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1. The heart-rate (HR) method for determining the energy expenditure of free-living subjects has been evaluated using a whole-body calorimeter in which individuals lived continuously for 27 h while carrying out normal daily activities. Eight male volunteers each occupied the calorimeter on at least two occasions when HR and energy expenditure were measured continuously. 2. After each session in the calorimeter a calibration was obtained using standard techniques by determining HR and heat production (HP) over periods of 10-15 min at several levels of activity. Energy expenditure in the calorimeter was then predicted, by each of five methods, from the mean HR in the calorimeter. Additionally, one session in the calorimeter was used to obtain a calibration and was used for predicting the subject's energy expenditure while in the calorimeter on other occasions. 3. Standard methods of prediction using one calibration point at rest and several points during activity were unreliable for predicting the energy expenditure of an individual. The 24 h HR was at the lower end of the calibration scale and there were considerable over-estimates or underestimates of energy expenditure, particularly during the night when the mean (+/- SD) difference between the actual and predicted HP was -66 +/- 38.6%. A linear regression fitted to points at the lower levels of activity improved the prediction of 24 h HP while a logistic plot reduced the error even further. The best estimate of energy expenditure was that obtained from a calibration over 24 h within the calorimeter; the mean (+/- SD) difference between the actual and predicted 24 h HP was +3 +/- 10.5% for light activity and -3 +/- 6.7% for moderate activity. Thus current procedures for calibrating subjects may lead to large errors which could be reduced by using a respiratory chamber.
The effects of two beta-adrenergic receptor blocking drugs, the non-selective propranolol and the beta1selective metoprolol, were studied on hemodynamics and plasma renin activity (PRA) of healthy volunteers in an ergometric exercise test. Oral doses of 160 mg of propranolol and 200 mg of metoprolol were tested against placebo. The drug plasma concentrations were determined. Heart rate and systolic blood pressure were equal and significantly lower during treatment with both active drugs when compared to placebo. The effect of drugs on exercise heart rate was correlated with the logarithm of drug plasma concentration with both propranolol and metoprolol. Propranolol, but not metoprolol, decreased the basal level of PRA. The ergometric exercise induced a significant rise in PRA after placebo but this increase was partially inhibited by the both active drugs. On the basis of these findings it is suggested that in man the basal level of PRA could be decreased mainly by blocking the beta2-adrenoceptors. Instead the exercise induced increase of PRA could be inhibited by blocking the beta1-adrenergic receptors.
To determine optimal heart rate for the maximal cardiac output at various levels of inotropy and blood volume, the relationship between heart rate (HR) and stroke volume (SV) was examined in anaesthetized dogs during right atrial pacing. Myocardial inotropy was raised by intravenous infusion of isoproterenol, a stimulator of adrenergic beta-receptors, and reduced by propranolol, an inhibitor of adrenergic beta-receptors. Circulating blood volume was increased by saline infusion. Within the range of optimal heart rate, SV and HR were inversely related: SV = k (HR0-HR), where k indicates the relationship between changes in SV and HR. The intercept with the HR axis is HR0. At constant HR a rise in inotropy increased SV and a fall in inotropy reduced SV. These changes in SV were eual at every HR, and k was therefore constant. In contrast, blood volume expansion increased SV more at low than at high HR (k increased), but HR0 was not significantly changed. Calculated maximal cardiac output: k.HR02/4, and optimal heart/rate: HR0/2, agreed with observations when maximal cardiac output was raised from 1900 to 4500 ml/min by increasing blood volume and inotropy. Optimal HR was not influenced by changes in blood volume, but was increased from 160 to 200 beats/min by increasing inotropy. We conclude that the optimal heart rate and the maximal cardiac output can be predicted from the linear relationship between SV and HR during right atrial pacing.
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1 The effects of a 5-min period of sustained mental arithmetic upon blood pressure and heart rate were determined in several groups of healthy subjects and hypertensive patients. 2 The arithmetic produced significant increases in heart rate and blood pressure (both systolic and diastolic) in both normotensive and hypertensive subjects. 3 The blood pressure changes were neither attenuated nor enhanced by the prior administration of basis. 4 In subjects habituated to the test the heart rate increase was unaffected by the drugs, but in those less familiar with the test it was usually attenuated. 5 Although the beta1-adrenoceptor selective blocker, metoprolol, caused decreases in baseline values for blood pressure and heart rate similar to those observed with the use of the two non-selective blockrs, it was shown in a double-blind crossover comparison with propranolol that the haemodynamic changes provoked by the mental arithmetic were not less in the presence of beta1-receptor blockade than when both beta1- and beta2-receptors were blocked. 6 These findings suggest that, during beta2-adrenoceptor blockade, the haemodynamic effects of minor mental stress are not exaggerated because of uncompensated alpha-receptor mediated vasoconstriction, such as occurs following adrenaline infusion.
