1. Resistance exercise and microgravity are conditions that produce changes in skeletal muscles

2. Functions of musculoskeletal system Provide the basic form and shape of organism Mechanical function of support Means of protection for vulnerable organs Allows body movement Provides a set of levers Heat production

3. Homeostatic functions of skeletal system Maintain a constant state- invloves behavioral responses to environmental changes Erythrocytes and other formed elements of the blood produced in bone marrow Stores minerals – calcium and phosphorus

4. Characteristics of muscle fibers Irritability Contractibility Extensibility Elasticity

5. Figure 19.1 The power a muscle is capable of generating reflects its functional capabilities

6. Figure 19.2 Quadriceps muscles of the anterior thigh

7. Figure 19.3 A needle biopsy is used to obtain samples of muscle tissue

8. Structural; basis of contraction Fascia Connective tissue components Nerve and blood supply Components of a skeletal muscle fiber

9. Figure 19.8 Major muscles of the lower leg

10. Structure of Skeletal Muscle (continued)

11. (coninued)

12. Mechanisms of Contraction Each myofibril contains myofilaments. –Thick filaments: A bands contain thick filaments (primarily composed of myosin). –Thin filaments: I bands contain thin filaments (primarily composed of actin). –Center of each I band is Z disc.

13. Sliding Filament Theory of Contraction (continued)

14. Excitation-Contraction Coupling (continued) Ca 2+ attaches to troponin. Tropomyosin- troponin complex configuration change occurs. Cross bridges attach to actin.

15. Mechanisms of Contraction (continued) Sarcomere: –Z disc to Z disc. –M lines: Produced by protein filaments in a sarcomere. –Anchor myosin during contraction. Titin: –Elastic protein that runs through the myosin from M line to Z disc. Contributes to elastic recoil of muscle.

16. Mechanisms of contraction- sliding filament theory A band – thick filaments I band – thin filaments Myosin cross-bridges extend out from the thick filaments to the thin filaments Activity of c-b Sequence of events in stimulation and contraction of muscle

17. Sliding Filament Theory of Contraction (continued) Muscle contracts: –Occurs because of sliding of thin filaments over and between thick filaments towards center. Shortening the distance from Z disc to Z disc. A bands: –Contain actin. Move closer together. –Do not shorten. I bands: –Distance between A bands of successive sarcomeres. –Decrease in length. H bands shorten. –Contain only myosin. –Shorten during contraction.

18. Contraction Myosin binding site splits ATP to ADP and P i. ADP and P i remain bound to myosin until myosin heads attach to actin. P i is released, causing the power stroke to occur. Power stroke pulls actin toward the center of the A band. ADP is released, when myosin binds to a fresh ATP at the end of the power stroke.

19. Contraction (continued) Release of ADP upon binding to another ATP, causes the cross bridge bond to break. Cross bridges detach, ready to bind again. Synchronous action: –Only 50% of the cross bridges are attached at any given time.

20. Contraction (continued)

21. Role of Ca 2+ in Muscle Contraction Muscle Relaxation: –[Ca 2+ ] in sarcoplasm low when tropomyosin blocks attachment. Prevents muscle contraction. Ca 2+ is pumped back into the SR in the terminal cisternae. –Muscle relaxes.

22. Muscle in vivo Twitch Summation Tetanus Fatigue

23. Muscle Response to Varying Stimuli More rapidly delivered stimuli result in incomplete tetanus If stimuli are given quickly enough, complete tetanus results Figure 9.15

24. Muscle Twitch Comparisons Figure 9.14b

25. Treppe: The Staircase Effect Figure 9.18

26. Twitch, Summation, and Tetanus (continued)

27. Motor unit Motor end plate Excitation –contraction coupling Synaptic cleft Neuromuscular junction Motor unit recruitment

28. Motor Unit When somatic neuron is activated, all the muscle fibers it innervates contract with all or none contractions. Innervation ratio: –Ratio of motor neuron: muscle fibers. Fine neural control over the strength occurs when many small motor units are involved. Recruitment: –Larger and larger motor units are activated to produce greater strength.

