Your SlideShare is downloading. ×
muscles
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×
Saving this for later? Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime – even offline.
Text the download link to your phone
Standard text messaging rates apply

muscles

627
views

Published on

qwer

qwer

Published in: Technology, Business

0 Comments
0 Likes
Statistics
Notes
  • Be the first to comment

  • Be the first to like this

No Downloads
Views
Total Views
627
On Slideshare
0
From Embeds
0
Number of Embeds
0
Actions
Shares
0
Downloads
7
Comments
0
Likes
0
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide

Transcript

  • 1. Ch 12 can be done in one lecture
  • 2. Chapter 12: MusclesReview muscle anatomy (esp. microanatomyof skeletal muscle) Developed by John Gallagher, MS, DVM
  • 3. Terminology: sarcolemma t-tubules sarcoplasmic reticulum myofibers, myofibrils, myofilaments sarcomere
  • 4. More Terminology: Tension Contraction Load Excitation-contraction coupling Rigor Relaxation
  • 5. Anatomy Fig 12-3
  • 6. More Anatomy Fig 12-3
  • 7. Myofibrils = Contractile Organelles of Myofiber Contain 6 types of protein: Actin Contractile Myosin Tropomyosin Regulatory Troponin Titin Accessory Nebulin Fig 12-3 c-f
  • 8. Fig 12-3
  • 9. Titin and Nebulin Titin: biggest protein known (25,000 aa); elastic! » Stabilizes position of contractile filaments » Return to relaxed location Nebulin: inelastic giant protein » Alignment of A & M Fig 12-6
  • 10. Sliding Filament Theory p 403 Sarcomere = unit of contraction Myosin “walks down” an actin fiber towards Z- line » ? - band shortens » ? - band does not shorten Myosin = motor protein: chemical energy  mechanical energy of motion
  • 11. The Molecular Basis of Contraction Rigor State Compare to Fig 12-9 myosin affinity changes due to ATP binding ATP ADP + Pi Tight binding between ATP bindsG-actin and myosin  dissociation No nucleotide bound
  • 12. Released energy changes angle between head & long axis of myosinMyosin head acts as RelaxedATPase Rotation and weak muscle state binding to new G-actin when sufficient ATP
  • 13. Power stroke begins ADP released as Pi released Tight binding to actinMyosin crossbridge movement pushes actin
  • 14. Regulation of Contraction by Troponin and Tropomyosin Tropomyosin blocks myosin binding site (weak binding possible but no powerstroke) Troponin controls position of tropomyosin and has Ca2+ binding site  Ca2+ present: binding of A & M Fig 12-10  Ca2+ absent: relaxation
  • 15. Rigor mortis Joint stiffness and muscular rigidity of dead body Begins 2 – 4 h post mortem. Can last up to 4 days depending on temperature and other conditions Caused by leakage of Ca2+ ions into cell and ATP depletion Maximum stiffness  12-24 h post mortem, then?
  • 16. Initiation of Contraction Excitation-Contraction Coupling explains how you get from AP in axon to contraction in sarcomereACh released from somatic motor neuron at the Motor End Plate AP in sarcolemma and T-Tubules Ca2+ release from sarcoplasmic reticulum Ca2+ binds to troponin
  • 17. Details of E/C Coupling Nicotinic cholinergic receptors on motor end plate = Na+ /K+ channels Net Na entry creates EPSP + AP to T-tubules DHP (dihydropyridine) receptors in T- tubules sense depolarization Fig 12-11
  • 18. Excitation- Contraction CouplingFig 12-11 a
  • 19. DHP (dihydropyridine) receptors open Ca2+ channels in t-tubulesIntracytosolic [Ca2+] ContractionCa2+ re-uptake into SRRelaxation Fig 12-11 b
  • 20. Muscle Contraction Needs Steady Supply of ATP  Where / when is ATP needed?  Only enough ATP stored for 8 twitches » Phosphocreatine may substitute for ATP Twitch = single contraction relaxation cycle
  • 21. Where does all this ATP come from? Phosphocreatine: backup energy source C(P)Kphosphocreatine + ADP creatine + ATP CHO: aerobic and anaerobic resp. Fatty acid breakdown always requires O2 – is too slow for heavy exercise » Some intracellular FA
  • 22. Oxidative onlyMuscle Fiber Oxidative orClassification glycolytic
  • 23. Muscle Adaptation to Exercise ( not in book)Endurance training: More & bigger Resistance training: mitochondria  More actin & myosin proteins & more More enzymes for sarcomeres aerobic respiration  More myofibrils More myoglobin muscle hypertrophy no hypertrophy
  • 24. Muscle Tension is Function of Fiber Length Sarcomere length reflects thick, thin filament overlap Long Sarcomere: little overlap, few crossbridges  weak tension generation Short Sarcomere: Too much overlap limited crossbridge formation  tension decreases rapidly
  • 25. Force of Contraction (all-or-none) Increases With » muscle-twitch summation » recruitment of motor units Mechanics of body movement covered in lab only Fig 12-17
  • 26. Smooth muscle A few differences » Innervation by varicosities » Smaller cells » Longer myofilaments » Myofilaments arranged in periphery of cell Cardiac muscle contraction covered later