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MSK > 20 - Physiology 3 > Flashcards

20 - Physiology 3 Flashcards

1
Q

What should I know?

A
  1. Different types of muscle contraction
  2. (DRAW) force-length and force-velocity relationship and relate to power output
  3. Energetics of contraction
  4. Myasthenia Gravis and Duchennes Muscular dystrophy
  5. Define muscle fatigue and causes
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2
Q

What is isometric contraction?

A

> NO external shortening takes place

> force of the weight = the force developed by the muscle

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3
Q

What is isotonic contraction?

A

> movement takes place
there is a mismatch between the tension generated by the contracting muscle and the load and so the muscle changes length

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4
Q

What are the 2 types of isotonic contraction?

A

Eccentric - muscle actively lengthens as load>muscle

Concentric - muscle actively shortens as muscle>load

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5
Q

Isotonic Concentric Contraction

A

> shorten
muscle force>load force
lifting a weight, cycling, swimming, push up

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6
Q

Isotonic Eccentric Contraction

A

> lengthen as resists load
muscle force < load force
climbing down a mountain, running down a hill, downwards motion of a push up, uncurling a bicep controlled

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7
Q

What type of muscle contraction causes a lot of Delayed Onset Muscle Soreness (DOMS)?

A

Eccentric (lengthening)
> strengthening exercises involve eccentric contractions
> they cause a lot of damage, injury and soreness

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8
Q

How is muscle growth aided?

A

Eccentric muscle damage causes the release of cytokines that may aid muscle growth

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9
Q

What are isolated muscle studies?

A

> Muscles put at a fixed length and an electrical stimulus is applied to the muscle by electrodes to initiate contraction
can measure the force produced by a muscle at different fixed lengths

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10
Q

Describe the Force - Length Relationship

A

> force developing cross bridges are formed in the region of filament overlap
when the muscle is stretched there is less filament overlap so force decreases as length increases
when you decrease the length there is an interaction between thin filaments, thick filaments and the Z Discs so force decreases
there is an optimal length where there is an optimal/maximal formation of X Bridges as myosin heads are opposite actin binding sites

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11
Q

What is the optimal length of sarcomeres?

A

2.1-2.2 um

We subconciously move our muscles to this length

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12
Q

What is the passive force component of the total force of muscle contraction?

A
  • the applied force to stretch muscle

- the passive force reflects the elastic properties of the CT matrix (and cytoskeleton)

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13
Q

Relationship between passive and active force?

A
  • reciprocal

- passive force increases and active force decreases and length increases

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14
Q

What is the active force?

A

The twitch force

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15
Q

How is the force-length relationship predicted?

A

With the Sliding Filament Theory

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16
Q

What is the current theory for Delayed Onset Muscles Soreness (DOMS)?

A

> that not all sarcomeres lengthen evenly during eccentric contraction
once a sarcomere gives way it will be massively stretched and so will develop less force
the weakest sarcomeres in series will LENGTHEN FIRST in eccentric contraction and give way first leading to the ‘popping sarcomere theory’

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17
Q

Describe the Force-Velocity Relationship

A
  • as load increases the velocity the muscle shortens should decrease
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18
Q

If the load on a muscle is constant then the velocity of shortening should be…

A

Constant. This is isotonic contraction.

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19
Q

Isometric contraction…

A

> Occurs when the maximum force developed by the cross bridges is balanced by the applied force
there is no movement and so there is no velocity
no velocity or distance moved so no power output by the muscle

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20
Q

Eccentric contraction…

A

force applied ? X bridge resulting in the muscle stretching

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21
Q

How do you calculate the power output of a muscle?

A 
F = ma
Work (J) = Fd
Power (W) = work/time
= Fd/time
= Force x Velocity 
> power is dependent on the rate of muscle shortening
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22
Q

How do you calculate the power of an isometric contraction?

A

No movement
No work
No power

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23
Q

When is maximum force developed?

A

Fo/optimal force is developed when there is no shortening = isometric contraction

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24
Q

When is the velocity of shortening maximum?

