1. Skeletal muscle
    • Striatied
    • attached to bones
    • support and movement of skeleton
    • voluntary somatic NS
  2. smooth muscle
    • nonstriated/syncytial
    • hollow viscera
    • around organs and vessels single cells and small clumps
    • propel or regulate flow
    • involuntary intrinsic activity
    • regulated by atutonomic NS
    • hormones
  3. cardiac muscles
    • striated/syncytial
    • heart
    • propels blood through circulatory system
    • involuntary
    • intrinsic activity
    • regulated by autonomic NS
    • hormones
  4. Structure and function of skeletal muscle
    • attached to bone
    • cells: held in parallel 10-100um in diameter, >20cm long, formed by fusion of mononucleated myoblasts in utero
    • cell membrane- sarcolemma (inner plasmalemma, outer basement membrane)
    • normal subcellular organelle- mitochondria, golgi apparatus, ER, lysosomes, ribosomes, myofibrils
  5. what is the functional breakdown of a skeletal muscle?
    • skeletal muscles
    • muscle fibre
    • myofibril
    • repeated sarcomeres (think and thin fillaments)
  6. arrangement of filaments w/in skeletal muscle fibre that fives rise to striated appearance
    • think and thin filaments
    • Z line
    • M line
    • H zone
    • I band
    • A band
  7. Sliding filament theory of contraction
    • move thick and thin filaments relative to eachother
    • A band has NO change in size!
  8. cross bridge cycle
    • 1) activated myosin- ATP split to ADP store energy in myosin fibre)
    • 2) forms crossbridge w/ actin (liberation and use of energy)
    • 3) confomational change causes myosin to move/bend, causes release of ADP
    • 4) to bread crossbridge neet ATP! go back to right angle
  9. Regulation of the contractile process in skeletal muscle
    • resting state: tropomyosin attached to troponin attached to Ca2+ binding site in front of myosin binding site on actin. blocking myosin.
    • must move troponin out of way to used actin/myosin binding site
    • Ca2+ binds to troponin moving it away.
    • increases intracellular Ca2+ allows contraction
    • **in theory- Ca2+ pumps should relase enough- but doesn't, b/c it goes right back again
  10. Sacoplasmic reticulum
    • (see image)
    • has extension to extracellular surface
    • lateral sacs (store Ca2+)
    • SR wraps around sarcomeres- has a lot of Ca2+ w/in
    • T tubule (pass through transversly)
    • some Ca2+ released will come back in again to reverse contraction must remove Ca2+ back to SR
    • T- tubules important to get ALL arts of muscles cell- even deep)
    • ATP Ca2+ pumps always active
  11. AP and SR
    • electrical signal (AP) passes through- see typical AP- passes across cell membrane opens voltage gated ca2+ channels, releasing Ca2+ into cell- alowing contraction pathway
    • triad- combo of t tubule and lateral sacs
  12. signal transmission at neuromuscular junction
    neurone usually makes contact in MIDDLE of muscle cell. each muscle cell is stimulated by ONE motor neurone but 1 motor neurone may inovate >1 muscle cell
  13. isometric vs isotonic
    • isometric: load increases as muscle contracts. cross bridge cycle proveds tension (life something too heavy- provides tension but no shortening- no movement relative to eachother)
    • isotonic: LENGTH decreases but load remains CONSTANT. crossbridge cycle provides movement (tone of muscle is the same- shorten muscle, but load hasn't changed. movement relative to eachother.)
