Chapter 2: Neromuscular Physiology Flashcards by Reizo Miranda

It is the result of the concentration difference of ions across a selectively permeable membrane that is caused by diffusion.

MEMBRANE ACTION POTENTIAL

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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

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Resting membrane potential before the action potential begins.

Polarized stage

RESTING STAGE

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Rise of the potential in the positive direction caused by SODIUM inflow

DEPOLARIZATION

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Re-establishment of the normal negative resting membrane potential (RMP).

REPOLARIZATION

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An overshoot of the RMP toward negativity.

HYPERPOLARIZATION

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These are necessary actors in causing depolarization and repolarization.

VOLTAGE GATED Na AND K CHANNELS

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When the membrane potential becomes less negative, it activates the activation gate causing sodium ions to pour inward.

ACTIVATION

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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

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Gate of the potassium channel is closed and potassium ions are prevented from passing through.

RESTING STATE

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When the membrane potential becomes less negative causing opening of the gate to allow potassium diffusion. However, it happens with a delay.

SLOW ACTIVATION

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What is the threshold for stimulation?

-65mV

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Required sudden rise is?

15 - 30mV

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Any initial rise in the membrane potential will lead to a?

positive feedback cycle that would open the sodium channels.

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Rising voltage in MP causes

more Na channels to open.

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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

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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.

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It occurs through the mechanism of Na-K pump

RE-ESTABLISHING RMP

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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

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Low membrane potential can not fully close the gates

REPETITIVE DISCHARGE

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is due to K leak channels

HYPERPOLAROZATION

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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.

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The potential remains near the peak of the potential for many milliseconds before repolarization begin.

PLATEAU

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slow opening allows for prolonged
depolarization

CALCIUM (slow) CHANNELS

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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 s**horten 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 fibe**r 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 processe**s 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

**PSEUDO**HYPERTROPHY

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

1. ATRIAL MUSCLE 2. VENTRICULAR MUSCLE 3. 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

1. ATRIAL 2. 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**

Chapter 2: Neromuscular Physiology Flashcards

(109 cards)