Decline In Heart Rate Research Articles

Exercise and the Elderly

Data from cross-sectional studies suggest that VO2max declines in adulthood at a rate of 0.40-0.45 ml.kg-1.min-1 per year in males and 0.30 ml.kg-1.min-1 per year in females. Longitudinal studies suggest that the loss is much greater for males, approximating 1.0 ml.kg-1.min-1 per year or more. The rate of loss may be greater in sedentary compared to active individuals. The decline in VO2max with age appears to be inevitable, and a major contributing factor may be the decline in maximal cardiac output. A reduced maximal heart rate is a consistent finding, and this may be due to decreased end-organ sensitivity to catecholamines. Maximal stroke volume may or may not decrease, and physical training status may be a determining factor. The most recent evidence suggests increased dependence upon the Frank-Starling mechanism, resulting in an increased stroke volume to offset the decline in maximal heart rate. Cardiac output is thought to be maintained in this manner. Use of this mechanism may depend upon the absence of underlying disease. Therefore, investigators who vigorously screen potential subjects for occult coronary disease may report findings different from those who do not. Maximal a-vO2 difference may or may not decline in the elderly. The research is divided, and there is support for both beliefs. Several factors typical of the elderly, including a decline in muscle mass, increased blood distribution to the skin during exercise, and a potentially lower capillary/fiber ratio, would contribute to a lower a-vO2 difference. On the other hand, in those subjects with reduced cardiac output, there may be greater dependence upon a-vO2 difference during maximal exercise. Pulmonary function does not appear to limit VO2max, although the elderly may be less efficient while breathing during exercise. However, the higher ventilation and higher ventilatory equivalent for oxygen observed during submaximal exercise could be due to higher relative stress in the elderly. Elderly males and females are capable of demonstrating a training effect in response to endurance training regardless of previous physical activity patterns and current training status. The degree of change with training, expressed in relative terms, appears to be comparable to that demonstrated by younger subjects. Physiological factors contributing to an increased VO2max as a result of training appear to be similar in elderly and younger subjects, with the possible exception of no change in maximal a-vO2 difference in the elderly. This point is somewhat controversial.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of a drag-reducing polyelectrolyte of microscopic linear dimension (Separan AP-273) on rat hemodynamics.

Separan AP-273, a polydisperse, high molecular weight (10(5)-10(7) dalton range), anionic polyacrylamide, demonstrates polymer drag reduction (Toms effect) in the flows of several substances including blood. That is, under appropriate conditions, pipe flow can be increased markedly for a given pressure gradient, sometimes threefold or more, by nanomolar concentrations of linear macropolymers. The effect of intact and degraded Separan was tested in the open-chest, anesthetized rat, and left ventricular and carotid pressures, aortic blood flow (electromagnetic flow probe on ascending aorta), and the electrocardiogram were recorded. The results indicate that aortic flow, which in control animals was about half the flow reported for conscious rats, increases markedly after injection of Separan. The effect on blood pressure after an initial fall was variable, but the slope of arterial diastolic pressure was consistently steepened. Electrocardiographic changes were unremarkable except for a slow decline in heart rate. Although secondary reflexes undoubtedly influenced the results, the primary mechanism of the polymer appears to involve a reduced resistance to flow. The results are compatible with the proposal that the Toms effect, or some variant of it, is operative in vivo under favorable conditions. If this view is correct, then Separan and two other chemically different macropolymers with similar hemodynamic effects and physical attributes, i.e., linearity and molecular lengths approaching 100 micron, might be prototypes of a novel category of cardiovascular drugs.

Aging of modulation of heart rate.

We postulated that measurements of autonomically mediated fluctuations in heart rate might provide a quantitative probe of biological aging. We used power spectrum analysis of instantaneous heart rate while 33 male subjects matched their breathing to a metronome at 15 breaths/min. Measurements were made in supine and standing position. Total power and its two major components, high- and low-frequency power, declined with age in both positions but at different rates. High-frequency power that represents parasympathetically mediated respiratory sinus arrhythmia declined linearly in supine position only in subjects 9-28 yr with a slope of -0.796, which was significantly different from zero at P = 0.0007. The absolute value of high-frequency power in standing position was approximately 60% of that in supine, a difference that was statistically significant (P = 0.01). Low-frequency power that represents beta-adrenergically mediated heart rate fluctuations, especially in standing position, declined linearly to 62 yr of age (P = 0.0001). Mean heart rate increased 17.2 beats/min, and diastolic blood pressure increased 8 mmHg in the entire group in the standing compared with supine position. There were no significant differences in these changes above and below 30 yr of age. We conclude that the influence of the two major mechanisms that modulate heart rate decline at significantly different rates with aging.

Cardiovascular unwinding, type A behaviour pattern and locus of control.

Three studies are reported, in which subjects were exposed for a period of three minutes to a threat of possible shock. On average subjects showed higher heart rates before the trial than after the trial, and higher rate during the first minute of the trial than the final minute. Results are reported here which show that Type A behaviour pattern and internal locus of control are consistently related to less decline in heart rate.

