muscular contraction mbbs and other science. Pptx

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1. molecular basis of muscle contraction Dr. Alok Kumar Yadav

2. Skeletal Muscle Structure

3. Skeletal Muscle Fiber

4. Sarcomere

5. Actinin filament

6. Myosin filament

7. Review of thin and thick filament structure

8. Effect of calcium ions after release from Sarcoplasmic reticulum

9. ATP as source of energy for muscle contraction After ATP has bound to myosin head, binding of Myosin to Actin molecule takes place.

10. Mechanism of muscles contraction Excitation-contraction coupling Process by which AP on surface of cell membrane triggers contraction of muscles fiber using calcium ions.

11. Cont… Muscle fiber is stimulated Ca 2+ release via ryanodine receptor Thin filaments move to middle of sarcomere Quantum release of Ach Generation of end plate potential Transmission of AP on sarcolemma Movement of AP in T tubules Voltage changes sensed by dihydro- pyridine receptors Initial of contraction

12. Sliding filament mechanism of muscle contraction When a muscle cell contracts, thin filaments slide past thick filaments, and sarcomere shortens. Walk Along Theory or the Ratchet Theory

13. Shortening of the Muscle Decrease in I-band and H-band, A-band stays the same

14. Event during muscle relaxation

15. Chemical changes during skeletal muscle contraction Described in following heading:- source of energy for muscle contraction Efficiency of muscle contraction Heat production during muscle contraction Muscle fatigue Rigor mortis Heat rigor

16. 1. Source of energy for muscle contraction 1.Reconstitute ATP ADP+Phosphocreatine = ATP 2.Reconstitute both ATP and phosphocreatine Glycogen pyruvic acid + Lactic acid 3.Oxidative metabolism End products of glycolysis + cellular food stuff ENERGY LIBERATES Rapid enzymatic breakdown oxygen ATP

17. 2. Efficiency of muscle contraction Percentage of input energy to muscle that converted in to work instead of heat . Maxim efficiency- muscle contract slowly or without any movement. Less than 25%, remainder becoming heat. Fenn effect- muscle uses extra energy in proportion to work.

18. 3. Heat production during muscle contraction Av hill- 1922-sensative thermocouples Work + Heat + ATP Efficiency -percentage of total energy spent for work Isotonic contraction- Higher Isometric contraction-Lesser TYPES OF HEAT 1.Resting heat 2.Initial heat Activation heat and shortening heat 3.Relaxation heat 4.Recovering heat Muscle contraction Input energy

19. 4. Muscle fatigue Inability of muscle to sustain given amplitude of contraction . Seen - prolonged & strong contraction of muscle. Causes: 1. Reduction in central command. 2.Transmission of nerve signal through nmj diminish. 3.Interruption of blood flow through a contracting muscle. 4. Rate of depletion of muscle glycogen

20. 5. Rigor mortis State of contracture of muscles of after death due to depletion of ATP. Cause:- Muscles cells unable to prevent ca 2+ ions entry . ATP required to cause separation of cross bridges from actin filament during relaxation. Muscles in rigor until muscle proteins deteriorate (15-25hrs) Autolysis –released enzymes from lysosomes. Temperature – events occur rapidly .

21. 6. Heat rigor Shortening of muscle when exposed to heat above 50 ⁰, related to coagulation of muscle protein. Demonstrated- isolated muscle preparation.

22. Smooth muscle Structure of smooth muscle Group of smooth muscles fibbers behave as syncytium.

23. Functional organization Fibres is of three type 1.Circular 2.Circular and Longitudinal 3.Circular,Longitudinal,Oblique. Types of smooth muscle Single-unit smooth muscle Multi unit smooth muscle

24. Ionic basic of smooth muscle contraction The process of excitation and contraction is very slow in smooth muscles because of poor development of ‘L’ tubules (sarcoplasmic reticulum). Sequence of event by which excited plasma membrane of a muscle fibre leads to cross-bridge activity by increasing sarcoplasmic Ca2+ ions. Three different mechanisms- 1. Electro-mechanical coupling. Excited through sarcolemmal depolarization 2. Pharmaco-mechanical coupling. Exited through chemical agent. 3. Mechano-mechanical coupling. Excited through stretch

