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Physiology > 11. 12.Skeletal muscle, contraction, electromechanical coupling , muscle fatigue > Flashcards

11. 12.Skeletal muscle, contraction, electromechanical coupling , muscle fatigue Flashcards

1
Q

Basic characteristics of skeletal muscles

A

Attached at skeletal bones

striated

Innervated by somatic nervous system

Contraction under voluntary control

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2
Q

What are functions of skeletal muscle

A

Reflex and voluntary movements

Respiration-contraction of diaphragm and external intercostal

Regulate body temperature (thermogenesis)- heat generated during contraction - shivering when body temp low

Controls entrance (mouth) and exit (anus) orifices- voluntary control of food and fluids and rid urine/faeces

Help movemnt of venous blood to heart

Support and protect visceral organs

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3
Q

They are made of muscle fibers. what are these called

A

myofibers (each fiber is a single cell)

  • Elliptical, multinucleated and nuclei just below sarcolemma

*The cytoplasmic surface of the cell membrane is
covered by a protein called dystrophin, which
provides mechanical stabilization during cell
contractions.

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4
Q

Composition of a myofiber

A

Individual fibres surrounded by connective tissue ENDOMYSIUM

Muscle fibers grouped together in fascicles surrounded by PERIMYSIUM

Fascicles bundle together to form whole muscle surrounded by epimysium

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5
Q

What do myofibers (myocytes) contain in their cytoplasm that helps with contractility

A

myofibrils

1 micrometer thick

divided into thick and thin myofilaments

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6
Q

What are myofibrils
What is their main structural and functional unit

A

Cell organelles responsible for muscle contraction

Sarcomere

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7
Q

What are the components of myofibers

A

cell memebrane= sarcolemma (surrounded by ECM forms basal lamina)

Cytoplasm= sarcoplasm ( has glyccogen granules, myoglobin, sarco retic and mysofibrils)

ER= Sarcoplasmic reticulum (storage for Ca2+

T tubules ( sarcolemmal invaginations conducts excitation from sarcolemma to myofibrils)

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8
Q

What causes the striated appearance

A

repeating dark and light bands in myofibrils

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9
Q

What are the thick and thin filaments of sarcomeres

A

thick= myosin

thin= actin

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10
Q

myosin composition

A

6 polypeptide chains
2 heavy 4 light

heavy chain = long tail and globular head. the tails form double helix

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11
Q

What are properties of myosin heads

A
  1. Bind to active center of actin
  2. Binding site for ATP
  3. Binding site for light chains
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12
Q

Actin is a globular protein froming double helix

What blocks its active center

A

Tropomyosin

Bound to tropomyosin is troponin (3 subunits I,C,T)

I= prevents removal of tropomysoin when there no signal
C= receives signal from calcium ions
T= bind the other sununits to topomyosin

*Troponin moves tropomyosin when there is a impulse

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13
Q

As well as contractile proteins what other proteins are there

A

Cytoskeletal proteins

Corrects arrangement of thick and thin filaments

Titin and nebulin are longitudinally arranged cytoskeletal protein

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14
Q

What are the 6 physiological properties of skeletal muscle

A
  1. excitability
  2. Conductivity
  3. Contractility
  4. elongation
  5. Elasticity
  6. Generation of heat
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15
Q

How are skeletal muscles excited

A

nerve impulses reach them along motor neurones of somatic system

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16
Q

The axons reach the muscle by what site

A

Neuromuscular juntion

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17
Q

Sarcomere bands

A

Z lines= ends of the sarcomere
DARK: a-actinin homodimer

I band= either side of z line
LIGHT: thin actin filaments

A band=located in middle of sarcomere
large diameter so restricts light
DARK: Thick myosin

M line= where the myosin filamets join tail
to tail

H zone= where thick and thin filaments
dont overlap (A and I band)
LIGHT

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18
Q

What bit of the sarcomere contracts

A

Only I band shortens

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19
Q

What does it mean the myo-neuronal synapse is 1:1?

A

Each impulse in the presynaptic cell triggers an action potential in the postsynaptic structure without the need for temporal or spatial summation, as in most CNS cells.

