Chapter 2: Neromuscular Physiology Flashcards
It is the result of the concentration difference of ions across a selectively permeable membrane that is caused by diffusion.
MEMBRANE ACTION POTENTIAL
This are rapid changes in the membrane potential that spread rapidly along the nerve fiber membrane
It begins with a sudden change from the normal resting negative membrane potential to a positive potential and ends vice versa.
ACTION POTENTIAL
Resting membrane potential before the action potential begins.
Polarized stage
RESTING STAGE
Rise of the potential in the positive direction caused by SODIUM inflow
DEPOLARIZATION
Re-establishment of the normal negative resting membrane potential (RMP).
REPOLARIZATION
An overshoot of the RMP toward negativity.
HYPERPOLARIZATION
These are necessary actors in causing depolarization and repolarization.
VOLTAGE GATED Na AND K CHANNELS
When the membrane potential becomes less negative, it activates the activation gate causing sodium ions to pour inward.
ACTIVATION
The same stimuli for activation also closes the inactivation gate. However, closes a few 10,000ths of a second after the activation gate open.
INACTIVATION
Gate of the potassium channel is closed and potassium ions are prevented from passing through.
RESTING STATE
When the membrane potential becomes less negative causing opening of the gate to allow potassium diffusion. However, it happens with a delay.
SLOW ACTIVATION
What is the threshold for stimulation?
-65mV
Required sudden rise is?
15 - 30mV
Any initial rise in the membrane potential will lead to a?
positive feedback cycle that would open the sodium channels.
Rising voltage in MP causes
more Na channels to open.
Excitable membrane excites adjacent membranes
An action potential elicited at any one point on an excitable membrane usually excites adjacent portions of the membrane
PROPAGATION OF ACTION POTENTIAL
Nerve of Muscle Impulse
A segment of the membrane is depolarized
Positive** charges spread** 1-3mm through the fiber
Rise in membrane potentials leads to a positive feedback cycle
Newly depolarized areas produce more local circuits and travels the length of the fiber.
It occurs through the mechanism of Na-K pump
RE-ESTABLISHING RMP
Either all depolarized or none depolarized
The depolarization process travels over the entire membrane if conditions are right, but it does not travel at all if conditions are not right.
Allows the spread of depolarization to stop.
ALL OR NOEN PRINCIPLE
Low membrane potential can not fully close the gates
REPETITIVE DISCHARGE
is due to K leak channels
HYPERPOLAROZATION
REPETITIVE DISCHARGE
A low membrane potential leads to** influx of sodium and calcium**
Action potential occurs and membrane repolarizes
Hyperpolarization causes a delay before depolarization occurs again.
The potential remains near the peak of the potential for many milliseconds before repolarization begin.
PLATEAU
slow opening allows for prolonged
depolarization
CALCIUM (slow) CHANNELS
slow activation
leads to delayed repolarization
POTASSIUM CHANNELS
Viscid intracellular fluid
AXOPLASM
Its membrane is the one that conduct the action potential.
CENTRAL CORE
AXON
Has Myelin Sheath → electrical insulator
*
Has Node of Ranvier →uninsulated area
between sheaths
*
Seen in large fibers
*
Conduction velocity: 100 m/sec
MYELINATED FIBERS
Flow of electric currents through the Nodes of Ranvier only allows impulse to jump along the fiber.
Increases velocity of impulses and conserves energy for the axon
SALTATORY CONDUCTION
Has no Myelin Sheath
*
Has no Node of Ranvier
*
Seen in small fibers
*
Conduction velocity: 0.25 m/sec
UNMYELINATED FIBERS
Stimuli that barely reached the level required to elicit an action
Below the stimuli
ACUTE SUBTHRESHOLD POTENTIAL
Stimuli that barely reached the level required to elicit an action potential, but occurs only after a latent period.
THRESHOLD POTENTIAL
A new action potential cannot occur in an excitable fiber as long as the membrane is still depolarized
REFRACTORY PERIOD
period during which a second action potential cannot be elicited even with a strong stimulus.
