answer a equation about anatomy lactur

profilesalzari
kine_2560_muscle_s14.ppt
Home>Nursing homework help>answer a equation about anatomy lactur

GOALS Ch 9

What do all muscle cells have in common?

What are some common terms used to describe muscle cells?

What are major muscle functions?

How do muscle cells differ? (p. 310-11, 9th ed) Compare the three types of muscle tissue: location, voluntariness, rhythmicity, etc

MUSCLE SIMILARITIES (Cardiac, smooth & skeletal)

  • 1. Skeletal and smooth cells elongated
  • 2. Contraction dependent on myofilaments

Actin and myosin

  • 3. Terminology: myo- and sarco- = muscle

Sarcolemma = cell membrane

Sarcoplasm = cell cytoplasm

Sarcoplasmic reticulum (SR)= endoplasmic reticulum

*

Special characteristics of muscle

Exhibit excitability/irritability = ability to receive & respond to stimulus

Contractility = ability to shorten forcibly w. Stimulation

Elasticity= ability of muscle to recoil & resume resting length after being stretched

Extensibility= ability to be stretched

General Muscle Functions

  • Produces movement by contraction [all]

Actin slides into myosin

  • Maintains posture [skeletal
  • Stabilizes joints [skeletal]
  • Generates heat [skeletal]
  • Forms valves in internal organs [ smooth]
  • Pumps blood [cardiac]
  • Moves urine [smooth]

MUSCLE DIFFERENCES (in 3 types). Make a table to describe these:

  • Location
  • Structure of cells
  • Function
  • Means by which activated to contract
  • Aerobic
  • Source of calcium
  • Number of nuclei, etc... .

1. Skeletal Muscle Characteristics

Skeletal description

  • Longest muscle cell
  • Attached to skeleton
  • Voluntary control
  • Striations
  • Multinucleated
  • Tires easily
  • Calcium from SR

Skeletal muscle: striations

1. Skeletal muscle Characteristics

  • Aerobic & anaerobic

[with and without oxygen]

  • T-Tubules

[new organelle in muscle]

  • Can display tetany

locked contraction

  • No pacemaker

[ no contracting by itself]

2. Cardiac Muscle

  • in heart wall = myocardium

Involuntary; self-exciting (has pacemaker)

Striations; single nucleus per cell

Rhythmic (75 bpm) ; Slow contraction

Aerobic only!

Cardiac Muscle

Two sources of Calcium/Ca++: from SR [inside] and from ECF [outside]

FYI:

100 bpm = tachycardia;

<60 bpm = bradycardia

3. Smooth muscle

Walls of hollow visceral organs

No striations; single nucleus per cell

Involuntary; self exciting & rhythmic

3. Smooth muscle

Slow, sustained contraction = peristalsis [of food, urine, etc]

Has pacemakers

Mainly aerobic

Calcium from SR and ECF

GOALS: Detail Skeletal Muscle

  • Describe the layers of connective tissue coverings.
  • Describe nerve and blood supply to skeletal muscle.

What is the difference between direct and indirect attachments?

Of origin and insertion?

1. Connective tissue wrappings of skeletal muscle

Endomysium =surrounds each muscle fiber

Perimysium = collagen sheath around fascicle = bundle of muscle cells

Epimysium = outer coat around perimysium of dense connective tissue; can bind to

Deep fascia = outermost layer that binds muscle into groups

Fascia

  • All connective tissues continuous

with each other and

with tendons

  • Reinforce muscle
  • Provide entry/exit routes for blood vessels

*

2. Nerve & blood supply of skeletal muscle

  • Muscle:

Supplied with nerve ending to contract

Needs rich blood supply for:

oxygen and glucose delivery (artery) &

waste [CO2, ..] pick up (veins)

Blood vessel (artery) and nerve enters center of muscle and branches into connective tissue

3. ATTACHMENTS:

  • Most muscles span joints & have at least 2 attachments to bone

1. INSERTION = End that moves

2. ORIGIN = End that is stationary; usually proximal

DIRECT ATTACHMENTS

= Epimysium fused to periosteum of skeleton


INDIRECT ATTACHMENTS= Epimysium extends beyond muscle as

1. tendon

2. Aponeurosis = broad connective tissue sheet

GOALS: Skeletal Muscle Cell

  • Describe the detailed parts of a skeletal muscle cell.
  • Examine the structure of sarcoplasmic reticulum and t-tubules.
  • Describe the characteristics of actin and myosin.
  • How do the regulatory proteins troponin and tropomyosin affect actin ?

