1. Characteristics: Location, cell shape, nuclei per cell, innervation, connections to adjacent myofibers, arrangement of actin and myosin, regulation of cross bridges, sources of Ca++, response to injury, twitch duration, etc. Different types of muscles for different tasks! S 1

2. S 2 Synonyms: NMJ = neuromuscular junction Myoneural junction Motor end plate

3. Fig. 09.15 1 AP in motor axon releases sufficient ACh for 1 AP in skeletal muscle. Nicotinic Myasthenia gravis and loss of nAChRs EPP S 3

4. Fig. 09.11b Terms: Myofiber, myofibril, myofilament Thick myofilament = myosin Thin myofilament = actin S 4

5. Fig. 09.12 The concentration of free calcium is directly related to force of contraction in skeletal muscle Thus we need to understand the cellular mechanism of contraction… cell biology flashbacks… High fAP leads to accumulation of Ca++ in sarcoplasm because Ca++ ATPase doesn’t return all Ca++ to SR quickly enough. S 5

6. YouTube Videos Role of ATP in muscle Creepy Muscle demo Sarcomere contraction Powerstoke in muscle I Role of ATP in muscle Creepy Muscle demo Sarcomere contraction Powerstoke in muscle I S 6

7. Fig. 09.08 Two roles of ATP: 1) Energy for powerstroke & 2) Necessary for detaching myosin from actin Crossbridge cycling continues as long as ATP and Ca++ present. S 7

8. Classes of Myofibers based on Twitch Duration Each skeletal muscle fiber express only one of two different myosins isozymes: Fast twitch = rapid hydrolysis of ATP means crossbridges cycle faster Slow twitch = slower hydrolysis, isozyme catalyzes the reaction slower Isozymes not modified by athletic training! S 8 Contraction velocity also affected by load!

9. Fig. 09.02 dArk band = aligned myosin filaments lIght band = absence of myosin filaments S 9 Myofilaments

10. S 10

11. Fig. 09.03 S 11

12. Fig. 09.04 S 12

13. Fig. 09.05a S 13

14. Fig. 09.05b Contracted S 14

15. Fig. 09.05a Image if the sarcomeres were stretched? How would the number of cross bridges capable of binding to actin be affected? How would the overlap affect the tension produced? S 15

16. 1QQ # 13 Answer one. 1.Suppose there was a mutation that rendered troponin incapable of binding Ca++. Would that embryo survive? Why or why not? 2.What would happen if you injected Ca++ into a skeletal myofiber? 3.For our twitch recordings in lab, what events (in the proper sequence) were occurring during the latent period? 4.Why is peak tetanic tension 3-5 times greater than peak twitch tension? How is Ca++ involved?

17. Fig. 09.16 S 16

18. Length-tension Relationship So….. Tension produced by a single myofiber varies depending on sarcomere length. S 17

19. Link to cytosolic calcium concentration, release, and reuptake? Muscle kinetics S 18

20. Fig. 09.20 So….. Tension produced by a single myofiber varies depending on frequency of Action Potentials. S 19 Why does this plateau? Why is peak TETANIC tension so much greater than peak TWITCH tension?

21. Muscle Metabolism Classification of Myofiber types – Speed of myosin ATPase – Metabolic sources of ATP – Fatigability S 20

22. Classes of Myofibers based on Twitch Duration Each muscle fiber express only one of two different myosins isozymes: Fast twitch = rapid hydrolysis of ATP means crossbridges cycle faster Slow twitch = slower hydrolysis, isozyme catalyzes the reaction slower Myosin isozymes not modified by athletic training! S 21

23. Classes of Myofibers based on Metabolic and Enzyme profiles Oxidative: at peak activity rely on full aerobic cellular respiration – many mitochondria, enzymes for oxidative phosphorylation, numerous capillaries, lots of myoglobin (red) Glycolytic: at peak activity rely on glycolysis – few mitochondria, many glycolytic enzymes, large store of glycogen, fewer capillaries, little myoglobin (white) S 22 Metabolic and Enzyme profiles CAN BE modified by athletic training!