A

> When there is no force developed

> maximum velocity of shortening reflects the maximum rate of cross bridge turnover

25
Q

When is power output the greatest in isotonic contraction?

A

> rate of delivery of mechanical energy

> greatest at 1/3 of the maximum isometric force

26
Q

What is the most important contractile property of muscle that limits maximum sprinting speed?

A

The force-velocity relationship

27
Q

When is contraction most efficient and what is muscle efficiency for humans?

A

> 1/3 the maximum rate of shortening

> human muscle efficiency is 20-25%

28
Q

What is the most important function of muscle?

A

To shorten against a load and so do work. The rate at which this work is done is the muscles power output.

29
Q

Skeletal muscle has the greatest…

A

variation in the breakdown of ATP from moment to moment. ATP breakdown can change from 20 to several 100 fold between rest and activity
> in order to sustain contractile activity skeletal muscle metabolism must produce molecules of ATP as quickly as they break it down

30
Q

What are the 3 sources of ATP in muscle and when are they used?

A 
1. Creatine Phosphate > Creatine + ATP (Creatine Kinase)
> 10 - 30 seconds/immediate system
2. Oxidative Phosporylation (FAs + AAs)
> few minutes/short term system
> provides most of the ATP
3. Glycolysis
> 5 minutes +/long term system 
> used at peak activity (anaerobic)
31
Q

What are the 3 types of fibre types?

A
  1. Type 1 fibres (slow twitch)
  2. Type 2a fibres (fast oxidative/hybrid)
  3. Type 2b fibres (fast glycolytic)
32
Q

Type 1/Slow Twitch Fibres?

A
  • red in colour due to myoglobin
  • lots of mitochondria as is aerobic (efficient slow metabolism)
  • very resistant to fatigue
  • abundant in posture muscles and endurance athletes
  • lower rate of ATP turnover
33
Q

Type 2a/ Fast Oxidative/ Hybrid Fibres

A
  • hybrid of both type 1 and type 2 fibres
  • red and lots of mitochondria
  • uses both aerobic and anaerobic metabolism
  • more prone to fatigue than type 1
34
Q

Type 2b Fibres/Fast Glyolytic

A
  • white
  • produce ATP slowly by anaerobic metabolism
  • capable of short, fast bursts of power and fatigue rapidly (inefficient)
  • can turn into Type 2a fibres with resistance training
  • high rates of ATP turnover
35
Q

What are 3 causes of muscular weakness?

A
  1. Muscle fatigue
  2. Muscular Dystrophy
  3. Sarcopenia
36
Q

What is muscle fatigue?

A
  • Muscle fatigue is a failure to maintain the required or expected power output leading to a reduced muscle performance/force outcome
  • for example a decline in muscle function as they are used intensively and repeatedly
37
Q

What are the causes of muscle fatigue?

A
  • The aetiologies/causes of muscle fatigue are not yet clearly established
  • there are a range of potential sites where fatigue can occur from the brain (motivation) through to the myofilament interactions
38
Q

What do performance enhancing techniques used by athletes target?

A

They target pathways that are ASSUMED to cause muscle fatigue e.g. creatine supplements, carb loading, high altitude (increasing the oxygen carrying capacity of the blood by increasing ox phos)

39
Q

How is muscle fatigue clinically relevant?

A
  • limits ability to carry heavy objects for any time
  • limits athletes achievement of maximal performance
  • some pathologies like heart failure
40
Q

What are some potential sites of fatigue?

A
  • excitatory input to high motor centres
  • excitatory drive to lower motor neurons
  • motor neuron excitability
  • neuromuscular transmission
  • sarcolemma excitability
  • ECC
  • contractile mechanism
  • metabolic energy supply and metabolite accumulation
41
Q

Central Fatigue includes…

A
  1. Decreased activation from the CNS (may include psychological/motivational issues)
  2. Decreased number of motor units recruited
42
Q

Peripheral fatigue affects the…

A

Cellular mechanisms that control force
> calcium concentration (released from the SR)
> sensitivity of myofilaments to calcium (means more calcium is required)
> slower cross bridge cycling

43
Q

What controls calcium sensitivity?