ABSOLUTE REFRACTORY PERIOD
period after the absolute refractory wherein a second action is inhibited, but not impossible to elicit
RELATIVE REFRACTORY PERIOD
Thin membrane covering the muscle fiber which fuses a tendon fiber at the end of each muscle
SARCOLEMMA
MUSCLE COMPOSITION
MUSCLE–> FASCICLE–> MUSCLE FIBER–> MYOFIBRIL
covering of each muscle
EPIMYSIUM
covering of each fascicle
PERIMYSIUM
covering of each myofibril
ENDOMYSIUM
A springy protein that maintains the side- by-side relationship of actin and myosin
TITIN
ntracellular fluid in the spaces between the myofibrils
SARCOPLASM
Regulates calcium storage, release and reuptake
SARCOPLASMIC RETICULUM
A portion of the myofibril that lies between two successive Z disks
SARCOMERE
Also known as the thick filament
Anisotropic (A) bands
It has cross bridges
MYOSIN
contains myosin as well
as some actin filaments
ANISOTROPIC (A) BANDS
Also known as the thin filament
Isotropic (I) bands
ACTIN
composed oF pure actin
filaments
ISOTROPIC (I) BANDS
proteins that passes crosswise across the myofibril and attaches the myofibrils to one another
Z DISK
Area of pure myosin
H ZONE
a line that bisects the H Zone
M LINE
Myosin molecules are composed of two heavy chains and four light chains.
TAIL & HEAD
two heavy chains wrapped spirally around and forms a double helix
TAIL
composed of 2 heads and each is formed by 2 light chains and the end of the heavy chains is folded bilaterally
HEAD
tails of the myosin molecules bundled together
BODY
part of the bodies of each myosin molecule
ARM
protrude to the sides
HEAD
collective term for the arm and head
CROSS-BRIDGES
flexible points of the cross-bridges; exit and head
HINGES
it is the backbone of the filament
F-ACTIN
it serves as attachment for ADP molecules
G-ACTIN
it is wrapped around F-actin; at rest, it lies on top of the active binding sites of actin strands
Tropomyosin
it is attached to the tropomyosin and is believed to attach tropomyosin to actin
TROPONIN
has high affinity for actin
TROPONIN I
has high affinity for tropomyosin
TROPONIN T
has high affinity for calcium
TROPONIN C
inhibits actin and myosin via calcium ions
TROPONIN- TROPOMYOSIN COMPLEX
GENERAL MECHANISM OF MUSCLE CONTRACTION
Action potential travels along a motor nerve to its endings causing Ach release
Ach binds with Ach channels causing Na to diffuse inside muscle membrane leading to another action potential
Action potential travels through the center of the fiber activating the sarcoplasmic reticulum to release Ca
Ca causes the actin and myosin to slide alongside each other causing contraction
Ca is pumped back and stored until it is used again. This causes cessation of contraction.
MOLECULAR CONTRACTION: THE SLIDING FILAMENT THEORY
ATP binds with the heads of the cross bridges and is cleaved, but cleaved products remain in the head
**Calcium bonds with the troponin-tropomyosin complex **uncovering the active sites causing actin and myosin bond
Power stroke and Walk-along mechanism takes place
Once power stroke occurs, cleaved products are released causing detachment of the head from the actin
Release of cleaved products causes attachment and cleavage of a new ATP leading to new energy causing again a power stroke
Cycle continues until the actin pulls the Z membrane up against the ends of the myosin or the load becomes too great
is produced when the
sarcomere is at 2.0-2.2 micrometers
produced at normal length and 2x length
MAXIMUM TENSION
produced when the muscle is** fully shortened or fully lengthened**
when length is ½ normal
MINIMAL TO NO TENSION
RELATIONSHIP WITH LOAD
Velocity of contraction is inversely proportional with load.
Muscles do not shorten or lengthen
during contraction
ISOMETRIC
Muscles shorten or lengthen but the tension remains constant throughout contraction
ISOTONIC
Muscle lengthens throughout the contraction
ECCENTRIC
Muscle shortens throughout the contraction
CONCENTRIC
It is identified as all muscle fibers innervated by a single nerve fiber depending on the function of the muscle.
