General physiology lecture 3

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  •   This is the presentation for Muscle Physiology for Human Anatomy and Physiology II at Oklahoma City Community College.
  • There are three types of muscle tissue in the body. Skeletal muscle is the type that attaches to our bones and is used for movement and maintaining posture. Cardiac muscle is only found in the heart. It pumps blood. Smooth muscle is found in organs of the body such as the GI tract. Smooth muscle in the GI tract moves food and its digested products.
  • Skeletal muscle attaches to our skeleton. *The muscle cells a long and cylindrical. *Each muscle cell has many nuclei. *Skeletal muscle tissue is striated. It has tiny bands that run across the muscle cells. *Skeletal muscle is voluntary. We can move them when we want to. *Skeletal muscle is capable of rapid contractions. It is the most rapid of the muscle types.
  • Cardiac muscle tissue is only found in the heart. *Cardiac cells are arranged in a branching pattern. * Only one or two nuclei are present each cardiac cell. *Like skeletal muscle, cardiac muscle is striated. *Cardiac muscle is involuntary. *Its speed of contraction is not as fast as skeletal, but faster than that of smooth muscle.
  • Smooth muscle is found in the walls of hollow organs. *Their muscle cells are fusiform in shape. *Smooth muscle cells have just on nucleus per cell. *Smooth muscle is nonstriated. *Smooth muscle is involuntary. *The contractions of smooth muscle are slow and wave-like.
  • In this unit we will primarily study skeletal muscle. Each muscle cell is called a muscle fiber. Within each muscle fiber are many myofibrils.
  • Dark and light bands can be seen in the muscle fiber and also in the smaller myofibrils. An enlargement of the myofibril reveals that they are made of smaller filaments or myofilaments. *There is a thick filament called myosin and *a thin filament called actin. Note the I band, A band H zone or band and Z disc or line. These will be discussed shortly.  
  • A small section of a myofibril is illustrated here. Note the thick myosin filaments are arranged between overlapping actin filaments. *The two Z lines mark the boundary of a sarcomere. The sarcomere is the functional unit of a muscle cell .We will examine how sarcomeres function to help us better understand how muscles work.
  • A myosin molecule is elongated with an enlarged head at the end.
  • Many myosin molecules form the thick myosin filament. It has many heads projecting away from the main molecule.
  • The thinner actin filament is composed of three parts: actin, tropomyosin and troponin.
  • Here is a sarcomere illustrating the thin actin and thick myosin filaments. The area of the sarcomere has only myosin is called the H band.
  • Here is another diagram of a sarcomere. Note the A band. It is formed by both myosin and actin filaments. The part of the sarcomere with only actin filaments is called the I band. This is a sarcomere that is relaxed.
  • This sarcomere is partially contracted. Notice than the I bands are getting shorter.
  • The sarcomere is completely contracted in this slide. The I and H bands have almost disappeared.
  • Which filament has moved as the sarcomere contracted? Note the thick myosin filaments have not changed, but the thin actin filaments have moved closer together.
  • The string of green circles represents an actin filament. There are binding sites in the filament for the attachment of myosin heads. *In a relaxed muscle the binding sites are covered by tropomyosin. The tropomyosin has molecules of troponin attached to it. *Calcium, shown in yellow, will attach to troponin. *Calcium will change the position of the troponin, tropomyosin complex. *The troponin, tropomyosin complex has now moved so that the binding sites are longer covered by the troponin, tropomyosin complex.
  • The binding sites are now exposed and myosin heads are able to attach to form cross bridges.*  
  • This diagram shows the microanatomy of skeletal muscle tissue again. *The blue sarcoplasmic reticulum is actually the endoplasmic reticulum. It stores calcium. *The mitochondria are illustrated in orange. They generate ATP, which provides the energy for muscle contractions.
  • The next few slides will summarize the events of a muscle contraction. The nerve impulse reaches the neuromuscular junction (myoneural junction).
  • Acetylcholine is released from the motor neuron.
  • Acetylcholine binds with receptors in the muscle membrane to allow sodium ions to enter the muscle.
  • The influx of sodium will create an action potential in the sarcolemma. Note: This is the same mechanism for generating action potentials for the nerve impulse. The action potential travels down a T tubule. As the action potential passes through the sarcoplamic reticulum it stimulates the release of calcium ions. Calcium binds with troponin to move tropomyosin and expose the binding sites. Myosin heads attach to the binding sites of the actin filament and create a power stroke. ATP detaches the myosin heads and energizes them for another contraction. The process will continue until the action potentials cease. Without action potentials the calcium ions will return to the sarcoplasmic reticulum.  
