CONTRACTILE TISSUES. medical physiologyptx

this presentation will help in better understanding of contractile tissue physiology

1. CONTRACTILE TISSUES PRESENTER: EMILY M KYUKO H56/44542/2023 LECTURER: PROF. F.BUKACHI INSTITUTION:THE UNIVERSITY OF NAIROBI DEPARTMENT:MEDICAL PHYSIOLOGY MSCN CLASS 2023/2024

2. LEARNING OBJECTIVES Describe the different types of contractile tissues. State functions of muscular tissues. State the structure and properties of contractile tissues. Explain the physiology of excitation and relaxation of smooth muscles, cardiac muscles and skeletal muscles.

3. INTRODUCTION Muscle cells can be excited like neurons. This can be mechanically, chemically or electrically. Contraction is by proteins; actin and myosin

4. MUSCULAR TISSUE TYPES OF MUSCULAR TISSUE Three types of muscular tissue include; Skeletal Cardiac Smooth

5. MUSCULAR TISSUES SKELETAL MUSCLE TISSUE M ost skeletal muscles move bones Skeletal muscle tissue is striated: Alternating light and dark bands (striations) as seen when examined with a microscope W orks mainly in a voluntary manner Its activity can be consciously controlled Some are controlled subconsciously to some extent E.g.: the diaphragm alternately contracts and relaxes without conscious control

6. TYPES OF MUSCULAR TISSUE cont; Cardiac Muscle Tissue Found only in the walls of the heart Striated like skeletal muscle Action is involuntary Contraction and relaxation of the heart is not consciously controlled Contraction of the heart is initiated by a node of tissue called the “pacemaker” Smooth Muscle Tissue Located in the walls of hollow internal structures Blood vessels, airways, and many organs Lacks the striations of skeletal and cardiac muscle tissue Contraction is usually involuntary

7. Comparison of Structure and Properties of Muscle Tissue Types Tissue Histology Function Location Skeletal Long cylindrical fiber, striated, many peripherally located nuclei Voluntary movement, produces heat, protects organs Attached to bones and around entrance points to body (e.g., mouth, anus) Cardiac Short, branched, striated, single central nucleus Involuntarily Contracts to pump blood Heart Smooth Short, spindle-shaped, no evident striation, single nucleus in each fiber Involuntary movement, moves food, involuntary control of respiration, moves secretions, regulates flow of blood in arteries by contraction Walls of major organs and passageways

8. FUNCTIONS OF MUSCULAR TISSUE Producing Body Movements Walking and running Stabilizing Body Positions Posture Moving Substances Within the Body Heart muscle pumping blood Moving substances in the digestive tract Generating heat Contracting muscle produces heat Shivering increases heat production

9. PROPERTIES OF MUSCULAR TISSUES These are properties that enable muscle to function and contribute to homeostasis ; Excitability Ability to respond to stimuli Contractility Ability to contract forcefully when stimulated Extensibility Ability to stretch without being damaged Elasticity Ability to return to an original length

10. SKELETAL MUSCLE TISSUE Connective Tissue Components Fascia Dense sheet or broad band of irregular connective tissue that surrounds muscles Epimysium The outermost layer Surrounds numerous bundles of fascicles Perimysium Separates 10-100 muscle fibers into bundles called fascicles Endomysium Separates individual muscle fibers from one another Tendon Cord that attach a muscle to a bone Aponeurosis Broad, flattened tendon

11. Descriptive Video

12. SKELETAL MUSCLE STRUCTURE AND FILAMENTS MICROSCOPICALLY Each muscle fiber is multinucleated and behave as a single unit It contains bundles of myofibrils surrounded by sarcoplasmic reticulum -SR( stores calcium ions , release of Ca ++ triggers a contraction) Each myofibril contains interdigitating thick and thin filaments arranged longitudinally in sarcomeres for contraction function. Repeated units of sarcomere form unique banding pattern in striated muscle A sarcomere runs from Z line to Z line (the basic functional unit of a myofibril)

13. THE FILAMENTS There are two types of filaments in the skeletal muscle namely; 1. Thick filament 2 . Thin filament 1.THICK FILAMENTS Are present in A band in the center of the sarcomere Contains myosin Each myosin has two heads attached to a single tail Myosin heads bind ATP and ACTIN, they are involved in cross-bridge formation

