Understanding Muscle Contraction and Neural Control: A Comprehensive Overview

1. Note: there are slides before these that we will take up.

2. Neuron Membrane Potential Muscle Membrane Potential Muscle Tension 1 2 3 4 5 6 7 8 9 10 96 97 98 99 100

3. Types of Muscle Contraction Concentric Isometric Eccentric

4. Types of Muscle Contraction Force (g) 1.6 1.4 1.2 1.0 0.8 0.6 0.4 0.2 Maximal Isometric tension 0.8 0.6 0.4 0.2 0 0.2 0.4 0.6 0.8 Shortening(m/s) Concentric Lengthening (m/s) Eccentric Velocity

5. Functional Classification of Muscles • Agonists:prime movers; responsible for the movement • Antagonists:oppose the agonists to prevent overstretching of them • Synergists:assist the agonists and sometimes fine-tune the direction of movement

6. Functional Classification of Muscles In the control of muscular contraction, muscles rarely function in isolation

7. Control of Muscular Contraction • How is this all coordinated??? • How much force? • How fast? • Which muscles? • The answer relies on use of specific: • Motor Units • Fibre Types • Feedback Loops

8. Muscle Fibre Types • 2 main categories: • Type I (Slow Twitch, Slow Oxidative, SO) • Type II (Fast Twitch) • More than one type of fast twitch fibre • Classified based on contractile speed and metabolic properties Type IIa(Fast Oxidative/Glycolytic, FOG, Fatigue Resistant) – slowest contractile speed of fast twitch fibres Type IId/x or IIb (Fast Glycolytic, FG, Fatigueable) – fastest contractile speed of fast twitch fibres (note: little Type IIbfound in humans)

9. Fibre Type Characteristics

10. Fibre Types Characteristics Type IIx/d 50 40 30 20 10 0 Tension Type IIa Type I 50 100 150 200 Time (msec) stimulus

11. Motor Units • Recall: All fibres of a motor unit are of the same type • It appears that the motor neuron determines fibre type • ST motor units are smaller (i.e. less fibres), therefore generate less force than FT motor units • Different muscles have different fibre compositions probably related to function

12. % ST Fibres Fibre Types Differ within Muscles For example: % ST in different muscles reflects function

13. Motor Units • Recall: different muscles have different fibre compositions probably related to function • Typically, successful athletes have fibre type profiles that may vary with event

15. $ 1,000,000 Question??? • It appears that the proportion of various fibre types can influence an athlete’s success, which begs the question…. … Is this a function of training or genetics???

16. % of Slow Twitch Fibres in Sets of Twins TWIN A 80 60 40 20 0 identical fraternal TWIN B 0 20 40 60 80

17. Training/Detraining Muscle

18. Resistance Training and Gains in Muscular Fitness • Muscle is very plastic (adaptable), increasing in size and strength with training and decreasing with immobilization • Strength is a function of muscle size. • Remember, more cross-bridges = more force.

19. Neural Control of Strength Gains All increases in strength possess some neural mechanisms: 1. Recruitment of motor units • Increased number of motor units recruited from increased neural drive • Synchronicity of motor unit recruitment is improved

20. Motor Unit Recruitment • Motor units are recruited in order of smallest to largest motor neuron – “Hennman’s Size Principle” • Slow twitch motor units, with smaller motor neurons, are recruited first in graded contractions • Fast twitch motor units are recruited as the force required increases

21. Neural Control of Strength Gains All increases in strength possess some neural mechanisms: 1. Recruitment of motor units • Increased number of motor units recruited from increased neural drive • Synchronicity of motor unit recruitment is improved 2. Increased frequency of discharge from the a-motor neuron

22. Wave Summation

23. Neural Control of Strength Gains All increases in strength possess some neural mechanisms: 1. Recruitment of motor units • Increased number of motor units recruited from increased neural drive • Synchronicity of motor unit recruitment is improved 2. Increased frequency of discharge from the a-motor neuron 3. Decrease in autogenic inhibition 4. Reduction in the coactivation of agonist and antagonist muscles 5. Morphological changes in the neuromuscular junction

24. Neuromuscular Junction (NMJ) Fig 3.5

25. Long-term strength increases are largely the result of muscle fiber hypertrophy Muscle Hypertrophy Transient hypertrophy is the increase in muscle size that develops during and immediately following a single exercise bout Fluid accumulation in the interstitial and intracellular space from the blood plasma H H H H H H H H H H H H H H O O O O O O O

26. Long-term strength increases are largely the result of muscle fiber hypertrophy Muscle Hypertrophy Transient hypertrophy is the increase in muscle size that develops during and immediately following a single exercise bout Fluid accumulation in the interstitial and intracellular space from the blood plasma Chronic hypertrophy is the increase in muscle size after long-term resistance training Increased size: (Fiber Hypertrophy) Increased # muscle fibers (Fiber Hyperplasia)

27. Microscopic Views of Muscle Cross Sections Before and After Training Photos courtesy of Dr. Michael Deschene's laboratory.