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20
Q

Mechanism of neuromuscular junction

A
  1. AP travels down motor neuron and causes depolarization
  2. Depolarization causes Ca2+ channels to open and calcium to enter presynaptic terminal
  3. Ca2+ and snare complex Ach is extruded into synaptic cleft
  4. Ach binds to receptors on post synaptic membrane ( mototr end plate)
  5. This causes Na+/ K+ channels to open = depolarization= EPSP=AP in adjacent muscle tissue
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21
Q

Excitation/contraction coupling

A

AP in mucle cell travels along sarcolemma until it reaches T TUBULES

DIHYDROPYRIDINE RECEPTORS are located in t tubules

AP causes conformational change to DHP

Causing Ca2+ channels to open ( RYANODINE RECEPTORS) or sarcoplasmic reticulum

Calcium ions go into bind to troponinc to move tropomyosin and expose actin myosin head

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22
Q

What is the result of the coupling mechanism

A

Ca2+ leave SR and bind to tropinin C

Causes removal of tropomyosin from active sites of actin

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23
Q

So which is the link between excitation and contraction

A
  1. Release of Ca2+ from SR
  2. Binding of actin to myosin =contraction
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24
Q
A
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25
Q

Sliding filament theory of Huxley and Niedergerke

(baso how is the contraction executed)

A

Tropomysosin is removed from the active centers

ATP molecule binds to myosin head then is degraded to ADP and P by myosin ATPASE

Possible binding of myosin to actin = CROSS BRIDGES

These cross bridges increase 200X the
ATPase activity of myosin head.

When ADP and P detatch from myosin head, it tilts 45’.

This tilt causes the bound actin to slide towards centre of sarcomere

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25
Q

How is the acto myosin head disassembled

A

When new ATP molecule binds to myosin head

This is then degraded to ADP and P and process starts again

26
Q

Depending whether tension or length changes, what are the types of contractions

A

ISOMETRIC CONTRACTION=No movement Only tension changes at steady length, muscle doesnt chnage length but tension increases

ISOTONIC CONTRACTION= length changes under steady tension.

26
Q

What is is Lymn Taylor cycle

A

It represents the sequence of
biochemical reactions that convert
the energy released by ATP into
motion.

26
Q

Therefore, what are the 2 prerequisites for binding of actin to myosin

A
  1. Ca2= needed to displace tropomyosin from actin active centre
  2. Breaking down ATP on myosin head to ADP and P. Then release of this causes head to tilt and pull actin filaments for contraction
27
Q

What are the 2 types of isotonic contraction

A

concentric= muscle shortens

Excentric= muscle lengthens

28
Q

What happens during concentric contraction

A

Lifts a load of a weight lesser than the max tension of the muscle
Muscle length shortens
Like doing bicep curl

29
Q

What happens during eccentric contraction

A

Lifts a load that exceeds 1.6-1.8 times the max tension of the muscle
Length of muscle increases even though active tension greater

E.g Descending down the stairs or lowering a load in hand

Max muscle active tension is greater during eccentric contraction eg can lower heavier load than lift it
Therefore can cause muscle damage like muscle fever

30
Q

What damage to muscles can eccentric contraction

A

Delayed onset muscle soreness ( muscle fever)

Bc you can lower a heavier load with your hand than you can lift

31
Q

What happens during isometric contraction

A

muscles increases tension muscle length does not

These static contractions are performed by muscles that maintain upright position of body or stabilize joint position

32
Q

How do both these contractions occur during lifting of a load

A

When a load is to be lifted, the muscle first contracts isometrically until it develops tension EQUAL to the load

Then it lifts the load by contracting isotonicaly ( muscle shortens and lengthens)

33
Q

Relationship btw speed and concentric contraction

A

As the lod increases, speed of contraction decreases

when the load becomes
equal to the maximum isometric tension
(maximum force), the speed becomes zero.

eg holding a heavy dumbell but cant flex it up)

34
Q
A
35
Q

How is active tension generated

A

when actin filaments bind to mysoin filaments ]

It is greatest when the isometric
contraction occurs at the optimal length
of the muscle, which corresponds to the
length at rest.

36
Q

How is passive tension generated

A

Generated by structural proteins called Titin, elastic and collagen fibers

It is generated by stretch

baso u reach optimal length of muscle and u try to stretch it further

37
Q

When is the highest active tension generated

A

at sarcomere lenth 2-2.2 micrometres

This is where max overlap of thin and thick filaments

2.2 micrometres is length of sarcomere at rest

38
Q

Depending on frequency of impulses to muscle, what type of contractions can we get

A

Muscle twitch= single isotonic contration
Impulse is longer than contration and relaxation duration. Each impulse finds the muscle in relaxed state and makes new contraction

Tetanus= impulse excites muscle before it completely relaxes from previous contraction so increases amplitude tetanic contraction

39
Q

Difference btw incomplete and complete tetanus

A

Incomplete= Impulse finds muscle in relaxation phase
serrated graph

Complete= when impulse finds muscle in contracted state
smooth graph

40
Q

Phases of single isotonic contraction

A

Latency period - this is the time from
the beginning of the stimulus to the
beginning of contraction.

b. Contraction phase - the ascending part
of the curve; and

c. Relaxation phase - the descending part
of the curve.

