The Cardiovascular and Respiratory Systems

The heart is myogenic - it generates/controls its own electrical impulse called the cardiac impulse.

1. Cardiac impulse initiated from the SA node (pacemaker) in right atrium.

2. Impulse passes through right and left atrium walls to AV node, causing both atria to contract; this is known as 'artial systole'.

3&4. AV node conducts impulse down through bundle of HIS...

5. down through the left and right bundlebranches to the apex of heart.

6. Impulse travels up around ventricle walls via pukinje fibres, causing both ventricles to contract; this is known as 'ventricular systole'.

Cycle continues. SA node initiates the next cardiac impulse

1. Both atria fill with blood. AV valves closed.

2. Atrial blood pressure rises above ventricular pressure.

3. Rising blood pressure forces AV valves open an blood passively passes into both ventricles. Semilunar valves closed.

4. Both atria contract actively forcing the remaining atrial blood into ventricles.

5. Semilunar valves remain closed.

6. Both ventricles contract increasing ventricular pressure.

7. Aortic and pulmonary valves forced open. AV valves closed.

8. Blood forced out into; aorta to body tissues = stroke volume; pulmonary arteries to lungs. N.B. Only 40/50% blood is ejected at rest during ventricular systole (SV).

9. Diastole of the next cardiac cycle begins. Semilunar valves close preventing backflow of blood from aorta and pulmonary arteries.

Stroke volume:

Resting = 60/80 ml

Sub-maximal = trained160/200 ml and untrained 80/100 ml

Maximal = trained 160/200 ml and untrained 100/120 ml

Heart rate:

Resting = 70/72 bpm

Sub-maximal = Up to 100/130 bpm

Maximal = 220 - your age

Cardiac output:

Resting = 5 l/min

Sub-maximal = Up to 10 l/min

Maximal = 20-40 l/min

1. Resting heart rate: the average resting heart rate is 72.

2. Anticipatory rise: the heart rate increases even before exercise due to adrenalin.

3. Rapid increase in heart at start of exercise: Proprioreceptors in muscles and joints detect activity, chemoreceptors detect increase in carbon dioxide and lactic acid and increased effect of adrenalin.

4. Continued but slower increase: Continued effect of chemo and proprior receptors, increase in blood temperature and more venous return.

5a. Steady plateau/Slight fall (aerobic sub-max): Oxygen supply equal to the demand of muscles and baroreceptors slow down the heart rate to optimal level to meet oxygen demands

5b. Continued increase (anaerobic maximal): Continued action of all above actions and supply of oxygen does not meet the demand .

6. Rapid fall in heart rate: Decrease in stimulation from factors in 2,3 and 4 above.

7. Slower fall in heart rate: Heart rate elevated to aboce resting levels to help repay oxygen debt and to remove by-products like lactic acid.

Stroke Volume:

Stroke volume increases from values around 60-80 ml per beat at rest to maximal values of around 120 ml per beat during exercise. This increase is due to:

- increased capacity of heart to fill. Increase in venous return, which stretches ventricular walls and increases the filling capacity of the heart and hence the end diastole volume.

- increased capacity of heart to empty. A greater EDV provides a greater stretch on the heart walls which increases the force of ventricular systole (contraction on ventricles). This increases ventricular contractability which almost completely empties the blood from the ventricles, increasing SV.

Cardiac Output:

Cardiac output, being th product of stroke volume and heart rate (Q = SV x HR), increases directly in line with exercise intensity from resting values of 5l/min up to maximal values of 20-40l/min, to supply the increased demand for oxygen from the working muscles.

Cardiac Control Centre (CCC):

The meddulla oblongata in the brain contains the cardiac control centre (CCC), which is primarily responsible for regulating heart rate via the stimulation of the SA node.

The CCC is controlled by the autonomic nervous systtem (ANS), meaning that it is under involuntary control and consists of sensory and motor nerves from either the sympathetic or parasympathetic nervous system.

The three main factors that affect the activity of the CCC are:

• Neural control
• Hormonal control
• Intrinsic control

Neural:

Baroreceptors in aorta and carotid arteries. Increase in blood pressure results in a decrease in HR but neutralised due to demand for oxygen.

