Neuromuscular Adaptation

1. Neuromuscular Adaptation Muscle Physiology 420:289

2. Agenda • Introduction • Morphological • Neural • Histochemical

3. Introduction • The neuromuscular system readily adapts to various forms of training: • Resistance trainin • Plyometric training • Endurance training • Adaptations vary depending on type of training • Skeletal muscle adapts in many different ways • Morphological • Neural • Histochemical

4. Agenda • Introduction • Morphological • Neural • Histochemical

5. Morphological Adaptations • Morphology: The study of the configuration of structure of animals and plants • Most obvious morphological adaptation is increase in cross-sectional area (CSA) and/or muscle mass • Hypertrophy vs. Hyperplasia

6. Hypertrophy and Myofibrillar Proliferation • Two mechanisms in which protein is accumulated  muscle growth • Increased rate of protein synthesis -Myosin and actin added to periphery of myofibrils • Decreased rate of protein degradation -Proteins constantly being degraded -Contractile protein ½ life = 7-15 days -Regular and rapid overturn  adaptability

7. Hypertrophy and Myofibrillar Proliferation • Mechanism of action: • Myofibrils increase in mass and CSA due to addition of actin/myosin to periphery • Myofibrils reach critical mass where forceful actions tear Z-lines longitudinally • Myofibril splits

8. Figure 8.3 b, Komi, 1996

9. Figure 8.3 a, Komi, 1996

10. Hypertrophy and Myofibrillar Proliferation • Hypertrophy of different fiber types: • Fast twitch: -Mechanism: Mainly increased rate of synthesis -Potential for hypertrophy: High -Stimulation: Forceful/high intensity actions • Slow twitch: -Mechanism: Mainly decreased rate of degradation -Potential of hypertrophy: Low -Stimulation: Low intensity repetitive actions -FT may atropy as ST hypertrophy

11. FT ST FOG Figure 8.5, Komi, 1996

12. Hypertrophy and Myofibrillar Proliferation • Role of satellite cells • History: • First identified in 1961 – Thought to be non-functioning • Adult myoblasts • Believed to be myoblasts that did not fuse into muscle fiber • Called satellite cells due to ability to migrate

13. Brooks, et al., Fig 17.2, 2000

14. Brooks et al., Fig 17.3, 2000

15. Hypetrophy and Myofibrillar Proliferation • Satellite cell activation due to injury: • Dormant satellite cells become activated when homeostasis disrupted • Satellite cells proliferate via mitotic division • Divided cells align themselves along the injured/necrotic muscle fiber • Aligned cells fuse into myotube, mature into new fiber and replace old fiber

16. Figure 5.7, McIntosh et al. 2005

17. Hypertrophy and Myofibrillar Proliferation • Satellite cell activation due to resistance training: • Resistance training causes satellite cell activation as well • Interpretation: -Satellite cells repair injured fibers as a result of eccentric actions -Hyperplasia

18. Hyperplasia • Muscle fiber proliferation during development – 4th week of gestation  several months postnatal • Millions of mononucleated myoblasts (via mitotic division) align themselves • Fusion via respective plasmalellae (Ca2+ mediated) • Myotube is formed • Cell consituents are formed  myofilaments, SR, t-tubules, sarcolemma . . .

19. Evidence of Hyperplasia • Animal studies: • Cats: 9% increase in fiber number after heavy resistance training (Gonyea et al, 1986) • Quail: 52% in latissimus dorsi fiber number after 30 days of weight suspended to wing (Alway et al, 1989)

21. Evidence of Hyperplasia • Human study: MacDougall et al. (1986) • Method of estimation: • Fiber number Fn of total muscle area (CT scan) and fiber diameter (biopsy) • Compared biceps of elite BB, intermediate BB and untrained controls • Results: Range: • 172,000 – 419,000 muscle fibers • Means between groups not significant • Conclusion: • Large variation between individuals • Variation due to genetics

23. Other Morphological Adaptations • Angle of pennation • In general  as degree of pennation increases, so does force production • Why? • More muscle fibers/unit of muscle volume • More cross-bridges • More sarcomeres in parallel

25. Sarcomeres in series  displacement and velocity Sarcomeres in parallel  force Figure 17.20, Brooks et al., 2000

26. Figure 17.22, Brooks et al., 2000 Muscle length (ML) to fiber length (FL) ratio also an indicator of force and velocity properties of muscle

27. Training?

28. Other Morphological Adaptations • Capillary density: • High intensity resistance training: Decrease in capillary density • Endurance training: Increase in capillary density (body building) • Mitochondrial density: • High intensity resistance training: Decrease in mitochondrial density • Endurance training: Increase in mitochondrial density

29. Agenda • Introduction • Morphological • Neural • Histochemical

30. Neural Adaptations • Recall: • Motor unit: Neuron and muscle fibers innervated • Increasing force via recruitment of additional motor units  Number coding

31. Figure 9.6, Komi, 1996

32. Neural Adaptations • Recall: • Increasing force via greater neural discharge frequency  Rate coding • Maximum force of any agonist muscle requires: • Activation of all motor units • Maximal rate coding

33. Neural Adaptations • Timeline

34. Fig 20.8, Brooks et al. 2000

35. Neural Adaptations • Increased activation of agonist motor units: • Untrained subjects are not able to activate all potential motor units • Resistance training may: • Increase ability to recruit highest threshold motor units • Increase rate coding of all motor units

36. Neural Adaptations • Neural facilitation • Facilitation = opposite of inhibition • Enhancement of reflex response to rapid eccentric actions

37. Fig 20.10, Brooks et al., 2000

38. Neural Adaptations • Co-contraction of antagonists • Enhancement of agonist/antagonist control during rapid movements • Joint protection • Evidence: Sprinters greater hamstring EMG during knee extension compared to distance runners

39. http://www.brianmac.demon.co.uk/sprints/sprintseq.htm

40. Neural Adaptations • Neural disinhibition: • Golti tendon organs (GTO): • Location: Tendons • Role: Inhibition of agonist during forceful movements • Examples: • Muscle weakness during rehabilitation • Arm wrestling • 1RM

41. 1. High muscle tension GOLGI TENDON REFLEX 3. GTO activation 4. Inhibition of agonist 2. High tendon tension Figure 4.16, Knutzen & Hamill (2004)

43. Neural Adaptations • Progressive resistance training may inhibit GTO • Anecdotal evidence: • Car accidents • Hypnosis

44. Neural Adaptations • Resistance training vs. plyometric training • Load: • RT: Heavy • PT: Light • Velocity of movement: • RT: Low • PT: High • Stretch shortening cycle (SSC): • RT: Minimal • PT: Yes

46. Agenda • Introduction • Morphological • Neural • Histochemical

47. Histochemical Adaptations • Histochemistry: Identification of tissues via staining techniques • Recall

48. Table 12.8, McIntosh et al., 2005

49. Histochemical Adaptations • Muscle fiber distribution shifts • Generally believed that ST do not change to FT and vice-versa • Several studies have observed IIB  IIA in humans • Fiber shifts from ST to FT and vice-versa have been observed in animals under extreme conditions

50. Histochemical Adaptations • Chronic long term low frequency (10 Hz) stimulation of rabbit tibialis anterior • 3 hours: Swelling of SR • 4 days: Increased size/# of mitochondria, increased oxidative [enzyme], increased capillarization • 14 days: Increased width of Z-line, decreased SERCA activity • 28 days: ST isoforms of myosin and troponin, decreased muscle mass and CSA