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MD1 - Exercise Block > Exercise > Flashcards

Exercise Flashcards

1
Q

How does different muscle fibre types stain ?

A

Type 1 stains black in acid

Type 2 stains black in alkaline

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2
Q

What is the ratio of type I, IIa and IIx in untrained individuals

A

Type I, IIa, IIx 50-55, 30-35, 10-20% respectively

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3
Q

How soon does Muscle CSA and Myofib synth rate decline from inactivity

A

Starts to go down as soon as leg is in suspension. lose about 10cm^2 of muscle CSA over 20 days.

Myofib synth rate decline 0.06-0.02 after 10 days.

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4
Q

What are the Mitochondrial adaptations to exercise training

A
  • Increased mitochondrial density and oxidative enzymes
  • Reduced CHO use and lactate production
  • Increased fat oxidation
  • Enhanced endurance performance
  • Improved insulin action
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5
Q

What are the potential mechanism for mitochondrial adaptation?

A

Stimuli
- Ca2+, energy status, redox, tension, metabolites, hormones

Signalling
- AMPK, calcineurin, CaMK, MAPK, PKC, PKD

Transcriptional regulation

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6
Q

What stimuli induce GLUT4 expression?

A

Increase ADP, AMP

Reduced ATP, CP, Gly

Increased Ca2+

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7
Q

What is the main fuel for sprinting?

A

ATP and PCr

at 1m its 50-50 anaerobic and aerobic

at 2m its mostly aerobic

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8
Q

What are the fuels for endurance exercise?

A

At low energy exercise most is provided by fat

Require about 60-65% of workload max to optimise fat loss

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9
Q

How does fuel contribution change over time in fixed intensity exercise?

A

Initially 80% other CHO

Slowly use more Plasma glucose and fat over time

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10
Q

What are the factors influencing exercise metabolism

A

Intensity & duration

Diet

Training

Environmental temperature

Age & Gender

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11
Q

What is the definition of fatigue and how does it differ from weakness

A

Fatigue is a reversible reduction in force and power generation capacity

Weakness if fatigue at rest

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12
Q

What factors contribute to peripheral fatigue?

A
  • Reduced AP amplitude
  • Myoibrilar protein sensitivity reduction by increase P, reduced pH and increased ROS
  • Increased K+ and Na+
  • Inhibition in SR Ca2+ reuptake by increased P, ADP and ROS and reduced ATP
  • Inhibition of Ca2+ release by RyR due to CaP percipitation, increase Mg and reduced ATP, increased P
  • Reduced maximum Ca2+ activated force due to increased P
  • Reduced shortening velocity due to ADP
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13
Q

Is the mechanical limitation different for O2 uptake in athletes and untrained?

A

No

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14
Q

What is the VO2 max?

A

a measure of the maximum volume of oxygen that an athlete can use. It is measured in millilitres per kilogramme of body weight per minute (ml/kg/min)

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15
Q

What is the cardiovascular responses to exercise?

A

Increase O2 to skeletal and cardiac muscle

Facilitate CO2 and heat removal

Maintain MAP and BP

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16
Q

What is the cause of exercise hyperaemia?

A

Metabolic vasodilator from contracting skeletal muscle, endothelium (K+, Adenosine, H+, NO, PGI) and RBC (ATP)

Muscle pump

“Conducted vasodilation”

Functional sympatholysis (Metabolites desensitise the sympathetic signals)

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17
Q

What is the mechanism for increased oxygen extraction in athletes?

A

Most of the increase in VO2 max is due to the increase in CO. There is minimum oxygen extraction.

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18
Q

What is systolic and diastolic an indirect measure of ?

A

CO and MAP respectively

19
Q

What is cardiovascular drift and what are the causes of it?

A

Cardiovascular driftis the term that describes the physiological changes in heart function during prolonged exercise. During prolonged exercise, stroke volume steadily drops as the heart rate increases. Stroke volume is the amount of blood the heart pumps with every beat.

  • Increased HR and decreased SV
  • Hyperthermia
  • Dehydration
  • Increased plasma adrenaline
  • Peripheral displacement of BV due to cutaneous vasodilation
20
Q

What are the neural control of circulation

A

Peripheral

  • Baroreceptors
  • Muscle chemoreceptors
  • Muscle mechanoreceptors

Central (Central command and set basic patterns of effector activity)

  • Motor cortex
  • Subthalamus
  • Spinal motor systems
21
Q

What is the autonomic control during exercise?

A

At first it is the inhibition of vagal control and followed up the activation of sympathetic control leading to diversion from visceral organs to skeletal muscle.

