Lecture 33: Cardiovascular Response to Exercise and Physiological Adaptations Flashcards

(49 cards)

1
Q

What is the overall effect on the heart during exercise?

A
  • Decrease parasympathetic activity
  • Increase sympathetic activity
  • Increase CO
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2
Q

What happens to our heart rate during exercise? Give the units.

A

beats/min
▪ Increases from resting rate (~60bpm)
▪ Max HR = 220 – age
▪ Increases by 3-4 times

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3
Q

What happens to stroke volume during exercise? Give the units.

A

mL/beat
* Increases from resting volume (~70mL)
* Increases by 1.5-2 times

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4
Q

What happens to cardiac output during exercise? Give the units.

A

Volume/min
▪ HR x SV
▪ Increases from resting ~5 L/min
▪ Max ~40 L/min in elite athletes
▪ Increases by up to 8 times

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5
Q

What is the overall effect on vessels during exercise?

A
  • Increase sympathetic output to veins and arterioles in abdominal organs and kidneys
  • Increase vasoconstriction in abdominal organs and kidneys
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6
Q

What blood flow redistribution occurs during exercise?

A

Global vasoconstriction
Local vasodilation

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7
Q

How does cardiac distribution change from rest to exercise?

A

Blood distribution % to:
* Skin increases slightly
* Heart & brain decreases (but more blood flow as CO has increased but % is lower)
* Viscera decreases
* Skeletal muscle increases

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8
Q

Why is blood redistributed to skeletal muscle?

A

Largest increase in blood flow; to provide O2 and nutrients, and remove CO2 and waste products

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9
Q

Why is blood redistributed to skin?

A

For heat loss

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10
Q

Why is blood redistributed to the heart and brain?

A

Increased blood flow for the heart to meet increased demands

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11
Q

Why is blood redistributed away from abdominal organs?

A

They’re less active during exercise

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12
Q

What causes global vasoconstriction?

A
  • Exercise stimulates SNS
    ▪ Noradrenaline released from sympathetic nerve terminals, binds to ⍺1 & ⍺2 receptors
    ▪ Vasoconstriction of arterioles
    ▪ Reduces blood flow
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13
Q

What is functional sympatholysis?

A

Local vasodilation of skeletal muscle overrides the vasoconstriction from sympathetic vasoconstrictor nerves

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14
Q

What are the 3 mechanisms of local vasodilation/decreasing TPR?

A
  1. Working muscle metabolites act on smooth muscle of skeletal muscle arterioles
    causing vasodilation: metabolic regulation/active hyperemia
  2. Muscle contraction compresses the outside of blood vessels causing reflexive vasodilation: mechanical feed-forward vasodilation
  3. Adrenaline binds to B2 adrenergic receptors on smooth muscle of skeletal muscle arterioles and causes vasodilation
    * Blood flow is increased to working muscles
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15
Q

What happens to MABP during moderate, steady-state exercise?

A
  • CO increase = TPR decrease
    ▪ MABP is relatively constant
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16
Q

What happens to MABP during high intensity exercise?

A
  • CO increase > TPR decrease
    ▪ MABP increases: mostly due to increase in systolic pressure
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17
Q

Normally, what is the result of stimulating baroreceptors?

A

Decreased sympathetic nervous activity

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18
Q

Describe the normal baroreflex (during rest):

A
  • Baroreceptors detect ↑ MABP and ↑ AP firing
    ▪ Activation of barosensitive neurons in medulla
    ▪ Inhibit SNS central command
    ▪ ↓ SNS output to the heart and blood vessels
    ▪ MABP ↓ returning to normal set point
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19
Q

Describe the baroreflex during exercise:

A
  • Mechano- and chemoreceptors in exercising muscle send info to the exercise ‘central command’
    ▪ MABP set point ↑
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20
Q

What 2 responses occur during the exercise pressor response?

A
  1. Exercise ‘central command’ activates neurons to inhibit barosensitive neurons in the medulla
    ▪ MABP ↑ but there’s no inhibition of the SNS central command
    ▪ ↑ sympathetic output to the heart and blood vessels
  2. Exercise ‘central command’ directly
    stimulates SNS central command to ↑ SNS output

▪ MABP ↑ to exercise set-point

21
Q

How can muscle fibre types change with anaerobic training?

A
  • More Type IIa – fast oxidative glycolytic
  • More Type IIx/b – fast glycolytic
22
Q

How can muscle fibre types change with anaerobic training?

A

More Type I - slow oxidative

23
Q

What is anaerobic training and when do adaptations occur?

A
  • High intensity, low rep training
    ▪ Anaerobic glycolytic
    system
    ▪ Adaptations occur within 3 weeks
24
Q

What are the 2 overall goals of anaerobic training?

