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PHGY 209 > Muscle Physiology > Flashcards

Muscle Physiology Flashcards

1
Q

What are the three types of muscle?

A

Skeletal, cardiac, and smooth

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2
Q

Function of skeletal muscle?

A

Posture and locomotion (under conscious control)

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3
Q

Function of cardiac muscle?

A

Responsible for the rythmic contractions of the heart

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4
Q

FUnction of smooth muscle?

A

Involuntary contraction in blood vessels, gut, bronchi and uterus

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5
Q

How are muscles attached?

A

Each muscle is attached to a tendon on either end, which are in turn attached to bones

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6
Q

What does muscle contraction do? (skeletal)

A

Shortening of the muscle pulls on tendons, in turn causing flexion of joints

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7
Q

Skeletal muscle composition?

On the most surface level

A

Each skeletal muscle is composed of long thin cells called muscle fibers - multinucleated cells

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8
Q

How are skeletal muscle fibers generated (development)?

A

Fusion of a large number of myoblasts (precursor cell) - each myoblast has one nucleus, so that when fused, the muscle fiber is multinucleated

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9
Q

What are skeletal muscle fibers composed of?

A

Myofibrils - cylindrical bundles

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10
Q

Describe myofibril composition?
from the side || cross section

A

Myofibril is composed of alternating light I bands and dark A bands.
The I bands are all marked down the middle by a Z-line.
The Z-lines demark the sarcomere (contractile unit)
**lattice of the thin/thick filaments that form the sarcomere

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11
Q

Describe the composition of the sarcomere?

A

Contractile unit
Made of two types of overlapping filaments:
-Thick filaments (one end of the A band to the other)
-Thin filaments (attached to Z lines, extending across I and into A)
Thin and thick filaments are attached by crossbridges

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12
Q

What is the I-band?

A

Section of the sarcomere containing only thin filaments

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13
Q

What is the H-zone?

A

Section of the sarcomere containing only thick filaments

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14
Q

What is the A-band?

A

Overlap of thin and thick filaments
Forms the lattice structure

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15
Q

What are thin filaments made off?

A

Actin - each actin filament being madde of globular acting subunits (helix)

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16
Q

What are thick filaments made off?

A

Myosin - long strand with a head group
**note: two heavy myosin strands form a myosin II molecule
A bunch of myosin then form the thick filaments

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17
Q

What is the sliding filament model? Explain how it works

A

Theory explaining muscle contraction
-ATP = myosin dissociation
-phosphorylation = conformational change to active state
-attachment
-power stroke + dissociation of ADP+P
*repeated, non synchronized process powered by ATP hydrolysis

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18
Q

What drives the sliding filament model? What is the alternate name?

A

The cross bridge cycle is driven by ATP binding/hydrolysis to the myosin head groups
1. ATP binds to myosin head - dissociation of myosin head from actin
2. ATP hydrolysis occurs - change in conformation of myosin head group
3. Binding of myosin head group (thick) to actin (thin)
4. Power stroke occurs - ADP and P are removed during this step

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19
Q

What initiates the volontary contraction of muscle? +pathway

A

Motor control regions of the brain -> axons in spinal cord -> motor neurons in spinal cord -> efferent fibers (motor neurons)

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20
Q

What is a motor unit?

A

A motor neuron and the group of muscle fibers it innervates

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21
Q

Where do motor neuron synapses go to?
How many muscle fibers are innervated by a single motor neuron?

A

Approximately the middle of the muscle fiber
Anywhere between 10 and a thousand dependent on muscle

22
Q

Where does sensory input & motor output exit the spinal cord?

A

Sensory input: dorsal horn (back)
Motor output: Ventral horn (stomach)

23
Q

Name of the neurotransmitter ?
receptor ?
at neuromuscular junctions?

A

Acetylcholine (ACh)
nicotinic acetylcholine receptors

24
Q

Explain the process of neuromuscular transmission

A
  1. Action potential in the motor neuron
  2. Acetylcholine release at presynaptic cleft across synaptic cleft
  3. Na+ influx through activated nicotinic acetylcholine receptors
  4. Depolarization of the endplate - action potential is reached
  5. Fiber action potential (whole fiber contracts)
25
Q

What are T-tubules? Where are they found?

A

ring-like invaginations of the plasma membrane that are essential for muscle contraction found on the exterior of the myofibril

26
Q

What is the sarcoplasmic reticulum? Where are they found?

A

specialized organelle in muscle cells that stores and releases Ca2+ to control muscle contraction and relaxation found on the exterior of the myofibril

27
Q

What is excitation-contraction coupling?

A

process that links the electrical activity of muscles to their mechanical contraction

28
Q

How does excitation-contraction coupling work?

