Cardiovascular responses to exercise Flashcards

1
Q

What are the primary functions of the CVS?

A

Deliver O2 to contracting skeletal muscle

Remove CO2 & heat from contracting skeletal muscle

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2
Q

What is increased muscle blood flow during exercise primarily due to?

A

Vasodilator metabolites and action of muscle pump

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3
Q

How does CO increase?

A

Increased HR & SV

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4
Q

How is the circulation during exercise controlled?

A

Involves “central command” and feedback from contracting muscles and key receptors (eg. baroreceptors) interacting with the autonomic nervous system (ANS).

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5
Q

How does exercise training affect the heart (adaptations)?

A

Remodels the heart to enhance stroke volume and promotes skeletal muscle angiogenesis.

  • Increased max CO, maximal SV (CO due to SV)
  • Reduced HR, maximal HR goes down slightly, reduced submaximal HR
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6
Q

What are the roles of the heart during exercise? (& what is Ficks’ equation?)

A

Increase O2 supply to skeletal and cardiac muscle
Facilitate CO2 and heat removal
Maintain MAP (MAP = Q x TPR)

***Ficks’ equation: VO2 = Q x (CaO2 - CvO2)
Oxygen consumption = CO * diff in [ ] of arterial vs venous blood

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7
Q

What is the distribution of CO & blood flow during exercise?

A

Decreased splanchnic and renal flow

Cerebral blood flow is maintained (or could be slightly increased)

Coronary and muscle blood flow increases

Skin blood flow increases, however at maximal exercise, maintaining MAP/blood flow to brain takes precedence, so a decrease in skin blood flow can be observed. (Potential overheating)

Cardiac output and O2 uptake will both increase. For every L of increased O2 uptake, there is a 5L increase in CO.

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8
Q

What are the factors affecting exercise hyperaemia?

A
  • Metabolic vasodilators from contracting skeletal muscle, endothelium and/or RBC
  • Muscle pump
  • “Conducted vasodilation”
  • Functional sympatholysis
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9
Q

What are the vasodilator metabolites?

A
  • K+, H+, adenosine, ATP
  • ROS
  • NO, prostacyclin, prostaglandin E2
  • Endothelial derived hyperpolarising factor (action of cytochrome P-450 2C)
  • ATP released from RBC
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10
Q

What are the cardiovascular responses to exercise in trained vs untrained?

in terms of: CO, VO2max

A

At submaximal intensities, there is no difference between a trained/untrained person.

However, athletes have higher maximal CO (more capillaries & mt) and therefore greater VO2 max.

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11
Q

HR vs SV during exercise? (trained vs untrained)

A

HR is slower to begin with and during exercise in athletes when compared with the sedentary.

Stroke volume of athletes is also higher.

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12
Q

What blood pressure changes in response to increasing exercise intensity?

A

An increase in exercise intensity causes a shortening of the cardiac cycle. TPR is usually weighted towards diastolic pressure, however during exercise, shortening of the cardiac cycle causes a shortening of diastole and therefore ventricular filling time - resulting in suboptimal filling at high exercise intensities.

As TPR leans more towards systole than normal, as does MAP, therefore MAP will increase during exercise.

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13
Q

What happens to blood O2 content during exercise in the legs?

A

90% of it goes to contracting muscle, therefore mixed venous O2 content gets closer to femoral venous O2 content, which is desaturated very quickly due to the leg muscles.

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14
Q

Does the heart fatigue?

A

The heart is quite resilient and has lots of mt and capillaries, unlikely to fatigue. In the event of a marathon, may possibly cause ventricular dysfunction, but more likely a reduction in ventricular filling.

Stroke volume is decreased slightly because of the suboptimal filling.

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15
Q

What are the cardiovascular responses to prolonged (leg) exercise?

A

Increase in:
HR and TPR

Decrease in:
Blood volume, arterial BP, CO, skin blood flow, SV, forearm blood flow

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16
Q

What factors are involved in cardiovascular drift during prolonged exercise?

A
  • Increased HR & decreased SV
  • Hyperthermia
  • Dehydration
  • Increased plasma [adrenaline]
  • Peripheral displacement of blood volume due to cutaneous vasodilation
17
Q

What is the effect of fluid ingestion on cardiovascular drift?

A

Fluid ingestion attenuates cardiovascular drift.

HR and rectal temperatures are higher with dehydration.

18
Q

What is involved in the neural control of the circulation?

A
Central command (involves motor cortex) -- feedforward
*anticipation of exercise resets baroreceptor to allow HR & BP to simultaneously increase

Baroreceptors, muscle chemosensors and mechanoreceptors modulate central command

19
Q

Autonomic control during exercise

A

Early on in exercise, subject to vagal control
But exercise turns off vagal control

Later on, sympathetic control (increase in NA):

  • decreased RBF, SBF
  • increased PRA (plasma renal activity), MSNA, lactate
20
Q

What was observed in the Dallas bed rest study?

A

3 weeks of bedrest inactivity (removal of orthostatic/gravitational stress) = 30 years of aging
*sedentary behaviour is bad for you

However will still respond to training both after exercise, and after 30 years of aging.

21
Q

What are the mechanisms of increased CO following training?

A

Expanded blood volume and albumin production (retain fluid), therefore better able to fill ventricles - Frank-Starling mechanism

Increased heart size (increased LV mass, chamber size, increased adrenergic sensitivity)

22
Q

What are the microvascular adaptations to exercise training?

A

increased capillary density and capillary recruitment for better oxygen delivery to muscle