  14. Effect of load on isotonic twitch
    • light load: larger distance shortened for longer time
    • medium load: smaller distance shortened for shorter time
    • heavy load: very small distance shortened for very short period of time (longer latent period, rate will be less, recovery longer)
  15. summation (mechanical)
    • unfused tetanus (more twitches- continously increasing)
    • tetanus (maintains Ca2+= maintain contraction for long time)
    • tension is generated due to increase of Ca2+ intracellular= more crossbridges= more contractions
  16. length tension relationships
    • max overlap= best tension- Normal held in body
    • 60% muscle length= too much overlap, disturbed ability to form crossbridges
    • 180% muscle length= unable to overlap/interact w/ eachother= no crossbridges formed= no tension
  17. energy considerations
    • phosphorylation of creatine phosphate
    • oxidative phosphorylation (aerobic glycolysis)
    • anaerobic glycolysis
  18. phosphorylation of creatine phosphate
    • immediate source of ATP
    • creatine phosphate + ADP <----> creatine + ATP
  19. oxidative phosphorylation (aerobic glycolysis)
    • ATP derived from glycogen, glucose and fatty acid metabolism
    • limited by: oxygen availability, substrate availability, enzyme reaction time
  20. Anaerobic glycolysis
    • initially muscle's glycogen stores broken down to lactic acid w/ the production of ATP
    • under conditions of heavy work, blood glucose broken down to lactic actid to ATP
    • not efficient but fast and does not require oxygen
  21. Three types of skeletal muscle
    • slow oxidative
    • fast oxidative
    • fast glycolytic
  22. Slow oxidative skeletal muscle
    • primary source of ATP: oxidative phos
    • Myosin ATPase activity: low
    • glycogen content: low
    • mitochondria: many
    • myoglobin: yes (red muscle)
    • capillaries: many
    • fatigue: resistant
  23. Fast oxidative skeletal muscle
    • primary source of ATP: oxidative phosphorylation
    • Myosin ATPase activity: high
    • glycogen content: medium
    • mitochondria: many
    • myoglobin: yes (red muscle)
    • capillaries: many
    • fatigue: intermediate
  24. Fast glycolytic
    • primary source of ATP: Anaerobic glycolysis
    • Myosin ATPase activity: High
    • glycogen content: High
    • mitochondria: few
    • myoglobin: low (white muscle)
    • capillaries: few
    • fatigue: rapidly
  25. factors affecting muscle tension (summary)
    • tension developed by each fibre:
    • AP freq.
    • fibre length
    • fibre diameter
    • fatigue
    • Number of active fibres:
    • number of fibres per motor unit
    • number of active motor units recruitment
    • (motor unit 1- slow oxidative
    • motor unit 2- fast oxidative
    • motor unit 3- fast glycolytic)
  26. Smooth Muscle (general)
    • Nucleated spindle shaped cells (1 nucleous)
    • lacks cross striations
    • cells DO contain thin and thick filaments but they are NOT arranged as in skeletal/cardiac muscle
    • 1/3 of the myosin and 2X actin of skeletal muscle
    • thick and think filaments exhibit cross bridge activity
    • contraction occurs via sliding filament mechanism, activated by cytosolic Ca2+ concentration
    • located around hollow viscera to propel things through (ex: blood vessels, terus, esophigous, GI, etc)
    • dense bodies w/ think fillaments
  27. Excitation contraction coupling in smooth muscle
    • Resting state: calmodulin (no troposin)- relationship w/ Ca2+ gives control to muscle. Myosin/actin binding site
    • Ca2+ calomdulin complex activiates myosin light chain kinase
    • phosphoylates myosin
    • contraction: (slower than skeletal) myosin interacts with actin (same effect as skeletal- just diff. route)
    • myosin phosphatase (dephos. to go back to resting- normal state/always present)
  28. additional specific features of smooth muscle
    • low ATPase activity- less is used
    • Latching- slowing down of cross bridge cycle (ONLY seen in smooth muscle)
    • calcium comes from the SR! small not organized and EXTRACELLULAR fluid- via chemical or voltage gated channels/ no sufficient to saturate all calmodulin
    • (has almost no SR- so not a good source of Ca2+. No T-tubules- too small of a cell.
    • will see calveoli indents on cell membrane.
