physio e3l4: ch 12 muscle physiology

skeletal muscle:

1. where is it

2. 3 exceptions

1. connected to two or more bones by tendons

2. 3 exceptions

   1. facial = to skin

   2. larynx = to cartilage

   3. other muscles like sphincters

3 connective tissues and what layer they surround

1. epimysium = continuous w/ tendon connective tissue

2. perimysium = divides muscle into fascicles (100s, 100s of myofibers/musclefibers)

3. endomysium surrounds muscle fibers

components of a muscle fiber (myofiber):

1. what is it

2. made of

3. sarcomere

4. how nucleated

5. sarcolemma

6. Transverse (T) tubule

1. a muscle cell

2. many myofibrils

3. smallest contractile unit of a muscle fiber

4. multinucleated and extend length of the muscle

5. sarcolemma = PM that surrounds muscle fiber

6. T Tubules = groove in the sarcolemma going down

components of a muscle fiber/cell (myofiber):

1. sarcoplasm

2. mitochondria

3. sarcoplasmic reticulum/lateral sacs

4. Triad

1. cytoplasm of muscle fiber

2. a lot for ATP

3. smooth ER that stores Ca+

4. T tubule groove b/t 2 sarcoplasmic reticulum (lateral sacs)

myofibers:

1. what is it and 2 parts

2. what do the 2 parts form

3. give what appearance to what two muscles

1. arrangement of thick and thin filaments, which are contractile proteins

   1. thick filament = myosin

   2. thin filament = actin

2. thick and thin filaments form sarcomeres

3. give striated appearance to skeletal and cardiac muscle

1. structure of a sarcomere

2. red and blue?

3. A band

4. H zone

5. M line

6. I (pronounced “eye”) band

7. z line

1. 1 sarcomere = Z- line → Z-line

2. red = myosin (thick), blue = actin (thin)

3. A band = has overlap of actin/myosin, dark band is the thick filament

4. H zone = myosin only

5. M line = anchors myosin, perpendicular to long axis

6. I band = actin only, light band

7. Z line = anchors actin, perpendicular to long axis

myosin (thick myofilament) structure:

1. 2 parts

2. orientation

3. binding sites

4. what does it look like

1. myosin tail = towards M line

2. myosin head = towards I band

   1. actin binding site

   2. nucleotide binding site for ATP and ATPase

myosin (thick myofilament) structure:

1. 2 forms of myosin head?

2. how to move b/t them?

3. how is myosin arranged?

2. myosin head 2 forms

   1. high E = when connected to ADP + P

   2. low E = when ATP

3. low E → high E via ATP hydrolysis by ATPase

4. 2 myosin bound at tails = m line crossbridges

actin (thin filament) structure:

1. 3 parts structure

1. G-actin mC = each contains myosin binding site

2. F actin = fibrous string made of G actin mC’s

3. double helical actin strands = made of F actin

   1. anchored at Z line

tropomyosin and troponin:

1. what do they both do

2. what are they/purpose of each

1. both are myofiber regulatory proteins

2. tropomyosin = overlaps binding sites on actin for myosin

   1. covers myosin binding site on G actin mCs

3. troponin complex

   1. attaches to tropomyosin

   2. binds Ca+ reversibly = regulate skeletal muscle contraction

titin:

1. what is it

2. what does it do

3. why important

4. what does it look like

1. myofiber structural protein

2. anchors thick filaments to thin filaments

3. provides sarcomere structural support and elasticity

2 parts muscle force generation

1. excitation-contraction coupling → cross bridge cycle

2. excitation-contraction coupling = how muscle contractions turned on/off

3. cross bridge cycle = how muscles generate force

1. what is muscle contraction

2. why?

3. what is happening at:

   1. A band

   2. I band

   3. H zone

4. how slide?

1. shortening of sarcomeres

2. overlapping actin and myosinn filaments slide past each other

3. sections

   1. A band = no change

   2. I band = shortens

   3. H zone = shortens

4. sliding due to cyclical formation and breaking of cross bridges = crossbridge cycle

excitation contraction:

1. where

2. 3 steps (w/o details)

3. ryanadine receptor acts like

4. what comes after excitation contraction?

