10.03 Muscle, Fuels and Fatigue Flashcards

1
Q

What are the major functions of skeletal muscle on the whole body level?

A
  • It can comprise up to 40% of total body mass
    • Loss of muscle mass in ageing and cancer cachexia is a major cause of death
  • Active generation of forces required for power, movement and posture
  • It is a major site for deposition of glucose and fatty acids
    • Once muscles have optimised their own stores of glucose, remainder in plasma is deposited in fat and taken up by the liver

Characteristics of skeletal muscle are important in detemining metabolic health

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2
Q

What is the evidence to support that contraction (use) of skeletal muscle has important systemic consequences?

A

Release of myokines ​from contracting skeletal muscle (IL-6 is a major example) that are able to alter fat, liver, brain and other organ functions

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3
Q

Desribe the relationship between type I muscle fibre composition and fat composition of the body

A

The more type 1 fibres present, the less fat is present. This is thought to be due to their greater capacity to oxidise fat and use it as a fuel

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4
Q

Describe mitochondrial concentration in skeletal muscle in relation to glucose disposal in the muscles

A

The higher the mitochondrial mass in muscle, the more glucose is able to be deposited into the muscle (increased ability to utilise energy - oxidative capacity is increased)

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5
Q

What is the evidence to support the idea that muscle is an endocrine organ?

A

It is believed that the myokines and other important products released from exercised skeletal muscle is important.

Plasma transported from exercise trained mice to non-exercise mice confers an exercise phenotype to these mice

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6
Q

What are the human muscle fibre types?

A

Type I fibers are also known as slow twitch fibers produce repeated low-level contractions by producing large amounts of ATP through an aerobic metabolic cycle.

Type IIa fibers are also sometimes known as fast oxidative fibres and manufacture and split ATP at a fast rate by utilising both aerobic and anaerobic metabolism and so produce fast, strong muscle contractions, although they are more prone to fatigue than type I fibers.

Type IIx - fast glycolytic fibers produce ATP at a slow rate by anaerobic metabolism and break it down very quicky. This results in short, fast bursts of power and rapid fatigue.

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7
Q

How are the different fibre types seen in immunohistochemistry?

A

It depends on the pre-incubation method.

Myosin ATPase staining in sections. Type I fibres stain dark after acidic and Type II stain dark after alkaline due to differential acid/alkaline solubility.

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8
Q

How is immunoblotting used to determine muscle fibre types and levels?

A

The Type 1 fibres have myosin heavy chain 1 while type 2 fibres have myosin heavy chain II.

The troponin C levels is also different between the two muscles

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9
Q

Describe the properties of Type I muscle fibres in terms of the following:

A
  • Low Force
  • Slow Twitch
  • Low fatigue
  • Most abundant
  • High mitochondria
  • High vascularisation
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10
Q

Describe the properties of Type IIa muscle fibres in terms of the following:

A
  • The fast phenotype
  • Second most abundant
  • Highest fibre diameter area
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11
Q

Describe the properties of Type IIx muscle fibres in terms of the following:

A
  • Least abundant
  • These are the “explosive fibres - high power” seen in high amounts in sprinters
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12
Q

“Speed is born while Endurance is Made”

What is meant by this statement?

A

They type IIa fast phenotype can be trained to become more fatigue resistant which is what is required for endurance activities.

However the type IIx fibres required for sprinting and speed (high power, short duration events) is very difficult to “make” and train these fibres (born with them)

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13
Q

Describe Heddeman’s Size principle of muscle recruitement

A

Muscle fibres are progressively recruited in relation to the force of contraction.

  1. Type I fibres first
  2. Type IIa next
  3. Type IIx last

This is dependent on both the intensity and duration of force production

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14
Q

What is the composition of muscle fibre types in the 2 major types of athletes and normal untrained people?

A
  • Untrained people have about 50/50 twitch fibre ratios
  • Sprinters have low slow twitch and high fast twitch
  • Distance runners have high slow twitch and low fast twitch
    • Some evidence fast twitch a fibres can become more resistance to fatigue (superfibres)
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15
Q

Describe the distribution of the muscles for different athelete types.

Relate this to the genetics vs. training debate

A

Extremes (runners) had more slow twich in leg and kayakers more in arm than legs likely due to training But the genetics impact (positve reinforcement) that they were better at one than the other is liekly due to genetics

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16
Q

Describe the changes to muscle architecture in response to training

A
  • Max voluntary contraction increases (early changes due to neuromuscular junction recruitment and then later due to hypertrophy)
  • The cross sectional area takes time to occur
  • Change in fascicle length also occurs (generation of greater force)
17
Q

Describe the relationship between muscle disuse and muscle mass

A

Muscle mass reduction occurs very quickly with disuse (30% reduction of muscle mass in the ICU w/ patients in a coma)

And unilateral casting also causes significant decrease.

18
Q

Draw and explain the major cascade leading to muscle architecture changes

A

Signaling protein mamallian target of rapomysin; mTOR protein (protein synthesis controller) is under regulation of IGF (insulin is not essential, amino acids are)

This increase in mTOR protein expression leads to protein synthesis and prevention of muscle protein degradation

19
Q

How does exercise training affect mitochondria in skeletal muscle?

