1. Anatomy and Physiology 2211K - Lecture 4

2. Slide 2 – Cytology of a muscle fiber

3. Slide 5 – Protein filaments

4. Slide 4 – Actin molecule

5. Slide 7 – Myosin molecule

6. Slide 8 – Tropomyosin and troponin

7. Slide 9 - Tinin

8. Slide 10 - Nebulin

9. Slide 3 - Myofibrils

10. Slide 4 – Myofibrils II

11. Slide 16 – Sarcomere

12. Slide 12 – Energy molecules II

13. Slide 12 – Nucleosides NTP + ADP NDP + ATP Nucleoside triphosphate (NTP) is a general name for all energy molecules such as ATP, TTP, CTP, GTP, UTP Since the conformational change of the heavy meromyosin (e.g. as an result muscle contraction) is energized by ATP only, the remaining energy sources (e.g. TTP, CTP, GTP, UTP) could be salvaged in an emergency to recharge ADP As shown above, the nucleoside triphosphate (NTP) which are the remaining energy molecules of TTP, CTP, GTP, UTP could be utilized to recharge ADP by transferring its high energy bond Nucleoside diphosphokinase is the enzyme used to transfer the high energy bone and a phosphate from NTP to ADP thereby forming ATP Nucleoside diphosphokinase

14. Slide 13 – Creatine phosphate Creatine Phosphate + ADP Creatine + ATP Creatine phosphate is the major reserve energy source in muscles Creatine possesses a a high energy bond (and a phosphate) and it is formed when the muscle is at rest In an emergency, the high energy bond (and a phosphate) is transferred to ADP thereby reforming a charged energy molecule ATP Creatine kinase is responsible for transferring the high energy bond from creatine phosphate to ADP Creatine Kinase

15. Slide 14 – adenylate kinase ADP + ADP AMP + ATP As an last ditch effort to gain energy, your body will salvage even a spent energy molecule like Adenosine diphosphate (ADP) The enzyme adenylate kinase is used to transfer a phosphate from ADP to another ADP to create a new high energy bond or a recharged ATP Adenylate Kinase

16. Slide 18 – Neuromuscular junction

17. Slide 19 – sodium and potassium concentrations

18. Slide 18: Polarized

19. Slide 18: Ionotropic and metabotropic receptor

20. Slide 20: Reaching threshold

21. Slide 20 – Spread of action potential I Figure 17: Graphic illustration of the formation of an action potential. Please note that the ① pore of the ligand gated Na+ channel (red) will open after the binding of ACh which allows the initial influx of Na + and the generation of an electric impulse (red arrow). ② Subsequently, the electric impulse will spread down the membrane by causing the first voltage gated Na + channel to open which in turn will create another electric impulse and ③ opening another voltage gated Na + channel. ④ Like falling dominos, another electric impulse will be generated whereby causing other voltage gated Na + channel to open

22. Slide 22: DHP Receptor Figure 18: Graphic illustration of the interactions between DHP receptor, ryanodine receptor and calcium release channel. ① The generated action potential activates the DHP receptor which causes this voltage gated Ca ++ channel to open. ② Ca ++ cations from the extracellular matrix to flow into the cell. ③ The Ca ++ cations bonds to ryanodine receptor causing it to activate. ④ The activated ryanodine receptor trigger the opening of the calcium release channel thereby allowing the Ca ++ stored within the sarcoplasmic reticulum to be released into the sarcoplasm

23. Slide 21: muscle contraction summary I

24. Slide 24 – Cross bride and power stroke

25. Slide 24: muscle contraction summary II Figure 22: Graphic illustration of excitation- contraction coupling. ① Action potential arrives at the neuromuscular junction which causes AChE to be released via exocytosis. ② AChE diffuses cross the synaptic cleft and binds with nAChR and initiates an action potential. ③ Action potential travels to the t-tubules and activates the DHP receptor which in turn causes the sarcoplasmic reticulum to release Ca ++. ④ Ca ++ is released into the sarcoplasm and ⑤ binds with troponin which in turn moves tropomyosin away from the active site. Cross bridge is formed between the myosin and actin myofilament and actin-myosin cycling begins. ⑥ actin-myosin cycling results in the shortening of the sarcomere. The shortening of the sarcomere causes the shortening of the myofibril. ⑦ The shortening of the myofibril results in muscle contraction

26. Slide 23: Depolarized

27. Slide 26: Repolarization

28. Slide 27: return to polarization

29. Slide 22 – Return to polarization and muscle relaxation summary Figure 25: Graphic illustration of skeletal muscle relaxation. ① Acetylcholinesterase removed AChE which causes the nAChR to close. ② Lack of action potential causes the voltage gated Na + channel to close. ③ DHP receptor turns “off” which causes the reabsorption of Ca++ by the terminal cisternae and subsequent storage in the sarcoplasmic reticulum. ④ Removal of Ca ++ from TnC which causes troponin to return to its original shape. Regaining its shape, troponin moves tropomyosin back to its original conformation. Tropomyosin covers the active site of actin myofilament and severs the cross bridge. ⑤ Sarcomere and myofibril return to its relaxed state. ⑥ muscle relaxation

30. Slide 27 - Myoglobin

31. Slide 31: Cellular respiration overview

32. Slide: Anaerobic respiration

33. Slide 26 – Creatine phosphate

34. Slide 43 – oxygen debt and lactic acid

35. Slide 35: aerobic and anaerobic respiration overview

36. Slide 36 – Types of muscle

37. Slide 47 – Origin, insertion and joint

38. Slide 48 – Flexor and extensors

39. Slide 49 - fasia

40. Slide 40 – Smooth muscle