14. FILAMENTS cont , 2. THIN FILAMENTS Are anchored at the Z line Are present in I bands Interdigitate with thick filaments in a portion of the A band Contains actin , tropomyosin and troponin Troponin is the regulatory protein that permits cross-bridge formation when it binds to calcium ions Troponin is a complex of three globular proteins, which are;

15. TROPONINS TROPONIN T ; for tropomyosin. Attaches the troponin complex to tropomyosin TROPONIN I ; For inhibition. It inhibits the interaction of actin and myosin TROPONIN C ; for calcium ions. Is the calcium binding protein that permits interaction of actin and myosin

16. SKELETAL MUSCLE TISSUE Z discs Separate one sarcomere from the next Thick and thin filaments overlap one another A band Darker middle part of the sarcomere Thick and thin filaments overlap I band Lighter, contains thin filaments but no thick filaments Z discs passes through the center of each I band H zone Center of each A band which contains thick but no thin filaments M line Supporting proteins that hold the thick filaments together in the H zone

17. MUSCLE PROTEINS Myofibrils are built from three kinds of proteins 1) CONTRACTILE PROTEINS Generate force during contraction 2) REGULATORY PROTEINS Switch the contraction process on and off 3) STRUCTURAL PROTEINS Align the thick and thin filaments properly Provide elasticity and extensibility Link the myofibrils to the sarcolemma

18. CONTRACTILE AND REGULATORY PROTEINS Myosin Thick filaments Functions as a motor protein which can achieve motion Convert ATP to energy of motion Projections of each myosin molecule protrude outward (myosin head) Actin Thin filaments Actin molecules provide a site where a myosin head can attach Tropomyosin and troponin (regulatory proteins) are also part of the thin filament In relaxed muscle, Myosin is blocked from binding to actin Strands of tropomyosin cover the myosin-binding sites thus preventing formation of cross-bridges while at rest Calcium ion binding to troponin moves tropomyosin away from myosin-binding sites Allows muscle contraction to begin as myosin binds to actin

19. STRUCTURAL PROTEINS Titin Stabilize the position of myosin accounts for much of the elasticity and extensibility of myofibrils Dystrophin Links thin filaments to the sarcolemma

20. Skeletal Muscle

21. CONTRACTION AND RELAXATION OF SKELETAL MUSCLE THE SLIDING FILAMENT MECHANISM Myosin heads attach to and “walk” along the thin filaments at both ends of a sarcomere Progressively pulling the thin filaments toward the center of the sarcomere Z discs come closer together and the sarcomere shortens Leading to shortening of the entire muscle

22. Contraction and Relaxation of Skeletal Muscle

23. The Contraction Cycle The onset of contraction begins with the SR releasing calcium ions into the muscle cell Where they bind to actin opening the myosin binding sites

24. STEPS IN EXCITATION –CONTRACTION COUPLING IN SKELETAL MUSCLE Action potential ; action potential in the muscle membrane initiate depolarization of the T –tubules Depolarization of T-tubules opens ca2+ release channels in the nearby sarcoplasmic reticulum causing release of ca2+ from SR into intracellular fluid. Increase in intracellular calcium until it can cause change in troponin Calcium binds to troponin C on the thin filaments This causes a conformational change in troponin leading to the following events in cross-bridge cycle; Tropomyosin is moved out of the way Actin and myosin bind . Heads of cross-bridge pivot, the thin and thick filament slide over each other and ATP is hydrolyzed

25. EXCITATION-CONTRACTION COUPLING cont; Subsequently , the cross-bridges break and a new molecule of ATP bind to the myosin head to begin a new cycle cross-bridge cycling continues as long as ca2+ is bound to troponin C, and is sufficiently in high levels and ATP is available. Relaxation ; occurs when calcium uptake into the sarcoplasmic reticulum (SR) by ca2+ ATPase lowers the intracellular calcium ATP is consumed in the process of calcium uptake and during the cross-bridge cycle

26. Learning Video

27. Excitation–Contraction Coupling(summarized) An increase in Ca ++ concentration in the muscle initiates contraction A decrease in Ca ++ stops it Action potentials cause Ca ++ to be released from the SR into the muscle cell Ca ++ moves tropomyosin away from the myosin-binding sites on actin allowing cross-bridges to form The muscle cell membrane contains Ca ++ pumps to return Ca ++ back to the SR quickly Decreasing calcium ion levels As the Ca ++ level in the cell drops, myosin-binding sites are covered and the muscle relaxes

