cardiorespiratory adjustments in exercise Flashcards

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1
Q

3 muscle types

A

slow twitch - type I

fast twitch - type IIa and IIb

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2
Q

slow twitch is carried out by what process

A

oxidative phosphorylation

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3
Q

fast twitch is carried out by what process

A

relies on creatine phosphate to regenerate ATP

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4
Q

physical characteristics of slow twitch muscles

A

– good blood supply
– lots of mitochondria & myoglobin
– mainly postural but also used in endurance events

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5
Q

physical characteristics of fast twitch muscles

A

– not so dependent on blood supply or mitochondria
– large amount of glycolytic enzymes
– used in sprinting and “explosive” events

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6
Q

ATP pool required for contraction is regenerated from three sources

A

– cellular respiration (requires O2)
– creatine phosphate (4 – 5x that of ATP)
– muscle glycogen

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7
Q

when is creatine phosphate used

A

for short bursts of energy can be used to replenish ATP from ADP

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8
Q

when is glycogen used?

A

– large stores of glycogen can be broken down to provide substrate for glycolysis
– yields 2 ATP and 2 lactic acid molecules, enough to function if O2
is insufficient
– however, it is limited and eventually muscle must depend on cellular respiration

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9
Q

exercise intensity is defined in terms of

A

oxygen uptake

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10
Q

how does oxygen consumption change with work during dynamic exercise

A

in a linear manner

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11
Q

maximal oxygen consumption

A

VO2 Max

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12
Q

how is maximal oxygen consumption measured

A

incremental increases in exercise intensity

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13
Q

cardiorespiratory adjustment

A

• To facilitate O2 consumption and prevent fatigue there needs to be
the continued delivery of O2
to the muscle

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14
Q

what can a lack of oxygen during respiration lead to

A

lack of O2 means anaerobic respiration and lactate acidosis

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15
Q

• O2 delivery depends on three aspects

A
  1. Getting O2
    into the body and blood (respiration)
  2. Getting O2 from the lungs to the tissues (cardiovascular delivery)
  3. Getting O2 from the blood to the respiring tissues (O2 extraction)
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16
Q

how does the oxygen consumption and carbon dioxide production change during exercise

A

In exercise both O2 consumption and CO2 production increase

17
Q

how is oxygen delivery and CO2 removal facilitated during exercise

A

both respiratory rate and tidal
volume increase
– tachypnoea not hyperventilation

18
Q

how is respiratory function controlled

A

“chemically” controlled

– via peripheral and central chemorecptors

19
Q

how does peripheral receptor respond to adjustments and what does it respond to?

A

drive peripheral receptor due to increase in acidity

lead to hyperventilation

20
Q

anaerobic threshold

A

The anaerobic threshold is when demand for O2 exceeds delivery
– tissues start to respire anaerobically

21
Q

how can glycolysis continue

A

NADH must be recycled back to NAD+
– done by lactate dehydrogenase converting pyruvate to lactate
drops pH
increasing acidity
metabolic lactic acid acidosis
stimulates peripheral chemoreceptors and increased ventilation

22
Q

what drives cardiovascular adaptation

A

SNS

23
Q

How does SNS help adapt cardiovascular

A

Increase in cardiac output and the redistribution of blood flow
– SNS increase in heart rate and stroke volume as well as vasoconstriction
• Direct sympathetic action on heart rate and contractility
• Increased venous return and therefore stroke volume
– due to increased muscle pump, respiratory pump and venoconstriction
• Sympathetic vasoconstriction and metabolite vasodilatation alter
pattern of distribution
– away from GI, renal and to working muscle and heart

24
Q

hyperaemia

A

dilate all capillary vessel when there is greater surface area for perfusion and decrease in perfusion distance to accommodate greater oxygen demand
greater concentration gradient
no change in solute diffusity

25
Q

how does increased CO2 and H+ and temp affect oxygen delivery to tissue

A

reduce affinity for Hb - Bohr effect - shift dissociation curve to the right
promote oxygen delivery to tissue

26
Q

how is oxygen debt repaid

A

– fast: re-phosphorylation of ATP/creatine
– slow: lactate conversion back to glucose/glycogen
– ultraslow: increased metabolic rate after exercise

27
Q

oxygen debt

A

as the VO2

in excess of resting after exercise

28
Q

3 stages in which oxygen debt is incurred

A

– depletion of ATP, depletion of creatine phosphate then the build up of lactic acid

29
Q

why is there such thing as an oxygen debt

A

Adaptations aim to supply O2 to match demand during exercise - but when exercising is over the initial deficit will need to be repaid

30
Q

how does training affect muscle

A

increase muscle strength and resistance to fatigue
muscle hypertrophy - larger muscle fibres not hyperplasia - getting more muscle fibres
increased glycolytic and oxidative capacity - increased glycogen, ATP , phospho-creatinine, mitochondrial enzymes

31
Q

cardiorespiratory effects of training

A

Bradycardia and cardiac remodeling
reduced blood pressure - enhances endothelial function, inc. muscle capillary density
increased myoglobin and 2,3,BPG
reduced ventilation at same work rate - shift in anaerobic threshold

32
Q

other effects of training

A

increase VO2 max and O2 debt and anaerobic threshold

33
Q

during what time period can significant improvement be seen

A

8-10 weeks
30 min sessions, 2/3 times per week
60% max O2 consumption

34
Q

what will training not improve

A

– VO2 or the cardiac output at rest
– diffusing capacity or the haemoglobin concentration
– maximum heart rate