Regional vascular responses to gradual reductions in right atrial pressure and aortic pressure were investigated in nine men. In each study, lower body negative pressure was applied in a ramp of -1 mm Hg/min for 40-50 minutes. During the range from control to -20 mm Hg, right atrial pressure (4 studies) fell from 4.2 mm Hg to -0.6 mm Hg; heart rate was slightly reduced (2 beats/min), and aortic mean pressure and pulse pressure (6 studies) were unchanged. The maximal rate of rise of aortic pressure showed no consistent trends. Forearm blood flow (30 studies) fell with the onset of lower body negative pressure and reached 67% of the control value by -20 mm Hg. Splanchnic blood flow (14 studies) was significantly reduced by -7 mm Hg and fell to 89% of control by -20 mm Hg. During the range from -20 to -50 mm Hg, right atrial pressure continued to fall. Aortic mean pressure fell slightly or was unchanged in four subjects and fell dramatically at -35 mm Hg in two subjects. Aortic pulse pressure began to fall at about -20 mm Hg and fell linearly thereafter. Heart rate paralleled aortic pulse pressure (r=-0.86 to -0.93). Forearm blood flow fell to 55% and splanchnic blood flow fell to 65% of control at -50 mm Hg. Thus, significant vasoconstriction occurred without measurable change in arterial blood pressure. We concluded that low-pressure baroreceptors, presumably in the cardiopulmonary region, initiate splanchnic and forearm vasoconstriction with more pronounced vasoconstriction occurring in the forearm.KEYS WORDS peripheral circulation heart rate lower body negative pressure blood pressure regulation forearm blood flow splanchnic blood flow low-pressure baroreceptors • A major cardiovascular adjustment to moderate hemorrhage is increased sympathetic outflow to the heart and various vascular beds. Traditionally this adjustment has been associated with carotid sinus and aortic baroreceptors (1) which clearly play important roles in regulating arterial blood pressure. More recently, however, stretch receptors in the cardiopulmonary region (low-pressure baroreceptors) have been implicated in the mediation of reflex responses to hemorrhage in dogs, cats, and rabbits (2-4). In humans, simulation of hemorrhage by mild degrees of lower body negative pressure can evoke marked forearm vasoconstriction without significant changes in heart rate, aortic mean pressure, aortic pulse pressure, or maximal rate of rise of aortic blood pressure (dP/dt max) (5). It appears that reduced pressures in the cardiopulmonary region accompanying lower body negative pressure must be the stimulus for the reflex vasoconstriction. Previous studies in man (6, 7) have implicated low-pressure baroreceptors in the reflex release of forearm vasoconstrictor tone accompanying increases in thoracic blood volume induced by postural or respiratory maneuvers.We attempted to determine whether the vasoconstriction seen in forearms during a mild degree of lower body negative pressure, which was insufficient to measurably affect arterial blood pressure, was evide...

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Haemodynamic and ventilatory responses, during multilevel bicycle exercise and during multilevel symptomlimited treadmill exercise, were compared in 8 patients with coronary heart disease and in one sedentary middle-aged man, at known percentages of each subject's maximal oxygen uptake (Po2max), determined on a treadmill.When comparisons were made at the same percentages of Vo2max on treadmill or bicycle, we found higher arterial mean pressure, heart rate, pressure-rate product, peripheral vascular resistance, and pulmonary ventilation during bicycle exercise. Cardiac output was the same and stroke volume was lower on the bicycle.We conclude that in terms of arterial blood pressure and pressure-rate product, all conditions being as mentioned above, bicycle exercise constitutes a greater stress on the cardiovascular system at any given oxygen uptake than does treadmill exercise.

Eight women and 4 men, mean age 71.1 years, examined by a clinical check-up participated in a bicycle ergometer training program (12 weeks with 3 training sessions per week). Symptom limited ergometric bicycle tests were performed before and after the training period. The training work load was continuously controlled by maintaining the training heart rate according to 60% of the maximum work load of the first test. To hold the training heart rate (HR) on a constant level the work load had to be increased systematically during the whole training period up to 180% of the level at the beginning. The working time in each training session was increased from 2 X 10 mm at the beginning up to 2 X 20 min after the sixth week. The maximum work load (+ 16%) and the maximum oxygen uptake (+ 11%) increased significantly. The submaximal HR decreased significantly. In contrast there was no significant difference in maximum HR and maximal change of base excess between the initial exercise test and the control study at the end of the training program. This indicates that the increased exercise capacity represents a real endurance training effect and not only an increase in the degree of exhaustion. We conclude that also in healthy people between 67-76 years a significant endurance effect is possible when the training work load and training time is increased systematically according to the rules of training sciences.

Maximal oxygen uptake V O O2 max ) and functional aerobic impairment (FAI) were determined by treadmill test in 42 men with coronary heart disease and in 11 slightly older healthy men. Patients were separated according to occurrence or nonoccurrence of angina with exercise. At rest and at four levels of submaximal exercise on a bicycle ergometer, cardiac output (Q), using the direct Fick principle, heart rate (HR), mean systemic and pulmonary arterial pressures, and arterial-mixed venous oxygen difference (A-V O 2 D) were evaluated in relation to relative aerobic requirement (% V o o2 max ). Q was highly correlated with V o o2 , and both the level and the rate of change of Q were lower in patients with angina at all submaximal workloads. Stroke volume (SV) and HR were significantly restricted at the higher workloads. Although peripheral resistance was increased, there was no compensatory increase in A-V O 2 D. Both restricted SV and reduced HR are responsible for cardiovascular components of the abnormal FAI found in patients with myocardial ischemia due to coronary arterial disease.

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The polarcardiographic responses to exercise in normal men, young and middle-aged, have been compared with those of men who show ischemic responses on the electrocardiogram. Changes in the ST-vectors are the most significant. These changes have been reduced to a single numerical quantity based on the spatial magnitude of the vector at the end of the QRS complex and the spatial direction of a vector occurring at a clearly specified time during the period of the ST-segment. The assets of polarcardiography are that it enables study of direction and nwgnitude of ST-vectors in a time sequence. Thus it provides information of clinical importance which cannot be obtained by either electro-or vectorcardiography.