The physiologic sequelae of chronic dynamic exercise.

The physiologic results of acute dynamic exercise include complex neurologic, hormonal, pulmonary, and cardiovascular adjustments that provide an integrated response perfectly matching oxygen supply with oxygen demands. Long-term repeated bouts of dynamic exercise of sufficient intensity and duration yield predictable changes in anatomy and physiology. These changes affect active skeletal muscle and the heart. Changes in skeletal muscle include an increased capillary blood volume, increased mitochondrial density, increased oxidative pathway enzymes, and more efficient regulation of blood flow. These adaptations result in an increased oxidative capacity and more favorable fuel utilization. Oxygen extraction increases, accounting for up to 50 per cent of the increased maximal oxygen consumption, and endurance improves. Following chronic dynamic exercise the heart beats slower and has a larger stroke volume at rest and throughout a broad range of work intensities. The maximal cardiac output increases substantially, accounting for up to 50 per cent of the increased maximal oxygen consumption. The metabolic and biochemical changes found in skeletal muscle are not found in cardiac muscle. Changes found in isolated cardiac muscle do not always correlate with heart performance. The separation of central and peripheral factors in assessing heart performance is difficult because preload and afterload are major determinants of heart function and are altered by chronic dynamic exercise. Ischemia is a major stimulus for the development of coronary collateral vessel development in animals. Because dynamic exercise does not induce ischemia in normal humans, collateral vessel development may only occur in those with coronary heart disease. However, there is no convincing evidence that chronic dynamic exercise results in physiologically important coronary collateral vasculature in patients with angina. Improved work capacity is predictable following chronic dynamic exercise in patients with coronary heart disease. Although the rate pressure product that produces angina does not change following training, heart rates are lower at matched absolute workloads and the maximal consumption of oxygen increases. Changes in heart function are largely secondary to peripheral changes in these patients.