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4 Clinical Physiology > L8 Muscle > Flashcards

L8 Muscle Flashcards

1
Q

What determines the strength of a muscle contraction?

A
  1. Cross Sectional Area
  2. # and type of fibers within the muscle
  3. Frequency of muscle fiber stimulation
  4. Thickness of each muscle fiber
  5. Resting length of muscle fibers
  6. Velocity of movement
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2
Q

What kind of muscle design is the strongest?

A

pennate

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3
Q

Hennemann’s Size Principle

A
  1. When a weak contraction is desired, smaller motor units are recruited
  2. Stronger contraction is wanted, progressively larger motor units are recruited
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4
Q

Is this recruitment pattern the same when using electrical stimulation to cause a muscle contraction?

A

NO
activate Type 2 motor unit first

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5
Q

Multiple motor unit summation

A

different numbers of motor units are brought into play to produce gradations of strength

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6
Q

Type of muscle fibers stimulated to contract

A
  1. Muscle fiber type is determined by MOTOR NEURON
  2. Somatic motor neuron innervates only one type of muscle fibers
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7
Q

Slow Twitch Fibers

A

Type 1

High Oxidative Capacity
Resistant to Fatigue

postural control muscles are mainly type 1

motor neurons have a slower conduction rate

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8
Q

High Oxidative Capacity of Type 1

A

rich capillary supply
lots of mitochondria and aerobic enzymes
high concentration of myoglobin

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9
Q

Myoglobin

A

iron and oxygen binding protein

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10
Q

Resistant to fatigue type 1 fibers

A

postural muscle s

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11
Q

Fast Twitch Fibers

A

Type 2 Fibers, phasic

Lower oxidative capacity
Fatigue quickly

gastroc, biceps, extraocular muscles are type 2

motor neurons have faster conduction rate

conduction velocity is fast, cell body size is large

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12
Q

Lower oxidative capacity Type 2 Fibers

A

Fewer Capillaries, mitochondria

Lower concentration of myoglobin

High concentration of glycolytic enzymes and large glycogen stores

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13
Q

Subpopulations of Type 2 Fibers

A

Type 2a
Type 2b
Type 2x

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14
Q

Type 2a Fibers

A

slowest, for endurance

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15
Q

Type 2b fibers

A

don’t exist in humans

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16
Q

Type 2x fibers

A

fastest, sprint/interval activities

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17
Q

How is it determined what muscle fibers you have?

A

Specific muscle (gastroc vs core)
genetics
age
training

you cannot convert type 1 to type 2, you can convert between the type 2 subtypes

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18
Q

Structure of skeletal muscle

A

composed of fibers/cells
multinucleate

Myofilaments–> Myofibrils –> Muscle fiber

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19
Q

Myofibril

A

subunit of muscle cell that consists of successive sarcomeres

single sarcomere contains many longitudinal myofilaments

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20
Q

Sarcomere

A

Z to Z, basic unit of striated muscle contraction

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21
Q

H band

A

thick filaments, composed of myosin

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22
Q

I band

A

thin filaments, composed of actin

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23
Q

A band

A

overlap of thick and thin filaments

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24
Q

Z line/disc

A

center of each I band

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25
Q

What happens to the sarcomere during contraction?

A

Distance between Z lines shortens

Successive A bands move closer together

I bands slide over and between H bands, decreasing length

26
Q

Contraction Steps (ATP)

A
  1. globular head of myosin splits ATP
  2. ADP and P bound to myosin until myosin attaches to actin
  3. Phosphate is released, causing myosin to perform a power stroke
  4. Filaments slide
  5. ADP is released when myosin binds to new ATP, breaking cross bridge
  6. ATP is hydrolyzed, myosin head returns to original conformation
27
Q

Excitation-contraction Coupling

A
  1. Action potential travels down motor neuron to axon terminal
  2. Voltage gated calcium channels open, so calcium diffuse into terminal
  3. Rise in intracellular calcium causes release of AcH into NMJ
  4. Ach binds to nAch receptors in motor end plate, leading to EPP
  5. EPP leads to action potentials that travel into T-tubules
  6. AP causes calcium to be released from SR
  7. Calcium binds to troponin, allows tropomyosin to move, myosin can bind to actin
28
Q

Motor end plate

A

specialized region of sarcolemma at the NMJ with increased nACH receptors

binding of ACh to NaCh reeptors produces an end-plate potential, if it is enough, AP is produced

29
Q

Terminal Cisternae

A

Calcium in relaxed muscle is stored within expanded portions of the SR

30
Q

Transverse tubules

A

terminal cisternae are separated by a narrow gap which are the T-Tubules

narrow membrane tunnels that are continuous with the sarcolemma

31
Q

Sarcoplasmic reticulum

A

modified endoplasmic reticulum, consisting of sacs and tubes that surround each myofibril

32
Q

Structure of thin filament

A

F actin is composed of subunits of actin called G-actin

F actin are arranged in a double row and twisted to form a helix

33
Q

Tropomyosin

A

protein that lies within the groove between the F-actin chains

34
Q

Troponin

A

complex of 3 proteins that is attached to tropomyosin, not actin

35
Q

Role of Ca in muscle contraction

A

Ca binds to troponin, which triggers tropomyosin to move. Allows actin to be revealed, causing power strokes

36
Q

How does skeletal muscle relaxation occur?

