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Muscle Anatomy and Physiology

Muscle Anatomy and Physiology. The Neuromuscular Junction / Motor Unit. Anatomy: Max=>Min. Muscle, fasciculus, fiber, fibrils, filaments Epimysium, perimysium, endomysium “Bundles within bundles”. Contractile units: SARCOMERES. Thin: actin, troponin, tropomysim Thick : myosin

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Muscle Anatomy and Physiology

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  1. Muscle Anatomy and Physiology The Neuromuscular Junction / Motor Unit

  2. Anatomy: Max=>Min • Muscle, fasciculus, fiber, fibrils, filaments • Epimysium, perimysium, endomysium • “Bundles within bundles”

  3. Contractile units:SARCOMERES • Thin: actin, troponin, tropomysim • Thick: myosin • Z-lines, A-band, I-band, H-Zone

  4. Motor Units • Motor Neuron + Muscle fiber(s) • TERMS: • Twitch: Single contraction & relaxation of a motor unit • Tetanus: Sustained contraction by summing “twitches” • Recruitment: Smooth moves – How many units needed?

  5. How Many Units? • The number of Motor Units recruited for a task depends on: 1. Demand 2. Duration

  6. Excitation - Contraction Coupling • Pre-Synaptic Terminal (Nerve): Acetylcholine released • Post-Synaptic Terminal (Motor Endplate): Ach stimulates by binding =>Muscle fiber depolarization • Contraction!

  7. Excitation: • Resting Membrane Potential: Membranes separate charges: Polarized • Depolarization: Charge reversal across membrane

  8. Action Potential (AP) Depolarization travels along membrane AP travels along sarcolemma=> T-tubules => sarcoplasmic reticulum => Terminal Cisternae => Calcium released

  9. Sarcomeres Shorten HOW????

  10. Sliding Filament Theory • The Action Potential reaches the Terminal Cisternae • Calcium released binds to Troponin • Tropomysin “moves” out of the way • Myosin-Actin Crossbridges formed

  11. Contraction: • All-or-None “Twitch” • Sarcomere units shorten by thin and thick filaments “sliding” past each other

  12. The Physiology of Muscle Contraction and ATP

  13. Take “Five”: Draw and Label The Neuromuscular Junction: Page 158 *What is the chemical Neurotransmitter?

  14. One More Visit to that Neuromuscular Junction: • Acetylcholine released • Binds with Ach-Receptors – linked to Na+ Channels • Na+ influx – DEPOLARIZES Motor endplate • Causing an ACTION POTENTIAL • Etc. Etc. Etc.

  15. What Happens to the Acetylcholine? • Good Question Sherlock: • Homework: • Describe the fate of Acetylcholine • Think diabolically of poisons that could interfere with the normal function of the neuromuscular junction…

  16. Toxins: Neuromuscular Junction • Affecting Production, Release, Binding or degradation of Acetylcholine • Nerve Gas: Inhibit degradation • Black Widow Toxin: Massive release of Acetylcholine • Botulism: Inhibits Acetylcholine Release

  17. Death by Sarin: Acetylcholine accumulates in NMJ • Runny nose, eyes, drooling, sweating, • Difficulty breathing, tight chest • Nausea, vomiting, loss of “control” • Twitching, jerking, staggering • Headache, confusion, coma and convulsions

  18. Something Lighter Please • Check out this cool site for specific exercises! • http://www.exrx.net/Lists/Directory.html

  19. Muscle Energetics

  20. Where Does All That ATP Come From? • Energy for work is supplied by the breakdown of “FUELS” • FUELS: CHO, FAT, (PROT) • Glucose is preferred for intense work • Fats are the “slow burners” and use lots of Oxygen

  21. Energetics of Contraction - Continues • ATP-PC: fast, limited • Anaerobic Glycolysis: Cytosolic breakdown of Glucose without O2 – Forms Lactic Acid • Aerobic Oxidation: slow,but plentiful supply of ATP

  22. All Three Contribute APT at All times… • Supply Rate and Demand Rates • ATP-PC: Fastest Rate – 10 seconds max • Anaerobic Glycolysis: 2-5 minutes max • Aerobic (Oxidative Phosphorylation): Slowest rate, almost endless capacity

  23. The Marathon: • Hours of exercise possible • Uses ATP from aerobic (oxidative) sources • Oxygen Delivery!

  24. The Half-Mile…or: • More Intense • Bursts Lasting 2-5 minutes with rests • Using Anaerobic Glycolysis • Lactic Acid Buildup

  25. The Sprints and Jumps • Less than 10 seconds duration • Very Intense • Creatine Stores in Muscles contribute to CP-ATP production

  26. Creatine Phosphate: • Increase ATP-PC contribution of energy • Used in Maximum intensity-short term work • May extend work effort a few seconds…or repititions • Useless without training…

  27. One Last Crazy “Engebretsen Simulation” • 5 Volunteers to be the “Motor Neuron” • 1 Volunteer to be “Post-Synaptic Membrane” • 6 Sarcolemma-Triad volunteers • 2 Terminal Cisternae volunteers • The rest are sarcolemmas joining hands 

  28. Muscle Fatigue: • More Complicated than you think: • ATP depletion very rare: usually seen with max efforts - cramps • Lactic ACIDOSIS slows all functions • Psychological fatigue…Central perception of exhaustion

  29. II Myosin Fast, Force, Fatigue “White”: Glycogen Anaerobic Bigger I Myosin Slow, Endure “Red”: Myoglobin, mitochondria, Aerobic Smaller Muscle Fiber Types: Fast (II, IIa) vs Slow (I)

  30. We Made It!

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