MICROSCOPIC SKELETAL MUSCLE CELL/FIBER ANATOMY

  • sarcolemma = cell membrane
  • sarcoplasm = cytoplasm contains:

stored Glycogen = glucose polymer

Myoglobin = protein that stores oxygen in cell

Myofibrils = bundles of contracting myofilaments; densely packed

many nuclei

many mitochondria for energy

Sarcoplasmic reticulum chambers called cisternae full of Ca++

MICROSCOPIC SKELETAL MUSCLE CELL ANATOMY………….

transverse tubules = T-tubules =

channels from cell membrane deep into cytoplasm

- delivers electrical message of depolarization

causing Ca++ to exit cisterns into cytoplasm

  • Cells appear striated from muscle proteins:

actin, myosin, troponin, tropomyosin

Myofibril anatomy

  • Single muscle fiber can contain thousands of myofibrils
  • Myofibrils contain sarcomeres (functional unit of muscle cell/smallest contracting unit) arranged end-on-end
  • Sarcomeres made of myofilament proteins arranged in stripes in alternating I and A bands

Detail of myofilament proteins in sarcoplasm

1. Actin

“I” band; makes up most of thin filaments

Has sites for cross bridges w. myosin heads

Contains regulatory proteins

1. troponin: inhibits actin; can bind calcium

and rearrange

2. tropomyosin stiffens actin and blocks myosin binding sites in RELAXATION so myosin can’t attach

Z = midline dark area

slides during contraction

Detail of myofilament proteins in sarcoplasm

  • MYOSIN

“A” band, thick, dark

rodlike tail w. 2 globular heads =

Heads are site of cross bridges

ATP and actin binding sites

stationary during contraction

Myosin

GOALS

  • Describe the anatomy of the T-tubule and cisterns.
  • Trace the path down a t-tube to the cisternae [path depolarization will take].

Sarcoplasmic Reticulum Cisterns & T-tubule anatomy

  • SR cisterns = system of membrane tubules surrounding each myofibril

SR run longitudinally

  • Cisterns store Ca++ in relaxation and release Ca++ to cytoplasmic proteins during contraction
  • If cisterns where A & I bands meet, with mitochondria and glycogen, called = terminal cisternae

T-TUBULES ANATOMY………..

  • -indentation of sarcolemma at each I and A junction
  • tubes run from ECF into terminal cisternae

carries electrical depolarization message to release Ca++ from cisterns

  • Fyi: triads = cisternae-t-tube-cisternae

GOALS

Describe the 3 parts of the neuromuscular junction [NMJ] = where nerve supplies muscle

1. Motor Neuron of NMJ

  • neuron highly branched to each muscle; one to middle of each muscle fiber
  • Motor neuron has high concentration of

1. mitochondria

2. synaptic vesicles (sacs) containing neurotransmitter = ACh

  • when nerve “fires” it releases ACh from sacs; ACh flows into synaptic cleft of synapse

2. Synaptic cleft of SYNAPSE of NMJ

  • = gap or space between muscle & nerve filled with gel ECF
  • ACh diffuses across synaptic cleft to muscle

3. MUSCLE CELL OF NMJ

  • highly folded sarcolemma =motor end plate = where nerve fiber comes close to muscle
  • Motor plate has binding sites for Ach (blocked in disorders liked myasthenia gravis)
  • high concentration mitochondria
  • contains actin & myosin in cytoplasm for contraction

GOALS

  • What is coupling?
  • Follow depolarization to the cisternae.

What is the sliding filament theory?

  • Describe the events of contraction and relaxation.

Contraction coupling

  • Sequence of events by which an action potential along the sarcolemma leads to sliding of protein myofilaments.
  • First there is excitation with electricity….. by depolarization
  • Then this is coupled to sliding filaments of muscle contraction

SLIDING FILAMENT CONTRACTION

  • SLIDING FILAMENT THEORY
  • thin filaments slide past thicker myosin so that actin and myosin overlap to a greater degreeshortening of muscle

heads of myosin attach to actin, and de-attach,ratcheting motion; requires Ca++ [Ca++ rearranges troponin/tropomyosin with actin,”freeing” it to slide]

Depolarization path of action potential

  • 1. Neuron depolarization:

Na+ enters the neuron cytoplasm in small steps down to the end of the neuron.