A
  1. Neural stimulation stops
  2. ACh is broken down by actylcholinesterase within the NMJ
  3. SR stops releasing calcium and immediately resequesters calcium that was just released
37
Q

ACh is broken down…

A

AChE is an enzyme that metabolizes ACh into acetate and choline

38
Q

AChEIs

A

drugs that inhibit acetylcholinesterase, allows ACh to stay in the synaptic cleft longer

used in treatment of myasthenia gravis and alzheimer’s disease

39
Q

ADRs of AChEIs

A

DUMBBELSS

Diarrhea
Urination
Miosis
Bronchoconstriction
Bradycardia
Excitation
Lacrimation
Salivation
Sweating

40
Q

Muscle Fatigue

A

inability of a muscle to maintain the required tension for a given task or generate an expected power when a contraction is sustained

most likely due to accumulation of extracellular K+

41
Q

Moderate Exercise and Muscle fatigue

A

Failure at any site downstream or upstream can contribute to development of muscle fatigue

42
Q

Fatigue is multifactorial

A

Increased intracellular concentration of lactate, H+, inorganic phosphate

impaired Ca 2+ release

increased production of fatigue reactants

depletion of glycogen

43
Q

Central Fatigue

A

NMJ and upstream
fatiguing exercise changes brain concentrations of NTs, which decreases neural drive to muscle

increase perception of effort
decreased motivation
high serotonin, low dopamine

44
Q

Peripheral Fatigue

A

produced by changes at or distal to NMJ

AI diseases that target synaptic proteins
muscular dystrophies

45
Q

Central fatigue pathological conditions

A

MS, guillain barre, CIDP

46
Q

S/S of Muscle Fatigue

A

muscle discomfort, pain, cramping
tremor in contracting muscle
unintentional slowing of movement
altered quality of movement
decline in peak torque, EMG, MMT

47
Q

Muscle Fatigue Treatment

A

No single agreed upon treatment , fatigue must be evaluated based on many variables

massage, compression, NSAIDs, e-stim all treat the S/S

light aerobic exercise is more effective than total rest

48
Q

Endurance training increases…

A

lactate threshold

means it prolongs the time until an increasing proportion of energy must be derived from anaerobic glycolysis

49
Q

Muscle adaptations to aerobic/endurance training

A
  1. Increases # of mitochondria and aerobic enzymes in all muscle fiber types
  2. Increases # of type 2a fibers and decreases # of type 2B fibers
  3. Does NOT increase size of muscles
50
Q

Other adaptations of endurance training on muscles

A

improved ability to obtain ATP from OP
increased size and # of mitochondria
less lactic acid produced
increased myoglobin
increased triglyceride content
increased lipoprotein lipase
increased energy derived from fat
Lower rate of glycogen depletion
improved efficiency of O2 use
decreased type 2B fibers

51
Q

Muscle adaptations to resistance training

A

Hypertrophies type 2 muscle fibers

Increase in size and number of MYOFIBRILS

cell # increases mainly in animals, minimal in humans

52
Q

Smooth Muscle

A

found in almost every organ
major component of the walls of hollow organs

53
Q

Smooth muscle contraction

A

-arranged in circular or longitudinal layers
-lack of sarcomeres, no striations
-more thin vs thick (16:1)
-actin and myosin contract by unique regulatory mechanism

thin filaments/actin attach to either plasma membranes, dense bodies

54
Q

Myosin Heads of Smooth muscle fiber

A

arrangement of myosin heads to thin filaments is required for proper smooth muscle function

can still contract at very stretched lengths

must be able function when greatly stretched

55
Q

Urinary bladder

A

smooth muscle cels stretch 2.5 times their resting length

56
Q

Uterus

A

smooth muscle cells stretch 8 times their original length by end of pregnancy

57
Q

Differences between smooth and skeletal muscle

A
  1. smooth muscle cells produce graded depolarizations and contractions w/out producing APs
  2. Extracellular Ca enters through special channels in smooth
  3. Ca binds with calmodulin in smooth
  4. Calmodulin joins with myosin kinase
58
Q

Similarities between Smooth and Skeletal

A
  1. Depends on sharp rise in intracellular free Ca
  2. Greater the depolarization of smooth muscle, more Ca will enter the cell, stronger the contraction
  3. Myosin head binds with actin
  4. Relaxation occurs when Ca concentration decreases
59
Q

Single-unit smooth muscles

A

Most smooth muscles
many gap junctions
only some cells receive ANS innervation
have intrinsic electrical activity and contract in response to stretch

60
Q

ANS innervation of smooth muscles

A

entire surface of a smooth muscle contains receptors

ACh released along a stretch of an autonomic nerve fiber located a distance from smooth muscle cells

61
Q

Varicosities

A

regions of autonomic fiber that release NT

62
Q

Multiunit smooth muscles

A

contraction requires nerve stimulation
few if any gap junctions

arrector pili muscles in in skin
ciliary muscles attached to eye lens

4 Clinical Physiology (9 decks)

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