1. neuromuscular junciton

2. steps

   1. neurotransmitter activates muscle → AP travels down T tuble until it reaches voltage gated dihydrothymidine receptor (DHR)

   2. AP causes DHR to change shape → ryandine receptor to open (mechanically gated)

   3. ryandine receptor opens → Ca+ exits lateral sacs of sarcoplasmic reticulum

3. gate on sarcoplasmic reticulum

4. cross-bridge cycle

cross-bridge cycle:

1. 3 things present at the beginning

2. 6 ateps

3. why does rigor mortis happen

4. why does rigor mortis eventually relax?

1. beginning

   1. high Ca+ from SR/excitation contraction

   2. myosin in low E form (ATP)

   3. G actin bound to tropomyosin and troponin

2. cycle

   1. low E myosin (ATP) -(hydrolysis)→ high E myosin (myosin head conformation change)

   2. Ca+ binds troponin → troponin pulls/shifts trotropomycin, exposing the myosin binding site on actin

   3. exposed myosin binding sites bind High E myosin (ADP+P) → releases P

   4. releasing P → “Power Stroke” = myosin pulls actin

   5. after power stroke, ADP released = myosin and actin STUCK together in contraction, no movement (cross-bridge)

      1. rigor mortis = peak 12 hours, lasts 24 hrs, then will begin relaxing, fully relaxed 48 hours

   6. contraction stops when new ATP added to myosin (Low E) and separates from actin

enzymes break myofibers

how is the cross bridge cycle analogous to rowing a boat:

1. cross bridge or myosin head =

2. linking of myosin head to actin =

3. power stroke =

4. release of cross bridge =

1. oar

2. oar contact w/ water

3. oar pulling through water

4. oar out of water and repositioning

3 ways how to stop contraction? how pump?

1. stop APs = stops excitation

2. release Ca+ from troponin = tropomyosin covers myosin binding sites on actin

3. remove Ca+ from cytosol bay pumping it back into sarcoplasmic reticulum (storage)

   1. Ca+ - ATPase pump in the sarcoplasmic reticulum uses ATP

muscle activity across a joint:

1. stationary vs mobile

2. origin and insertion

3. muscles can only ___ not ___

4. how antagonistic

1. most muscles connect two bones via tendons. when muscle contracts, one bone is stationary, one bone moves

2. origin = muscle’s point of attachment POA to the ststationary bone

3. insertion = muscle’s POA to moveable bone

4. pull not push

5. combination of contraction and relax = flexor flexes, extensor relaxes

   1. motor unit stim and motor unit inhibition

1. 2 types of muscle fibers?

2. what are they

3. what do they do?

4. how innervated?

1. extra fusal fibers

   1. contractile cells of the muscle, outer

   2. generate force/skeletal muscle contraction

   3. innervated by alpha motor neurons

2. intrafusal fibers

   1. contractile cells of the muscle spindle, inner

   2. adjust sensitivity of muscle to stretch

   3. innervated by gamma motor neurons

muscle spindle:

1. what does it do

2. how controlled

3. AP frequency when:

   1. stretched

   2. relaxed

   3. contracted

1. detects changes in muscle length

2. sensitivity of sensory endings adjusted by action of intrafusl fibers

3. AP freq when:

   1. stretched = a lot of AP bc there’s load on the muscle

   2. relaxed = some AP bc of muscle tone=

   3. contracted = none

1. alpha and gamma motor neurons are _____

2. why?

1. coactivated

2. intrafusal fibers can’t detect stretch when they aren’t being activated/contracted

3. intrafusal fibers aren’t being stretched during a muscle contraction, so can’t detect stretch when flexing

4. ability to both flex + detect stretch recovered by coactivation of gamma (intrafusal activation) with alpha (extrafusal activation)

Golgi tendon organs (GTOs):

1. what are they

2. how do they work

3. why important

1. sensory capsules within tendons that detect passive tension/stretch

2. tendon stretch activates the GTO

3. provide reflex inhibition/relaxation of muscle to prevent injury from too much stretch/force

smooth muscle:

1. where is it found

2. what NS

3. 3 parts of structure

1. internal organs and BVs

2. autonomic

3. small spindle-shaped cells

4. nonstriated

5. gap junctions

6. varicosities on surface bc have gap junctions

smooth muscle:

1. how contract

2. 3 contraction structures different

3. range/axes of contraction?

