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Musculoskeletal Module > Lecture 23 > Flashcards

Lecture 23 Flashcards

1
Q

What 3x ways can you modulate the force of contraction?

A

Summation and Tetanus
Recruitment of Motor Units
Action of sympathetic Nervous system

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2
Q

Skeletal:

A

Shorter AP
Refractory period: short
Relaxation: when Ca taken back up to SR
Can stimulate multiple times before fully relaxed
-Single stimulas:150ms
Summation: Ca2+ is released with each stimulus, not removed rapidly, crossbridge cycle continues
Unfused Tetanus: some relaxation but not complete
Fused Tetanus: multiple stimulus, but multiple AP at N junction
-most contractions in body are due to sustained Tetani - Multiple burst of AP arriving at NJ

Modulate force of contraction by regulating interval between stimuli/AP

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3
Q

Weak contraction:

A

Fewer motor units recruited

Frequency of AP reduced

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4
Q

Isometric

A

NO external Shortening

Force weight = Force developed

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5
Q

Isotonic

A

contraction where Movement occurs
Mismatched Tension generated by the contracting muscle and the (constant) Load on the muscle (more tension than needed
a) Concentric- shortening muscle
b) Eccentric- produce force while lengthening

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6
Q

Concentric Isotonic contraction

A

Contracted Shortening

F.weight

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7
Q

Eccentric Contraction

A

F.weight > F.developed by muscle
-climbing down mountains, running down hilly, downward motion of pushups
-Muscle damage typically occurs DOMS
strengthening exercises
-growth aided due to eccentric m damage causes Cytokine release

Not all sarcomeres will legnthen evenly, the weaker sarcomeres will lengthen, and once stretched beyond optimal length will produce less force. Repetitive eccentric contraction, will lengthen and give way/pop first = Popping sarcomere theory and produce less work

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8
Q

DOMS

A

Delayed onset muscle soreness

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9
Q

Isolated force length Experiments

A

Electrodes applied to muscle to provide electrical stimulus
Force-length relationship
Stimulate muscle at different muscle lengths

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10
Q

Passive force

A

Nebulin and Titin
Sarcomeric Proteins -produce elastic properties of sarcomeres
Increased stretch = increase in passive force produced(not relying on cross bridge)

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11
Q

Force velocity

A

Rate of shortening = load vs velocity
heavier load= slower velocity of contraction
Load= max force produced by muscle = isometric(crossbirdge cycling but no shortening)
Continue to load with force- lengthen- Negative shortening (eccentric)

Force-velocity relationship is the most important contractile property of muscle that limits maximum sprinting speed

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12
Q

ATP breakdown

A

ATP breakdown varies in no other cell
Rest= ATP breakdown at BASAL level
Max activity= Basal 20-100 fold
Sustain contraction, need to produce ATP at same rate that they breakdown

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13
Q

3x sources of ATP in muscle

A
  1. Creatine Phosphate -give p to ADP. gets ATP from mitochondria to site of ATP consumption. Breatine phosphate smaller than ATP. Shuttle to ATP so more is generated
  2. Glycolysis. Glygocen.
  3. Oxidative Phosphorlylation
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14
Q

What are the 3x ATP sinks?

A

Myosin ATPase
Cerca ATPase
Na/K pump
Atp big molecule, simple diffusion too long

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15
Q

What are the 3x main consequences of different energy sources?

A

Immediate: Creatine phosphate
Short Term: Glycolytic/Glycolysis
Long Term: Aerobic/Oxidative (over few mins)

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16
Q

S fibres:

A

Type 1
Red - myoglobin
-lots of mitochondria (aerobic)
Posture and endurance muscles

17
Q

type IIa

A 
Fast Oxidative
hybrid of ii fibres
Red and lots of Mitochondira
both aerobic and anareobic
More prone than type 1
18
Q

F fibres

A 
Fast glycolytic
White
Anaerobic production of ATP slower
Short, fast bursts of fibres
--> can turn into Type IIa by Resistance training
19
Q

What is the relationship transition between Type IIa and b fibres?

A

Type IIb fibres cans turn into type IIa by Resistance Training

20
Q

What are 3x causes of muscle weakness?

A
  1. Muscle fatigue
  2. Muscular dystrophy
  3. Sarcopenia
21
Q

Muscle fatigue

A

failure to maintain required/expected POWER output

  • leads to reduced muscular performance
  • motivation
  • Potential sites between brain and contractile protein interactions
  • Athletes Target pathways that are assumed to cause muscle fatigue - to enhance performance
  • Carb loading
  • high altitude:max O2 by increase Hb
  • creatine supplementations
22
Q

Central fatigue

A

Decreased motivation/activation

decreased MN recruitment

23
Q

Peripheral fatigue

A

Cellular mechanisms

  • Ca transient (amount of SR Ca delivery per AP= amount of crossbirdge cycling)
  • less ca sensitivity of myofilaments
  • Slower crossbridge cycling
    1. accumulation of metabolites (ionic conc change)
    2. depletion of energy supplies to muscle (glycogen)(rate of ATP production)
24
Q

DMD Duchenne’s Muscular dystrophy

A

1/3500 Male live births
Normal at birth - diagnose at 4
abnormal gate
genetic mutation of Distrophin
Big stocky muscles- fewer muscle fibres
Increased Weakness and degeneration of skeletal muscle
10= wheelchair
20=respiratory failure -not if on ventilator
Die late 20s
Genetic technique cure
Cardiac involvement- Dilated Cardio myopathy
Distrofin gene = decreased distrophin in muscles
connected to proteins that link ECM to intracellular F.actin (actin Filaments)
when crossbridge cycling occurs/force produce, force is tranduced across membrane
Less Distrophin = Actin Filaments no longer Linked to membrane proteins
+ controls Channels/receptors (TripC channels- allow Ca2+ influx)
-High levels of Intracellular Calcium
-enzymes (creatine kinase) leaks out =leaky cell membranes
Increased membrane permeability = enzymes such as Creatine kinase leak out. And ions such a Ca2+ Leak in

25
Q

Age related loss of Muscle function

A 
early muscle mass and strength increase
old age have little muscle mass= muscle deterioration
=injury prone
Sarcopenia:
Poverty of flesh
-Primary consequence of agying
Muscle m: Body mass ratio decreased
Significant loss of strength
26
Q

Sarcopenia

A

Age related (intrinics changes) primary cause
-can be slowed
Immutable and Irreversible
Muscle mass: Body mass ratio decreases
More type 1, no change in mean XSA cross sectional area for Type I or Type II B
Decrease in capillary:fibre ratio - less o2 removal
Denervation fo FF fibres + Motor unit remodelling

Mice: Less NMJ proteins (decreased activation)
Less alpha MN numbers

New muscle formation ISNT impaired
Exercise and diet can SLOW progression

Musculoskeletal Module (27 decks)

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