Peter Jones is a 63-year-old man who, in his younger days, was a professional soccer player. With the training regimens that this involved he maintained a high level of physical fitness. For many years after his retirement as a football player he had kept himself active, particularly with regular games of golf. Recently he had found that this made him very tired. This was especially noticeable on the uphill sections of the course. He had also noticed that he became breathless when climbing the stairs in his house. This worried him because his father had died following a heart attack aged 58 years.

Peter knew that his father had smoked heavily from his teenage years and in his latter years had suffered considerably with angina. Apart from a very occasional cigarette Peter had effectively been a non-smoker and had not experienced episodes of angina. Nevertheless, he was concerned about the decline in his physical capacity which he felt could not just be attributed to advancing years. Peter, therefore, made an appointment to see his family doctor.

This scenario gives rise to the following questions:

1. What are the normal cardiovascular responses to exercise?

2. How can exercise capacity be improved by training?

3. What factors limit exercise ability with increasing age?

Increased extraction of oxygen from arterial blood (see Chapter 1) in exercising muscles will also contribute to the increase in oxygen delivery.

Initiation of the cardiovascular responses to exercise

Identification of the key physiological events at the initiation of dynamic exercise has long been contentious and is still the subject of debate, despite the existence of theoretical models for more than 100 years. Reflex control of the circulation normally relies on sensory information provided from baroreceptors and chemoreceptors (see Chapter 10). These same reflexes function during ongoing exercise, but mean arterial BP, Po₂ and Pco₂ do not change significantly at the start of exercise. The changes in cardiac function during exercise therefore occur too rapidly to be explained by activation of baroreceptor and chemoreceptor reflexes.

Areas within the medulla control the sympathetic and parasympathetic nerves which normally regulate heart rate and cardiac contractility as part of the baroreceptor reflex (see Chapter 10). At the start of exercise, the influence of central command over the medullary centres is to decrease vagal tone and to increase sympathetic drive, thus increasing heart rate. Part of this response may be an alteration in the operation of the baroreceptor reflex (see Chapter 10). Under normal conditions, this reflex keeps blood pressure relatively constant at a ‘set point’. During exercise, central command induced changes in this set point have the same effect as a blood pressure which is too low, hence leading to an increase in heart rate.

Reflex activation of the sympathetic nervous system also leads to peripheral vasoconstriction (see Chapter 9). This occurs particularly in the splanchnic and kidney circulations and in the vessels of non-contracting muscles. This helps to divert blood flow to active muscles. The central command mechanism is probably complemented by feedback from metabolite concentrations, particularly [K⁺], detected by chemoreceptors in contracting muscles and information from mechanoreceptors within moving joints and muscles.

Cardiovascular changes in sustained exercise

Cardiac output is a function of both heart rate and stroke volume. Figure 13.1 shows the effect of different intensities of dynamic exercise on cardiac output, heart rate and stroke volume in healthy young individuals. Intense exercise in trained athletes may require a fivefold increase in cardiac output. Changes in stroke volume reach maximum levels at a moderate exercise intensity (see below). Beyond this level, further increases in cardiac output are provided solely by increases in heart rate. Increased oxygen delivery to tissues is also achieved by increasing the extraction of oxygen from arterial blood (see Chapter 1). Thus, the arterial–venous oxygen content difference widens with increasing exercise intensity.

Fig. 13.1 Responses to sustained dynamic exercise. Typical plateau responses of heart rate, stroke volume and cardiac output to different intensities of sustained dynamic exercise in a fit young individual.

Maximum heart rate in intense exercise in a physically fit 20 year old ‘textbook person’ is 180–195 bpm. This figure changes with age so that maximum heart rate in a 10-year-old may be 210 bpm (see Chapter 12), whereas in a person aged 65 it is only about 165 bpm. Central command dominates heart rate control in mild exercise but, in more intense forms of exercise, autonomic reflexes (see Chapter 10) and the indirect effects of metabolites (see Chapter 9) generated in contracting muscles become increasingly important. Secretion of adrenaline (epinephrine) and noradrenaline (norepinephrine) from the adrenal medulla, and their effect on the sinoatrial node, also contributes to the increase in heart rate.

Stroke volume of the heart increases during dynamic exercise but reaches a maximum level at an exercise intensity of about half maximum O₂ consumption (Fig. 13.1). The extent of changes in stroke volume appears to vary with the type of dynamic exercise and the physical fitness of the individual. In trained individuals there may be relatively greater changes in stroke volume at lower workloads. In Chapter 4 the factors determining the stroke volume of the heart are identified as:

• preload effects (Frank–Starling mechanism)

• contractility effects

• afterload effects.

Increased filling of the right ventricle (increased preload) occurs as a result of increased contraction of limb muscles and therefore increased venous return to the heart. A simple, but often neglected, concept is that increases in cardiac output can only be achieved if there is an equivalent increase in venous return of blood to the heart, you can’t get out what you don’t put in! Sympathetic nervous system activation during dynamic exercise will lead to venoconstriction which also increases preload on the heart. When resting in a supine position, because there is less effect of gravity on venous return from the lower part of the body, stroke volume is already higher than in an upright posture. The cardiac output increases which occur during exercise in a supine position (e.g. swimming) are achieved almost entirely as a result of an increase in heart rate because stroke volume is already approaching maximum levels at the start of exercise.

Contractility increases in the heart are associated with an increase in myocyte intracellular [Ca⁺⁺] and lead to an increased force of ventricular contraction (see Chapter 4). Sympathetic nervous system activation in exercise and the release of adrenal medulla catecholamines will lead to increased contractility via activation of β-adrenoceptors. The modest increase in mean arterial blood pressure (Fig. 13.2

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