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Normal Animal > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

1
Q

Major properties of muscle

A

contractility
excitability
extensibility
elasticity

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2
Q

contractility

A

Ability of a muscle to shorten, accompanied by mechanical force generation: role in movement

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3
Q

excitability

A

capacity of muscle to respond to a stimulus

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4
Q

extensibility

A

Muscle can be stretched to its normal resting
length and beyond to a limited degree

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5
Q

elasticity

A

Ability of muscle to recoil to original resting length after being stretched

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6
Q

qualities of skeletal muscle

A

Attached to bones
– Nuclei are multiple per cell and peripherally located
– Striated
– Under voluntary and involuntary (reflex) control

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7
Q

What bundles of muscle fibers called

A

fascicle

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8
Q

What are tendons

A

– Fibrous connective tissue that connects muscle fibers, containing the contractile apparatus, to bones

–Serve as elastic anchors

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9
Q

what is a synergist?

A

Separate muscles that work together to cause a movement around a joint

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10
Q

What is a agonist?

A

Muscle causing a particular action (e.g., flexion) when it contracts

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11
Q

What is a antagonist?

A

a muscle working in opposition to agonist; typically relaxes during contraction of agonist

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12
Q

passive tension is exerted by

A

tendons - elastic components lying in series and parallel to contractile elements (muscle fibers)

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13
Q

For shortening during contraction

A

non-contractile parts of a muscle (tendons and surrounding connective tissue) are taut, owing to their elasticity

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14
Q

The net force of contraction includes both the…..

A

the active (ATP-dependent) and passive (elastic) contributions to shortening

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15
Q

muscle types (fiber)

A

parallel and pennate

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16
Q

Parallel muscle types

A

fiber arrangement– parallel to the longitudinal axis of the muscle, e.g. biceps brachii, etc.

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17
Q

Pennate muscle type

A

fiber arrangement— fibers are at an angle to the longitudinal axis of the muscle, e.g. deltoid, etc

(generate greater force but less range of motion)

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18
Q

connective tissue ___ muscle fibers

A

surrounds

organize muscle fibers and provide a parallel components of elasticity

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19
Q

Know where these are

muscle fiber, artery, nerve, vein, capillary, synapase (neuromuscular junction), axon of motor neuron, sarcolemma

A
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20
Q

Morphology of a muscle cell

A

~0.1 mm in diameter and several cms in length (big!!)
• Cylindrical in shape with tapered ends
• Elongated nuclei
– Located at the periphery of cells
– Lie just underneath the sarcolemma (plasma membrane)
• Is described as a multinucleated syncytium due to
its developmental origin as a fused aggregate of progenitor cells

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21
Q

during developments myoblasts ….

A

fuse to become myotubes

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22
Q

myoblasts

A

1 nucleus
lacks myofibrils (contractile proteins)

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23
Q

myotubes

A

develop myofibrils and other organelles for contraction

skeletal muscle fiber is formed by the fusion of numerous mononucleated cells

24
Q

Myofibrils

A

bundles of myofilaments packed within muscle fiber and are the contractile machinery

25
Q

sarcomere

A

the fundamental contractile structure

26
Q

understand this picture

A
27
Q

mechanism of contraction

A

Thick and Thin filaments slide in opposite directions via repeated cycles of binding interactions, individually shortening the sarcomeres and thereby the entire fiber

28
Q

describe Ca2+ induced cross-bridge formation using tropomyosin and troponin

A

In the absence of Ca2+, the thin filament protein tropomyosin (on the actin fiber) STOPS interaction between actin and myosin filaments

• Ca2+ binding to troponin (which is also on the actin fiber) promotes a change in the conformation of tropomyosin, allowing the myosin “head” access to its binding sites on actin

tropomyosin (and actin) is not about myosin until it gets a taste of ca2+ on its troponin site and then is obsessed

29
Q

steps of muscle contraction in terms of cross-bridge and its relation to ATP

A
  1. cross-bridge not attached to actin (has hydrolyzed ADP)
  2. Ca2+ allows cross-bridge to bond with actin
  3. change of orientation and loss of ADP and P cause filaments to slide
  4. ATP binding to myosin (cross-bridge) and they release from actin
  5. ATP is hydrolyzed and waiting back to 1
30
Q

Why does rigor mortis occur?

