Exercise And Ischaemic Heart Disease

The positive effects of being physically active when suffering from coronary artery disease was shown as early as the end of the 1700s. These findings were unfortunately lost to memory and it was not until the mid-1960s that exercise was used as therapy for coronary artery disease.

The first cardiac rehabilitation programmes based on physical training were then started, and the first  recommendations issued in 1980.

Acute physiological effect of exercise in ischaemic heart disease

The cardiovascular system’s immediate response to exercise is an increase in heart rate due to reduced activity in the parasympathetic nervous system (vagal slowing). This is followed by increased activity in the sympathetic nervous supply to the heart and the body’s blood vessels.

Relatively rapid heart rate during submaximal exertion or post-exercise recovery is often seen soon after a myocardial infarction or heart surgery. An unusually low heart rate during submaximal exertion can be due to beta blocker medications or an increase in stroke volume from the exercise.

The use of beta blockers, which lower the heart rate, limit the interpretation of heart rate response in exercise.

At an early stage during exercise, cardiac output increases through an increase in stroke volume due to an improved length-tension relationship in the heart muscle. This is called the Frank Starling mechanism, and involves an enhancement of force when the muscle fibre lengthens.

The lengthening of the heart muscle fibre is due to increased venous return flow. The increase in cardiac output occurs mainly through an increase in heart rate, meaning that when beta blocker therapy is given the maximal cardiac output becomes lower.


The presence of different rhythm disturbances (arrhythmias) is not uncommon in ischaemic heart disease. If the arrhythmias present at rest and disappear during exertion, they are usually benign. If, however, the arrhythmias increase during exertion, there is cause to stop the exercise and discuss further medical investigation.

Blood pressure

Systolic blood pressure rises with increased dynamic exercise as a result of the increased cardiac output. Diastolic blood pressure usually remains unchanged or is somewhat higher. It is important to note in the clinical work that, during auscultation, diastolic pressure can be heard right down to zero during exertion, and can thereby be a false reading.

An insufficient fall in blood pressure or elevation of blood pressure can occur during exercise. During ongoing exertion, a poor rise in blood pressure or a drop in blood pressure is due to impeded outflow in the aorta, severe left ventricle dysfunction, angina in the heart or beta blocker medication.

In certain individuals with heart disease, however, the blood pressure can increase (over and above the measured maximal exertion value) in the recovery phase.

If the exercise is stopped abruptly, some individuals may experience a substantial fall in systolic blood pressure. This drop in blood pressure is due to accumulation of venous blood and a delayed increase in peripheral resistance adjusted to the decrease in cardiac output.

Oxygen uptake in the heart

The oxygen uptake of the heart during exercise can be calculated using the so-called double product (rate pressure product = RPP), defined as the systolic blood pressure times the heart rate divided by 100.

There is a linear relation between the heart’s oxygen uptake and the heart’s blood supply that occurs primarily in the diastolic phase. During exercise, the blood flow to the heart muscle can increase up to five times the resting value. A

person with heart disease is usually not able to maintain adequate blood flow to the ischaemia-affected part of the heart and the heart’s metabolic requirements during exercise can thereby not be met, resulting in acute oxygen deficiency in the heart muscle, angina pectoris.

Skeletal muscle blood flow and peripheral resistance

The skeletal muscle blood flow can increase three-fold during exercise and the total peripheral resistance decreases due to increased vasodilatation in working skeletal muscle during exercise.

In the case of beta blocker therapy, a somewhat smaller increase in blood flow in the working muscle occurs, which is why the feeling of fatigue in peripheral musculature is greater in patients receiving beta blockers.

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