One of the more difficult concepts for students to understand is how the heart copes with the demands of exercise, and how training benefits the performer. For example, many students will learn that training produces an effect called bradycardia. But, how does bradycardia benefit a performer? How does having the heart beating slower help a performer? Let’s look at this aspect of the heart and also try to get a better understanding of Starling’s Law and cardio-vascular drift.
During exercise, heart rate increases in direct proportion to the amount of work undertaken. When the exercise is exhausting, a maximum heart rate is reached. An estimate of maximum heart rate may be calculated from the formula:
Maximum heart rate = 220 – age
When workloads are kept constant, such as when running on a treadmill at constant speed, the heart rate increases but eventually levels off, reaching a plateau. This is the steady state heart rate and indicates the optimal heart rate for the amount of exercise being undertaken. Increase or decrease the workload and a new steady state heart rate will develop within a minute or two.
There are two main terms used to describe the amount of blood leaving the heart during a contraction.
The cardiac output is the amount of blood leaving one ventricle in one minute. This increases dramatically when we exercise.
The stroke volume is the amount of blood leaving one ventricle per beat. Stroke volume also increases during exercise.
Another term that is sometimes used when talking about the heart is the ejection fraction. This is the proportion of the volume of blood in one ventricle that leaves the heart during a contraction (systole).
Cardiac output and stroke volume are related such that:
Cardiac output = stroke volume x heart rate.
Simple maths shows this relationship to the full.
The average stroke volume for a young adult is 70 cms3, and the average resting heart rate is something near 70 beats per minute.
The resting cardiac output is therefore 70 x 70 = 4900 cms3 per minute. This is the same as 4.9 dm3 per minute. Note the units: it’s a volume in a certain amount of time.
When individuals exercise, the heart rate increases. For students, a maximum heart rate of approximately 200 beats per minute is possible. Stroke volume also increases during exercise and can easily go up to 125 cms3.
This gives us an exercising cardiac output of 200 x 125 = 25,000 cms3 per minute or 25 dm3 per minute – more than 5 times higher than the resting cardiac output!
I like to show students what sort of volumes we are talking about here. A simple analogy is use the box in which reams of paper are packaged. That box has a volume of approximately 5 dm3. So at rest, a boxful of blood passes through the heart each minute, and this increases to over 5 boxes per minute during hard exercise.
The box comes in handy in the next part as well.
In order to understand cardiac mechanics, an idea of the weird physiology of cardiac muscle is needed. Not only can cardiac tissue, like any other muscle in the body muscle contract, it can also conduct nerve impulses. That’s why the sino-atrial node can initiate the cardiac cycle by sending nerve impulses through the atria to cause systole. Cardiac muscle has a third property; it is elastic, and when stretched, will return to its original shape with some force. Another analogy here would be an elastic band – the more you stretch it, the greater the force generated when it recoils.
The increase in stroke volume that occurs when exercising is mainly due to the fact that when we exercise, more blood enters the ventricles when the heart is relaxed (diastole), and the walls of the ventricles , being made up of elastic tissue, will stretch to accommodate the blood and then contract more forcefully; just like an elastic band. This is Starling’s Law of the Heart. The increase in blood flow into the heart is because of the increased venous return due to more blood flowing faster around the body.
The volume of blood in the body averages out at approximately 4-5 litres – about the same volume as that box! Most of the time, this blood is not all in circulation; some of it is in temporary storage in organs such as the liver and spleen, because at rest, it simply isn’t needed. When we exercise this stored blood in released into the general circulation, increasing the volume of blood circulating and so increasing the venous return.
So exercise increases venous return, which stretches the heart during diastole and produces a corresponding increase in the force of contraction of the heart resulting in an increase in stroke volume.
It’s a sequence of changes. Get students to rearrange cards or drag boxes on a whiteboard into the correct order.
Effects of training
Training, especially endurance training over months/years, makes the heart increase in size. This is mainly due to an increase in the thickness of the cardiac muscle of the left ventricle. Cardiac muscle, like skeletal muscle, gets bigger the more it is overloaded; it undergoes hypertrophy (also called ‘athlete’s heart’).
In power-trained athletes, the hypertrophy is not as great and is caused by both an increased thickness of the ventricular cardiac muscle, and an increase in the size of the ventricular chamber.
The hypertrophied heart is capable of increased filling during the diastolic (resting) phase and increased strength of contractions during the systolic phase.
Stroke volume also increases because of training. Training increases blood volume and hence there is a greater venous return during exercise.
Again it’s that sequence – more blood; increased venous return; greater diastolic filling; more stretch; more forceful contraction; greater stroke volume
Training reduces the resting heart rate. As mentioned before, a resting heart rate below 60 beats per minute is known as bradycardia.
Remember that cardiac output = stroke volume x heart rate. Training has little effect on resting cardiac output, because cardiac output is largely dependent on physique and metabolic rate. So if, as a result of training, stroke volume increases, but cardiac output remains essentially the same, the heart rate at rest must reduce.
Some students understand this better if numbers are used! So cardiac output at rest = 4900 cms3 per minute because heart rate = 70 beats per minute and stroke volume = 70 cms3 per minute.
If training increases the stroke volume to 100 cms3, and the resting cardiac output remains at 4900 cms3, resting heart rate falls to 4900 ÷ 100 = 49 beats per minute
The main benefit of training to the performer is that not only is resting heart rate reduced, but he or she will have a reduced heart rate at different workloads when compared to an unfit performer.
Remember again that we only have a boxful of blood available in our blood vessels. The essential role of this blood during exercise is to get as much oxygen to our muscles as possible. Students need to realise that the heart is also a muscle and therefore needs its own supply of oxygen being delivered by the blood. The faster the heart beats, the more blood/oxygen it requires.
Make another analogy! The heart is about the same size as a fist and also about the same size as a biceps muscle. Just think how hard an exercising heart is working – 150-200 contractions per minute; equivalent to contracting 3 times per second! Imaging how much oxygen that must require when you compare that to how quickly a biceps muscle gets tired having done just a few dozen contractions!
The less the heart contracts, the less blood/oxygen it needs and the more oxygen that is available for the working muscles. The fitter performer doesn’t ‘waste’ oxygen on their heart; they therefore have more available to their exercising muscles. This is why the slower (bradycardic) heart is beneficial to a performer. The fitter performer has a lower resting heart rate; they probably have a higher exercising heart rate as well – unfit people may be unable to exercise hard enough to get their heart rate up to its maximum. Fitter performers are said to have a greater heart rate range.
Resting heart rate
Maximum heart rate
Heart rate range
When exercise continues for a long period, the stoke volume begins to get smaller while the heart rate increases. There is also a slight increase in cardiac output during sustained exercise. These changes to cardiac function are called the cardio-vascular drift and are mainly caused by sweating.
Sweating causes a loss of fluid from the body. The difficult conceptual jump here is to appreciate that the fluid we call sweat actually comes from the blood. If you lose fluid from the blood, the blood volume must decrease, which will result in a decreased venous return. The decrease in venous return means less stretching of the cardiac muscle during diastole and hence Starling’s Law of the heart tells us that there will be reduced force of contraction and therefore a reduced stroke volume.
So during extensive exercise, lasting something like an hour, when stroke volume reduces because of sweating, but cardiac output remains essentially the same, because its steady state exercise, then heart rate needs to increase to maintain equilibrium. This is the main cause of cardio-vascular drift.
The slight increase in cardiac output that occurs during prolonged exercise is also due to sweating and the increased need for oxygen to provide energy for the production of sweat to cool the body.