BPK 305 - Lecture 18

Early response to exercise

1. Cerebral cortex planning and anticipating

2. Information is sent vie the hypothalamus to the cardiovascular centre's in the medulla

3. Increased sympathetic output

4. increased CO and vasoconstriction

What areas vasoconstriction before exercise?

- skin

- kidneys

- sphlanchic regions

- inactive muscles

Muscle depended events of arteries

- increased metabolites

- local vasodilation of active muscles

- decreased arterial pressure

- sensed by arterial baroreceptors

- increased SV, HR, vasoconstriction, and medullary sympathetic output

Increased medullary sympathetic output

- adrenaline release of adrenal medulla

- Activates β2 adrenergic receptors

in vasculature supplying skeletal muscle

- enhances vasodilation

What does increased core temperature do?

- detected by thermoreceptors in hypothalmus

- inhibition of dermal vasoconstriction

- increased blood flow to skin

Skeletal muscle dependent effects on veins

- skeletal muscle pump

- increased VR

- increased RAP

- increased EDP

- increased EDV

- increased SV

What limits oxygen consumption?

- uptake of O2 at the lungs

- delivery of O2 by blood flow

- extraction of O2 from the blood

How does O2 consumption change during exercise?

Increased 10-20 fold

Normal VO2 maxes

Healthy male: 45

Healthy female: 38

Elite male: over 85

Elite female: over 77

Self dog: 240

How does A-VO2 difference change with exercise?

4 fold increase

Why does A-VO2 difference change with exercise?

- increased capillary recruitment

- Bohr effect: increased HbO2 unloading due to high PCO2, decreased pH, increased temp

- increased mitochondrial respiration increases diffusion gradient

How much does CO change with exercise?

4-6 fold increase

What causes increased CO during exercise?

Increased HR and SV

How much does HR increase during exercise?

3 fold

Why does HR increase during exercise?

Sympathetic stimulation of the SA node

How much does SV increase during exercise?

1.3-2 fold

Why does SV increase during exercise?

- Increased contractility

- increased VR

Chronic cardiovascular training

- 3 to 4 times per week

- 30 to 60 minutes per session

- 60 to 70% VO2 max

- 4 months duration

What does training do to O2 delivery?

Training improves O2 delivery to peripheral tissues

What can be rate limiting for O2 consumption?

O2 delivery

What does trining do to stroke volume?

Increases

What does training do to heart rate?

Decreases fasting heart rate but max heart rate remains the same or possibly decreases

What does training do to cardiac output?

Increases it

What does training do to a-VO2 difference?

Slight increase

Why does oxygen extraction increase with training?

- increased capillarisation

- increased diffusion gradient due to increased mitochondrial content

How does training increase SV?

- heart gets stronger so the contractile force increases which increases the ejection fraction

- plasma volume increases which increases Vm and EDV

Which component of SV increase is more important?

Contractility

What does a decreased resting heart rate do?

More time in diastole increases time for filling and venous return

What happens to the effects of a decreased resting HR during max exercise?

They are lost

Exercise hypertrophy

- physiological hypertrophy

- increased heart mass

- normal or improved function

- reversible

CVD hypertrophy

- pathological hypertrophy

- increased heart mass

- reduced function

- irreversible

Eccentric hypertrophy

increased cell length

What does eccentric hypertrophy cause?

Ventricular dilation and increased wall thickness

When is eccentric hypertrophy seen?

Volume overload

- endurance exercise

- faulty valve

Concentric hypertrophy

Increased cel width

What does concentric hypertrophy cause?

Increased wall thickness and no dilation

When is concentric hypertrophy seen?

Pressure overload

- resistance training

- hypertension

Endurance athletes heart

- thickened LV walls

- LV dilation

Strength athletes heart

- Thickening of LV walls

- mild LV dilation

Combination athlete heart

- gross thinking of LV walls

- LV dilation

Hypertension heart

- thickening of LV walls

- no dilation in early stages

Dilated cardiomyopathy heart failure

- thinning of LV walls

- significant LV dilation

Hypertrophic cardiomyopathy heart

- gross thickening of LV walls

- no dilation or decrease in LV chamber size

pathological hypertrophy

- up regulation of fetal genes

- fibrosis

- cardiac dysfunction and increased mortality

- working against a constant higher afterload

physiological hypertrophy

- different molecular and structural profile

- normal organization of cellular structures

- no fibrosis

- often only transient bouts of higher afterload

Pathological hypertrophy signalling pathways

- Excessive AngII, Endothelin, NA activation of Gq

- activates hypertrophic gene expression

Physiological hypertrophy signalling pathways

- Insulin-like growth factor 1 (IGF1) activation of PI3-K

- PI3-K regulates cell growth and survival

Transgenic mice in physiological hypertrophy

- over-expression of IGF1/PI3-K

→ hypertrophy with normal cardiac function

- under expression of IGF1/PI3-K

→ less hypertrophy