Synaptic vesicles lyse at membrane of neuron

NT [Ach] is released into synaptic cleft of synapse

  • 2. Synaptic cleft neurotransmitter transmission:

Ach diffuses high to low, neuron to muscle

3. Skeletal muscle cell depolarization:

NT/Ach binds at motor end plate, & starts ‘local ion changes’, opening Na+ channelsmuscle cell inside becomes slightly less negative = local graded potential

Depolarization/actionpotential sweeps down sarcolemma into T-tubule into cell [1-2 millisec]

Cisterns release Ca++ which exits into cytoplasm

CONTRACTION

  • Ca++ binds to troponin which then changes shape
  • Myosin binding sites on actin exposed
  • actin is ‘let go” & it slides into myosin
  • actin binds to myosin heads in cross bridges; using ATP to de-attach = racheting motion
  • muscle shortens = contraction

Fyi: Cross Bridge Cycle,
Specific detail of myosin changes

  • 1. Cross bridge attachment (energized myosin attaches to actin)
  • 2. Working stroke (ADP and Pi are released, myosin head binds & pivots, pulling on actin)
  • 3. Cross bridge detachment (after new ATP binds to head, actin is let go

Fyi: Cross bridge cycle, Specific detail of myosin changes

  • 4. “Cocking” of myosin head (hydrolysis of ATP to ADP and Pi by ATPase gives energy and myosin head returns to high energy position, “cocked”
  • cycle repeats

  • Contraction (SLIDING) continues as long as there is Ca++ and ATP
  • Muscles shorten 30-35%

MAJOR EVENTS RELAXATION

  • Acetylcholinesterase (ACHase) on sarcolemma decomposes Ach
  • muscle no longer stimulated
  • Ca++ moves from cytoplasm into sarcoplasmic reticulum
  • cross bridges break
  • actin slides back out of myosin

RELAXATION ….

  • muscle lengthens
  • troponin & tropomyosin hold actin

Comparison of Ca++ in contraction and relaxation

  • Relaxation:

when Ca++ is low in the cell cytoplasm [high in cisterns], muscle is relaxed, & tropomyosin blocks actin

  • Contraction:

when Ca++ rises in the cell cytoplasm, it binds to troponin, it changes shape, tropomyosin moves, and actin is “freed” to slide

GOALS

  • Name the sources of ATP used in contraction.
  • Review production of ATP by glucose breakdown.
  • Describe the source of sugar available in the muscle cell.
  • Describe the delivery of oxygen to the muscle. What acts as a holding tank for oxygen in the cell?

ENERGY SOURCES FOR CONTRACTION

Where does muscle get ATP for cross-bridging in contraction?

1. stored ATP in muscle cell

2. stored creatine changed to creatine phosphate in muscle cell

These last a few seconds, & cell must make ATP from glucose

HOW DOES MUSCLE GET GLUCOSE?

  • Liver and muscle change glycogen to glucose & delivers it to muscle through blood.

GLYCOLYSIS IN MUSCLE CELL

  • glucose diffuses into muscle cell from blood
  • enzymes in cytoplasm change glucose to pyruvic acid (3C)
  • yield 2 ATP
  • pyruvic acid diffuses into mitochondria

KREBS CYCLE/AEROBIC RESPIRATION IN MUSCLE CELL

  • pyruvic acid changes to acetyl co-A
  • co-A enters Krebs cycle
  • O2 diffuses into cell and enters mitochondria & Krebs cycle coupled w. oxidative phosphorylations
  • products are heat, CO2 gas, 36 ATP, and H+ H2O

HOW IS OXYGEN SUPPLIED FOR KREBS CYCLE?

  • 1. Hemoglobin (Hb), a blood protein in red blood cell releases oxygen to muscle cell 2. Myoglobin (Mb), a protein in muscle cell,

1. stores O2 from blood in muscle cell temporarily

2. releases O2 to cytoplasm when blood vessel clamped in contracting muscle

GOALS

  • Explain how ATP is produced when oxygen delivery to the muscle cell is poor.
  • How is the liver affected?

