muscle 1.4 Flashcards

1
Q

in one single motor unit muscle fibers are..

A

all the same

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2
Q

does a muscle have only 1 fiber type

A

no it has all 3 motor unit types

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3
Q

2 factors of total muscle tension development

A

1) amount of tension developed by each fiber
(frequency-tension relation, length-tension relation, fiber diameter, fiber type, fatigue)

2) number of fibers contracting at any time (number of fibers per motor unit, number of active motor units)

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4
Q

small motor units vs large motor units

A

small motor units : total tension the muscle produces increases in small steps by activating more motor units

large motor units : total tension the muscle produces increases in large steps by activating more motor units

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5
Q

size of a motor neuron

A

the diameter of the neuronal cell body (diamteter of its axon)

type 1 smallest diameter = smallest tension
type 2a slightly larger diameter= larger tension
type 2x biggest diameter =greatest tension

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6
Q

what makes the smaller diameters in muscle fibre types produce less tension?

A

there is the same number of sodium ions entering to cause excitatory synapse, but the difference is there greater depolarization
-motor units are spread out over a smaller surface in muscle fibre types with smaller diameters

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7
Q

what determines the velocity that a single muscle fiber shortens

A

1) the load on the fiber -> load on the whole muscle
2) the speed of the myosin type expressed in the fiber -> type of motor units in the muscle

when you increase motor unit recruitment, the load decreases on each motor unit which increases both force and velocity

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8
Q

what happens if there is denervation atrophy

A

neuron to the skeletal muscle was destroyed

-progressively smaller in diameter and amount of contractile proteins they contain will decrease

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9
Q

what happens if there is disuse atrophy

A

when the muscle is not used for a long period of time

-same thing, smaller diameter, amount of contractile proteins decrease

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10
Q

what happens when you exercise the muscle

A

increase amount of contractile activity, increase in size (hypertrophy), changes in capacity of ATP production and subtype of myosin they express

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11
Q

low intensity/long duration exercise leads to

A
  • increase number of mithochondra in all muscle fibers
  • myosin composition MAY shift in fast fibres from 2X to 2A
  • increase in number of capillaries

all increase ability to sustain muscle contraction through OXIDATIVE metabolism

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12
Q

high intensity exercise

A
  • increase in diameter (hypertrophy) due to satelite cell activation and increased synthesis of actin and myosin filaments -> more fibrils
  • myosin in fast fibers could shift 2a to 2b
  • increase synthesis of glycolytic enzymes
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13
Q

can you increase strength without hypertrophy?

A

yes increase synchronous of muscle units, enhance ability to recruit fast glycolytic motor neurons

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14
Q

can you change proportions of fibers in a muscle

A

can change fibres 2A to 2x but not from type 1 to 2

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15
Q

tone

A

resistance training can enhance tone

  • more myofibrils are activated during RT, more energy being used = good for weight loss
  • RT enhances background motor unit firing
  • better at recruiting large motor units
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16
Q

transient hypertrophy

A

increase in muscle size that develops immediately following exercise (transitioning quickly)

17
Q

chronic hypertrophy

A

increase in muscle size due to long term strength training, muscle fibres increase size and increased recruitment of muscle fibres and activation

neural adaptations happen first then hypertrophy

18
Q

insulin like growth factor 1, anabolic steroids (androgens), myostatin

A

androgens influence on muscle strength and growth

myostatin is produced by skeletal muscle cells, it is a regulatory protein which inhibits muscle hypertrophy through negative feedback effect

-myostatin bad if you want to get big

-some people have myostatin deficiency

19
Q

effects of aging

A

maximum force a muscle can generate decliness 30-40% between 30-80 years old

  • average fibre diameter decreases, less PA
  • intensity and duration of exercise in older individuals doesnt produce as much change
20
Q

what causes exercise-induce muscle soreness

A

thought to be structural damage to the muscle cells and their membrane which activates the inflammation response

-releases histamines that activate endings of pain neurons in the muscle

eccentric produces most muscle soreness

21
Q

acute muscle soreness

A

pain due to ischemia (not enough blood flow; oxygen to the muscle) or accumulation of hydrogen ions or lactate

22
Q

doms

delayed onset muscle soreness

A

post - 12,24,48 hours after exercise

nothing to do with lactate, lactate gone after an hour

23
Q

creatine kinase

A

structural member of the M LINE

  • when the muscle is damaged it is torn apart and released
  • CK is often used as a marker for muscle damage
24
Q

what does strained muscle leads to

A

scar tissue

has collagen overtop which does not allow the muscle to stretch as nicely

25
Q

antagonist

A

groups of muscles that produce oppositely directed movements at joint

26
Q

fulcrum

A

point on which a lever rests or is supported and on which it pivots

27
Q

first class lever

A

fulcrum is between load and effort

eg. semispinalis doing flexion and extension at head

28
Q

second class lever

A

fulcrum at the end near the load

eg. soleus doing plantar flexion and dorsiflexion

29
Q

third class

A

fulcrum at the start near the effort

eg. biceps doing flexion and extension

skeleton is a lever and fulcrum system

30
Q

mechanical equilibrium of forearm

A

downward load x distance from the elbow = isometric tension exerted by the muscle X distance from the elbow

31
Q

muscle cramps

A

involuntary tetanic contractions of skeletal muscles

AP’s firing higher rates than normal, sensory receptors and motor neurons in the area activated

caused by : electrolyte imbalances in extracellular fuid, over exercise, dehydration, chemical imbalances, hormonal imbalances, cholesterol lowering medications

-spicy foods reduce excess AP = less cramping

32
Q

muscular dystrophy

A

genetic disease

  • progressive degeneration of skeletal and cardiac muscle fibres
  • absence of proteins that make up the costameres in striated muscle
33
Q

costameres

A

clusters of structural and regulatory proteins that link the Z disks of the outermost myofibrils to the sarcolemma and extracellular matrix

-allow you to have lateral transmission from sarcomere to extracellular matrix

help stabilize the muscle

34
Q

myasthenia gravis what is it? whats it caused by? treatment?

A

neuromuscular disorder charcterized by muscle fatigue and weakness that progressively worsened as the muscle is being used

caused from destruction of nicotinic Ach receptors proteins of the motor end plate, mediated by antibodies of a persons own immune system

treatment is adminestering acetylcholinesterase inhibitors, suprress immune function with glucocorticoids and removal of the thymus