot divide after first year. Repair occurs when: satellite cells and MSCs from bone marrow can produce some new cells if not enough cells produced, fibrosis occurs 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 by mitosis (hyperplasia) new fibers can form from stem cells in blood vessel walls

84 © 2012 Pearson Education, Inc. Aging of Muscle Tissue Beginning at age 30, skeletal muscle starts to be replaced by fat Reflexes slow Maximum strength decreases Some fibers change to slow oxidative

85 © 2012 Pearson Education, Inc. Rigor Mortis A fixed muscular contraction- body stiffening that occurs 2-7h after death and ends after 1-6 days Caused when: 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.

86 © 2012 Pearson Education, Inc. Abnormal Contractions Spasm: involuntary contraction of single muscle Cramp: involuntary and painful contraction of skeletal muscles due to electrolyte imbalance, insufficient hydration, fatigue

87 © 2012 Pearson Education, Inc. Muscle disorders and diseases Botulism: paralysis of skeletal muscles due to consumption of bacterial toxin that blocks release of Ach Tetanus: Caused by infection with Clostridium tetani that thrives in low oxygen environments Deep puncture wound-Bacteria produces toxin that affects CNS and motor neurons Toxin suppresses the inhibition of motor neuron activity leading to sustained powerful contractions Symptoms include headache, muscle stiffness, lockjaw, high mortality rate. Preventative Immunization: Tetanus shot

88 © 2012 Pearson Education, Inc. Muscle Diseases Myaesthenia gravis: progressive autoimmune disorder that causes progressive damage at the NMJ Antibodies bind and block some Ach receptors at the NMJ Results in weaker muscles that fatigue easily Mucsles of face and neck most commonly affected; Begins with double vision and difficulty swallowing. May progresses to paralysis of respiratory muscles and death Treatment: Inhibitors of acetylcholinesterase, steroids that reduce antibodies that are binding the ACh receptors More common in women 20 to 20 years of age

89 © 2012 Pearson Education, Inc. Muscle Diseases Muscular dystrophies: Inherited autoimmune disorder where the immune system blocks the receptors to ACh resulting in muscle weakness and atrophy Mutated gene on X chromosome; greater frequency in males than in females Appears by age 5 and by age 12, may be unable to walk Most common form is Duchenne muscular dystrophy: Mutation in dystrophin gene so little of this reinforcing protein in sarcolemma. Gene therapy is hoped-for treatment


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