  • A motor unit is all the muscle cells controlled by one nerve cell. This diagram represents two motor units. Motor unit one illustrates two muscle cells controlled by one nerve cell. When the nerve sends a message it will cause both muscle cells to contract. Motor unit two has three muscle cells innervated by one nerve cell.
  • Motor units come indifferent sizes. *The ratio is about one nerve cell to 100 muscle cells in the back. *Finger muscles have a much smaller ratio of 1:10. *Eye muscles have a 1:1 ratio because of the precise control needed in vision.
  • ATP or adenosine triphosphate is the form of energy that muscles and all cells of the body use. *The chemical bond between the last two phosphates has just the right amount of energy to unhook myosin heads and energize them for another contraction. Pulling of the end phosphate from ATP will release the energy. ADP and a single phosphate will be left over. New ATP can be regenerated by reconnecting the phosphate with the ADP with energy from our food.
  • Creatine is a molecule capable of storing ATP energy. It can combine with ATP to produce creatine phosphate and ADP. The third phosphate and the energy from ATP attaches to creatine to form creatine phosphate.
  • Creatine phosphate is an important chemical to muscles. *It is a molecule that is able to store ATP energy. *Creatine phosphate can combine with an ADP * to produce creatine and ATP. This process occurs faster than the synthesis of ATP from food.
  • Muscle fatigue is often due to a lack of oxygen that causes ATP deficit. Lactic acid builds up from anaerobic respiration in the absence of oxygen. Lactic acid fatigues the muscle.
  • Muscle atrophy is a weakening and shrinking of a muscle. It can be caused by immobilization or loss of neural stimulation.
  • Hypertrophy is the enlargement of a muscle. Hypertrophied muscles have more capillaries and more mitochondria to help them generate more energy. Strenuous exercise and steroid hormones can induce muscle hypertrophy. Since men produce more steroid hormones than women, they usually have more hypertrophied muscles.
  • Muscle tonus or muscle tone refers to the tightness of a muscle. In a muscle some fibers are always contracted to add tension or tone to the muscle.
  • Tetany is a sustained contraction of a muscle. It results from a rapid succession of nerve impulses delivered to the muscle.
  • This slide illustrates how a muscle can go into a sustained contraction by rapid neural stimulation. In number four the muscle is in a complete sustained contraction or tetanus.
  • The refractory period is a brief time in which muscle cells will not respond to stimulus.
  • The area to the left of the red line is the refractory period for the muscle contraction. If the muscle is stimulated at any time to the left of the line, it will not respond. However, stimulating the muscle to the right of the red line will produce a second contraction on top of the first contraction. Repeated stimulations can result in tetany.
  • Cardiac muscle tissue has a longer refractory period than skeletal muscle. This prevents the heart from going into tetany.
  • Isometric contractions produce no movement. They are used in standing, sitting and maintaining our posture. For example, when you are standing muscles in your back and abdomen pull against each other to keep you upright. They do not produce movement, but enable you to stand.
  • Isotonic contractions are the types that produce movement. Isotonic contractions are used in walking and moving any part of the body.  
