Cardiovascular Response to Exercise

Oxygen Delivery During Exercise

• Oxygen demand by muscles during exercise is 15-25x greater than at rest

• Increased O2 delivery accomplished by:

  • Increased cardiac output

  • Redistribution of blood flow

    - From inactive organs to working skeletal muscle

  • Increased extraction of O2 at the tissue

How can we measure oxygen consumption (VO2)?

Fick Principle: VO2 = Q x a-vO2 diff

(“ O2 consumed = O2 delivered - O2 returned”)

A - VO2 difference

Fick Equation:

VO2 = (Q) * (A-VO2diff)

a-VO2 Difference and Increased VO2max

• Improved ability of the muscle to extract oxygen from the blood (peripheral adaptations)

  • Increased blood flow

  • Increased capillary density

  • Increased mitochondrial number

• Increase is not due to elevation of arterial oxygen content

Prolonged Exercise

• Cardiac output is maintained

• Gradual decrease in stroke volume

  • Due to dehydration and reduced plasma volume

• Gradual increase in heart rate

  • Cardiovascular drift

Summary of Cardiovascular Control During Exercise

• Initial signal to “drive” cardiovascular system comes from higher brain centers

  - Central command

• Fine-tuned by feedback from:

  - Chemoreceptors

  • Sensitive to muscle metabolites (K+, lactic acid)

  - Mechanoreceptors

  • Sensitive to force and speed of muscular movement

  - Baroreceptors

  • Sensitive to changes in arterial blood pressure

How does VO2max increase with endurance training?

Typical increase of ~15-20% with training

• Dependent on baseline levels

• Dependent on age & health

• Genetic implications

How does VO2max increase with endurance training? (CENTRAL adaptation)

• Stroke volume increase (explains 50% of change in VO2max)

• Results in reduction in HR for SAME WORKLOAD

How does VO2max increase with endurance training? (PERIPHERAL adaptation)

• Enhanced extraction

• Increased [MITO] and enzyme action

• Increased capillary density

Increase in Preload (EDV)

• Increased plasma volume

• Increased venous return - due to longer filling time (heart rate lower at rest and submaximal loads)

• Increased ventricular chamber size - allows for maximal filling

Decrease in Afterload (heart doesn’t have to work against as much back pressure to get the blood out) - decreased resistance to flow to muscle

• Decreased arterial constriction - more optimal dilation/constriction in trained muscles

• Increased maximal muscle blood flow with no change in mean arterial pressure

Detraining and VO2max

• Decrease in VO2max with ending of training

  - Decreased SVmax

  • Rapid loss of plasma volume

• Decrease in maximal a-VO2 difference

  • Decreased mitochondira

  • Decreased oxidative capacity of muscle

    - Decrease in Type IIa fibers and Increase in Type IIx (more faster and powerful) fibers

When we are exercising do we want a HIGH A-VO2 difference or LOW A-VO2 difference?

HIGH A-VO2 difference

If the heart rate goes up, and we want to keep the same Q (cardiac output) then…

(Q = HR x SV)

the stroke volume needs to go down

If stroke volume goes up and we want to maintain the cardiac output then…(Q)

(Q = HR x SV)

heart rate needs to decrease

Cardiac output (Q) goes up with?

Intensity

Anything that influences these factors will also influence stroke volume:

Preload

Afterload

Contractility

Fick Principle

About oxygen consumption. Depends on how much oxygen we’re delivering to the muscles, and how much oxygen they are extracting from the blood.

AVO2 difference

After training we have a larger AVO2 difference—meaning the muscles are doing a better job of extracting oxygen from the blood

Stroke volume accounts for…?

50% of the increase in VO2 max following a training program

Does HRmax change in the response of exercise?

No

What influences venous return?

• Diameter of the vein—venoconstriction from nervous system

• Skeletal Muscle Pump—squeezes the veins to help blood get through

• Respiratory Pump—as we inhale and exhale pressure is changing in our thoracic cavity