Chemoreceptors in muscles, aorta and carotid arteries. Decrease in pH, increase in pp carbon dioxide and decrease in pp oxygen.

Proprioreceptors in tendons, muscles and joints. An increase in motor activity means HR and SV increases.

Intrinsic:

Temperature - Increase in temperature leads to an increase in HR.

Venous Return - Increase in VR leads to increase in HR and SV (Starling's Law)

Hormonal:

Adrenalin from the adrenal glands. Stimulates A Node directly via blood leading to an increase in HR and SV.

The impact of regular participation in physical activity and a healthy lifestyle, in relation to the heart is:

• Increased SV decreasing resting heart rate to maintain the same Q at rest.
• Increased  potential max Q increases the supply of oxygen during exercise.
• Increased potential intensity/duration of physical activity.
• Bradycadia (<60) more efficient/healthy heart, under less strain at rest over the period of a lifetime.
• Arguably slows down the heart's deterioration in efficiency due to the natural ageing process.
• Improved length of an individual's quality of life (not necessarily longevity).
• Increased size/strength of force of contraction (Hypertrophy).

• All blood vesses have three layers exceot for single-walled capillaries.
• Artey and arteriole walls have a large muscular middle layer of involuntary smooth muscle to allow them to vasodilate (widen) and vasoconstrict (narrow) to alter their shape and size to regulate blood flow.
• Arterioles have a ring of smooth muscle surrounding the entry to the capillaries into which they control blood flow. Called precapillary sphincters, this ring of smooth muscle can vasodilate and vasoconstrict to alter their shape and size to regulate blood flow.
• Capillaries have a very thin, one-cell-thick layer to allow gaseois exchange to take place.
• Larger veins have pocket valves to prevent the back flow of blood and direct blood in one direction back to the heart.
• Larger veins have pocket valves to prevent back flow of blood and direct blood in one direction back to the heart.
• Venules and veins have a much thinner muscular layer, allowing them to venodilate (widen) and venoconstrict (narrow) to a lesser extent, and a thicker outer layer to help support the blood that sits within eahc valve.

Venous return is the deoxygenated blood returning to the heart. Starling's Law of the heart states that 'Stroke volume is dependant upon venous return'. Hence, if VR increases SV/Q increases and if VR decreases, SV/Q decreases.

Five venous return mechanisms help maintain and increase VR during exercise to ensure SV/Q are suffiecient to supply the demand for oxygen during exercise:

1. Pocket valves

2. Skeletal muscle pump

3. Respiratory pump

4. Smooth muscle

5. Gravity

- Blood pressure is the pressure exerted by the blood against the arterial blood vessel walls.

- Blood pressure is normally expressed as systolic over diastolic.

- Systolic Bp represents ventricular systole.

- Diastolic Bp represents the ventricular diastole.

- The average resting Bp is 120 over 80 mmHg.

- mmHg = millimetres of mercury.

- Blood pressure is also expressed as:

blood flow (Q) x resistance

- Blood pressure is measured sing a sphygmomanometer.

Endurance (aerobic) Training:

Systolic -

• Sub-maximal: Systolic increases in line with exercise intensity and may plateau during sub-mas work (around 140-160 mmHg).
• Maximal: Systolic continues to increase in line with intensity, from 120mmHg to above 200mmHg during exhaustive exercise intensity.

Diastolic -

• Sub-maximal: Diastolic changes little during sub-max.
• During gross muscle activities like rowing localised muscular diastolic Bp may fall to around 60-70mmHg.
• Maximal: Diastolic may increase a little as exercise intensity reaches maximum levels.

Isometric (resistance) Training:

Heavy weight-training involving isometric contractions causes a marked increase in both systolic and diastolic which can exceed 480/350 mmHg. Resting Bp after resistance training tends to not change and may decrease.

CHD is the single largest cause of death in the Western world and in linked to a more sedentary lifestyle. Five primary risk factors associated with developing CHD are:

• Physical inactivity
• High blood pressure
• Smoking
• High blood lipids (diet)
• Obesity

CHD os two or three times more likely in inactive sedentary individuals. Inactivity is a major risk factor for CHD, doubling the risk of a heart attack. There is a cause-and-effect relationship between physical inactivity and CHD. Lifelong involvement in an active lifestyle will help maintain significant protection from CHD.