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In sedentary individuals, the decrease in heart rate (HR) at a respiratory exchange ratio (R) of unity (HR/R = 1) is lost after 8 weeks of moderate-intensity exercise training. The purpose of this investigation was to examine the effect of training on HR/R = 1, using the exercise intensity (EI) at R = 1 (EI/R = 1) and the HR at a set EI (HR/EIS). In nine healthy volunteers, these indices showed small measurement variability and detected changes associated with 16 weeks of training in that EI/R = 1 and VO2/R = 1 increased, whereas HR/EIS, HR/R = 1 and HR/VO2 decreased. All of these changes were reversed when training ended. In a second trial in a further nine volunteers, the training programme was extended to 20 weeks, and again showed that the decrease in HR/R = 1 failed to progress after 8 weeks despite continued changes in other indices (increases in VO2/R = 1 and decreases in HR/VO2 elevation). The loss of HR/R = 1 decrease was attributed to equal and opposite effects on HR/EIS and EI/R = 1. However, the decreases in HR/EIS showed the same trend as HR/R = 1, with a lack of progression beyond 8-16 weeks. These findings suggest that different indices of cardiorespiratory fitness have different patterns of change and limitations during training. Those which rely on decreases in submaximal HR fail to detect adaptation during continued training. Using submaximal exercise test indices, detection of such changes is better achieved by the measurement of decreases in HR/VO2 elevation and increases in VO2/R = 1 values.

Evidence is presented to show that cardiac output is little affected by changes in heart rate but the heart volumes, systolic and diastolic, are inversely related. Heart rate is controlled by changes in efferent nerves, sympathetic and vagal, which are in turn controlled from central and reflex sources. An argument is presented showing that reflexes from receptors in the atria control heart volumes by affecting, in the short term heart rate, and in the long term water intake (thirst) and urine flow, and therefore blood volume. Explanations of the mechanisms involved are presented.

The alpha 1-adrenoceptor antagonist indoramin is proposed to reduce arterial blood pressure without a concomitantly significant increase in heart rate (HR). The present study involves assessment of the effect of alpha 1-adrenoceptor antagonism in patients with mild hypertension on the HR/oxygen consumption (Vo2) relationship, which has previously been shown to indicate improvement in cardiorespiratory fitness following exercise training. A total of 16 patients with a systolic blood pressure of 140-200 mm Hg and diastolic blood pressure of 95-110 mm Hg were examined. A double-blind, placebo-controlled study design was utilized. Following initial observations, the patients were randomized into one group (a) of seven patients who were given a placebo, indoramin, and finally placebo, and a second group (b) of nine patients who were given the two agents in the reverse order, i.e., indoramin, placebo, indoramin; each intervention lasted for 2 weeks and indoramin was given in a dose of 75 mg/day. Indoramin caused a reduction in the elevation of the computed regression line relating HR to Vo2 (a shift to the right), such that at the same HR a greater Vo2 was attained in 11 of the 16 patients in comparison with the baseline exercise test. Pooled results showed a shift of the HR/Vo2 regression line to the right when indoramin was compared with baseline (p less than 0.05) or placebo. In the same patients, indoramin caused a decrease in arterial blood pressure during exercise relative to baseline or placebo periods, and a decrease in the HR during exercise relative to baseline period, but not when compared with placebo periods.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of 4 beta-adrenoceptor blocking drugs on blood pressure and on exercise tachycardia were compared in a within-patient study of patients with uncomplicated essential hypertension. Twelve patients were treated with propranolol, practolol and atenolol and 7 of the same patients also received oxprenolol. Each patient received each drug separately, withdrawing each drug before starting the next, and each patient was titrated to the lowest attainable blood pressure and heart rate with each compound. All 4 drugs caused reductions in both systolic and diastolic blood pressure and in the heart rate induced by exercise. The maximum reduction by each drug in both systolic and diastolic blood pressure was the same. There were small but significant differences in the effects on heart rate between those drugs which had intrinsic sympathomimetic activity and those which did not have this property.

