14 The magnitude of the increase depends on multiple factors, including age, baseline exercise capacity, characteristics of the training regimen, whether or not training and testing are done with the same task (training specificity), and genetic factors.
The primary effect of aerobic exercise training is to increase maximal exercise capacity or V̇ o 2max by increasing maximal SV and maximal A-V O 2 Δ.
This makes sense because the greater the exercise stress relative to V̇ o 2max, the greater the catecholamine spillover, and the greater the HR and SBP response are. 14,16 Consequently, MO 2, or the internal work rate, 18 is not determined by the physical task or the absolute V̇ o 2 but by the V̇ o 2 relative to maximal capacity. Whereas Q is determined by the absolute V̇ o 2 or the external work rate, the HR and systolic blood pressure (SBP) response, and therefore the “double product,” an index of myocardial oxygen requirements (MO 2), are determined by the V̇ o 2 requirements of a physical task relative to maximal capacity or the percent V̇ o 2max. The cardiovascular response to exercise in patients with CAD mimics the normal response, although maximal capacity is often reduced by decreases in maximal SV or HR, exercise-limiting symptoms such as angina pectoris or claudication, or deconditioning from inactivity and bed rest. 15 Consequently, maximal exercise capacity or V̇ o 2max is a surrogate measure of maximal Q and SV. 14 The cardiac response to physical activity is tightly coupled to V̇ o 2 so that a 1-L increase in V̇ o 2 elicits an ≈6-L increase in Q. Increases in A-V O 2 Δ are produced by flow redistribution from metabolically less active tissue to the exercising muscle, hemoconcentration from fluid loss into the exercising muscle interstitial space, and increased O 2 extraction over the active muscle bed. The increase in Q is produced by increases in both heart rate (HR) and stroke volume (SV). 15 Rearranging the Fick equation (cardiac output =V̇ o 2 times arterial-venous O 2 difference ) demonstrates that V̇ o 2 is determined by the product of Q and A-V O 2 Δ. The response of the circulatory system is designed to match the V̇ o 2 requirements. The absolute oxygen demand, and therefore the absolute rate of V̇ o 2, is determined by the physical task or the external work rate 18 and the individual’s mechanical efficiency in performing that task. Physical activity increases the body’s oxygen demand measured as the ventilatory oxygen uptake or V̇ o 2. Only the most salient points are repeated here. The principles of exercise physiology, 14 their clinical import, 15 and their application to patients with atherosclerotic CAD 16,17 have been summarized. This review discusses the benefits of exercise training for patients with atherosclerotic cardiovascular disease.
#Farsky trainer trial
13 The reasons for this underutilization are not defined but probably include health professionals’ underestimation of the benefits of exercise, a lack of training in exercise therapeutics among many healthcare providers, poor financial reimbursement, the absence of reimbursed advocates for exercise therapy, 13 and the absence of a sufficiently large randomized clinical trial documenting a reduction in cardiac events.
Referral rates are even lower among women and older patients. 2 Despite these benefits, exercise training is rarely prescribed for cardiac patients, as evidenced by the fact that only ≈20% 11,12 of qualified patients are referred to formal cardiac rehabilitation programs. 7–10 A recent randomized, controlled comparison of exercise training and angioplasty in selected patients with angina documented fewer cardiac events in the exercise subjects over the year of follow-up. 6 Meta-analyses of exercise-based, cardiac rehabilitation studies have suggested that exercise training reduces cardiac mortality in coronary artery disease (CAD) patients.
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