iphy 3430 11 01 11 muscle system n.
Skip this Video
Loading SlideShow in 5 Seconds..
IPHY 3430 11-01-11 MUSCLE SYSTEM PowerPoint Presentation
Download Presentation
IPHY 3430 11-01-11 MUSCLE SYSTEM

Loading in 2 Seconds...

play fullscreen
1 / 17

IPHY 3430 11-01-11 MUSCLE SYSTEM - PowerPoint PPT Presentation

  • Uploaded on

IPHY 3430 11-01-11 MUSCLE SYSTEM. MUSCLE SYSTEM 1. contributes to homeostasis by moving materials from one place to another (blood, food, urine, fetus) 2. contributes to energetics by using ATP for muscle contraction.

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

IPHY 3430 11-01-11 MUSCLE SYSTEM

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript

MUSCLE SYSTEM 1. contributes to homeostasis by moving materials from one place to another (blood, food, urine, fetus)2. contributes toenergetics by using ATP for muscle contraction.

TypesStriated--Skeletal and Cardiac muscleUnstriated--Smooth muscleOther organs involved: brain, motor neurons

Excitation-Contraction Coupling1. Action potential from brain causes release of acetylcholine at neural muscular junction2. ACH binds to receptor on muscle membrane, causing increased permeability of muscle membrane to Na+3. Increased permeability to Na+ causes action potential to occur in muscle membrane4. Action potential spreads over entire surface of muscle membrane, down into t-tubules 


5. Action potential in t-tubules causes Ca++ to be released from vesicles on sarcoplasmic reticulum6. Ca++ binds to troponin, causing tropomyosin to slide off active sites on actin cross-bridge binding sites7. Exposed actin sites bind to myosin cross bridges, which were previously energized by breaking ATP by myosin ATPase8. Binding of actin and myosin causes cross bridge to bend, causing actin to slide inward.


9. ADP and Pi released from cross bridge10. New ATP molecule attaches to myosin ATPase breaking bond between actin and cross bridge , so cross bridge returns to original conformation11. ATP split which energizes cross bridge12. Cross bridge binds to new actin site and slides actin even further inward13. Continued action brings actin over myosin, resulting in muscle contraction


Muscle relaxation1. Brain ceases action potential down motor neuron2. No more ACH is released3. No more binding of ACH on muscle receptor causes no more action potentials4. With no more action potentials, Ca++ is actively transported back into vesicles 5. As Ca++ drops in cytoplasm, Ca++ bound to troponin falls off, and tropomyosin rolls back over actin sites6. Actin slides back into original position


Problems at neuromuscular junction:1. Nerve gas inhibits ACH esterase2. Curare binds to ACH site3. Myasthenia gravis--ACH receptor destroyed by immune system4. Botulism--blocks release of ACH5. Hypothermia--blocks release of ACH


How force of contraction is varied in muscleTemporal summation



Frequency of action potential


Spatial summation


# of motor units recruited