   1. 3 reasons why?

1. sliding-filament mechanism of contraction

2. non-striated, no sarcomeres, has dense bodies that also have thick and thin filaments

3. longer range of contraction and multiple axes of contraction

   1. longer actin/myosin

   2. myosin heads whole length

   3. multiple directions of contraction

smooth muscle excitation contraction:

1. 5 steps

1. Calcium dependent calcium release:

   1. most Ca+ enters from extracellular via voltage gated Ca+ channel in PM

   2. extracellular Ca+ triggers release of SR Ca+

   3. Ca+ binds calmodulin

   4. Ca+-malmodulin binds/activates myosin light-chain kinase (MLCK)

      1. phosphorylated MLCK → myosin ATPase active → cross bridge cycle

      2. phosphatase unphosphorylates MLCK → no myosin ATPase activity → no cross bridge cycle

smooth muscle excitation contraction:

1. 2 differences from skeletal?

1. depends on extracellular Ca+

   1. no T tubule → DHP → ryanadine receptor → Ca+ from SR

2. Ca+ binds calmodulin instead of troponin

1. 3 ways relax smooth muscle.

2. contraction time in smooth muscle

1. phosphatase removes phosphate from myosin

2. Ca removed from cytoplasm via

   1. Ca-ATPase or

   2. Ca/Na counter transport (secondary active)

1. slower than skeletal

smooth muscle neural regulation:

1. excitatory or inhibitory?

2. what determines response?

3. neurotransmitter release from?

1. both

2. response depends on receptor type

3. varicosities

multi unit smooth muscle:

1. where?

2. gap junctions? synchronous?

3. each fiber acts ___

   1. 3 ways how

1. large airways, arteries, eye (ciliary/iris)

2. no gap junctions = not synchronous

3. individually

   1. own innervation (varicosity touches every cell not just on surface)

   2. no recruitment

   3. no tone

single unit smooth muscle:

1. where?

2. gap junctions? synchronous? innervates how many cells?

3. each fiber acts ___

1. most common, intestine, blood vessels, respiratory tract

2. yes and yes, varicosity on the surface (innervates few cells) bc has gap junctions

3. contract together as a unit

single unit smooth muscle:

1. pacemaker cells

2. tone

3. graded contractions

4. stretch reflex

1. pacemaker cells = spontaneous depolarizations by itself

2. tone = level of contraction w/o stimulation

3. graded contractions = no recruitment

4. stretch reflex = sudden or prolonged stretch induces relaxation = protection

spontaneous demoralizations:

1. what muscle type

2. 2 types

   1. pacemaker potentials

      1. why

   2. slow wave potentials

      1. why

1. smooth and cardiac

2. pacemaker potentials = spontaneous depolarizations to threshold

   1. permeability to Na+, Ca+, K+

3. slow wave potential = cycles of graded potentials at Vm bc of Na+ permeability

cardiac muscle:

1. how “intermediate b/t skeletal and smooth?”

   1. 2 like skeletal

   2. 3 like smooth

   3. 1 like both

1. like skeletal

   1. striated w/ sarcomeres

   2. troponin-tropomyosin regulation

2. like smooth

   1. gap junctions (within intercalated disks)

   2. pacemaker cells

   3. innervated by autonomic NS (varicosities)

3. like both

   1. Ca+ from extracellular fluid and SR

cardiac muscle:

1. length of AP

2. summation? why?

3. what type of refractory period?

1. length of AP = length of contraction

2. no summation due to long refractory period

3. absolute (absolutely not going to get AP)

1. normal AP v. cardiac muscle AP?

2. compare steps (normal 3, cardiac3)

1. skeletal/smooth

   1. depolarization = Na+ in

   2. apex of AP = Na+ channels close

   3. drop = K+ leaving leak channels

2. cardiac has a long refractory period

   1. depolarization = same

   2. apex = same

   3. plateau = k+ leaving leak channels AND Ca+ entering