  • This concludes the presentation on Muscle Physiology
  • General physiology lecture 3

    1. 1. Muscle Physiology Lecture 3
    2. 2. Muscular Tissue <ul><li>Skeletal Muscle </li></ul><ul><li>Cardiac Muscle </li></ul><ul><li>Smooth Muscle </li></ul>
    3. 3. Skeletal Muscle <ul><li>Long cylindrical cells </li></ul><ul><li>Many nuclei per cell </li></ul><ul><li>Striated </li></ul><ul><li>Voluntary </li></ul><ul><li>Rapid contractions </li></ul>
    4. 4. Cardiac Muscle <ul><li>Branching cells </li></ul><ul><li>One or two nuclei per cell </li></ul><ul><li>Striated </li></ul><ul><li>Involuntary </li></ul><ul><li>Medium speed contractions </li></ul>
    5. 5. Smooth Muscle <ul><li>Fusiform cells </li></ul><ul><li>One nucleus per cell </li></ul><ul><li>Nonstriated </li></ul><ul><li>Involuntary </li></ul><ul><li>Slow, wave-like </li></ul><ul><li>contractions </li></ul>
    6. 6. SKELETAL MUSCLE CELL <ul><li>“ Striated ”; striped appearance is because of the </li></ul><ul><li>orderly arrangement of the thin and thick filaments </li></ul><ul><li>that makeup the majority of the contractile proteins. </li></ul><ul><li>The contractile proteins are made of 3 types of </li></ul><ul><li> filaments; </li></ul><ul><li>1. THIN FILAMENT </li></ul><ul><li>2. THICK FILAMENT </li></ul><ul><li>3. ELASTIC FILAMENT </li></ul>
    7. 7. CONTRACTILE PROTEINS <ul><li>THIN FILAMENT </li></ul><ul><li>Has 3 parts; </li></ul><ul><li>i) ACTIN PROTEIN </li></ul><ul><li>(i.e. the main molecule of this filament). </li></ul><ul><li>FUNCTION : Binds to myosin head. </li></ul><ul><li>ii) TROPONIN </li></ul><ul><li>FUNCTION : Regulatory function by binding to Ca 2+ </li></ul><ul><li>iii) TROPOMYOSIN </li></ul><ul><li>FUNCTION : Has a regulatory function by blocking/ unblocking </li></ul><ul><li>the binding site of actin to the myosin head </li></ul>
    8. 8. Microanatomy of Skeletal Muscle Each muscle cell is called a muscle fiber. Within each fiber are many myofibrils.
    9. 9. ARRANGEMENT OF CONTRACTILE PROTEINS IN SKELETAL MUSCLE
    10. 11. Z line Z line
    11. 12. A myosin is elongated with an enlarged head at the end.
    12. 13. CONTRACTILE PROTEINS <ul><li>THICK FILAMENT </li></ul><ul><li>– made of myosin protein </li></ul><ul><li>- has 2 main parts </li></ul><ul><li>i) MYOSIN HEAD - forms cross-bridge with actin. </li></ul><ul><li>ii) MYOSIN TAIL – forms the shaft of thick bands. </li></ul>
    13. 14. Many myosin molecules form the thick myosin filament. It has many heads projecting away from the main molecule.
    14. 15. The thinner actin filament is composed of three parts: actin, tropomyosin and troponin.
    15. 16. H Band This sarcomere illustrates the thin actin and the thick myosin filaments. The area of the sarcomere has only myosin is called the H bond
    16. 17. Sarcomere Relaxed Here is another diagram of a sarcomere. Note the A band. It is formed by both myosin and actin filaments. The part of the sarcomere with only actin filaments is called the I band. This is a sarcomere that is relaxed.
    17. 18. Sarcomere Partially Contracted This sarcomere is partially contracted. Notice that the I bands are getting shorter.
    18. 19. Sarcomere Completely Contracted The sarcomere is completely contracted in this slide. The I and H bands have almost disappeared.
    19. 20. Which filament has moved as the sarcomere contracted? Note the thick myosin filaments have not changed, but the thin actin filaments have moved closer together.
