1. Muscle Physiology

2. Muscle Tissues differ in structure, but share common function Figure 12-1: Three types of muscles What do all muscle tissues have in common in terms of their structure and function? pg. 407

3. Smooth muscle cells may function independently, or as a unit p. 433 See also p. 392 What is moving between cells, indicated by the arrows?

4. Smooth muscle is effective at decreasing the diameter of the lumen in a hollow organ p. 435 Ca +2 binds to calmodulin in the cytosol (not thin filaments). This activates a kinase associated with the myosin filaments, and then myosin ATPase. Note the globular heads along the entire length of the thick filament.

5. Muscle cells and connective tissue arranged to produce movement at a joint Figure 12-3a-1: ANATOMY SUMMARY: Skeletal Muscle pg. 410 What changes (in structure and function) would occur in this muscle with anaerobic training? Can you explain why? See also the concept map on pg. 400

6. The architecture of skeletal muscle fibers is complex because of their size Figure 12-3b: ANATOMY SUMMARY: Skeletal Muscle Pg. 411

7. Communication (using stored Ca +2 ) requires a complex membrane system Pg. 412 Figure 12-4: T-tubules and the sarcoplasmic reticulum Why is this important?

8. Myofibrils: Site of Contraction Figure 12-3c-f: ANATOMY SUMMARY: Skeletal Muscle What are the functions of Troponin and Tropomyosin? Pg. 414 What/where is myosin ATPase?

9. The Functional Unit of Contraction: the Sarcomere Figure 12-5: The two- and three-dimensional organization of a sarcomere A single power stroke of myosin cross bridges shortens the muscle cell by only @ 1%. Why isn’t muscle contraction “jerky”? Muscles may shorten up to @ 70% of their resting length! Pg. 413

10. The interaction of voltage and mechanical events allows myofilaments to interact Figure 12-11a: Excitation-contraction coupling Is the DHP receptor sensitive to voltage, mechanical change, or a ligand? p. 418

11. Troponin pulls Tropomyosin away from binding sites when Ca +2 is present Figure 12-11b: Excitation-contraction coupling These figures are also included in your packet, on page 113.

12. ATP must be present on myosin, before myosin can bind to actin Figure 12-9 (steps 1 & 2): The molecular basis of contraction Pg. 416 This stage is very short-lived. In other words, a molecule of ATP must bind to the myosin head in order for it to be “locked and loaded”; ready to interact with actin. See also pp. 111-112 in your packet. 1 2

13. Myosin uses an ATPase to split ATP, but hangs onto ADP and P i for a short time Figure 12-9 (steps 3 & 4): The molecular basis of contraction Hydrolysis of ATP results in the binding of the myosin head to the actin filament, but no movement has occurred yet. Of all the energy consumed during muscle contraction, only @ 25% is realized as external work (i.e. 75% is lost as heat!). 4

14. Release of P i causes a conformational change in the myosin head, now attached to actin Figure 12-9 (steps 5 & 6): The molecular basis of contraction The release of the phosphate group causes a conformational change in myosin, pulling the actin toward the center of the sarcomere. Almost done… What is the role of the Na-K pump? Actin A single power stroke of myosin cross bridges shortens the muscle cell by only @ 1%. Why isn’t muscle contraction “jerky”? Muscles may shorten up to @ 70% of their resting length! 6 5

15. Myosin releases ADP, but is still bound to actin until a new ATP arrives… 7 8 What happens if there is no ATP available?

16. Troponin & Tropomyosin A Troponin test is often ordered to determine the severity of heart muscle damage following a cardiac event, such as MI. Explain how this may be helpful. p. 415

17. Timing of Electrical & Mechanical Events What ions are moving (and through what kind of ion channel) during the depolarizing phase of the motor neuron? How quickly does contraction begin after the sarcolemma depolarizes? p. 419 Myogram of Single Muscle Twitch

18. ATP can be produced via 3 methods Aerobic Respiration Oxygen Glucose Fatty acids 30-32 ATPs Anaerobic Respiration Fast = power (…but) 2 ATP/glucose Phosphocreatine (CrP)  ATP What is oxygen debt? How does a cell repay its oxygen debt? Pg. 420

19. ATP can be produced rapidly by the action of Creatine Kinase Figure 12-13: Phosphocreatine This process is referred to as the “phosphagen system”. Explain why. What does a “kinase” do? How does it apply in this case? Pg. 420

20. Cellular Energy Stores in Human Muscle R.W. McGilvery, Biochemistry, a Functional Approach, W. B. Saunders, Philadelphia 1970 How is it possible that you get more power (ATP/time) with fermentation, when a cell produces only 2 ATP per molecule of glucose by this metabolic pathway? Why aren’t proteins/amino acids listed?

21. The Cori Cycle Muscle cell (or RBC) 2 Pyruvate Where do these reactions take place in the cell? What is this process called? How long do you think this cycle could be maintained? Explain why. Is this method of ATP production more or less efficient than aerobic respiration? The Cori Cycle may take place in a limited way inside muscle cells, to delay acidosis.

22. Substrate usage as a function of exercise duration Explain the differences in muscle vs. plasma sources of substrates. Could there be hormones involved?

23. Substrate usage as a function of exercise duration Plasma fatty acids Plasma glucose

24. Relationship between Oxygen Consumption and Work O 2 consumption increases 23X! Explain the changes (or lack there of) in these organs.

25. Overview: Muscle Cell Metabolism p. 815 Identify the phosphogen system… anaerobic energy production…aerobic energy production. Which substrates can be used in each? Identify the Cori cycle, and explain

26. CONTROLLING SKELETAL MUSCLES

27. The “final common pathway” in voluntary muscle movement receives 3 kinds of info. Describe the three “levels” of direct control over motor neurons that innervate skeletal muscles: 1.Spinal reflexes 2.Cortical (pyramidal) pathways 3.Subcortical (extrapyramidal pathways) Relate this information to the GPSP at these motor neurons. a.k.a. “pyramidal pathway” p. 461

28. Muscle Proprioceptors See also pg. 114 in your packet

29. Proprioceptors detect change in length and tension Figure 13-3: Sensory receptors in muscle What part of the CNS do these receptors send information to, regarding position or a change in position? Pg. 450

30. Tonic Activity of the Muscle Spindle (producing muscle tone in a muscle at rest) p. 452 The sensitivity of the muscle spindle depends on…? List some other inputs to the alpha motor neuron.

31. Muscle Spindle sends more frequent APs in the Stretch Reflex Does this reflex change the length of the muscle? Explain. Do these receptors adapt? Pg. 452

32. Co-activation of Alpha and Gamma Motor Neurons What would happen to the firing rate of the primary afferent neuron if the gamma motor neuron was not functioning? p. 453

33. Coactivation of pyramidal and extrapyramidal tracts maintains sensitivity

34. Golgi Tendon Reflex prevents injury Pg. 454 What neurotransmitter is released by the interneuron, and how does it inhibit the alpha motor neuron?

35. Summary: Integration of Muscle Reflexes