A
  1. Increase strength - due to muscle hypertrophy
  2. Increase anaerobic capacity - due to sarcoplasmic hypertrophy & increased lactate threshold
25
What is muscle hypertrophy?
Increase in size and strength of skeletal muscles - Within a whole muscle each muscle cell/fiber gets bigger because each muscle fibril gets bigger
26
What does increased contractile strength come from?
Increasing the SIZE of muscle cells/fibers (rather than adding more muscle fibres)
27
What 3 factors increase the size and strength of skeletal muscles?
1. Increased protein synthesis ▪ More actin and myosin added to each muscle fibril: more contractile strength 2. Satellite cell activity ▪ Proliferate and fuse to existing fibers to make each muscle fiber bigger 3. Sarcoplasmic hypertrophy ▪ Increased volume of the sarcoplasm and sarcoplasmic components
28
What is micro-trauma theory?
* Damage of muscle fibers ▪ 'Micro’ tears in small areas of a muscle fiber (not the whole muscle)
29
What repairs muscle fibres and how do they do this?
Satellite cells ▪ Myogenic stem cells (build muscle) and are quiescent until activated ▪ Activated and migrate to heal micro tears ▪ Span micro tear to prevent further damage, differentiate into myoblasts and fuse with existing muscle fibers adding new myofibrils and more nuclei -> Increasing size of fibre -> More protein (actin and myosin) synthesis (nuclei) -> Increasing contractile strength
30
What is sarcoplasmic hypertrophy?
▪ Increased volume of sarcoplasm ▪ No direct change in contractile strength ▪ Increased capacity for anaerobic glycolysis
31
What is increased anaerobic capacity?
* Increased ATP & substrate stores (creatine phosphate, glycogen) ▪ Increased enzymes for anaerobic glycolysis
32
What is myostatin?
* Increased with inactivity ▪ Causes atrophy ▪ Prevents excessive muscle growth ▪ Myogenesis regulator
33
What is an increased lactate threshold?
Increase in exercise intensity before reaching lactate threshold
34
What are myostatin inhibitors?
▪ Prevent muscle atrophy ▪ Could be used as a performance enhancer
35
What is muscle atrophy?
Decrease in size and strength of skeletal muscles due to inactivity or denervation
36
What type of training increases lactate threshold?
▪ High volume, maximal steady-state, interval workouts (80-90% of VO2max) ▪ Uses the anaerobic glycolysis energy system, producing lactate
37
What muscle modifications does the build up of lactate/lactic acid trigger?
* Muscle fibres get better at tolerating lactate build up (buffering) ▪ Increased transport of lactate out of muscle cells + improved body systems to clear lactate from blood and use it as a fuel source ▪ Lactate accumulation reduced
38
What is the benefit of training to increase lactate threshold?
Improved performance for both endurance athletes and speed & power
39
What is aerobic training and when do adaptations occur?
* Low intensity training, high rep, longer duration endurance training ▪ Oxidative phosphorylation systems ▪ Adaptations occur within 4-6 weeks
40
What is the overall goal of aerobic training?
Increase aerobic capacity - aerobic threshold and VO2max
41
What is an increased aerobic threshold?
Sustain a higher level of exercise intensity for longer before needing to use anaerobic glycolysis and therefore increasing lactate production
42
What is an increased VO2max?
Increased physical fitness, greater performance during aerobic endurance exercise
43
How does VO2 change with exercise intensity?
Increase until maximum level = VO2max * Max O2 consumption at max exercise level
44
What effect does aerobic training have on VO2 max and what are the benefits of this?
* Increases with aerobic training ▪ Limited by age ▪ Improved cardiovascular health ▪ Reduced risk of heart disease, diabetes, cancer, and stroke
45
How can VO2 max be increased?
1. Increasing O2 SUPPLY to exercising muscle: cardiovascular adaptations 2. Increasing ability of exercising muscle to USE O2 to make ATP: muscle cell metabolic adaptations
46
What effect does aerobic training have on heart rate?
* Max HR unchanged (determined by age) * Resting HR decreased, higher output at lower HR * Increased HR range during exercise
47
What effect does aerobic training have on stroke volume?
* Increased SV at rest and during exercise * Remodelling of ventricular walls: moderate hypertrophy, increased ventricular volume & increased contractility
48
What effect does aerobic training have on cardiac output?
Increase in max CO due to increases in HR and SV
49
How does aerobic training result in an increased oxidative ATP synthesis capacity?
* Change in muscle fiber type to more type I fibres (oxidative) * Increased production of oxidative enzymes * Mitochondria biogenesis (make more mitochondria): increased oxidative phosphorylation