Cardiac Output

Cardiac output is increased during exercise by increases in both heart rate and stroke volume. Heart rate increases in response to withdrawal of vagal (parasym-pathetic) tone and increased sympathetic stimulation of p1-adrenergic receptors in pacemaker regions of the heart. Heart rate increases within seconds of the start of exercise or even in anticipation of exercise. Heart rate reaches steady state in 2 to 3 minutes at exercise rates below the anaerobic threshold, in proportion to the increase in VO2. Heart rate at VO2max can be estimated for normal subjects as: frequency (beats/min) = 220 - age (years).

Increased heart rate has a positive inotropic effect on cardiac contractility due to the staircase (or Treppe) mechanism (see Fig. 9 in Chapter 11), which increases stroke volume. Sympathetic stimulation of ^-adrenergic receptors on the ventricles also increases cardiac contractility and stroke volume. Stroke volume reaches the maximum level at about 40% of VO2max, so further increases in cardiac output occur by increasing heart rate.

Myocardial oxygen consumption increases with heart rate and stroke volume, and reaches its maximal level during exercise. The myocardium extracts most of the oxygen from the coronary circulation during exercise so there is no extraction reserve (see later discussion). This explains why exercise in patients with coronary artery disease causes angina pectoris, a painful response to metabolic changes in the myocardium when flow is limited.

An increase in cardiac output cannot be sustained unless venous return also increases. Exercise increases venous return by several mechanisms. Rhythmic contractions during exercise can create a so-called muscle pump, which moves blood out of the veins past the one-way valves (see Fig. 8 in Chapter 17). Decreased intrathoracic pressure with large inspiratory efforts also promotes venous return. Venoconstriction from sympathetic stimulation of ^-adrenergic receptors in the veins causes the venous return curve to shift upward, and arterial vasodilation in exercising muscle beds (explained below) further increases the slope of the venous return curve (see Fig. 11 in Chapter 14). Finally, the increase in venous return leads to increased stroke volume due to the Frank-Starling mechanism, which is an increased contractile response to increased cardiac filling (see Fig. 4 in Chapter 13).

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