Mam Phys Lab Final

kymograph

first machine invented to measure physiological events

who invented the kymograph?

Carl Ludwig

limitations of kymograph

• length of record was limited

• could only record one event at a time

• messy

recording oscillographs

electronic machines used to produce a permanent record of a physiological event

BIOPAC is a computerized version of

recording oscillograph

recording channel

functioning unit of the recording oscillograph

sensing device

picks up information from the experimental set up

• can be an electrode or transducer

electrode

device used to detect electrical events (EKG, ECG, “pin,” “sleeve,” etc.)

transducer

transforms non-electrical signal into an electrical signal that the computer can understand

transducers convert ____________ energy from muscle contraction into __________ energy

mechanical; electrical

what is the processor of the BIOPAC system

MP36

processor

takes the electrical signal from the transducer; has two components (coupler and amplifier)

two components of processor

coupler and amplifier

coupler of processor

alters the electrical signal so it can be recognized by the rest of the recording channel

amplifier

this amplifies (boosts) the signal received proportionally so it can be measured

reproducer

device for making a permanent recording of a physiological event (computer screen, printer, etc.)

three components of a recording channel

1) sensing device

2) processor

3) recorder

for recorder: when signal is received from a sensing device, the life is deflected in _____________ to the strength of the signal

proportion

the reproducer of the BIOPAC system is the

computer and the software

recording oscillographs must be ______________ before use

balanced & calibrated

balancing recording oscillographs

matches the signal from the sensing device with the processor; like setting bathroom scale to zero

calibrating recording oscillograph

standardizes the recording channel; lets use quantify results; like setting increments on bathroom scale

stimulators

devices for administering controlled electrical signals to an excitable tissue in order to elicit a response

stimulators are devices for administering a _______________________________ to an excitable tissue in order to elicit a response

controlled electrical signal

threshold stimulus

lowest stimulus that will elicit a physiological response

stimulator variables

1) intensity

2) frequency

3) duration

intensity

the strength of a stimulus measured in volts

frequency

the number of impulses administered per second measured in Hz

duration

the length of time each impulse lasts

duration is the _________ of time ______ impulse lasts (ms)

length; each

duration is _______ total length of time impulses are administered to a subject

NOT

motor unit

motor neuron and all the muscle fibers it innervates

functional unit of muscle contraction

motor unit

three parts of motor unit

1) neuron

2) neuromuscular junction (NMJ)

3) muscle fibers

basic unit of skeletal muscle

muscle fiber

plasma membrane surrounding a muscle fiber

sarcolemma

extended the entire length of a fiber but are arranged in compartments called sarcomeres

myofilaments

primary component of thin myofilament

actin

prevents actin and myosin from binding together

tropomyosin & troponin

primary component of the thick myofilament

myosin

sliding filament theory

1) myosin cross bridge attached to the actin myofilament

2) myosin head pivots and bends as it pulls on the actin filament, sliding it toward the M line

3) new ATP attached to the myosin head, cross bridge detaches

4) as ATP is split into ADP and Pi, cocking of myosin head occurs

in order for muscle fiber to contract, stimulus must be delivered to _______

neuron

when the AP reaches the end of the neuron, _____________________ and ________ rushes into neuron at ______

VR Ca2+ channels open; Ca2+; NMJ

influx of Ca2+ causes vesicles filled with ____________ to fuse with the neural membrane (in muscle contraction)

Ach

Ach is released to _________ where it binds to _______________ on sarcolemma of muscle fiber

NMJ; nicotinic

what happens when Ach released to NMJ and nicotinic receptors?

causes AP on sarcolemma by opening CR Na+ channels

Ach causes muscle contraction after binding to nicotinic receptors in NMJ because this causes an AP on sarcolemma by opening __________________

CR Na+ channels

what are the three parts of a normal curve for muscle twitches

1) latency

2) contraction

3) relaxation

latency

short delay between when a muscle receives an electrical impulse (AP) and when it actually begins to develop tension or change length (contract)

multi-unit summation

recruit more motor units as stimulus strength increases

what is the maximal stimulus?

stimulus strength where you have recruited all the possible motor units and the force of contraction has reached its max

does force of contraction increase with increasing stimulus in multi-unit summation?

Yes, until you reach the maximal stimulus where you’ve recruited all the possible motor units, then force of contraction reaches its plateau

first neurons excited are ________________

lowest thresholds

increasing the strength of the stimulus, step-by-step, will bring more and more _________________ into action

neurons (and motor units)

if you add additional, stronger stimuli once motor unit summation has been achieved, what is the effect?

no effect on force of contraction

role of Ca2+ in muscle contraction

1) activated myosin ATPase that allows ATP to bind to active site and be split = release energy that bends myosin head out and up

2) binds to troponin of actin polymer = troponin-tropomyosin complex changes shape = expose binding sites on actin filament that form cross-bridges

as long as Ca2+ is present in sarcomere and bound to troponin ….

muscle will continue to contract

ATP functions in contraction/relaxation of muscles

1) supplies energy that allows for contraction

2) initiate relaxation by powering Ca2+ ATPase in SR that clears Ca2+ from sarcomere = cross-bridges break = relaxation begins

what happens if you give a second stimulus during the absolute refractory period?

a second impulse will NOT be produced

if you increase the frequency of stimulation in muscle cell, it will…. (think wave summation)

contract again before cell has completely relaxed

with wave summation, second contraction is added to the first, resulting in….