    20. 22. SLIDING FILAMENT THEORY
    21. 23. SLIDING FILAMENT THEORY <ul><li>A better understanding of how muscle contracts can </li></ul><ul><li> be demonstrated by the interaction between the </li></ul><ul><li> contractile proteins in muscle as demonstrated by </li></ul><ul><li> the sliding filament mechanism model. </li></ul><ul><li>(STEP WISE) </li></ul><ul><ul><li>Myosin heads are activated </li></ul></ul><ul><ul><li>HOW? – Myosin head hydrolyses (breakdown) ATP to ADP + Pi </li></ul></ul><ul><li>NB: Part of myosin head acts as ATPase. </li></ul><ul><li>ATPase is an enzyme that splits ATP to ADP and Pi (free phosphate group) through hydrolysis reaction . </li></ul><ul><li>Hydrolysis of ATP transfers energy from ATP to myosin head (so myosin head becomes activated ). </li></ul><ul><li>Activated myosin head binds to ADP and is ready for </li></ul><ul><li>actin binding (= cross bridge) </li></ul>
    22. 24. SLIDING FILAMENT THEORY <ul><li>2. Activated myosin head binds rapidly to myosin- binding sites on actin </li></ul><ul><li>3 . Myosin head still bonded to actin; </li></ul><ul><li>i) Changes its shape </li></ul><ul><li>ii) Moves towards the center of sarcomere </li></ul><ul><li> NB. i) and ii) called power stroke </li></ul><ul><li>4 . Myosin head is still bonded to actin </li></ul><ul><li>- ADP released from myosin head </li></ul>
    23. 25. SLIDING FILAMENT THEORY <ul><li>5. ATP binds to the myosin in the myosin-actin complex </li></ul><ul><li>6. Myosin head detaches from actin </li></ul><ul><li>7. Myosin head hydrolyses ATP to ADP + Pi </li></ul><ul><li>8. Steps 2 – steps 8 is repeated </li></ul>
    24. 27. Contraction: The Sliding-Filament Theory <ul><li>Sarcomeres change length when muscle contracts or is stretched = correspond the change in muscle length </li></ul><ul><li>A bands (corresponds to length of thick filaments) maintains constant length when muscle shortens vs. </li></ul><ul><li>I bands & H-zone (zones where actin & myosin do not overlap in the resting muscle) become shorter </li></ul><ul><li>When muscle is stretched, A bands again maintain a constant length and I bands & H zone become longer </li></ul>
    25. 28. Contraction: The Sliding-Filament Theory con’t <ul><li>Neither the myosin thick filaments nor the actin thin filaments change in length when a sarcomere shorted/stretched but it is the extent of over-lap between actin & myosin filaments that changes = became the basis of the sliding-filament theory </li></ul><ul><li>Sarcomeres shorten during muscle contraction as thin filaments actively slide along thick filaments i.e. thin filament are pulled closer to center of sarcomere & because they are firmly anchored in Z-disks, sarcomere shortens & vice versa = when muscle relaxes/stretched, the overlap between thin & thick filaments is reduced and sarcomeres elongate. </li></ul>
    26. 29. Binding Site Tropomyosin Troponin
    27. 30. The binding sites are now exposed and myosin heads are able to attach to form cross bridges. Myosin
    28. 32. Neuromuscular Junction
    29. 33. NEUROMUSCULAR JUNCTION <ul><li>DEFINITION -Is the junction between the terminal of a motor neuron and a muscle fiber. </li></ul><ul><li>- The neuromuscular junction is also called the myoneural junction . </li></ul><ul><li>It is a kind of chemical synapse . The terminals of </li></ul><ul><li>motor axons contain thousands of vesicles filled with </li></ul><ul><li>acetylcholine ( ACh ). </li></ul><ul><li>The ACh are released when n erve impulses (action potentials) traveling down the motor neurons of the </li></ul><ul><li>sensory-somatic branch of the nervous system. The end </li></ul><ul><li> result is that it causes the skeletal muscle fibers at </li></ul><ul><li>which they terminate to contract. </li></ul>
    30. 35. Acethy Acethylcholine is released from the motor neuron.
    31. 36. Acetylcholine Opens Na + Channel
    32. 37. Excitation-Contraction Coupling
    33. 38. EXCITATION- CONTRACTION COUPLING <ul><li>(SEQUENCE OF EVENTS) </li></ul>
    34. 39. EXCITATION- CONTRACTION COUPLING
    35. 40. EXCITATION- CONTRACTION COUPLING (cont’d)
    36. 41. EXCITATION- CONTRACTION COUPLING (cont’d)
    37. 42. Muscle Contraction Summary <ul><li>Nerve impulse reaches myoneural junction </li></ul><ul><li>Acetylcholine is released from motor neuron </li></ul><ul><li>ACh binds with receptors in the muscle membrane to allow sodium to enter </li></ul><ul><li>Sodium influx will generate an action potential in the sarcolemma </li></ul>
    38. 43. Muscle Contraction Continued <ul><li>Action potential travels down T tubule </li></ul><ul><li>Sarcoplamic reticulum releases calcium </li></ul><ul><li>Calcium binds with troponin to move the troponin, tropomyosin complex </li></ul><ul><li>Binding sites in the actin filament are exposed </li></ul>
    39. 44. Muscle Contraction Continued <ul><li>Myosin head attach to binding sites and create a power stroke </li></ul><ul><li>ATP detaches myosin heads and energizes them for another contraction </li></ul><ul><li>When action potentials cease the muscle stop contracting </li></ul>
    40. 45. Motor Unit All the muscle cells controlled by one nerve cell
    41. 46. MOTOR UNIT <ul><li>DEFINITION - Is a motor neuron plus all skeletal muscle </li></ul><ul><li>fiber it stimulates </li></ul><ul><li>So one skeletal muscle can have many motor units. </li></ul><ul><li>We generally see 2 patterns; </li></ul><ul><li>1. MUSCLES CONTROLLING PRECISE MOVEMENTS </li></ul><ul><li>2. MUSCLES CONTROLLING POWERFUL GROSS MOVEMENTS </li></ul>
    42. 47. Motor Unit Ratios <ul><li>Back muscles </li></ul><ul><ul><li>1:100 </li></ul></ul><ul><li>Finger muscles </li></ul><ul><ul><li>1:10 </li></ul></ul><ul><li>Eye muscles </li></ul><ul><ul><li>1:1 </li></ul></ul>Motor units come in different sizes. The ratio is about one nerve cell To 100 muscle cells in the back. Finger muscles have a much smaller Ratio of 1:10. Eye muscles have 1:1 ratio because Of the precise control needed in vision.