28. ACh diffuses across synaptic cleft, binds to its receptors in the motor end plate, and triggers a muscle action potential (AP). Nerve impulse arrives at axon terminal of motor neuron and triggers release of acetylcholine (ACh). Synaptic vesicle filled with ACh ACh receptor Acetylcholinesterase in synaptic cleft destroys ACh so another muscle action potential does not arise unless more ACh is released from motor neuron. Ca 2+ Muscle action potential Nerve impulse SR Contraction: power strokes use ATP; myosin heads bind to actin, swivel, and release; thin filaments are pulled toward center of sarcomere. Troponin–tropomyosin complex slides back into position where it blocks the myosin binding sites on actin. Muscle relaxes. Ca 2+ active transport pumps Ca 2+ release channels in SR close and Ca 2+ active transport pumps use ATP to restore low level of Ca 2+ in sarcoplasm. Ca 2+ binds to troponin on the thin filament, exposing the binding sites for myosin. Muscle AP travelling along transverse tubule opens Ca 2+ release channels in the sarcoplasmic reticulum (SR) membrane, which allows calcium ions to flood into the sarcoplasm. Elevated Ca 2+ 1 2 3 4 9 5 6 7 8 Transverse tubule

29. CONTROL OF MUSCLE TENSION 1.Twitch Contraction * The brief contraction of the muscle fibers in a motor unit in response to an action potential Twitches last from 20 to 200 msec Latent period (2 msec) A brief delay between the stimulus and muscular contraction The action potential sweeps over the sarcolemma and Ca ++ is released from the SR Contraction period (10–100 msec) Ca ++ binds to troponin Myosin-binding sites on actin are exposed Cross-bridges form

30. ??read on * Treppe * Recruitment *tetany

31. Control of Muscle Tension cont, Relaxation period ( 10–100 msec) Ca ++ is transported into the SR Myosin-binding sites are covered by tropomyosin Myosin heads detach from actin Muscle fibers that move the eyes have contraction periods lasting 10 msec Muscle fibers that move the legs have contraction periods lasting 100 msec Refractory period When a muscle fiber contracts, it temporarily cannot respond to another action potential Skeletal muscle has a refractory period of 5 milliseconds Cardiac muscle has a refractory period of 300 milliseconds

32. Types of Contractions Isotonic contraction The tension developed remains constant while the muscle changes its length Used for body movements and for moving objects Picking a book up off a table Isometric contraction The tension generated is not enough for the object to be moved and the muscle does not change its length Holding a book steady using an outstretched arm

33. Types of Contractions Eccentric contraction Occurs when the total length of the muscle increases as tension is produced Concentric contraction The muscle shortens, thereby generating force

34. MUSCLE METABOLISM Muscle Fatigue Inability of muscle to maintain force of contraction after prolonged activity FACTORS THAT CONTRIBUTE TO MUSCLE FATIGUE ARE;- Inadequate release of calcium ions from the SR Depletion of creatine phosphate (rapidly mobilizable reserve of high-energy phosphates in skeletal muscle & brain). Insufficient oxygen Depletion of glycogen and other nutrients Buildup of lactic acid and ADP Failure of the motor neuron to release enough acetylcholine

35. CARDIAC MUSCLES Like skeletal muscles they are striated. Z lines are present. At each intercalated disc the cell membranes fuse with one another in such a way that they form permeable communicating junctions ( gap junctions ) that allow almost totally free diffusion of ions.

36. CARDIAC MUSCLE cont; Gap junctions provide low resistance bridges for transmission of excitation from one cell to another allowing cardiac muscle to function as a syncytium. A typical cardiac muscle has a single centrally placed nucleus, although a few may have two or more nucleus . They are involuntary, self excitatory. The T tubules in a cardiac muscle cell are short and broad do not form triads like in like in skeletal muscles. The t tubules allows the heart cells to contract more forcefully by synchronizing calcium release throughout the cell.