WHAT HAPPENS WHEN O2 TO CELL RUNS OUT? EPOC

  • no more krebs cycle
  • EPOC =oxygen debt=excess postexercise oxygen consumption

when no O2, pyruvic acid increases

Pyruvic acid cannot diffuse out of cell

Pyruvic changes to lactic acid to diffuse out of cell to blood

blood carries lactic acid to liver

EPOC/ OXYGEN DEBT IN LIVER

  • Liver runs glycolysis ‘backwards’: changes lactic acid back to pyruvic acid, & adds ATP to change it back to glucose
  • Therefore liver uses its ATP
  • Body in oxygen debt until

1. Liver replaces its ATP

2. Muscle replaces its creatine phosphate & original ATP

3. Mb oxygen reserves replenished

4. glycogen replenished

GOALS

  • List some characteristics of the physiology of muscle contraction.

Contraction of a whole skeletal muscle

  • Force exerted by contracting muscle on an object = muscle tension
  • Force exerted on the muscle by the weight of the object = load
  • Motor unit=a motor neuron and all the branches to muscle fibers it supplies

Muscles exerting fine control have small motor units; large motor units to large muscles with less precise control, like hip

  • Force of muscle contraction affected by
  • 1. number & size of contracting muscle cells
  • 2. frequency of stimulation
  • 3. degree of muscle stretch
  • The greater the load, the slower the contraction.

GOALS

  • Define refractory period, muscle twitch, all or none response, and threshold.

MUSCLE RESPONSES IN AN ISOLATED MUSCLE: muscle twitch

  • Muscle twitch = response of motor unit to single action potential
  • 1. Threshold stimulus =

Minimum strength (stimulus) needed for contraction

Anything less than threshold gives no contraction

  • 2. ALL-OR-NONE-RESPONSE

If muscle gets threshold stimulus, contracts completely

If muscle gets greater than threshold, still contracts exactly same as threshold!!

No partial contraction of isolated muscle!!!!

FYI: MYOGRAM

  • = Graph of single contraction of isolated muscle lasting fraction of second
  • Phases of twitch

1. Latent/lag = period between threshold stimulus until contraction begins

2. Contraction = beginning to maximum contraction

3. Relaxation = maximum contraction to no contraction

4. Refractory = period after stimulation & contraction in which muscle will not respond. Can stimulate w. Threshold stimulus and no response!!!!

GOALS

  • Examine the terminology in following slides: rigor mortis, fatigue, ….

MUSCLE CONDITIONS

  • Tetany = sustained contraction; no relaxation period (in skeletal)
  • Fatigue = inability to contract muscle; increased lactic acid, low pH, high K+, usually not lack of ATP….
  • Cramp = prolonged spasms; lack of ATP; low Ca++. Drink water.
  • Tone = relaxed muscles always slightly contracted

Rigor mortis (rigor of death)

  • Muscles stiffen 3-4 hours after death
  • Peak rigidity 12 hours

Ca++ rises in muscle cells;

No ATP for detachment of actin from myosin

  • Rigidity decreases over 48-60 hours by bacterial degradation

TERMINOLOGY

  • Prime mover = muscle in a group responsible for most movement
  • Synergist = muscle in a group that assists prime mover
  • Antagonist = muscle in group that opposes prime mover

  • Origin = point of attachment of one end of muscle that is relatively immobile
  • Insertion = point of attachment of one end of muscle that moves
  • Insertion moves toward origin during contraction

NOMENCLATURE

  • Origin-insertion

Sternocleidomastoid

Origin = first - sternum

Insertion = last = mastoid process

  • Points of origin

Biceps

Two heads of origin (attachment)

  • Size

Pectoralis major (large)

Gluteus maximus and minimus

  • Shape

Deltoid (triangle); trapezius (trapezoid)

  • Action

Extensor digitorum (extends)

Flexor digitorum

TYPES OF CONTRACTION

  • Isotonic = muscle shortens w. Contraction
  • Isometric = muscle stays same length w. contraction

Velocity of contraction

  • Slow oxidative fibers
  • Fast oxidative fibers
    Fast glycolytic fibers

Activity Effects

  • Immobilization of muscles lead to atrophy (cell wasting or atrophy
  • Resistance exercise cause skeletal muscle hypertrophy (cell enlargement)
  • Regular aerobic exercise leads to increased endurance, increased strength,..

  • Review questions, 9th ed:
  • 1-5, 9-14

  • Short answer
  • 16,18, 20