1. In dogs anaesthetized with chloralose, small latex balloons were positioned at the left pulmonary vein-atrial junctions so as to stretch this region. By recording action potentials from slips of the cervical vagi it was established that distension of these balloons stimulated receptor endings in the atrial endocardium which discharged into the myelinated branches of the vagi i.e. Paintal type A, type B and Intermediate type receptors. 2. In other dogs, cooling the cervical vagus in steps of 2 degrees C reduced this response in vagal myelinated fibres. With twelve receptors the response to distension was reduced by 30% when the vagus was cooled to 16 degrees C, by 70% when cooled to 12 degrees C and abolished at 8--12 degrees C. 3. In a third group of dogs, distension of balloons at the pulmonary vein-atrial junctions resulted in a reflex increase in heart rate. Cooling the cervical vagi in these dogs in stages to 8 degrees C reduced this increase in heart rate. In nine dogs the response was reduced by 20% when the vagi was cooled to 16 degrees C, by 70% when cooled to 12 degrees C and abolished between 12 and 8 degrees C. 4. In a fourth group of dogs, distension of balloons at the pulmonary vein-atrial junctions was shown also to activate receptor endings in the atria which discharged into non-myelinated branches of the Vagi. In twelve receptors, cooling the cervical vagus in steps of 2 degrees C reduced this evoked increase in activity in non-myelinated fibres. These responses were abolished over a wide range of temperature unlike the responses observed above. 5. It is concluded that the increase in heart rate which follows distension of balloons at the pulmonary vein-atrial junctions is mediated solely by the Paintal-type receptors which discharge into the myelinated fibres in the vagi.

1. Stimulation of left atrial receptors by distension of the junctions between the pulmonary veins and the left atrium is known to cause a reflex increase in heart rate. It was suggested that the efferent path of this reflex was solely in the sympathetic nerves to the heart but more recently the existence of a vagal efferent component has been postulated by Albrook, Bennion & Ledsome (1972). 3. The junctions between the pulmonary veins and the levt atrium were distended before and after the administration of I.C.I. 66082 and bretylium tosylate. The response of an increase in heart rate was significantly decreased after the administration of I.C.I. 66082 (5 mg/kg) and abolished after the administration of bretylium tosylate (10 mg/kg). 3. It is concluded that the efferent pathway of the reflex is solely in the sympathetic nerves to the heart.

The effect of increasing heart rate by increasing the rate of atrial pacing in the absence of any reflex effects from atrial receptors, by cooling the vagi to 12 degrees C, was studied in two groups of dogs with different blood volumes. In one group of nine dogs with a high blood volume increasing heart rate, by an amount similar to that reflexly obtained in response to stimulation of atrial receptors, resulted in significant increases in urine flow and sodium excretion; in another group of eight dogs with a low blood volume similar increases in heart rate did not result in a diuresis or natriuresis. The findings suggest that the effects of an increase in heart rate in combination with differences in blood volume could contribute to the previously reported differences in the urinary responses that result from stimulation of atrial receptors in dogs with different blood volumes.

1. In anaesthetized dogs, distension of balloons so as to stimulate atrial receptors resulted in a reflex increase in heart rate. 2. Successive distensions of one, two and three balloons positioned in the left upper and middle pulmonary vein-atrial junctions and in the left atrial appendage resulted in a progressive increase in the magnitude of this response. 3. It is concluded that the magnitude of the increase in heart rate is related to the extent of receptor area stimulated.

1. Stretching the atrial appendages in anaesthetized dogs caused an increase in heart rate. This response was unrelated to changes in arterial blood pressure and left and right atrial pressures.2. The increase in heart rate was a reflex response; the afferent path was in the vagi and the efferent solely in the sympathetic nerves.3. The receptors involved in this reflex have been localized to the atrial appendages but there is no conclusive evidence as to their nature.

1. Localized distension of the junction between the superior vena cava and the right atrium without obstructing venous return caused an increase in heart rate.2. This increase in heart rate was a reflex response; the afferent path was in the vagi and the efferent solely in the sympathetic nerves.3. The receptors most likely to be stimulated by the distension of the junction between the superior vena cava and the right atrium are the right atrial receptors located on the endocardial surface of the intrapericardial portion of the superior vena caval-right atrial junction.

1. The chronotropic and inotropic responses of the dog heart to stimulation of the ansae subclaviae were studied.2. The maximum rate of rise of pressure in the left ventricle (dP/dt max) was used as an index of the inotropic changes.3. In experiments in which the secondary inotropic effects of changes in heart rate and blood pressure were prevented it was shown that, using stimuli which produced the same chronotropic response, stimulation of the left ansa subclavia resulted in an inotropic change which was about eight times greater than that which resulted from stimulation of the right ansa subclavia.4. In experiments in which heart rate and blood pressure were allowed to change freely it was shown that the secondary inotropic effects of changes in blood pressure and heart rate amounted to about 70% of the total inotropic change when the right ansa subclavia was stimulated and about 20% of the total change when the left ansa subclavia was stimulated.