BACKGROUND: Heart rate (HR) control in atrial fibrillation (AF) is commonly guided by resting HR measurements, usually with 12‑lead ECG or in-office pulse palpation. OBJECTIVES: We aimed to assess the reliability of resting HR measurements in AF patients with long-term ambulatory ECG and activity monitoring. METHODS: We included patients who had recorded a full-disclosure ambulatory ECG with a mobile cardiac telemetry device equipped with an accelerometer (PocketECG, MEDICALgorithmics, Poland), with at least 95% AF. Resting HR samples (≤20 per individual/day) were collected as 10-s daytime (8 am to 8 pm) measurements after ≥10 min of rest. These samples were compared to each individual's mean daytime resting HR. RESULTS: In 832 patients (median age 77 (interquartile range (IQR) 69-83) years, 42% women) with a median registration duration of 13 days (IQR 7-22), the population mean daytime resting HR was 85 (±15) beats per minute (bpm). A single resting HR differed from the mean daytime resting HR by a mean of ±10.4% (IQR 3.6-14.4%). When the mean daytime resting HR was ≥110 bpm, 29% of resting HR samples were < 110 bpm, and when the mean daytime resting HR was 80-109 bpm,11% of samples were ≥ 110 bpm. Resting HR measurement variability decreased to 5.3% (IQR 1.9-7.5%) when four resting HR samples were averaged. CONCLUSION: In patients with AF, a single resting HR measurement often differs substantially from the mean daytime resting HR. When a precise measurement is clinically relevant, repeated resting HR sampling or ambulatory monitoring can address this measurement imprecision.
Tracheobronchial clearance of inhaled 6mum Teflon particles (density 2 gm/cu cm) tagged with technetium 99m was studied in healthy subjects by external measurement of the radioactivity in the lungs for two hours. Clearance, salivary secretion, blood pressure, and heart rate were determined in eight subjects after double-blind, subcutaneous administration of 0.25 mg terbutaline sulfate, a beta-adrenoceptor stimulating compound and vehicle, respectively, in a crossover study. Terbutaline produced a marked increase in clearance and a slight increase in heart rate, but had no important effect on salivary secretion or blood pressure. The result indicates that the blood concentrations of catecholamines might be of importance for the regulation of the mucociliary transport rate.
We attempted to correlate inotropic and eletrophysilogic digitoxin effects with serum digitoxin concentrations during 8 hr after a single dose. Eight pentobarbital-anesthetized Labrador dogs were given 2.0 mg digitoxin intravenously. Left heart catheterization and His bundle registration were performed. acing and programed electrical stimulation were used to determine heart rate-independant changes in dP/dt, intra-atrial, atrioventricular (AV), His-Purkinje, and intraventricular conduction velocity. The effective (A-ERP) and functional (A-FRP) refractory periods of the atrium and the functional nodal refractory period (AV-FRP) were measured. Serum digitoxin concentrations were determined by radioimmunoassay. Median serum digitoxin half-time was 5.7 hr. The dP/dt increased after digitoxin, with maximum values after 2 hr. Digitoxin concentration correlated with the inotropic response after 4 hr. Heart rate fell significantly within 2 min and remained below control values for the 8 hr observation period concimitant with an increase in AV-nodal conduction time and AV-ERP increased significantly in the late elimination phase, while A-FRP increased slightly initially and remained high. No consistent correlation was found between the electrophysilogic variables and serum concentrations. We conclude that the two main effects of digitoxin, the inotropic and electrophysiologic, are dissociated in the elimination phase after a single dose.
The effect of long-term storage in polyvinyl chloride bags on the biological activity and the chemical stability of isoproterenol was studied. A freshly prepared solution of isoproterenol, isoproterenol solution stored for six months and isoproterenol stored for 30 months were infused into the coronary circulation of 14 isolated rabbit hearts; heart rates were determined. Spectrophotometric studies to determine stability at various pH levels were also done. Aging of the solutions at pH 4 and at a concentration of 4 microgram/ml caused no significant impairment of their potency. Solutions above pH 6 were unstable.
