BVMS1

• Striatied
• attached to bones
• support and movement of skeleton
• voluntary somatic NS

• 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

• striated/syncytial
• heart
• propels blood through circulatory system
• involuntary
• intrinsic activity
• regulated by autonomic NS
• hormones

• 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

• skeletal muscles
• muscle fibre
• myofibril
• repeated sarcomeres (think and thin fillaments)

• think and thin filaments
• Z line
• M line
• H zone
• I band
• A band

• move thick and thin filaments relative to eachother
• A band has NO change in size!

• 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

• 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

• (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

• 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

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

• 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.)

• 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)

• 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

• 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

• phosphorylation of creatine phosphate
• oxidative phosphorylation (aerobic glycolysis)
• anaerobic glycolysis

• immediate source of ATP
• creatine phosphate + ADP <----> creatine + ATP

• ATP derived from glycogen, glucose and fatty acid metabolism
• limited by: oxygen availability, substrate availability, enzyme reaction time

• 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

• slow oxidative
• fast oxidative
• fast glycolytic

• primary source of ATP: oxidative phos
• Myosin ATPase activity: low
• glycogen content: low
• mitochondria: many
• myoglobin: yes (red muscle)
• capillaries: many
• fatigue: resistant

• primary source of ATP: oxidative phosphorylation
• Myosin ATPase activity: high
• glycogen content: medium
• mitochondria: many
• myoglobin: yes (red muscle)
• capillaries: many
• fatigue: intermediate

• primary source of ATP: Anaerobic glycolysis
• Myosin ATPase activity: High
• glycogen content: High
• mitochondria: few
• myoglobin: low (white muscle)
• capillaries: few
• fatigue: rapidly

• 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)

• 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

• 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)

• 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)

• 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

• single unit
• multi unit

• 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)

• 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

• 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)

• 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)

• 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****

• 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+)

• 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)

• 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