Motor Unit
Small motor units are stimulated in preference of larger units initially
SIZE PRINCIPLE
When a muscle begins to contract after a long period of rest, its initial strength of contraction may be as little as one half its strength 10 to 50 muscle twitches later
TREPPE (STAIRCASE EFFECT)
It is the adding together of individual twitches to increase the intensity of overall muscle contraction.
SUMMATION
Increasing the number of motor units contracting
MULTIPLE FIBER SUMMATION
Increasing the frequency of contraction
FREQUENCY SUMMATION
A single, sudden contraction lasting a fraction of a second
TWITCH
Completely smooth and continuous muscle contraction due to rapid contractions fusing together
TETANY
Rapid, irregular and unsynchronized contraction that can be seen
FASICULATION
Rapid, irregular and unsynchronized contraction that cannot be seen
FIBRILLATION
Tautness of muscles even at rest
*
It results from a low rate of impulses coming from the spinal cord.
MUSCLE TONE
Results mainly from inability of the contractile and metabolic processes of the muscle to continue supplying the same work output
MUSCLE FATIGUE
leads to almost complete muscle fatigue within 1 to 2 minutes
INTERRUPTION OF BLOOD FLOW
Increase of the total mass of a muscle
*
It is due to repeated forceful contractions
*
Increased synthesis of muscle contractile proteins, splitting of myofibrils and increase in glycolytic enzymes
HYPERTROPHY
Decrease of the total mass of a muscle
*
It is due to a muscle disuse or denervation
ATROPHY
Increase in the number of muscle fiber
HYPERPLASIA
Replacement of contractile tissue with fibrous tissue or fatty tissue.
CONTRACTURE
False increase in muscle mass
*
Due to the replacement of muscle with fibrous or fatty tissue
PSEUDOHYPERTROPHY
Muscle contracture in dead caused by loss of ATP
RIGOR MORTIS
Internal extensions which penetrates the muscle fiber in order to allow propagation of action potential
T-TUBULES
Regulates calcium release, storage and
reuptake
Sarcoplasmic Reticulum
Excitatory neurotransmitter that excites the muscle fiber membrane
ACETYLCHOLINE
It destroys acetylcholine
ACETYCHOLINESTERASE
Pumps calcium back to the sarcoplasmic reticulum
CALCIUM PUMP
Composed of discrete, separate smooth muscle
Example: Ciliary muscle of the eye, iris muscle of the eye, piloerector muscles
Each fiber is Separated from each
other by a thin layer of membrane
MULTI-UNIT
Also called syncytial or visceral smooth muscle
Contain gap junctions
mass of smooth muscle fibers that
contract together as a single unit
UNITARY
Cardiac Muscle is composed of three (3) major types
- ATRIAL MUSCLE
- VENTRICULAR MUSCLE
- CONDUCTIVE MUSCLE FIBERS
Exhibit automatic rhythmical electrical discharge in the form of AP or conduction of the AP through the heart and contract only feeble
CONDUCTIVE MUSCLE FIBERS
Cell membranes that separate individual cardiac muscle cells from one another
INTERCALATED DISCS
Permeable communicating junctions that allow rapid diffusion of ions
*
Allow ions to move with ease so that action potentials travel easily
GAP JUNCTION
Collection of cells that work together such as the cardiac muscle
SYNCYTIUM
2 syncytium in the heart
- ATRIAL
- VENTRICULAR
ACTION POTENTIAL IN CARDIAC MUSCLE
Phase 0 (Depolarization)
Fast Na channels open, Na influx
*
Phase 1 (Initial Repolarization)
Fast** K** channels open, K efflux
*
Phase 2 (Plateau)
Ca channels open and K channels close, Ca influx
*
Phase 3 (Rapid Repolarization)
Ca channels close and slow K channels open, K efflux
*
Phase 4 (RMP)
Around -88 mV or -90 mV