25. Calcium-calmodulin Complex Stimulation of ATPase activity of myosin in smooth muscle is different from that in skeletal muscle. In smooth muscle, the myosin has to be phosphorylated for the activation of myosin ATPase. Phosphorylation of myosin occurs in the following manner: 1. Calcium, which enters the sarcoplasm from the extracellular fluid combines with a protein called calmodulin and forms a calcium-calmodulin complex 2. It activates calmodulin-dependent myosin light chain kinase . 3. This enzyme in turn causes phosphorylation of myosin followed by activation of myosin ATPase 4. Now, the sliding of actin filaments starts. Phosphorylated myosin gets attached to the actin molecule for longer period. It is called latch-bridge mechanism and it is responsible for the sustained contraction of the muscle with expenditure of little energy. Relaxation of the muscle occurs due to dissociation of calcium-calmodulin complex.

26. Event of smooth muscle contraction and relaxation Ca2+ influx into the smooth muscle cell Binding of Ca++ with Calmodulin-dependent MLCK Phosphorylation of myosin Increased myosin ATPase activity Myosin binds with actin resulting in cross –bridge formation Dephosphorylation of myosin by MLCP Latch-bridge state (sustained contraction)or, slow relaxation

27. Cont… Latch phenomenon Mechanism by which smooth muscle can maintain high tension without actively contracting allow long term maintenance of tone .

28. Properties of smooth muscle A. Anatomical properties 1.Lack of striation 2.Absence of tension 3.Absence of T- tubules 4.Absence of well –developed NMJ B. Electrical properties 5.Presence of of jap junction 6.Excitability 7.Variable RMP 8.Variable action potential C. Mechanical properties 9.Slow and prolonged contractile response-less energy 10.Length -tension relationship- Not linear (jagged line) 11.Force –velocity relationship 12. Marked shortening

29. Applied 1. MUSCULAR DYSTROPHY Muscular dystrophy is a disease characterized by progressive degeneration of muscle fibers, without the involvement of the nervous system. Mostly it hereditary origin. M uscles fail to regenerate, resulting in progressive weakness and confinement to a wheelchair. Eventually, death occurs. 2 . Myopathies . Metabolic myopathies Inflammatory myopathies 3. Focal dystonia- faulty contraction Spasmodic torticollis and cervical dystonia Nystagmus 4. Myotonia.

30. Duchenne Muscular Dystrophy Duchenne muscular dystrophy is a sex-linked recessive disorder. It is due to the absence of a gene product called dystrophin in the X chromosome. Dystrophin is necessary for the stability of sarcolemma. This disease is characterized by degeneration and necrosis of muscle fibers and degenerated muscle fibers are replaced by fat and fibrous tissue. Common symptom muscular weakness. Enlargement of muscles (pseudohypertrophy). In severe conditions, the respiratory muscles become weak, resulting in difficulty in breathing and death.

31. Becker Muscular Dystrophy Becker muscular dystrophy is also a sexlinked disorder. It occurs due to the reduction in quantity or alteration of dystrophin. Common features of this disorder are slow progressive weakness of legs and pelvis, pseudohypertrophy of calf muscles, D ifficulty in walking, fatigue and mental retardation.

32. Hypertonia Hypertonia or hypertonicity is a muscular disease characterized by increased muscle tone and inability of the muscle to stretch. Hypotonia Hypotonia is muscular disease characterized by decreased or lost muscle tone. Muscle offers very little resistance to stretch . Muscle becomes flaccid

33. LAMBERT-EATON SYNDROME Disorder of neuromuscular junction caused by development of antibodies against calcium channel in the nerve terminal, resulting in reduction in the release of quanta of acetylcholine. This disease is commonly associated with carcinoma. So, it is also called carcinomatous myopathy. characterized by several features of myasthenia gravis. In addition, the patients have blurred vision and dry mouth.

34. McARDLE DISEASE McArdle disease is a glycogen storage disease (accumulation of glycogen in muscles) due to the mutation of genes involving the muscle glycogen phosphorylase, necessary for the breakdown of glycogen in muscles. Muscular pain and stiffness are the common features of this disease.