Stroke volume and cardiac output

Stroke volume (SV) is the amount of blood pumped out of the heart (left ventricle - to the body)
during each contraction measured in mL/beat (millilitres per beat). Therefore cardiac output (Q),
the amount of blood leaving the heart each minute, measured in L/minute, can be calculated by
multiplying stroke volume by heart rate (Q = SV x HR).
The stroke volume and hence cardiac output will determine the amount of blood being circulated
and therefore how much oxygen will reach working muscles.
Stroke volume
The ability of the body to make oxygen-rich blood available for working muscles is the biggest
factor affecting aerobic performance. The more blood that the heart can eject per heart beat, the
more work an individual will be able to do.
Aerobic training, over a period of time, has a substantial effect on stroke volume and, therefore,
on the individual's future aerobic performance. Training causes the size of the heart to increase,
noticeably, the ventricles. The walls of the ventricles also become thicker and stronger. This
allows for more blood to enter the heart and more powerful contractions and therefore more
blood to be ejected during each contraction.
For all heart rate levels, from rest to maximal exercise, training increases an individual's stroke
volume and this is more evident during sub-maximal and maximal exercise as the ventricle fills
more completely.
Cardiac output
When a trained and untrained athlete are working at the same heart rate (beats per minute) the
trained athlete will have a much higher cardiac output than an untrained one (can be over double
for elite endurance athletes during maximal exercise). This is a direct result of a higher stroke
volume in the trained athlete. However the trained person works more efficiently as the body
adjusts the heart rate to meet the blood demands, so it is then seen that the cardiac output at rest
and during sub-maximal exercise are often quite similar as the extra stroke volume is offset by
the decrease in heart rate (this is why trained athletes have a lower exercise heart rate).
Control of Heart Rate
Heart rate is normally determined by the pacemaker activity of the sinoatrial node (SA node)
located in the posterior wall of the right atrium. The SA node exhibits automaticity that is
determined by spontaneous changes in Ca++, Na+, and K+ conductances. This intrinsic
automaticity, if left unmodified by neurohumoral factors, exhibits a spontaneous firing rate of
100-115 beats/min. This intrinsic firing rate decreases with age.

Heart rate is decreased below the intrinsic rate primarily by activation of the vagus nerve
innervating the SA node. Normally, at rest, there is significant vagal tone on the SA node so that
the resting heart rate is between 60 and 80 beats/min. This vagal influence can be demonstrated
by administration of atropine, a muscarinic receptor antagonist, which leads to a 20-40 beats/min
increase in heart rate depending upon the initial level of vagal tone.
For heart rate to increase above the intrinsic rate, there is both a withdrawal of vagal tone and an
activation of sympathetic nerves innervating the SA node. This reciprocal change in sympathetic
and parasympathetic activity permits heart rate to increase during exercise, for example.
Heart rate is also modified by circulating catecholamines acting via 1-adrenoceptors located on
SA nodal cells. Heart rate is also modified by changes in circulating thyroxin (thyrotoxicosis
causes tachycardia) and by changes in body core temperature (hyperthermia increases heart
rate).
SA nodal dysfunction can lead to sinus bradycardia, sinus tachycardia, or sick-sinus syndrome.
The maximal heart rate that can be achieved in an individual is estimated by
Maximal Heart Rate = 220 beats/min age in years
Therefore a 20-year-old person will have a maximal heart rate of about 200 beats/min, and this
will decrease to about 170 beats/min when the person is 50 years of age. This maximal heart rate
is genetically determined and cannot be modified by exercise training or by external factors.