29. Motor Unit (continued) Each somatic neuron together with all the muscle fibers it innervates. Each muscle fiber receives a single axon terminal from a somatic neuron. Each axon can have collateral branches to innervate an equal # of fibers.

30. Neuromuscular Junction Figure 9.7 (a-c)

31. Synaptic vesicles containing neurotransmitter molecules Axon of presynaptic neuron Synaptic cleft Ion channel (closed) Ion channel (open) Axon terminal of presynaptic neuron Postsynaptic membrane Mitochondrion Ion channel closed Ion channel open Neurotransmitter Receptor Postsynaptic membrane Degraded neurotransmitter Na + Ca 2+ 1 2 3 4 5 Action potential Figure 11.18 Synaptic Cleft: Information Transfer

32. Excitation-Contraction Coupling Na + diffusion produces end-plate potential (depolarization). + ions are attracted to negative plasma membrane. If depolarization sufficient, threshold occurs, producing APs.

33. Figure 9.10 ADP PiPi Net entry of Na + Initiates an action potential which is propagated along the sarcolemma and down the T tubules. T tubule Sarcolemma SR tubules (cut) Synaptic cleft Synaptic vesicle Axon terminal ACh Neurotransmitter released diffuses across the synaptic cleft and attaches to ACh receptors on the sarcolemma. Action potential in T tubule activates voltage-sensitive receptors, which in turn trigger Ca 2+ release from terminal cisternae of SR into cytosol. Calcium ions bind to troponin; troponin changes shape, removing the blocking action of tropomyosin; actin active sites exposed. Contraction; myosin heads alternately attach to actin and detach, pulling the actin filaments toward the center of the sarcomere; release of energy by ATP hydrolysis powers the cycling process. Removal of Ca 2+ by active transport into the SR after the action potential ends. SR Tropomyosin blockage restored, blocking myosin binding sites on actin; contraction ends and muscle fiber relaxes. Ca 2+ 1 2 3 4 5 6

34. Muscle Metabolism: Energy for Contraction Figure 9.20

35. Metabolism of Skeletal Muscles Metabolism of skeletal muscle Lactate threshold: –% of max. 0 2 uptake at which there is a significant rise in blood [lactate]. Healthy individual, significant blood [lactate] appears at 50– 70% V 02 max. During light exercise: –Most energy is derived from aerobic respiration of fatty acids. During moderate exercise: –Energy is derived equally from fatty acids and glucose. During heavy exercise: –Glucose supplies 2/3 of the energy for muscles. Liver increases glycogenolysis. During exercise, the GLUT-4 carrier protein is moved to the muscle cell’s plasma membrane.

36. Metabolism of Skeletal Muscles (continued) Oxygen debt: –Oxygen that was withdrawn from hemoglobin and myoglobin during exercise. –Extra 0 2 required for metabolism tissue warmed during exercise. –0 2 needed for metabolism of lactic acid produced during anaerobic respiration. When person stops exercising, rate of oxygen uptake does not immediately return to pre- exercise levels. –Returns slowly.

37. Metabolism of Skeletal Muscles (continued) Phosphocreatine (creatine phosphate): –Rapid source of renewal of ATP. –ADP combines with creatine phosphate. [Phosphocreatine] is 3 times [ATP]. –Ready source of high-energy phosphate.

38. Muscle Fatigue Any exercise induced reduction in the ability to maintain muscle to generate force or power. –Sustained muscle contraction fatigue is due to an accumulation of ECF K +. Repolarization phase of AP. During moderate exercise fatigue occurs when slow- twitch fibers deplete their glycogen reserve. Fast twitch fibers are recruited, converting glucose to lactic acid. –Interferes with Ca 2+ transport. Central fatigue: –Muscle fatigue caused by changes in CNS rather than fatigue of muscles themselves.

