Myocardial oxygen uptake can be estimated during clinical exercise testing by the product of heart rate and systolic blood pressure, which is called the double product or rate-pressure product. Other, less important factors include external work performed by the heart, the energy necessary for activation, and the basal metabolism of the myocardium.Īccurate measurement of myocardial oxygen uptake requires cardiac catheterization to obtain coronary arterial and venous oxygen content. Myocardial oxygen uptake is primarily determined by intramyocardial wall stress (ie, the product of left ventricular pressure and volume, divided by LV wall thickness), contractility, and heart rate. In most cases, the ventilatory threshold is highly reproducible, although it may not be achieved or readily identified in some patients, particularly those with very poor exercise capacity. The ventilatory threshold is another measure of relative work effort, and it represents the point at which ventilation abruptly increases, despite linear increases in oxygen uptake and work rate. V̇ o 2 max is influenced by age, sex, exercise habits, heredity, and cardiovascular clinical status.
One metabolic equivalent (MET) is a unit of sitting/resting oxygen uptake (≈3.5 mL of O 2 per kilogram of body weight per minute [mL It is convenient to express oxygen uptake in multiples of sitting/resting requirements. V̇ o 2 maxrepresents the amount of oxygen transported and used in cellular metabolism. 6 It is considered the best measure of cardiovascular fitness and exercise capacity. Maximal oxygen consumption (V̇ o 2 max) is the greatest amount of oxygen a person can take in from inspired air while performing dynamic exercise involving a large part of total muscle mass. During staged exercise testing, oxygen uptake usually remains relatively stable (steady state) after the second minute of each intensity of exercise below the ventilatory threshold. Oxygen uptake quickly increases when dynamic exercise is begun or increased. Vagal reactivation is an important cardiac deceleration mechanism after exercise it is accelerated in well-trained athletes but may be blunted in deconditioned and/or “medically ill” patients. In the postexercise phase, hemodynamics return to baseline within minutes of termination. Cardiac output can increase as much as 4- to 6-fold above basal levels during strenuous exertion in the upright position, depending on genetic endowment and level of training. In normal subjects, this is not a limiting determinant of peak exercise capacity. The pulmonary vascular bed can accommodate as much as a 6-fold increase in cardiac output without a significant increase in pulmonary artery pressure. Diastolic blood pressure may remain unchanged or decrease to a minimal degree. As exercise progresses, skeletal muscle blood flow is increased, oxygen extraction increases as much as 3-fold, total calculated peripheral resistance decreases, and systolic blood pressure, mean arterial pressure, and pulse pressure usually increase. During strenuous exertion, sympathetic discharge is maximal and parasympathetic stimulation is withdrawn, resulting in vasoconstriction in most circulatory body systems, except for that in exercising muscle and in the cerebral and coronary circulations. At fixed submaximal workloads below ventilatory threshold in healthy persons, steady-state conditions are usually reached within minutes after the onset of exercise after this occurs, heart rate, cardiac output, blood pressure, and pulmonary ventilation are maintained at reasonably constant levels. In the early phases of exercise in the upright position, cardiac output is increased by an augmentation in stroke volume mediated through the use of the Frank-Starling mechanism and heart rate the increase in cardiac output in the latter phases of exercise is primarily due to an increase in heart rate. Customer Service and Ordering Information.Stroke: Vascular and Interventional Neurology.
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