    43. 48. ATP ATP is the form of energy that muscles and all cells of the body use. The chemical bond bet the last 2 phosphates has just the right amount of energy to unhook myosin heads and energize them for another contraction. Pulling of the end phosphate from ATP will release the energy. ADP and a single phosphate will be left over. New ATP can be regenerated by reconnecting the phosphate with the ADP with energy from our food.
    44. 49. Creatine <ul><li>Molecule capable of storing ATP energy </li></ul>Creatine + ATP Creatine phosphate + ADP
    45. 50. Creatine Phosphate <ul><li>Molecule with stored ATP energy </li></ul>Creatine phosphate + ADP Creatine phosphate is an important chemical to muscles. It is a molecule that is able to store ATP energy. It can combine with an ADP to produce creatine and ATP. This process occurs faster than the synthesis of ATP from food. Creatine + ATP
    46. 51. Muscle Fatigue <ul><li>Muscle fatigue is often due to lack of oxygen that causes ATP deficit </li></ul><ul><li>Lactic acid builds up from anaerobic respiration in the absence of oxygen. </li></ul><ul><li>Lactic acid fatigues the muscle. </li></ul>
    47. 52. MUSCLE FATIGUE <ul><li>DEFINE: Is when muscle is unable to maintain its strength of contraction or tension </li></ul><ul><li>WHAT HAPPENS AT CELL LEVEL? </li></ul><ul><li>Muscle can not produce enough ATP to meet its needs </li></ul><ul><li>FACTORS CONTRIBUTING TO MUSCLE FATIGUE </li></ul><ul><li>Insufficient oxygen </li></ul><ul><li>Depleted glycogen </li></ul><ul><li>Build-up of lactic acid </li></ul><ul><li>Failure for action potential in motor neuron to release enough ATP </li></ul>
    48. 53. Muscle Atrophy <ul><li>Weakening and shrinking of a muscle </li></ul><ul><li>May be caused </li></ul><ul><ul><li>Immobilization </li></ul></ul><ul><ul><li>Loss of neural stimulation </li></ul></ul>
    49. 54. MUSCLE ATROPHY <ul><li>DEFINITION – Is wasting away of muscles </li></ul><ul><li>DESCRIBE – Individual muscle fibers within muscle size caused by progressive loss of myofibrils. </li></ul>
    50. 55. Muscle Hypertrophy <ul><li>Enlargement of a muscle </li></ul><ul><li>More capillaries </li></ul><ul><li>More mitochondria </li></ul><ul><li>Caused by </li></ul><ul><ul><li>Strenuous exercise </li></ul></ul><ul><ul><li>Steroid hormones </li></ul></ul><ul><ul><li>such as testosterone </li></ul></ul><ul><ul><li>stimulate muscle </li></ul></ul><ul><ul><li>growth and hypertrophy </li></ul></ul>
    51. 56. <ul><li>MUSCLE MUSCLE </li></ul><ul><li>HYPERTROPHY ATROPHY </li></ul>
    52. 57. Muscle Tonus <ul><li>Also called muscle tone </li></ul><ul><li>It refers to the tightness of a muscle </li></ul><ul><li>In a muscle, some fibers always contracted to add tension or tone to the muscle. </li></ul>
    53. 58. Tetany <ul><li>Sustained contraction of a muscle </li></ul><ul><li>Result of a rapid succession of nerve impulses </li></ul>
    54. 59. What is a muscle twitch? <ul><li>The brief contractile response of skeletal muscle to a single maximal volley of impulses in the motor neuron supplying it is called a twitch. </li></ul><ul><li>It is the fundamental unit of recordable muscle activity. </li></ul><ul><li>The duration of a twitch is between 1/5 and 1/200 second, depending of the type of muscle </li></ul>
    55. 60. PHASES OF A MUSCLE TWITCH
    56. 61. What are the three phases of a muscle twitch? <ul><li>Latent phase- indicates the period between the time the stimulus is applied and the beginning of the contractile response (0.01 sec) </li></ul><ul><li>Contraction phase – follows the latent phase when the muscle responds to the stimulus by shortening (0.04 sec) </li></ul><ul><li>Relaxation phase – is the period when the muscle returns to its original length(0.05 sec) </li></ul>
    57. 63. Tetanus This slide illustrates how a muscle can go into a sustained contraction by rapid neural stimulation. In number 4, the muscle is in a complete sustained contraction or tetanus.