What are the consequences of this?

A

Increase in mitochondrial density and oxidative enzymes so you are better able to utilse energy (better oxidase and store CHO and fat and end up in muscles rather than in adipose tissue).

  • Reduced CHO use and reduced lactate production
  • Increased fat oxidation
  • Enhanced endurance performance
  • Improved insulin action
20
Q

What are the potential mechanisms by which these mitochondrial changes occur?

A
  • Response to stimuli (like high intracellular calcium levels, energy state, metabolites, hormones, tension, redox etc)
  • Leads to increased/changed signalling pathways (eg. AMPK, MAPK, PKC, PKD)
  • Causing differential transcriptional regulation, protein function and expression (eg. MicroRNAs, GEF, MEF2, PPARdelta)
21
Q

What is the hypothesised relationship between exercise and GLUT4 expression on muscles?

A

Exercise may induce GLUT4 expression (independent of insulin)

22
Q

Describe the generation of ATP in skeletal muscle

A
  • CHO glycolysis (anaerobic) - with production of lactic acid
  • LIPID/FAT oxidation (Aerobic)
  • PROTEIN catabolism and utilisation (aerobic)
  • CREATININE PHOSPHATE breakdown (starts and lasts a few seconds only) to produce ATP directly
23
Q

Why is ATP so important for skeletal muscle activity

A

It is required for the myosin ATPase and Na-K-ATPase (maintenance of the membrane potential) and Ca-ATPase (SERCA to maintain contraction cycle)

24
Q

Compare the relative power and capacity of the different sources of energy/fuel for muscles

A

Anaerobic systems (glycolysis) generates ATP very quickly (high rate) but have a very small capacity. They are the emergency high intensity sources. CHO oxidation/fat oxidation burns/generates energy better w/ CHO than fat.

Fat is virually unlimited as a source

25
Q

What is “hitting the wall”?

A

A sudden fatigue and loss of energy which is caused by the depletion of glycogen stores in the liver and muscles.

Running out of CHO (glycogen) and therefore can’t generate ATP aerobically so have to slow down at this intensity (occurs at 60-65% of max aerobic capacity) while fat metabolism begins to take over as the major source

In this situation, your body feel general weakness, fatigue, and manifestations of hypoglycemia, such as dizziness and even hallucinations

26
Q

Describe the changes in muscle energy fuels over time with sprinting

A

Anaerobic sources are most active during short energy sprints.

  • Creatine phosphate is very important in the initial few seconds but longer (lose Creatine) and then they become less efficient.
  • Anerobic glycolysis plays the major role for sprinting
27
Q

Describe the changes in muscle fuels over increasing INTENSITY of exercise

A

Aerobic utilisation: increasing exercise intensity, increases contribution from fat and increase reliance of carbohydrates (esp. muscle glycogen in humans)

28
Q

Describe the changes in muscle fuels over increasing DURATION of exercise (endurance)

A

There is a heavy reliance of CHO that decreases as you run out of glycogen the fat contribution increases and glucose

29
Q

What are some factors influencing exercise metabolism?

A
  • Exercise intensity and duration
  • Diet
  • Training
  • Environmental temperature: you burn more CHO in heat
  • Age and Gender

These effects are mediated by substrate availabiliy, hormone levels and biochemical characteristics of skeletal muscle

30
Q

What is the definition of fatigue?

A

Reduction in force and power generating capacity and the inability to maintain the required/expecte force or power output

It is not muscle weakness

31
Q

Describe the metabolic feedback from skeletal muscles that helps to regulate central fatigue

Complex interaction w/ brain and muscle and organs. Differentiate successful athletes is the central system (motivational centres). Exertional heat stress can cause death in these athletes

A

Muscle efferents to the CNS signal to the brain that lots of activity is taking place (especially breakdown products and build up of Phosphate, ATP breakdown products and acid) tells the brain to decrease activity as a protective mechanism.

Drugs blocking Type 3 and 4 feedback in contracting muscle. (afferent w/o blocking efferent)

Blockage: subjects went much harder early on - removal of inhibitory feedback. But eventually fatigued and ended up doing worse as brain was disconnected to muscles

Also works the other way (brain is motivating muscles)

32
Q

There are cellular mechanisms of muslce fatigue. What does this involve?

A

Excitation-contraction coumpling processes:

  • Altered transmission of the action potential
  • Ion imbalances
  • Build up of magnesium
  • Calcium sensititisation
  • Acidosis, ROS and biproducts impact functions
33
Q

How is muscle glyogen involved in fatigue?

A

Running out of glycogen is an important factor: leads to increase IMP (breakdown product of ATP signaling not resynthesising it at an effective enough rate) - why atheletes glycogen load

The more glycogen present in muscles the longer a person is able to exercise

34
Q

CHO ingestion improves exercise capacity - why is this?

A

Use CHO at high intensity and we don’t have much reserve in the body (it is stored in fat rather than CHO as it is more efficient as a storage)