Introduction: the whole-body response to exercise

Chapter 1 Introduction

the whole-body response to exercise

The basic pattern of cardiovascular response to acute exercise is straightforward. It is centred on the principle that the cardiovascular system fulfils three primary functions: to deliver nutrients and oxygen to cells of the body’s tissues, to remove metabolites from the same sites and to regulate heat exchange between body and environment so as to maintain a stable core temperature. It is self-evident that increased metabolic activity in skeletal muscles must require increased local blood flow and that this metabolic activity must produce heat that needs to be dissipated.

Ultimately, the absolute amount of work that an individual can perform depends on the capacity of the circulation to service muscle metabolism and to maintain thermal stability. The efficiency of muscle cell contraction can of course affect exercise performance and the time to fatigue, so factors such as the cellular concentrations of mitochondria and myoglobin must be taken into account. If we compare trained and sedentary subjects, then the difference in work capacity will be partly due to the adaptive effects of training on muscle cell metabolism. However, no degree of muscular adaptation can enhance aerobic performance unless there is concomitant cardiovascular adaptation and, in highly trained individuals, this increased capacity for aerobic activity is limited entirely by blood flow. Similarly, despite the multiple factors that contribute to fatigue, it is the encroachment on circulatory performance that has the most predictable and the most potentially serious consequences.

The amount of skeletal muscle activation that occurs during exercise must by definition be proportional to the activity of descending neural instructions from the cerebral motor cortex. This offers an ideal way by which circulatory responses can be regulated in proportion to the extent of motor activity, via collateral inputs from the descending motor axons onto the hindbrain nuclei that control the sympathetic nervous system. These inputs activate sympathetic outflows to the heart and peripheral blood vessels, increasing cardiac output and blood pressure. At the same time, a combination of local mechanisms in the microcirculation of the active muscles ensures that these vessels are relaxed so that the elevated cardiac and perfusion pressure gradient result in increased muscle blood flow. This situation is summarized, in its simplest form, in Figure 1.1 below.

Figure 1.1 Basics of the relationships between motor command of exercise and the associated muscle work and muscle blood flow.

The next few chapters will be concerned with the mechanisms by which these basic events take place, together with some of the practicalities of measuring them in human subjects. We shall progressively expand upon the flow diagram shown in Figure 1.1, aiming to finish up with a complete diagrammatic description of the interactions that occur during acute exercise. We shall then examine the ways in which circulatory efficiency limits exercise in different circumstances and some of the factors that can curtail exercise by interfering with circulatory function. Finally, we shall look at the ways in which cardiovascular adaptation to chronic exercise improves the efficiency of the acute exercise response, and how this adaptation is affected by exposure to different altitudes.

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Cardiovascular Physiology in Exercise and Sport