    58. 64. Refractory Period <ul><li>Brief period of time in which muscle cells will not respond to a stimulus </li></ul>
    59. 65. Refractory Period The area to the left of the red line is the refractory period for the muscle contraction. If the muscle is stimulated at any time to the left of the line, it will not respond. However, stimulating the muscle to the right of the red line will produce a second contraction on top of the first contraction. Repeated stimulations can result to tetany.
    60. 66. Refractory Periods Skeletal Muscle Cardiac Muscle Cardiac muscle tissue has a longer refractory period than skeletal muscle. This prevents the heart from going into tetany.
    61. 67. Isometric Contraction <ul><li>Produces no movement </li></ul><ul><li>They are used in standing, sitting and maintaining our posture. </li></ul><ul><li>For example when you are standing, muscles in your back and abdomen pull against each other to keep you upright. They do not produce movement, but enable you to stand. </li></ul>
    62. 68. Isotonic Contraction <ul><li>Isotonic contractions are the types that produce movement. </li></ul><ul><li>Used in </li></ul><ul><ul><li>Walking </li></ul></ul><ul><ul><li>Moving any </li></ul></ul><ul><ul><li>part of the body </li></ul></ul>
    63. 69. Fast and Slow twitch muscles 1. Slow twitch muscles are Type I or slow oxidative fibers or red muscles – are designed to sustain slow but long-lived muscular contractions and are able to function for long periods on aerobic activity. 2. Fast twitch muscles are white fibers or Type II – have larger diameter, more extensive sarcoplasmic reticulum, more folds in their neuromuscular junctions, more glycolytic enzymes, less myoglobin, and fewer mitochondria.
    64. 70. Subtypes of Fast Twitch Muscles <ul><li>Type IIa or intermediate fast twitch muscles- or fast oxidative glycolytic fibers (FOG)- because of their ability to display, when exposed to the relevant training stimuli; has the high capacity to contract under conditions of aerobic energy production. </li></ul><ul><li>Type IIb fibers are the “turbo chargers ” in our muscles and are also called fast glycogenolytic (FG) fibers since they rely almost exclusively on the short-term alactic/glycolytic energy system to fire them up. </li></ul>
    65. 71. MYSTHENIA GRAVIS
    66. 73. MYSTHENIA GRAVIS <ul><li>A characteristic symptom is fatigabilit y, which means that a </li></ul><ul><li> muscle that is used repeatedly starts to become weak.  </li></ul><ul><li>The symptoms usually start in the face and spread to the </li></ul><ul><li>other parts of the body as the disease progresses.  </li></ul><ul><li>Patients initially complain of drooping eye lids that gets </li></ul><ul><li>worst as the day goes on; they develop double vision, </li></ul><ul><li>difficulty talking, and difficulty chewing.  </li></ul><ul><li>All of these symptoms are worst with repeated use and </li></ul><ul><li>improve with rest.  </li></ul><ul><li>As the disease progresses the shoulders and the thighs </li></ul><ul><li>become week and the weakness could eventually spread to </li></ul><ul><li>the muscles that are used to breath; the patient could </li></ul><ul><li>develop shortness of breath and stop breathing if not </li></ul><ul><li>treated properly. </li></ul>
    67. 74. Next meeting Quiz on Muscle Physiology

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