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

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?

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

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

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

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

Sarcomeres Shorten HOW????

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

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

The Physiology of Muscle Contraction and ATP

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

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.

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…

Toxins: 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

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

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Muscle Energetics

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

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

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

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

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

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

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…

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

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

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

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