A

no ATP available for muscles to release and stop contracting

31
Q

sarcomere shortening is accomplished by ….

A

sliding of interdigitated myofilaments during power strokes of myosin cross-bridges

this leads to overall shortening of the muscle

relative force is dependent upon the number of functional myosin heads attaching to actin filaments

32
Q

during contraction… (filaments and sarcomeres)

A

a) Sarcomere length shortens

b) Thick filaments (A bands) remain the same length.

c) Distance between ends of thick filaments in adjacent sarcomeres(I bands) shorten.

d) Distance between ends of thin filaments within a sarcomere (H bands ) also shorten.

33
Q

How does action potential work on muscle

A

Transmission of electrical signals along the length of motor neurons or muscle fibers is accomplished by the action potential, a rapid net re-distribution of ions across the plasma membrane,

driven by concentration gradients, which depolarizes the membrane along length of cell

34
Q

resting membrane potential of motor neuron and muscle cell?

A

motor: -70mV
muscle: -90mV

35
Q

Ion channels: 2 critical properties that dictate function

A
  1. gating (opening/closing in response to a signal)
  2. selective permeability (each ion channel is restrictive to a certain ion: Na+, K+ etc)
36
Q

Phases of action potential (think of the neuro lecture) 4 steps

A

Resting potential – governed by Na+ and K+ gradients and relatively high resting permeability to K+; interior of cell relatively negative compared to outside

  1. depolarization – above a threshold value, Na+ channels open, allowing an influx (inward flow) of Na+; temporary overshoot into a reverse polarized state (interior positive)
  2. repolarization – voltage-gated K+ channels open, allowing an efflux of K+ (outward flow) and re-establishment of the resting potential
  3. hyperpolarization – overshoot of K+ efflux
37
Q

Membrane excitability and propagation of action potential (5 steps)

A

Think of the pump train. moving a signal down a membrane when the one next to it opens - depolarize, repolarize, hyperpolarize, back to normal

  1. At rest, the sarcolemma (plasma membrane) is polarized, owing to the action of the Na+/K+ ATPase and other ion pumps that establish ion concentration gradients across the membrane.
  2. Activation of the ACh receptor (AChR), a ligand-gated Na+/K+ channel, allows net inward flow of Na+ and outflow of K+, causing a local depolarization of the plasma membrane.
  3. The local depolarization is sensed by adjacent voltage-gated Na+ channels, which open in response
    to the change in membrane potential. The Na+ influx causes the depolarization to move laterally along the surface of the muscle fiber.
  4. The spreading local depolarization is sensed by neighboring voltage-ga`ted Na+ channels, which open accordingly, propagating the signal along the length of the muscle fiber.
  5. Repolarization is accompanied by transient inactivation of the voltage-gated Na+ channels, rendering them temporarily refractory to opening thus ensuring unidirectional spread of the action potential.
38
Q

Excitation-contraction coupling (ECC)

A

• Mechanism whereby an action potential causes
muscle fiber contraction
• Involves
–Sarcolemma (plasma membrane)
–“T tubules,” infoldings of the sarcolemma
–Sarcoplasmic reticulum, a Ca2+ reservoir within cells
–Ca2+, Troponin

39
Q

Calcium channels involved in ECC

A

DHPR and RyR

DHPR- lives in sarcolemma/t tubule, opens due to depolarizAtion, activates ryr

RyR- lives in sarcoplasmic reticulum membrane, releases stored Ca2+

40
Q

What is SERCA

A

the sarcoplasmic reticulumn Ca2+ ATPase

an ion pump protein that moves Ca2+ from the sarcoplasm into the SR and restores Ca2+ gradient to end contractile response

41
Q

How can the magnitude of force produced in whole-muscle contraction be controlled? (3)

A
  1. Varying numbers of motor units recruited for a contraction.
  2. Controlling the rate of stimulation (‘summation of twitches’).
  3. Initial length of muscle fibers (‘length-tension relationship’)

force generated depends on number of fibers engaged in contraction

42
Q

What is a motor unit?

