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Neural Activation of Skeletal Muscle

Neural Activation of Skeletal Muscle. Review Neuron Anatomy Resting Membrane Potential Action Potential Synapse: Facilitation and Inhibition Neuromuscular Junction Control of muscle fiber properties by the α -motoneuron a. Action potential pattern and quantity

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Neural Activation of Skeletal Muscle

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  1. Neural Activation of Skeletal Muscle • Review • Neuron Anatomy • Resting Membrane Potential • Action Potential • Synapse: Facilitation and Inhibition • Neuromuscular Junction • Control of muscle fiber properties by the α-motoneuron • a. Action potential pattern and quantity • b. Neurotrophic influences

  2. Muscle mechanicsIsometric contractions • Length-tension relationship (Po, Lo) • Lo – optimal length • Sarcomere length that provides for optimal overlap of the thick and thin filaments • Length < Lo – maximal force is production impaired • Length > Lo – tension does not drop appreciably until the length is extended by 10-15% • Po – maximal isometric force Brooks et al.

  3. Muscle mechanicsIsometric contractions Fast Twitch Slow Twitch Force S S S S S S S S S S S S S S S S Time

  4. Dynamic contractions Eccentric • Have to Compromise • Max force = loss in velocity • Max velocity = loss in force Isometric • Po – max isometric tetanic tension. Occurs when force curve crosses the y-axis and velocity becomes zero • ↓force → ↑Velocity • Eccentric force is 50-100% due to more force needed to detach crossbridges • Also causes muscle damage • Power = Load x Velocity • “0” power when there is no load or when load is too heavy to be moved Concentric McMahon, Muscles, Reflexes, and Locomotion, Princeton, 1984

  5. The larger the load, the less shortening S H O R T E N I N G V max No load Small load Medium load Large Load Very Large Load (no velocity) Time (from onset of stimulation)

  6. Muscle mechanics To review, determinants of force/power production by a muscle 1. # of motor units recruited (i.e., the cross-sectional area of the active muscle) - recruitment rule – smaller units first followed by larger 2. frequency of stimulation (i.e., rate coding) 3. length of the fibers relative to Lo 4. velocity (shortening and lengthening) a. myosin ATPase activity b. SR concentration 5. muscle architecture (consider pennation) a. orientation of fibers to the long axis b. the # of sarcomeres in series

  7. Neuron anatomy:axon structure • Cells body • Makes neurotransmitters • Axon - distribution • Myelin Sheath • Nodes of Ranvier • Dendrite McComas, Skeletal Muscle, Human Kinetics, 1996

  8. Neuron anatomy: classification Advantage? Advantage? Vick, Contemporary Medical Physiology, Addison-Wesley, 1984

  9. Generating resting membrane potential (150,000 Na+) Resting ~ -70mv Electrochemical Gradient High  Low Three major factors contribute to the resting membrane potential: 1. Na2+-K+ pump 2. Differential permeability of ions 3. Non-permeable ions (e.g., proteins) Brooks et al. – Fig. 18-2

  10. Na+/K+ Pump Resting Membrane Potential • Maintained primarily by active transport • Pump opens to the cytoplasm where it binds Na+, hydrolyses ATP • Decreased affinity for Na+ binding • uncovered binding sites for K+ • pump cavity closes to cytoplasm, opens to external solution • When K+ ion bind, phosphate dissociates and things return to normal • Each cycle pumps out 3 Na, 2 K in and uses 1 ATP

  11. Neuron anatomy: ion channels – general model McComas, Skeletal Muscle, Human Kinetics, 1996

  12. Neuron anatomy: Na+ channel At least 4 subunits for any Na+ channel to make a passage pore McComas, Skeletal Muscle, Human Kinetics, 1996

  13. Generating the Resting Potential • Gated channels closed, non-gated channels open allowing for diffusion • Diffusion Gradients • K+ normally diffuses out of cell • Na+ normally diffuses into the cell • Na+ K+ pump • to maintain a negative resting membrane potential • pumps 3 Na+ out, 2 K+ in Equilibrium potentials (Veq): Nernst equation For ion X: VeqX = 61.5 log10 [X]o/[X]i For K+: VeqK = 61.5 log10 [K]o/[K]I VeqK = 61.5 log10 [4]o/[135]I = 93.5

  14. Action potential First step is that Na+ channels open allowing Na+ into the cell. The membrane potential to become positive. A positive membrane potential opens voltage gated K+ channels allowing the K+ to flow out of the cell. Next the Na+ channels close, K+ channels are still open it allows the outflow of positive charge. When the membrane potential begins reaching its resting state the K+ channels close. The Na+ /K+ pump return cell to Resting Membrane Potential 3 4 Hyperpolarization Why under resting? Lost chemogradient Have electrogradient 5

  15. Action Potential • Resting membrane potential - permeability for K+ is 25x> Na+ so membrane potential is near equilibrium potential of K+ (-92mV) • Action potential - 20x more Na+ channels open (inward) than K+ channels (outward) so the membrane potential changes in a positive direction

  16. Action potential: saltatory conduction

  17. Rate Coding • Frequency Coding of Stimulus Intensity • The greater the generator potential, the greater the number of action potentials produced per unit time (i.e., the higher the frequency)

  18. Refractory Periods • Absolute Refractory Periods • time at which a 2nd depolarization cannot occur regardless of the stimulus strength • Na+ channels inactive and cannot respond • Membrane is not repolarized • Relative Refractory Periods • a greater than normal stimulus can create an action potential • Na+ inactivation gates must have returned to normal (open position) and K+ channels (non-gated & gated)

  19. The Role of Refractory Periods • Prevent ‘backfiring” • wave of depolarization spreads in all directions but cannot depolarize an area from which the stimulus is coming - otherwise there would be a continuous cycle of depolarization • Sensory Coding • frequency of action potentials from the sensory neuron to the CNS • the greater the stimulus, the earlier in the relative refractory period will be the next action potential

  20. Synapses: facilitation and inhibition Transmission at synapses involves release of a chemical neurotransmitter from the pre-synaptic terminal and binding to receptors on the post-synaptic neuron Brooks et al.

  21. Neuromuscular Junction Brooks et al.

  22. Neuromuscular junction * Animation

  23. Control of muscle fiber properties by the α-motoneurona. Action potential pattern and/or quantity b. Neurotrophic influences (substances released from the α-motoneuron that influence gene expression in the muscle fiber)

  24. Control of muscle fiber properties by the α-motoneuron: evidence for the control Cross-innervation Has the potential for complete myosin ATPase remodeling Adapt to match motor unit Fast Slow McComas, Skeletal Muscle, Human Kinetics, 1996

  25. Control of muscle fiber properties by the α-motoneuron: evidence for the control Chronic low electrical stimulation Created slow fiber type McComas, Skeletal Muscle, Human Kinetics, 1996

  26. Control of muscle fiber properties by the α-motoneuron: evidence for the control Chronic electrical stimulation - soleus Many pulses Low Hz few pulses High Hz Many pulses High Hz McComas, Skeletal Muscle, Human Kinetics, 1996

  27. Control of muscle fiber properties by the α-motoneuron: integrated model McComas, Skeletal Muscle, Human Kinetics, 1996

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