41
Q

Why can muscle contractions be summated

A

Because the duration of a single muscle
contraction (50 - 100 ms) significantly exceeds the
duration of a single AP generated in the
sarcolemma (5 ms).

So muscle cells can react to new APs

42
Q

How we define the motor unit of а muscle?

A

. muscle fibes innervated by 1 motor neurone

(The finer the movements of a muscle,
like fingers , the smaller the number of muscle cells in the 1 motor unit.)

(large motor units made of thousands of muscle fibres and common in muscles of back)

43
Q

Are all motor units used during contraction?

A

. Active units at 40% at any given time
.When stronger contraction is
needed, % of active motor units increases.

44
Q

What are the types of muscle fibres

A

slow twitch oxidative (type 1)
fast twitch oxidative glycolytic (type 2 A)
fast twitch oxidative glycolytic (type 2 B)

45
Q

shortening velocity of mucle fibres is determined by atp breakdown. what it like for each fibre?

A

slow twitch - breakdown small and slow. takes 3000ms
fast twitch - breakdown high so contraction relaxtion cycle only takes 30ms

46
Q

Properties of slow twitch fibres

A

. Performs contractions with little maximal force for long time without fatigue
. energy supplied by aerobic pathway.
. lots of mitochondria and myoglobin and well supplied
. red colour
. fibres small diameter for quick gas exchange
** (long back muscles for posture)

47
Q

Properties of fast twitch A

A

. rapid contractions, moderate force
. well vascularized and rich myoglobin
. red colour
. resistant to fatigue (has good oxidative pathwyas for ATP resynthesis

48
Q

Properties of fast twitch B

A

. rapid contraction BUT not for long time
. contractions of high maximal force
. ATP from anaerobic glycolysis of glycogen
. little myoglobin and mito
. white colour
.fibres large diameter
** ocular muscles

49
Q

Which muscle fiber is rare in humans

A

fast twitch 2a= contract faster, lots of glycogen
Anaerobic pathway and aerobic pathway bc pf MITOCHONDRIA

Fast twitch 2b doesnt hv mitochondria (also called white fibers)

50
Q

What represents muscle fatigue

A

REVERSIBLE decrease of muscle performance due to prolonged work

  • Increasing the refractory period
  • diminishing the force of contraction
  • slowing down the velocity of contraction and relaxation
51
Q

What are the causes of fatigue in fast muscle fibers

A

Occurs due to the depletion of glycogen stores and accumulation of lactic acid-ACIDOSIS

Inorganic phosphates released during the breakdown of creatine-phosphate
also may lead to muscle fatigue.

52
Q

Why does acidosis and ingorganic phosphtaes lead to muscle fatigue

A

Acidosis inhibits glycolysis (main source of energy for contraction)

BOTH also reduce the release of Ca2+ from the sarcoplasmic reticulum and the sensitivity of the contractile system to it.

53
Q

What causes muscle fatigue in slow fibers

A

Resistant to muscle fatigue

Mainly occurs if O2 diminshes

54
Q

What does central fatigue mean

A

Fatigue can occur throughout the
body as a result of changes of the
pattern of muscle stimulation by CNS
which decreases the neural drive to
the muscles, and leads to reduced
muscle activation.

55
Q

What does electromyography register

A

EMG registers electrical potentials generated in the muscle upon its
excitation, not its mechanical response!

56
Q

What are the types of EMG electrodes used in medicine

A

needle-like and surface electrodes.

57
Q

What is the difference between
the electrical potentials detected
by needle-like or surface
electrodes?

A

Needle-like electrodes can register electrical potentials generated by
one or several motor units.

While through surface electrodes, total potential from multiple motor
units is registered.

58
Q

What are the adv and disadv of needle electrodes

A

Needle electrodes can register the electrical potentials generated in one or
several motor units and are therefore preferred in neurological practice.

However, the method is invasive.

59
Q

What are the adv and disadv of surface electrodes

A

Surface electrodes register the total electrical potential generated by
multiple motor units.

The overall muscle response to stimulation and the inclusion of new motor
units can be examined.

However, no detailed information is available on the individual motor units.

60
Q

Clinical application of EMG

A
  1. Diagnose muscular and neuromuscular diseases:
    * muscular dystophy
    * myasthenia gravis (affect neuromuscular junc)
    * Carpal tunnel syndrome
    * Poliomyelitis (motor neurones)
  2. To guide the needle when injecting botulinum toxin or phenol into the muscles.
  3. prosthetic implants with myoelectric control
  4. monitor neuromuscular function during general anesthesia when using
    neuromuscular blocking drugs.
    (avoid crurare effect)

Physiology (20 decks)

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