37. CONT; Action potential in cardiac muscles makes the sarcolemma more permeable to extracellular calcium ions because their contractions require both intracellular and extracellular calcium ions. They are almost totally dependent on aerobic metabolism or the energy they need to continue the contracting. They have energy reserves inform of glycogen and lipid inclusions. Contain large number of mitochondria (40% of the cell volume) and myoglobin a muscle pigment that can function as oxygen storage mechanism

38. CARDIAC MUSCLE UNDER EM

39. ACTION POTENTIAL IN CARDIAC MUSCLES Resting membrane potential -80. Stimulation produces a propagated action potential that is responsible for initiating contraction. Depolarization proceeds rapidly and an overshoot of the zero potential is present, as in skeletal muscle and nerve, but this is followed by a plateau before the membrane potential returns to the baseline

40. Cont; In mammalian hearts, depolarization lasts about 2 ms , but the plateau phase and repolarization last 200 ms or more Where as the skeletal muscles does not a plateau the cardiac muscles have a prolonged plateau due opening of two types of channels fast sodium channels and slow calcium channels

41. ACTION POTENTIAL IN CARDIAC MUSCLES Calcium channels remain open for some time maintaining the long period of depolarization causing the plateau. Immediately after the onset of action potential the permeability of cardiac muscles to potassium decreases. This decreases the outflux of potassium this prevents early return of action potential to resting membrane potential Repolarization is due to closure of the Ca 2+ channels and a slow, delayed increase of K + efflux through various types of K + channels.

42. REFRACTORY PERIOD The refractory period of the heart is the interval of time, during which a normal cardiac impulse cannot re-excite an already excited area of cardiac muscle. The normal refractory period of the ventricle is 0.25 to 0.30 second, which is about the duration of the prolonged plateau action potential.

43. RELATIVE REFRACTORY PERIOD Relative refractory period is about 0.05 second during which the muscle is more difficult than normal to excite but nevertheless can be excited by a very strong excitatory signal

44. ECG AND ACTION POTENTIAL The P wave is caused by spread of depolarization through the atria, and this is followed by atrial contraction, which causes a slight rise in the atrial pressure curve immediately after the electrocardiographic P wave . About 0.16 second after the onset of the P wave, the QRS waves appear as a result of electrical depolarization of the ventricles, which initiates contraction of the ventricles and causes the ventricular pressure to begin rising. Therefore, the QRS complex begins slightly before the onset of ventricular systole.

45. ECG AND ACTION POTENTIAL Finally, one observes the ventricular T wave in the electrocardiogram. This represents the stage of repolarization of the ventricles when the ventricular muscle fibers begin to relax. Therefore, the T wave occurs slightly before the end of ventricular contraction

46. PHYSIOLOGY OF THE HEART Blood normally flows continually from the great veins into the atria; about 80% of the blood flows directly through the atria into the ventricles even before the atria contract. Then, atrial contraction usually causes an additional 20% filling of the ventricles. Therefore, the atria simply function as a primer pumps that increase the ventricular pumping effectiveness.

47. CONT; However, the heart can continue to operate under most conditions even without this extra 20 per cent effectiveness because it normally has the capability of pumping 300 to 400 per cent more blood than is required by the resting body. Therefore, when the atria fail to function, the difference is unlikely to be noticed unless a person exercises; then acute signs of heart failure occasionally develop, especially shortness of breath.

48. ACTION POTENTIAL IN THE HEART

49. CONTRACTION OF CARDIAC MUSCLES Contraction is similar with skeletal muscles with a few differences. An electrical stimulation in form of an action potential delivered in a rhythmic pattern triggers a release of calcium ions from the cells internal calcium stores and sarcoplasmic reticulum Signals from Sino atrial node causes contraction of heart muscles, the pace making signal generated travels through the right atrium to the atrioventricular node along Bundle of His to cause a contraction. Increase in calcium ions causes the cells myofilaments to slide past each other in a process called excitation contraction coupling.

50. CONTRACTION CONT; Action potential spreads out through cells and across the surface of sarcolemma via the gap junction. voltage gated calcium ions channels gets activated and open calcium ions gets into cytoplasm – free activates calcium ions attach to troponin and initiate contraction

51. SMOOTH MUSCLES Found in the eyes, esophagus, stomach, intestines, bronchi, ureter, bladder, and blood vessels. Uni nucleated Have no sarcomere. Involuntary Smooth muscle may contract spontaneously or rhythmically and can be induced by a number of physiochemical agents (hormones, drugs, neurotransmitters).