24. 3 Sources of ATP in muscle Creatine phosphate, then oxidative phosphorylation (OP) from glycogen, then OP from blood glucose, then blood fatty acids. If intense, switch to glycolysis… then take a breather… oxygen debt Powerstroking & Disconnecting crossbridges S 23

25. S 24

26. Fig. 09.03 Type IType II AType II B S 25

27. S 26

28. Type I Type IIA Type IIB What are the causes of fatigue? Depends on the type of activity… S 27

29. Causes of fatigue High intensity, short duration exercise – Conduction failure in t-tubules – Lactic acid accumulation – Accumulation of ADP and inorganic phosphate Low intensity, long duration exercise – As above, and – Depletion of muscle glycogen – Low plasma glucose (hypoglycemia) – Dehydration Control pathways: “willpower” – Common in couch potatoes S 28

30. So what are the ways a muscle (consisting of many myofibers) increases tension? S 29

31. Fig. 09.13 Motor unit = a single somatic motor neuron and all the muscle fibers in innervates S 30

32. S 31 But each motor unit has myofibers of the same type: I or IIA or IIB.

33. Fig. 09.26 Relationship between recruitment and motor unit type S 33 Size of somatic motoneuron cell body The Size Principle

34. Increasing tension in a whole muscle Frequency of stimulation of motor neuron Activate larger motor units Recruitment: activate more motor units These factors also influence actual tension – Fiber length (length-tension) relationship – Fiber diameter – Level of fatigue (state of activity) S 32

35. Types of Contractions Isometric = Same length Isotonic = Same tension S 34 Aka Lengthening contraction

36. Response to training Resistance training Type II change enzyme profiles: II A to II B Type II add more actin and myosin Type II increase cross-sectional area (hypertrophy) Endurance training – Type I increases vascularity – Type I increase number of mitochondria S 35

37. Fig. 09.24b Read section of King et al., 1999 that deals with analysis of muscle biopsy material in subjects taking Andro or placebo while resistance training. What changes were expected? What changes were observed? S 36

38. Consider blood flow to skeletal muscles during isometric contractions. Consider blood pressure during isometric contractions. S 37

39. The benefits of using trekking poles? S 38

40. Chapter 9 B Properties of Smooth Muscle How does smooth muscle differ from skeletal muscle? (innervation, membrane potentials, excitation-contraction coupling, twitch duration, fatigue, etc. (Table 9-6 p.287) What are the features of membrane potential of smooth muscle? (pacemakers and slow waves) What are the differences between single-unit and multi-unit smooth muscle? (location, spread of excitation) S 39 Who cares about smooth muscles?

41. Figure 9.34 Special situation: Dephosphorylation & latch bridge from SR and influx during Action Potential or graded potential Graded potentials result in graded contractions S 40 Slow twitch of SM due to slow action of myosin ATPase. Lack troponin Excitation-contraction coupling in Smooth Muscles Ca ++

42. Latchbridge =latch state S 41 Comparison of Twitch Duration Thankful for latch state! Crucial for long-term tension of sphincters.

43. Control of membrane potential by neurotransmitters, hormones, local factors for some smooth muscles (0 2, NO, pH, stretch, vasodilators ….) S 42 Slow waves and pacemaker potentials Often with pacemaker cells Intestinal tract, uterus, small diameter blood vesselsLarge airways of lungs, large arteries, ciliary muscle Comparison of Single-Unit and Multi-Unit Smooth Muscles

44. Intercalated Discs: mechanical attachments of cardiac myofibers to each other, with gap junctions (electrical synapses) to conduct AP Analogy: Falling dominoes S 43 Cardiac Myofibers

45. Plateau phase S 44

46. S 45 Why no tetanic contractions of cardiac muscle?

47. Figure 12.17 Calcium-induced calcium release Ca++ channels blockers: How and where do they work? When are they used? Excitation- Contraction Coupling What ends the twitch? S 46

48. Fig. 09.06 Know this table p. 287 S 47