A

Troponin-Inhibitory

44
Q

What are proposed causes of muscle fatigue?

A
  1. The accumulation of metabolites
  2. The depletion of muscle energy supplies such as glycogen, O2, ATP, Creatine Phosphate
    (as occurs during high intensity muscle activity)
45
Q

According to the accumulation theory of fatigue what does lactic acid do?

A
  • decreases calcium affinity for TnC
  • obstructs glycolysis
  • slows relaxation
    > have found that hydrogen ion IS important but NOT in vivo at 37 degrees
46
Q

According to the accumulation theory of fatigue what does a build up of T Tubular K+ do?

A

Decreases membrane excitability

> not likely in vivo

47
Q

According to the accumulation theory of fatigue what does a build up of NH4+ do?

A
  • decreases membrane excitability

- inhibits myosin ATPase

48
Q

According to the accumulation theory of fatigue what does a build up of Inorganic Phosphate do?

A
  • decreases SR calcium release
  • decreases SR calcium uptake
  • decreases myofilament sensitivity
  • inhibits the power stroke as this occurs when Pi dissociates
49
Q

According to the accumulation theory of fatigue what does a build up of ROS?

A

Increases protein damage

50
Q

What are the clinical features of Duchenne’s Muscular Dystrophy?

A
  • this inherited disorder is progressive and degenerative
  • muscles are normal at birth but there is rapid degeneration and weakness of muscle early in life
  • wheel chair by 10
  • respiratory failure by 20
  • cardiac involvement through dilated cardiomyopathy
  • often an increase in muscle mass when young (NOT number of fibres)
51
Q

How common is Duchenne’s Muscular Dystrophy?

A

1/3500 MALE live births (common - is X linked)

52
Q

What causes Duchenne’s Muscular Dystrophy?

A
  • caused by a mutation in the dystrophin gene which causes a loss of cytoskeletal protein dystrophin
  • dystrophin normally links the contractile proteins to the surface sarcolemma so is needed for structural support and enables the force developed by the contractile proteins to be transduced across the membrane and the muscle itself
53
Q

What is the early stage of Duchenne’s Muscular Dystrophy characterised by?

A
  • an increased membrane permeability as have lost dystrophin to link the contractile proteins to the surface sarcolemma
  • soluble enzymes such as creatine kinase leak out
  • ions such as calcium enter and can activate caspases
54
Q

Describe age-related loss of muscle function

A
  • muscle mass and strength deteriorates as we age
  • there is intrinsic age-related changes in muscle fibres that are immutable and irreversible despite exercise
  • activity DOES slow the progression
  • called Sarcopenia
55
Q

What is sarcopenia?

A
  • “poverty of flesh”
  • is a primary consequence of ageing where there is a muscle mass/body mass ration decrease
  • there is a loss of strength
  • with age the make up of the muscle changes. This can be IMPROVED with exercise
  • there is an increase in the % of Type 1 Slow Oxidative Fibres
  • a decrease in the capillary-fibre ratio (reflects the energy and oxygen demand
  • there is a denervation of the FAST fatiguable Type 2 fibres and motor units
  • motor unit remodelling
56
Q

What happens to the fibre type percentage and capillary-fibre ratio in age?

A

> increase in type 1 slow oxidative fibres

> decrease in the capillary-fibre ration due to change in demand

57
Q

Is new muscle formation affected in sarcopenia/old age?

A

No

58
Q

What are disorders of muscle cells?

A

Myopathies

  • frequent symptoms are hypertrophy and atrophy
  • often inherited
59
Q

What are muscular dystrophies?

A
  • group of inherited muscle diseases that are progressive and degenerative
  • often caused by a mutation in the genes encodingthe dystrophin-glycoprotein complex

MSK (29 decks)

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