39. Muscle Tone Muscle tone: –Is the constant, slightly contracted state of all muscles, which does not produce active movements –Keeps the muscles firm, healthy, and ready to respond to stimulus Spinal reflexes account for muscle tone by: –Activating one motor unit and then another –Responding to activation of stretch receptors in muscles and tendons

40. Isotonic Contractions In isotonic contractions, the muscle changes in length (decreasing the angle of the joint) and moves the load The two types of isotonic contractions are concentric and eccentric –Concentric contractions – the muscle shortens and does work –Eccentric contractions – the muscle contracts as it lengthens

41. Isotonic, Isometric, and Eccentric Contractions In order for a muscle fiber to shorten, they must generate a force greater than the opposing forces that act to prevent movement of that muscle insertion. Isotonic contractions: –Force of contraction remains constant throughout the shortening process. Velocity of muscle shortening decreases as load increases. Isometric contractions: –Length of muscle fibers remain constant, if the number of muscle fibers activated is too few to shorten the muscle. Velocity of shortening is 0.

42. Isotonic Contractions Figure 9.19a

43. Isometric Contractions Tension increases to the muscle’s capacity, but the muscle neither shortens nor lengthens Occurs if the load is greater than the tension the muscle is able to develop

44. Isometric Contractions Figure 9.19b

45. Muscle Metabolism: Energy for Contraction ATP is the only source used directly for contractile activity As soon as available stores of ATP are hydrolyzed (4-6 seconds), they are regenerated by: –The interaction of ADP with creatine phosphate (CP) –Anaerobic glycolysis –Aerobic respiration PLAY InterActive Physiology ®: Muscle Metabolism, pages 3-15

46. Isotonic, Isometric, and Eccentric Contractions (continued) Force-velocity curve: –Inverse relationship between force opposing muscle contraction and velocity of muscle shortening. Eccentric contractions: –Force exerted on a muscle to stretch, it is greater than the force of muscle contraction. Muscle will lengthen as it contracts.

47. Slow- and Fast-Twitch Fibers –Skeletal muscle fibers can be divided on basis of contraction speed: Slow-twitch (type I fibers). Fast-twitch (type II fibers). Differences due to different myosin ATPase isoenzymes that are slow or fast.

48. Slow- and Fast-Twitch Fibers (continued) Slow-twitch (type I fibers): –Red fibers. –High oxidative capacity for aerobic respiration. –Resistant to fatigue. –Have rich capillary supply. –Numerous mitochondria and aerobic enzymes. –High [myoglobin]. Soleus muscle in the leg.

49. Slow- and Fast-Twitch Fibers (continued) Fast-twitch (type IIX fibers): –White fibers. –Adapted to respire anaerobically. –Have large stores of glycogen. –Have few capillaries. –Have few mitochondria. Extraocular muscles that position the eye. Intermediate (type II A) fibers: –Great aerobic ability. –Resistant to fatigue. People vary genetically in proportion of fast- and slow-twitch fibers in their muscles.

50. Characteristics of Muscle Fiber Types

51. Figure 19.10 Record speeds achieved by athletes decrease with age

52. Figure 19.11 Remodeling of motor units with aging

53. Figure 19.12 Dystrophin connects F-actin of the cytoskeleton to the sarcolemma

54. Figure 19.13 Costameres

58. Figure 19.4 VEGF responses to a single bout of endurance exercise

59. Figure 19.5 Endurance training increases the number of mitochondria

60. Figure 19.6 Changes in fast fiber types during training and detraining

61. Figure 19.7 Stretch or stretch combined with electrical stimulation increased protein synthesis

62. Effects of endurance training –Improve ability to obtain ATP from oxidative phosphorylation –Increase size and # of mitochondria –Less lactic acid produced per given amount of exercise –Increase myoglobin count –Increase intramuscular triglyceride content –Increase lipoprotein lipase –Increase proportion of energy derived from fat –Lower rate of glycogen depletion during exercise –Improve efficiency in extracting O2 from blood