Muscle Physiology Slide Notes Flashcards

1
Q

The limiting factor in muscle contraction

A

Calcium

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2
Q

Utilize more extracellular Ca2+ than intracellular

A

Cardiac and smooth muscle

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3
Q

Skeletal muscle function begins in the

A

Motor cortex (in cerebral cortex)

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4
Q

Connect brain to regions of the spinal cord

-where motor signals leave the ventral root

A

Rubrospinal and reticulospinal tracts

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5
Q

ACh receptors that are specific to skeletal muscle

A

Cholinergic-nicotinic receptors

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6
Q

Allows for calcium to be released from the SR

-a voltage gated Ca2+ channel

A

DHPR-RyR complex

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7
Q

Decreasing the amount of sarcoplasmic Ca2+ results in

A

Muscle relaxation

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8
Q

Transports calcium out of the cell and sodium into the cell

-a secondary mechanism to move calcium out of the cell

A

NCX

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9
Q

The biggest mechanism for sequestering Ca2+ back into the SR

A

SERCA

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10
Q

In skeletal muscle, crossbridge cycling is driven by

A

Intracellular Ca2+

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11
Q

Changes in Ca2+ are directly proportional to changes in contractility. These different levels of contraction are called the

A

Inotropic state

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12
Q

Allows for influx of Ca2+ into the myocardium

A

Type L channel

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13
Q

Targets bone and the kidneys and increases bone resorption, which increases plasma concentration of Ca2+

A

Parathyroid hormone (PTH)

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14
Q

Causes motor neuron and skeletal muscle hyperexcitability an Na+ channel stabiity

-can lead to muscle spasm

A

Hypocalcemia

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15
Q

Raises the threshold for voltage-gated Na+ channels which leads to muscle and neuron hypoexcitability

A

Hypercalcemia

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16
Q

The opposition to displacing load

A

Afterlod

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17
Q

Force generated to counter afterload

A

Preload

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18
Q

The preload is greater than the afterload and work is performed in

A

Isotonic Contraction

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19
Q

In cardiac muscle, the preload is the ability for

A

Ventricles to contract

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20
Q

In cardiac muscle, the afterload is

A

Aortic BP and pulminary arterial pressure

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21
Q

Blood only leaves the ventricles if

A

Preload > afterload

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22
Q

The maximal force a muscle can generate

A

Muscle tetanus

23
Q

Phenomenon due to muscle elasticity

-stretch in muscle

A

Passive tension

24
Q

Reaches a maxima shortly after contraction and then declines

-shows us that muscle generates most of its power early in contraction

A

Active tension

25
Q

If muscles are not starting from L0, but rather from a shorter length, the power the muscle can generate will be

A

Lower than if it were at L0

26
Q

Greatest at intermediate loads where F and V are moderate

A

Power

27
Q

Describe the orderly recruitment principle

A

We want to move a load, so type 1 fibers are recruited and we are in a stage of isometric contraction, then some type 2 fibers are recruited and we get an isometric to isotonic conversion. Then a large amount of type 2 fibers are recruited and we reach maximal force of muscle contraction. But then after 50msec or so, we recruit type 1 fibers because they are the only ones with the oxidative capacity to sustain prolonged contraction

28
Q

Musculotendon assessment mechanisms tell us if it is ok to keep contracting or if we need to stop. What are the two systems we have in place for this assessment?

A
  1. ) Golgi tendon organs

2. ) Muscle spindles

29
Q

Stress sensors that will decrease muscle contraction via type 1b afferent fibers if necessary

A

Golgi tendon organs (GTOs)

30
Q

Monitor change in muscle length and rate of change in length

A

Muscle spindles

31
Q

What are the components of the intrafusal fibers of muscle spindles?

A
  1. ) Bag fibers

2. ) Chain fibers

32
Q

What are bag fibers innervated with?

-Tells us about change in muscle length and provides us with proprioception

A

Type 1a afferents

33
Q

Tells us about static length

A

Type II afferents (in chain fibers)

34
Q

An increase in muscle fiber diameter

-predomiant

A

Hypertrophy

35
Q

An increase in number of muscle fibers

-less common

A

Hyperplasia

36
Q

Activated in response to stimuli induced by workload

  • stimulate myoblasts
A

Satellite cells

37
Q

The main source of muscle regeneration and growth

A

Satellite cells

38
Q

Released due to anaerobic and aerobic work and function in autocrine and paracrine hypertrophy myogenesis

A

Myokines

39
Q

Myokines promote

A

Osteogenesis, anti-inflammatory interactions, and insulin secretion

40
Q

Have direct anabolic and anti-catabolic effects by

Increasing: Satellite cell proliferation and GH and IGF-1 levels

Decreasing: Glucocorticoid activity

A

Anabolic androgen steroids (i.e. testosterone and dihydrotestosterone)

41
Q

Induces increase in nitrogen balance, proteogenesis, and increased hepatic IGF-1

A

Growth Hormone (GH)

42
Q

Ubiquitously expressed in skeletal muscle and increases proteogenesis and regeneration of muscle

A

IGF-1

43
Q

Are less effective without eachother, i.e. they are synergists

A

GH and IGF-1

44
Q

What are three catabolic factors?

A
  1. ) Excess Ca2+
  2. ) Glucocorticoids
  3. ) Myostatin
45
Q

Released as part of the immune/anti-inflammatory response and function to increase proteolysis and type II fiber atrophy

A

Glucocorticoids

46
Q

Stress induced hormones that decrease activity of IGF-1

A

Glucocorticoids

47
Q

Comes from the adrenal cortex and causes release of myostatin

A

Cortisol

48
Q

Expressed within satellite cells where it blocks cell cycle progression and inhibits proliferation of satellite cells

A

Myostatin

49
Q

Inhibition of myostatin results in

A

Unregulated muscle growth

50
Q

Muscle fatigue will prevent cross-bridge cycling. What are two factors that will lead to muscle fatigue?

A
  1. ) Decreased pH (affects type II fibers)

2. ) K+ efflux

51
Q

Which type of muscle fiber is most affected by aging?

A

Type II fibers

52
Q

Has slow wave and spike potentials and is innervated by autonomic nerve fibers

A

Visceral smooth muscle

53
Q

In visceral smooth muscle, what is the effect of the following stimulation:

  1. ) Sympathetic
  2. ) Parasympathetic
A
  1. ) relaxation

2. ) contraction

54
Q

In vascular smooth muscle, epinephrine and norepinephrine activate α1 adrenoreceptors which lead to

A

Inhibition of SERCA, resulting in increased sacoplasmic Ca2+ and thus vasoconstriction