A

a motor neuron plus all muscle fibers that it connects

43
Q

What are graded contractions

A

produced by variations in the number of motor units activated (varying degrees of force)

44
Q

What are innervation ratios?

A

(fibers per neuron) can vary based on functional requirements of muscle in question.

45
Q

Effect of stimulation rate on force of contraction

A

Twitch’
–Stimulated by a single isolated electrical stimulus
–Generates a fractional force of contraction that decays as fiber relaxes

• Summation of twitches
–More frequent stimuli, each producing units of contractile force
–Next stimulus arrives before relaxation from previous stimulus is complete, allowing summation

• Tetanic contraction
–Frequency high enough to produce steady contraction (no opportunity for relaxation) and maximal force development

46
Q

Length-tension relationship (in a isolated muscle fiber)

A

Force exerted depends on the number of myosin heads engaged in cross- bridge cycling with actin filaments

• The tension that a muscle generates varies with its length at the time a stimulus to contract is received

forms bell curve
(peak force occurs when there is maximum potential for overlap of thick and thin filaments…. greatest number of myosin head/actin interactions to occur)

47
Q

why is muscle a major consumer of chemical energy and metabolites

A

• Cross-bridge recycling
• Pumping of Na+, K+, Ca2+ and other ions
• Synthesis of contractile proteins

48
Q

Length- Tension relationship (in a muscle unit)

A

• Force generation capacity increases when the muscle is initially stretched
• The force generated by active sliding filaments is combined
with the shortening contributed by passive elastic components (tendons) that have been stretched

49
Q

Stretch-Shortening Interactions

A

• When a muscle is stretched prior to contraction, the resulting contraction is more forceful than in the absence of a pre-stretch.

• Elastic recoil: the effect of the series elastic component of the actively stretched muscle

• Stretch reflex in muscle stretched to an extreme: via an autonomic nervous signal to contract and thus shorten, protecting the muscle tissue

50
Q

3 types of skeletal fibers (most muscles have all 3)

A

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

51
Q

Fast fibers

A

high myosin ATPase activity, thus more rapid crossbridge cycling and high shortening velocity. Fatigue rapidly.

52
Q

slow fibers

A

slow myosin ATPase activity and lower shortening velocity. Fatigue more slowly.

53
Q

oxidative fibers

A

numerous mitochondria, high capacity of oxidative phosphorylation. ATP production dependent on blood borne oxygen and fuel; contain myoglobin, increases rate of oxygen capture in the fiber.

54
Q

glycolytic fibers

A

have few mitochondria but a high concentration of glycolytic enzymes and glycogen (polymer of glucose stored as fuel reserve in skeletal muscle and liver). Larger and have more thick and thin filaments and therefore can develop more tension. Fatigue rapidly.

55
Q

Effects of exercise on skeletal muscle

A

exercise increases:
– size (hypertrophy) of muscle fibers
– numbers of myofilaments
– capacity for ATP production
• Low intensity exercise affects oxidative fibers
- mitochondria and capillaries

• High intensity exercise affects glycolytic fibers
- diameter of actin and myosin and production of glycolytic enzymes

• Fiber types may be able to interconvert
• Fatigue is associated with energy (ATP) depletion, loss of efficiency in Ca2+ storage and release.

56
Q

mechanisms of exercise-induced changes in skeletal muscle

A

loss of muscle fibers w/ age

muscles get bigger due to thickening of fibers and addition of myofibrils

mechanical stress on muscles activates genes to produce more myosin and actin and gain more nuclei

57
Q

What is atrophy

A

muscle wasting or loss
due to inactivity, disease, aging

(depressed protein synthesis, enhanced proteolysis or both)

can be very detrimental

Normal Animal (18 decks)

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