larger total amount of force

temporal/wave summation

tension generated by muscle is added over a period of time in which the muscle is not allowed to completely relax

with wave summation, if frequency of stimulation is high enough….

muscle will have no chance to relax at all

maximum sustained muscle contraction is called….

tetany

during tetany, all _____________ are firing as rapidly as possible and the _____________ of the muscle is generated

motor units; maximum tension

what is this showing?

wave summation & generation of tetany

what is this showing?

multi-unit summation

if you decrease temperature, what happens to enzyme function?

decreases

acetycholinesterase

breaks down Ach in NMJ

myosin ATPase

converts chemical energy into directed mvmt and can be viewed as a molecular motor

SERCA pump

acts to transport Ca2+ ions from cytosol back to the SR following muscle contraction

what happens when you decrease the function of AchE?

• increases Ach contact with nicotinic receptors

• increase stimulation of Ca2+ release

• increase length of contraction

what does this show

effect of decreased AchE function

what happens when you decrease functionality of myosin ATPase?

• decreased ratcheting

• decreased force

• increased contraction time

what does this show

decreased myosin ATPase function

what happens if you decrease functionality of SERCA pump

• increased time of Ca2+ in sarcoplasm

• increased ratcheting

• increased contraction

• decreased sequester rate of Ca2+ = prolongs residence in sarcomere

• increased relaxation time = prolongs Ca2+ residence in sarcomere

what does this show

decreased SERCA pump functionality

what happens during muscle fatigue?

• ATP depleted

• decreased ratcheting

• decreases contractile force

what does this show

muscle fatigue after tetany

if a muscle is continuously stimulated, it will _______

fatigue

fatigue

a transient and recoverable decline in muscle force and/or power with repeated or continuous muscle contractions

what are the possible initial causes of fatigue?

1) the nerve itself might fatigue from being overstimulated and no longer able to produce an AP (ionic [ ] prevent this from being physiological reality)

2) NT might be depleted and thus the AP couldn’t be transmitted across the synapse to the muscle

3) muscle itself could fatigue as result of many factors (reatine phosphate degredation, altered pH from lactic acid buildup, buildup of inorganic phosphate from ATP hydrolysis, deleterious effects of Ca2+ release and uptake from SR)

local anesthetics

stabilize lipid bilayer = more rigid and less flexible

lidocaine

local anesthetic that makes it harder for ion channels in bilayer to change shape and makes it hard for nerves to generate an AP

muscle cell membrane receptors that respond to Ach

nicotinic

D-tubocurare

binds to nicotinic receptors, blocks Ach from binding = no Na+ channels opened = hinders AP transmission

the site of first fatigue is the ______ due to __________________

NMJ; depletion of Ach

site of first fatigue interpret

after nerve fatigue, switch to muscle shows an increase in force; this means that the site of fatigue is the NMJ and not the muscle itself because the direct muscle stimulation bypasses the NMJ and Ach (limiting factor)

mechanical stimulus of nerve

damages the membrane and allows Na+ to rush in, depolarizing the membrane and causing an AP without electrical stimulation

what happens when you mechanically stimulate the nerve?

the 1st pinch breaks the the neurolemma, and broken neurons can’t generate APs meaning following contractions will be lower in force

in our lab how did we do mechanical stimulus?

distal then proximal; if we did proximal then distal, the distal contraction would be much less because the AP would have to travel over the damaged proximal portion

interpreting mechanical stimulus of the nerve

1st pinch breaks neurolemma of neurons, ions freely flow into neuron causing AP; broken neurons can’t generate AP’s so fewer neurons available to respond so force of contraction will be lower

effect of lidocaine & ether on nerve and muscle contraction

• excitable membrane stabilizers make membrane more ridged

• interfere with lipid matrix

• Na+ and K+ channel controls are impaired

• Na+ and K+ cannot cross the nerve membrane

• Decreasing muscle contraction, till action potentials cannot be generated

with lidocaine added to the nerve, strength of contraction increases because no longer dependent upon an AP (and Ach) from the nerve

decreases Ach released = decreased # of AP = muscle contractions become weaker

what does this show?

muscle contractions from nerve stimulation decreases after lidocaine addition; switch back to muscle and the contraction force isn’t affected because the lidocaine was only added to the nerve, not the muscle

simplified effect of lidocaine

interfered with the lipid bilayer, impairing Na+ and K+ channels (force decreases with nerve stimulation, increases back to normal when switched to nerve)

d-Tc (curare)

nicotinic muscle isoform receptor type blocker

how does curare work?

d-Tc competes with Ach for the Ach receptors on the surface of the muscle cell membrane; doesn’t cause depolarization; it blocks the receptor, which prevents a normal response (contraction)

curare simplified

blocks N1 receptors at muscle; see no change when added to the nerve, because no N1 receptor; when injected into the muscle, contraction decreases in nerve stimulation but increases slightly when switched to muscle (may not go all the way back to normal due to excess fluid)

interpretation of curare

• d-Tc added to the sciatic nerve —> strength of contraction

  • No change: no nicotinic receptors on nerve surface

• d-Tc injected into the muscle + nerve stimulated

  • strength of contraction decreased

  • released Ach has fewer nicotinic receptors to bind to on the sarcolemma

• flipped to direct muscle stimulation, bypassing need from Ach = strength of contraction increases and remain constant