Mean arterial pressure, cardiac output and heart rate were determined in eight male New Zealand white rabbits while conscious and after being anesthetized with halothane plus nitrous oxide for 15 minutes. Delivery of the anesthetic agent was stopped and the measurement repeated at 15, 30, 60 and 210 minutes. In a separate experiment blood samples were obtained for plasma renin activity in six rabbits before anesthesia, after 15 minutes of halothane plus nitrous oxide administration, and again 210 minutes after cessation of the anesthesia. Later, this experiment was repeated with the same rabbits except that they were allowed to breathe room air instead of the anesthesia. The halothane anesthesia resulted in decreased mean arterial pressure and cardiac output, but these returned to the preanesthetic levels by 15 minutes after stopping the anesthesia. Heart rate increased during halothane administration, and although it tended to return toward control levels after cessation of the halothane, heart rate was still elevated 210 minutes later. Halothane plus nitrous oxide produced an increase in plasma renin activity, which then subsided to normal by 210 minutes following anesthesia; breathing room air did not result in increases in plasma renin activity. These studies revealed that although short-term anesthesia with halothane plus nitrous oxide resulted in cardiovascular changes in rabbits, after cessation of the anesthetic agent the cardiovascular system quickly returned to normal.
Baroreflex control of heart rate was determined during three awake control situations and during two depths of halothane anesthesia in man. Baroreflex function was quantiated by calculating the pressor test slope from the R-R interval change on the ECG produced by a pharmacologically induced pressor response. During the three awake control situations the subjects breathed room air or 100 per cent O2 spontaneously or 100 per cent O2 with ventilation controlled. Mean (+/- SD) slopes obtained were 15.1 +/- 4.5, 15.6 +/- 6.8 and 18.4 +/- 9.9, respectively. No significant difference in baroreflex function slope was observed. During light halothane anesthesia (0.7 per cent endtidal) baroreflex function was significantly depressed (mean slope = 2.5 +/- 1.5), and it was abolished at 1.1 per cent end-tidal halothane (mean slope = 0.03 +/- 0.04). It is concluded that halothane anesthesia produces depression of baroreflex control of heart rate in man.
Five subjects who had been training vigorously for 2 mo worked 5 min on the cycle ergometer at 1,480 +/- 100 kpm/min and at 1,920 kpm/min on separate days. Plasma norepinephrine (NE), blood lactate, and heart rate were determined during the postexercise periods. The same subjects were also tested at 1,480 +/- 100 kpm/min after a 2-mo detraining period, when subjects did not train. At 1,920 +/- 80 kpm/min, plasma NE was 4 ng/ml at the end of exercise. The NE concentration increased slightly in the first min postexercise, then decreased with a half-time of 2.8 min between 1 and 11 min postexercise. Detraining for 2 mo did not markedly affect the rate of disappearance of NE in the postexercise period in these five subjects. Between 11 and 30 min postexercise (1,480 +/- 100 kpm/min), heart rate was 25 beats/min higher after detraining, while NE was not significantly different. These data provide evidence that more rapid recovery of heart rate in trained individuals during this period is not likely due to a more rapid recovery from the sympathetic response to exercise.
Four groups of normotensive subjects were used in an experiment designed to: (a) replicate earlier data, (b) determine whether heart rate and respiration rate changes accompanied the development of acquired bi-directional diastolic blood pressure responses, and (c) investigate whether males and females acquired diastolic blood pressure responses at differential rates. Observations were carried out over one baseline and eight consecutive one-hour training sessions. Analyses of the blood pressure scores revealed subjects were able to acquire a bi-directional response, thereby confirming earlier reports. From subsequent analysis of the heart rate and respiration rate scores and from intercorrelations between diastolic blood pressure, heart rate, and respiration rate, no consistent relationships or patterns emerged. Comparisons of male and female blood pressure performance failed to yield evidence of reliable sex differences.
Data was collected from two men who attempted an 80 km run. Measurements of aerobic power (VO2 max) and determinations of heart rate (HR) and submaximal oxygen consumption (VO2) during treadmill running were carried out one week before the run. Throughout the 80 km run, HR was recorded by telemetry and used together with the laboratory data to estimate VO2 as a percentage of VO2 max. One subject completed the 80 km distance at 58% of VO2 max, the other subject, operating at 74% of VO2 max, was obliged to retired after 55 km. The data in this and other studies indicate that the high energy costs reported for the marathon (70-85% of VO2 max) cannot be sustained over the 80 km distance but that about 60% of VO2 max can be continued for seven hours and longer.
Measurements of aortic input impedance in the rat, dog, and man suggest a new hypothesis to explain the inverse correlation between rate and body size: that pulse wavelength and arterial length are matched in a way that minimizes cardiac work. The optimal rate is fast enough to avoid the high impedances produced by reflections at relatively low frequencies, yet slow enough to permit orderly excitation and recovery of the myocardium.
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