Exercise training has special significance for individuals with CAD because the changes promote lower myocardial oxygen demand at any given workload. These include lower heart rate, lower systolic blood pressure, and lower circulating catecholamines. The benefits of these adjustments can be demonstrated by the greater amount of work that can be done before angina and/or ischemic ST depression occurs. Moreover, several provocative studies suggest that there is an improvement in myocardial oxygen supply (ie, coronary blood flow) at a given level of myocardial oxygen demand after training. There are many mechanisms, or combinations thereof, that may explain these findings, which are discussed in the section below. demonstrates the positive effects of conditioning exercise on angina.
The increase in peak cardiac output is due to an increase in both stroke volume and peak heart rate, which differs from normal subjects, whose peak heart rate usually does not change. Changes in peak heart rate may reflect a greater level of effort applied during follow-up testing. In subjects with cardiac disease, the submaximal cardiac output may be lower at a given workload, with maintenance of V̇2 by widening the arteriovenous V̇2 difference after training. Such a result suggests improved overall efficiency for delivery of oxygen to the tissues. Studies have found that participation in a home exercise training group (compared with a control group) by physically disabled men with CAD significantly improved peak exercise LV ejection fraction and fractional shortening between baseline and 6 months. Another study revealed that in men with CAD, the increment in rest to peak LV ejection fraction improved with 1 year of training only in those performing high-intensity training (85% V̇2 max) but not in those performing low-intensity training (50% V̇2 max). This improvement occurred in subjects with both depressed (≤50%) and those with normal (>50%) LV ejection fractions. The increase in stroke volume that occurs with short-term training is likely attributed to augmentation of blood volume and, hence, ventricular preload. However, most studies involving patients with severe impairment of LV systolic function attribute the training effect to peripheral rather than central changes.
Most major CAD clinical events are accompanied by coronary thrombosis. Emerging evidence suggests that exercise training favorably affects this process, in particular, the fibrinolytic system. In one study, strenuous endurance exercise for 6 months in healthy older patients resulted in a significant improvement in hemostatic indices, with a reduction in plasma fibrinogen levels, an increase in mean tissue plasminogen activator, an increase in active tissue plasminogen activator, and a reduction of plasminogen activator inhibitor. Short- and long-term exercise affect platelet activation. Platelet activation is important in the pathophysiological mechanisms of unstable coronary syndromes and acute MI. Available data suggest that short-term exercise can lead to increased platelet activity, especially in sedentary individuals, but regular, long-term exercise may abolish or reduce this response.
Skeletal muscle changes after exercise training include increases in oxidative enzyme concentration, capillary density, myoglobin concentration, muscle glycogen, and adaptation of muscle fiber type to a higher percentage of type I fibers. All potentially contribute to greater capacity to use oxygen and to better endurance.
|Study Design:||Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Parallel Assignment
Masking: Open Label
Primary Purpose: Prevention
|Official Title:||Heart Failure: A Controlled Trial Investigating Outcomes of Exercise Training (HF-ACTION)|