Objective-To investigate whether physiological cardiac reserve can be measured in man without invasive procedures and whether it is a major determinant of exercise capacity. Design-Development of method of measurement and an observational study. Setting-A regional cardiothoracic centre. Subjects-70 subjects with a wide range of cardiac function, from heart failure patients to athletes. Methods-Subjects underwent treadmill, symptom limited cardiopulmonary exercise tests to measure aerobic exercise capacity (represented by Ṽ O 2 max) and cardiac reserve. Cardiac output was measured non-invasively using the CO 2 rebreathing technique. Results-Cardiac power output (CPO max ) at peak exercise was found to be significantly related to aerobic capacity: CPO max (W) = 0.35 + 1.5Ṽ O 2 max (l/min), r = 0.87, p < 0.001. It also correlated well with exercise duration (r = 0.62, p < 0.001), suggesting that cardiac reserve is a major determinant of exercise capacity. In the study, cardiac reserve ranged from 0.27 to 5.65 W, indicating a 20-fold diVerence between the most impaired cardiac function and that of the fittest subject. Conclusions-A non-invasive method of estimating physiological cardiac reserve was developed. The reserve was found to be a major determinant of exercise capacity in a population of normal subjects and patients with heart disease. This method may thus be used to provide a clearer definition of the extent of cardiac impairment in patients with heart failure. (Heart 1998;79:289-294)

SUMMARY1. Previous work has shown that physiological increases in mean aortic root pressure, which change the pressure in both the coronary circulation and the left ventricle, result in reflex vasodilatation. This study was undertaken to attempt to localize the reflexogenic area mainly responsible for the reflex.2. In anaesthetized, artificially ventilated dogs, cannulae connected to perfusion systems were inserted in the ascending aorta, left ventricular apex and left atrium. This allowed us to change the pressures in: (a) the aortic root including both the coronary arteries and the left ventricle; (b) aortic root and coronary arteries, at constant ventricular pressure; and (c) in the ventricle, with mean (although not pulse) aortic pressure constant. Aortic and carotid baroreceptors were perfused at constant pressure and reflex responses were determined from changes in perfusion pressures (flows constant) to a vascularly isolated hindlimb and to the remainder of the systemic circulation.3. Combined changes in mean aortic root (coronary arterial) and ventricular systolic pressures consistently resulted in decreases in perfusion pressures. A change in only mean aortic root (coronary arterial) pressure, with ventricular pressure constant, also resulted in decreases in perfusion pressures and these were only a little smaller than those to the combined stimulus. Changes in ventricular systolic pressure resulted in responses averaging only about 30 % of those to the combined stimulus.4. Setting mean aortic root or ventricular systolic pressures at different levels did not affect the responses to changes in pressures in the other region.5. These results show that physiological increases in pressure in the aortic root and coronary arteries, in the absence of changes in pressure in the left ventricle, cause reflex vasodilatation. The relatively small response occurring when ventricular pressure was changed could be due either to a contribution from ventricular receptors or to a change in the stimulus to coronary receptors resulting from changes in the ventricular or aortic pulse.6. We conclude that the reflex effects of increases in mean aortic root pressure are due mainly to stimulation of coronary arterial baroreceptors. MS 1970 J. K. A. AL-TIMMAN AND OTHERS

SUMMARYIn healthy human subjects the immediate responses of pulse interval and the steady-state responses of arterial blood pressure and cardiac output to changes in carotid sinus transmural pressure were determined before and during the application of a subatmospheric pressure to the lower part of the body. Increases in carotid sinus transmural pressure, effected by applications of subatmospheric pressure to the neck (neck suction) resulted in prolongation of pulse interval and decrease in blood pressure; opposite responses were obtained to application of a positive pressure (neck pressure). Application of lower body negative pressure resulted in a decrease in pulse interval (heart rate increase) but little change in blood pressure. During lower body negative pressure, the responses of pulse interval to neck pressure were reduced but those to neck suction were unaffected; the responses of blood pressure to neck suction were enhanced but those to neck pressure were unaffected. From experiments in which cardiac output was also determined, it was seen that lower body negative pressure reduced cardiac output, increased calculated total body vascular resistance and augmented the resistance response to neck suction although not to neck pressure. These results are compatible with the view that application of lower body negative pressure does not change the sensitivity of the baroreceptor reflex and that the changes in the responses are due to non-linearities of the stimulus-response curves.

Contrary to expectation, the aerobic exercise capacity of patients was found to be greater with the lower dose of lisinopril, suggesting that therapy with ACE inhibitors for heart failure may require tailoring the doses to the individual to optimize functional benefits in relation to the assumed prognostic benefits.