28. Myonuclear Domains • Theory of myonuclear domains: • Each myonuclei supports a finite area of the muscle cell. In order for hypertrophy to occur, you need more nuclei!! • Where might they come from?

29. Fiber Hyperplasia • Muscle fibers can split in half with intense weight training (cat research) • Each half then increases to the size of the parent fiber • Conflicting study results may be due to differences in the training load or mode • Satellite cells may also be involved in the generation of new skeletal muscle fibers • Hyperplasia has been clearly shown to occur in animal models; only a few studies suggest this occurs in humans too

30. Muscle Atrophy and Decreased Strength Atrophy = decrease in size Immobilization, Disuse, Neural Disorders • Decreased rate of protein synthesis • Decreased strength • Decreased cross-sectional area • Decreased neuromuscular activity • Affects both type I and type II fibers, with a greater effect in type I fibers. WHY? • Muscles can recover when activity is resumed

31. Muscle Atrophy and Decreased Strength Cessation of Training • Decreased strength • Little change in fiber cross-sectional area (but … type II fiber areas tend to decrease) • Maintenance training is important to prevent strength losses

32. Muscle Soreness and Recovery

33. Muscle Soreness Acute Muscle Soreness • Felt during the later stages and immediately after exercise • Can result from accumulations of exercise end-products such as increase H+ and edema (fluid build up in the muscle)

34. Muscle Soreness Delayed-Onset Muscle Soreness (DOMS) • Felt in the days following heavy or unaccustomed exercise • Eccentric muscle action is the primary initiator of DOMS – not directly related to lactic acid (lactate)

35. DOMS • It is possible that the damage leading to DOMS is caused by excessive amounts of Ca2+ in the muscle cell – enters through tears in the sarcolemma • Ca2+ can activate proteases (e.g. Calpain) which can digest structural proteins • Ca2+ can also activate phosolipase which can lead to further damage of the lipid membrane

36. DOMS and Performance Loss in strength can be associated with: 1. Physical disruption • Z-line streaming, focal damage 2. Failure in ECC • Tears in sarcolemma. can hinder nerve impulse conduction • Triad disruption. 3. Loss of contractile proteins • Actin and myosin, as well as structural proteins

37. DOMS post-strenuous exercise pre-exercise • Muscle sample taken immediately after a marathon • Shows cell membrane (sarcolemma) disruption

38. DOMS post-strenuous exercise pre-exercise • Muscle sample taken immediately after a marathon • Shows Z-line streaming

39. DOMS and Performance • Force-generating capacity of injured muscles is decreased • Strength loss may persist for days or weeks

40. Recovery and Protection from DOMS • Once muscle damage and soreness has occurred, the muscle adapts such that it is protected against subsequent soreness • This adaptation can last 3-4 weeks, with some reporting as long as 6 months • This adaptation is associated with smaller losses in strength and decreased blood CK following exercise of the same intensity as the original damaging bout

41. Inflammation and Repair • Neutrophils (a type of white blood cell, WBC) enter the injured area and help to clean up the site of damage these release cytokines • By 10-15 days many fibres have become necrotic (dying) and mononucleated inflammatory cells become prominent • After 2-3 weeks, much of the damage has been repaired by regeneration of fibre segments – this involves satellite cells

42. Inflammation and Repair Control 1 Day 4 Days 3 Days 7 Days 14 Days

43. Inflammation and Repair

44. The Satellite Cell Responseto Muscle Injury Reprinted, by permission, from T.J. Hawke and D.J. Garry, 2001, “Myogenic satellite cells: Physiology to molecular biology,” Journal of Applied Physiology 91: 534-551.

45. Inflammation and Repair • Upon activation, satellite cells migrate to the necrotic area and differentiate into myoblasts • Similar to embryonic development, these myoblasts form myotubes (precursors to muscle cell formation) • As the myotubes extend, they reach the intact “stumps” of the damaged fibres and the fibres become continuous • The entire inflammation and repair process can take 30 days!