A
  1. Activation of the ryanodine receptor by an action potential from the T-tubules allows for the efflux of Ca2+ from the sarcoplasmic reticulum to the cytoplasm
    *cytoplasm between SR and T-tubes
  2. Ca2+ binds to troponin on the thin filaments
  3. Conformation change of the troponin moved the assocaited tropomyosin away from the myosin binding site on actin
  4. Cross bridge between thin and thick filaments occurs - contraction of fibers can happen
29
Q

Name of muscle contraction caused by a single action potential? What is the relationship of ________ to the action potential?

A

Twitch
It lags behind the action potential, due to the delay in excitation contraction coupling

30
Q

What does the duration of a muscle contraction reflect?

A

The time it takes for the Ca2+ concentration in the muscle cell to return to baseline (after the efflux from the sarcoplasmic reticulum)

31
Q

Name of force generated by a muscle?
(Q1) exerted by a whole muscle is called?
What is it?
The additive effect of all the twitches is called what?

A

Tension
Recruitment
Increase in the number of active fibers
Summation

32
Q

What is summation? What does it result in?

A

-Process by which a muscle’s force increases when it’s stimulated multiple times without enough time to fully relax
(accumulation of action potentials)
-Sustained contraction of the muscle - tetanus

33
Q

What is recruitment, why is it important?

A

CNS activates motor units to produce a muscle contraction (motor unit recruitment)
Increases muscle tension

34
Q

Main requirement if muscle fiber activity?

A

Large amounts of energy - skeletal muscle energy metabolism

35
Q

What can be achieved from the premade ATP within a muscle fiber?

A

A few twitches
ATP -> ADP

36
Q

What is the next step after the use of premade ATP in skeletal muscle energy metabolism? What can be achieved from this step?

A

Transfer of P from creatine phospate to ADP -> ATP
Few seconds of muscle activity
(Creatine phospate -> Creatine | via creatine kinase)

37
Q

What occurs after the use of creatin phosphate in skeletal muscle energy metabolism? Where is this coming from?

A

(hitting prolonged muscle activity)
ATP levels are sustained by glycolysis and oxidative phosphorylation
Fuel is provided by glycogen in the muscle and glucose&fatty acids in the blood

38
Q

Three types of skeletal muscle fibers?

A

-Fast glycolytic fibers
-Slow oxidative fibers
-Fast oxidative fibers

39
Q

What is + function of fast glycolytic fibers?

A

Myosin with high ATPase activity - no myoglobin
“white muscle”
Generation of large force over short periods of time

40
Q

What is + function of slow oxidative fibers?

A

Myosin with low ATPase activity - contains myoglobin to facilitate oxygen transport from blood
“red muscle”
Generation of low levels of force over long periods of time

41
Q

What is + function of fast oxidative fibers?

A

Intermediate of fast glycolytic fibers and slow oxidative fibers
“Fast” myosin and oxidative metabolism

42
Q

What pathways of skeletal muscle energy metabolism do fast glycolytic fibers use?

A

-premade ATP
-conversion of creatine phosphate
-conversion of glycogen via glycolysis into lactic acid
**lactic acid goes to blood

43
Q

What pathways of skeletal muscle energy metabolism do slow oxidative fibers

A

-premade ATP
-conversion of creatine phosphate
-Glucose and glycogen conversion by glycolysis & oxygen (-> myoglobin) and fatty acids into oxidative phosphorylation

44
Q

Function of muscle fatigue? Mechanisms responsible for?

A

Protects the muscle from damage
NOT caused by ATP depletion
There are a number of incompletely understood mechanisms
-changes in ion gradients
-change in pH from lactic acids
-depletion of glycogen
-failure of command signals from CNS (central command fatigue)

45
Q

What is muscles response to exercise?

A

Dependent on exercise type
-Low intensity: increase in fiber mitochondria, vascularization (increased ability of muscle fiebrs to extract ATP energy through oxidative metabolism)
-High intensity: increase in diameter of fast glycolytic fibers and muscle hypertrophy

46
Q

What is muscle hypertrophy?

A

increase in the size, density, and shape of skeletal muscles (muscle building)

47
Q

What causes muscle soreness after exercise?

A

inflammation in response to muscle damage

48
Q

What causes muscle changes post exercise?

A

Release of ‘factors’ by damaged tissue

49
Q

What is morphologically unique to smooth muscle?

A

Lacks striation due to less order within myosin and actin
(as opposed to cardiac and skeletal muscles)

50
Q

What activates smoot muscle contraction?

A

Ca2+ release from the SR or from membrane calcium channels;
Binding to calmodulin activates myosin light chain kinase causing;
Activation of smooth muscle myosin

51
Q

What regulates contraction of smooth muscle?

A

Extracellular signals:
hormones and neurotransmitters of the autonomic nervous system

PHGY 209 (5 decks)

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