52. SMOOTH MUSCLES CONT; Contain both thick and thin filaments They are not arranged in in orderly sarcomeres. Arranged diagonally . Have no regular pattern and no striations. Contain caveolae in the sarcolemma instead of T Tubules

53. CONT; Sarcoplasmic reticulum contains only small amount of stored calcium, Remaining calcium comes from ECF Filaments attach to dense bodies and stretch from one dense body to another. The motor innervation of smooth muscle is exclusively autonomic, either parasympathetic or sympathetic

54. SM CONT; Dense bodies function in the same way as two discs During contraction the filaments pull on the dense bodies causing a shortening of the muscle fiber. Instead of Z lines, there are dense bodies in the cytoplasm and attached to the cell membrane, and these are bound by α- actinin to actin filaments

55. SM CONT; Smooth muscle also contains tropomyosin, but has no troponin . Calmodulin a protein used to bind calcium ions in the cytosol instead of troponin. Calmodulin then activates myosin kinase which phosphorylates myosin.

56. STRUCTURE OF SMOOTH MUSCLE Physical structure of smooth muscle. The fiber on the upper left shows actin filaments radiating from dense bodies. The fiber on the lower left and at right demonstrate the relation of myosin filaments to actin filaments .

57. TYPES OF SMOOTH MUSCLES There are two broad categories of smooth muscle cells: 1. Unitary smooth muscle contraction is synchronized by gap junctional communication to coordinate contraction among many cells. Found primarily on hollow viscera EXAMPLE the intestine, the uterus, and the ureters.

58. CONT; 2 . Multiunit smooth muscle contraction is coordinated by motor units, functionally similar to skeletal muscle. Found in the iris of the eye. With few or no gap junctional bridges

59. CONTRACTION IN SMOOTH MUSCLES Slower than skeletal but lasts longer. Prolonged calcium in the cell provides continued contraction. Calcium ions moves slowly out of the muscle fiber, delaying relaxation

60. CONT; This is important in the GI system where a steady state is maintained on the contents state is maintained on the contents of the stomach. Food in the digestive system stretches intestinal walls initiating peristalsis In the walls of the blood vessels which maintain a steady pressure on blood. Action potential from autonomic nervous system. Pupils constrict due to increased light energy. Epinephrine causes relaxation of smooth muscles in the airway and in some blood vessel walls

61. CONTRACTION OF SM SUMMARIZED Binding of acetylcholine to muscarinic receptors Activation of calmodulin -dependent myosin light chain kinase Increased myosin ATPase activity and binding of myosin to actin Contraction

62. CONT; Phosphorylation of myosin Increased influx of Ca2+ into the cell Dephosphorylation of myosin by myosin light chain phosphatase Relaxation, or sustained contraction due to the latch bridge and other mechanisms

63. COMPARISON OF SMOOTH MUSCLE AND SKELETAL MUSCLE CONTRACTION Slow Cycling of the Myosin Cross-Bridges. The rapidity of cycling of the myosin cross-bridges in smooth muscle i.e. their attachment to actin, then release from the actin, and reattachment for the next cycle is much slower than in skeletal muscle. The frequency is as little as 1/10 to 1/300 that in skeletal muscle . Low Energy Requirement to Sustain Smooth Muscle Contraction . Only 1/10 to 1/300 as much energy is required to sustain the same tension of contraction in smooth muscle as in skeletal muscle.

64. Cont; Slowness of Onset of Contraction and Relaxation of the Total Smooth Muscle Tissue . A typical smooth muscle tissue begins to contract 50 to 100 milliseconds after it is excited, reaches full contraction about 0.5 second later, and then declines in contractile force in another 1 to 2 seconds, giving a total contraction time of 1 to 3 seconds. This is about 30 times as long as a single contraction of an average skeletal muscle fiber. Maximum Force of Contraction Is Often Greater in Smooth Muscle Than in Skeletal Muscle . Latch Mechanism Facilitates Prolonged Holding of Contractions of Smooth Muscle .

65. REFFERENCES Ganongs review of physiology 23 rd edition Medical physiology by Guyton . Guyton and Hall Textbook of Medical physiology Google.