Correlated with the increase in adrenaline

22
Q

What is the mechanisms for increased CO following training?

A

Increased BV (Frank starling mechanism)

Increased heart size (increased LV mass and chamber size)

Increased adrenergic sensitivity

23
Q

What is the microvascular adaptations to exercise training?

A

Increased capillary density and increased capillary recruitment

24
Q

What is the respiratory responses to exercise

A

Maintain O2 saturation

CO2 removal

Acid base balance

Fluid and temperature balance

25
Q

What is the VT1 and VT2

A

VT1
Start getting CO2 not for aerobic metabolism but from the buffering of lactic acid

VT2
Get hot, adrenaline, potassium, even more CO2. (hyperventilation)

26
Q

What is the cause of exercise hyperpnea?

A

Motor cortical activation

Muscle afferents (spindles, type II & IV)

CO2 flux to the lung

Increased K+, H+, lactate

Elevated catecholamines and temp

No role for O2

27
Q

What is the cause of exercise ventilation following training?

A

Reduced blood lactate/H+

Low plasma K

Lower plasma catecholamines

Reduce activation of muscle afferents

Reduced central drive

28
Q

What are the limitations to maximal VO2?

A

Respiration

Central circulation

Metabolism

Peripheral circulation

29
Q

What are the benefits of fluid ingestion?

A

Increased BV

Decreased HR

Increased SV and CO

Lower core temp

Lower plasma Na and osmolarity

Reduced muscle glycogen use

Enhanced exercise performance

30
Q

What are the uses for cardiopulmonary exercise testing?

A

Exercise capacity/fitness

Disease risk

Differential diagnosis

Assessment of severity of disease

pre-operative risk

disability evaluation

rehabilitation/exercise prescription

effectiveness of therapy

31
Q

What factos contribute to VO2max

A

Lungs

Heart and circulation

Muscle

Mitochondria

32
Q

How do you indirectly measure VO2

A

By using oxygen pulse, VO2 in relation to heart rate.

VO2/Heart beat = SV (oxygen pulse)

33
Q

What is lactate an indicator of?

A

Hypoxia, biomarker for mismatch of O2 delivery to muscle

34
Q

What is the physical work capacity?

A

The power output at a given heart rate

e.g. PWC150 is the power output at 150 HR

35
Q

What is endurance correlated to and what are the evidence?

A

Endurance time can be correlated with Cytochrome oxidase and VO2 max.

49% of variation of endurance can be explained by VO2max
81% of variation Muscle oxidative capacity (cytochrome oxidase)

Took a group of rats and depleted them of iron, slowly gave iron back.
VO2 max is largely determined by oxygen delivery. This is the major driving factor increasing the VO2 max. Despite the increase in change of VO2 max there is less change in endurance.

Endurance is correlated with muscle pyruvate oxidate/muscle oxidative capacity

36
Q

What is the lactate threshold correlated to?

A

VO2 max and Muscle oxidative capacity

However, LT is more correlated with muscle oxidative capacity

37
Q

What is the determinant of endurance in well-trained cyclists?

A

Lactate threshold

38
Q

What are the principles of exercise prescription?

A

Readiness/Risk evaluation

Volume
Frequency/Intensity/Duration

Adaptation
Overload/progression

Specificity

39
Q

How does exercise training change insulin action?

A

Insulin signalling

Glut4 expression

Hexokinase. glycogen synthase activity

Muscle oxidative capacity

Muscle blood flow

Capillary density/recruitment

NO/NOS

*no change in distal part of insulin receptor pathway (insulin receptor, PI3K tyrosine kinse)

40
Q

What is the expression of GLUT4 like in T2DM?

A

Down regulated in adipose tissue in T2DM

No change in muscle

41
Q

What is GLUT4 expression like in exercise?

A

Exercise increase GLUT4 in adipose tissue and skeletal muscle

42
Q

How are myokines and adipokines involved in CVD?

A

Adipokines = Negative effect for CVD (TNFa, CRP, low grade systemic inflammation)
Myokines interact with adipose tissue and interact directly with CVD RF, some of the systemic benefits of exercise is due to the release in myokines (stored in exosomes).

Exosomoes have systemic and autocrine effects

43
Q

What cytokine do muscles release?

A

IL-6, thought to have anti-inflammatory effects

44
Q

What are the risks associated with exercise?

A

Sudden cardiac death

Exercise induced bronchospasm

Musculoskeletal injury

DOMS

Exertional rhabdomyolysis

Exertional hyperthermia/hypothermia

Proteinuria

MD1 - Exercise Block (3 decks)

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