    • can regulate function of smooth muscle by amount of Ca2+ into cell)
  29. What activates excitation contraction coupling in smooth muscles?
    • 1) spontaneous electrical activity
    • different forms of AP shape (spike or plateau), no neuron activity has inherent activity. slow leekage eventually drives cell- nothing "controlling"
    • cells are linked by electrical gap junctions- so activity in one cell spreads to all others
    • 2) innervation by autonomic nervous system: control inherent activity, 2 diff. neurons (each swelling has neurotransmitters to release)
    • 3) hormones: oxytocin, seratonin
    • 4) local chemical factors: O2, CO2, H+ concentrations
    • 5) stretch: physical stretch can induce contraction
  30. classfications of smooth muscle (2)
    • single unit
    • multi unit
  31. Single unit smooth muscles
    • AP propagated from cell to cell via gap juntions
    • may develop spontaneous action potentials
    • activity altered by hormones
    • innervation varies, may be limited to areas containint pacemaker cells
    • activiated by stretch
    • (intestine, repro tract, small diameter blood vessels)
  32. Multi unit smooth muscles
    • little or no propagation of action potentials
    • activity closely regulated by neural imputs
    • degree of contraction dependent upon number of units activated and summation of neural imputs
    • activity altered by hormones
    • not activated by stretch
    • (large airways to lungs, large arteries, hairs on skin)
    • low if any gap junctions
  33. 3 types of cardiac muscle cels
    • Pacemaker cells: small plate, few organelles (sinoatrial node, atrioventicular node)
    • Conductors: short, broad, oriented end to end, few lateral connections (bundle of his, purkinje fibres)
    • contractile myocardial cells: bulk- thinker in ventricles than atria (muscle)
    • (striated, multiple cells which branch and interconnect, cells joined at intercalated disks)
    • cells are very small w/ single nucleaus--have T-tubules more extensive (pass elec. signal very quickly)
  34. the contractile muscle cells of the heart...
    • operate as 2 functional syncitia
    • separated by a layer of NON-CONDUCTING connective tissue
    • AP starts at SA node
    • spreads over atria
    • passes through connective tissue (via the bundle of his)
    • signal slowed
    • spreads through ventricles
    • (Atria and ventricals will contract seperately)
    • SA (AP)--> AV--> His--> PF
    • (need double contract to act as pump)
  35. action potentials w/in cardiac muscle
    • 1) pacemaker potential (slow)- decrease K, increase Na/Ca permeability
    • 2) AP- inward Ca2+ flow
    • 3) repolarisation
    • (long AP- when reach threshold- very few Na+ channels open- instead generating Na+ levels by Ca2+ movement)
    • AND
    • (contractile cells)
    • 1) Depolarisation: increase Na, decrease K permeabiliy (very quick!)
    • 2) initial repolarisation: closure of fast Na channels
    • 3) maintained depolarisation: Na, Ca influx (slow channels)
    • 4) repolarisation: closure of slow channels, influx of K
    • (stable RMP- ventricular cells are "slaves" to pacemakers- *****1 AP last 100-200ms****
  36. excitation contraction coupling in cardiac muscle
    • Ca2+ diffuses INTO cell as part of the AP and stimulates the opening of Ca2+ regulated Ca2+ channels in the SR
    • The AP timulates the opening of voltage gated Ca2+ channels
    • Ca2+ binds to troponin (thin filaments) but troponin not saturated
    • myosin binding sites exposed
    • contraction
    • active transport of Ca2+ back into SR and out of cell (terminate)
    • (Ca2+ comes from extracellualar- free Ca2+)
  37. factors affecting heart rate
    • Slope of pacemaker potential:
    • sympathetic NS increase
    • parasympathetic NS decrease
    • warming Increase
    • cooling decrease
    • minimum membrane potential:
    • parasympathetic NS
    • Ach-hyperpolarisation (lower= decreased HR, hight = increased HR)
  38. Factors affecting Stroke volume
    • 1) starlings law of the heart: increased stretch of the ventricular muscle due to increased diastolic filling leads to increase force of contraction- length-tension relationship at rest, cardiac muscle fibres are at less than optimal length
    • 2) faster ventricular contraction and relaxation: adrenaline from sympathetic NS and adrenal gland affects pacemaker potential, AND contractile force for any given end diastolic voume.
    • increased Calcium permeability, Ca release from SR, increase cross bridge formation- faster contraction- faster Ca2+ reuptake- faster relaxation
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