Heart rate in humans during underwater swimming with and without breath-hold

Heart rate was monitored, by way of radiotelemetry, from 6 male subjects of mean age (±SE) 24 ± 1 years and of mean mass 73.5 ± 2.5 kg. Measurements were made in a 25 m pool at a water temperature of 28°C. Resting heart rate was 67 ± 3.7 beats · min −1 and when the subjects submerged themselves completely in the pool, but remained inactive, there was a prompt, gradual reduction in heart rate which reached 48 ± 2.6 beats · min −1 within 30 sec and 40 ± 2.6 beats · min −1 within 59 ± 5.6 sec (maximum duration). When they propelled themselves under water for 33 sec by kicking their legs and breathed through a snorkel tube, heart rate increased progressively to a value of 118 ± 4.1 beats · min −1 at 28 sec. However, when they performed the same manoeuvre while holding their breath, there was an initial increase in heart rate to 106 ± 5.7 beats · min −1 within the first 10 sec. This was followed by a decline in heart rate which was more rapid than that recorded during inactive submersion and which eventually reached 48 ± 4.4 beats · min −1 at mean underwater duration of 33 ± 1.8 sec. It is concluded that during the first 10–15 sec of underwater breath-hold swimming in humans, the cardiovascular response (as indicated by heart rate) is similar to that seen during a similar level of exercise while breathing air. From then on there is a progressively more intense bradycardia which is probably indicative of an oxygen conserving response consisting of reduced perfusion of most of the body except the heart, CNS and active locomotory muscles. The degree and rate of onset of this proposed oxygen conserving response are influenced by the intensity of the exercise performed while under water and whether or not the period of underwater breath-hold swimming is preceded by exercise.

The effect of D-Ala-2-Me-Phe-4-Met-(O)-OL enkephalin on blood pressure, heart rate and digoxin-induced arrhythmias in the guinea pig

The cardiovascular effects of D-Ala-2-Me-Phe-4-Met-(O)-01 enkephalin were investigated after its administration into the fourth cerebroventricle of the guinea pig. This enkephalin is a synthetic Met-enkephalin analog that is more resistant to degradation and has a high affinity for opioid receptors. It produced a significant increase in blood pressure and decline in heart rate. At high concentrations, 100 ug/kg plus 100 ug/kg/hr in the fourth ventricle, it produced bradyarrhythmias that were sometimes fatal. At doses that did not alter survival or produce arrhythmia, namely 30 ug/kg plus 25 ug/kg/hr in the fourth ventricle, the response to digitalis was assessed. Significant leftward shifts in the relationships between digoxin and arrhythmia occurrence and development of fatal arrhythmias were observed. Thus, D-ala-2-Me-Phe-4-Met-(O)-01 enkephalin has definite cardiovascular effects that include potentiation of digoxin arrhythmias.

Loss of nocturnal decline in blood pressure after cardiac transplantation.

Twenty-four hour noninvasive ambulatory blood pressure and heart rate monitoring was performed on patients who underwent orthotopic cardiac transplantation, as part of the investigation of the de novo hypertension that developes in such patients. Patients with essential hypertension served as control subjects. The results demonstrated a highly significant loss of the usual decline in blood pressure and heart rate during sleep in the transplant patients. A similar loss of nocturnal decline in blood pressure was noted in a group of 10 patients with autonomic neuropathy secondary to diabetes mellitus. The de novo hypertension associated with cardiac transplantation is probably multicausal. Impairment of renal function by cyclosporin-A with associated salt and water retention and persistent elevation of the systemic vascular resistance in the presence of a restored normal cardiac output by the "new" heart are major factors. In addition, loss of the normal nocturnal decline in blood pressure and heart rate, which probably is related to the denervated state of the transplanted heart, may play an important role in blood pressure control.

Alterations in cardiovascular structure and function with advancing age

The greatest difficulty in studying the effects of aging on cardiovascular structure and function lies in separating the effects of aging itself from those of the inextricably entwined disease processes and life-style changes that accompany aging. Age-related stiffening of the arterial tree results in an increased systolic blood pressure, which appears to impose a greater load on the heart. Probably as an adaptive mechanism to maintain normal wall stress, a modest age-associated concentric left ventricular hypertrophy develops, which approximates 30% between ages 25 and 80. The decrease in mitral valve E-F slope and increase in the left atrial dimension, which are seen with advancing age, may be construed as the consequences of a thicker-walled, less compliant left ventricle. Systolic left ventricular function, measured at rest either by echocardiography or radionuclide techniques, is unaffected by aging. Aerobic exercise capacity, whether measured as total work performance or maximal oxygen consumption, declines with age, although in subjects who maintain a high level of physical activity, the decline appears to be approximately half of the 10 % per decade decrease seen in sedentary persons. An age-related decline in maximal exercise heart rate has been a universal finding. Although several studies over the past 4 decades have found cardiac output to decrease with age, both at rest and during exercise, a recent study of subjects carefully screened to exclude latent coronary artery disease found no such decline in cardiac output. In these subjects, the age-related decline in maximal heart rate and systolic emptying at peak exercise was offset by an Increased utilization of the Frank-Starling mechanism. An attractive hypothesis for explaining the hemodynamic profile of a decreased maximum heart rate, increased preload and decrease in ejection fraction at maximal effort, despite elevated norepinephrine levels, is an age-associated, diminished end-organ responsiveness similar to β-adrenergic blockade.

Differences between Saimiri sciureus and Callicebus moloch in physiological responsiveness: Implications for behavior.

The New World primates Callicebus moloch and Saimiri sciureus differ markedly in life modes. Physiological responsiveness (heart rate, cortisol) of these related taxa was compared in two situations that differed in the presumed degree of stress imposed, exposure to a novel environment and physical restraint. In both situations, Saimiri exhibited higher initial levels of heart rate and corticosteroids. In addition, the species differed in their patterns of response to both situations. Saimiri maintained initial heart rate levels across a 1-hour exposure period, whereas Callicebus showed a marked and continuous decline in heart rate. Adrenocortical activity increased in both species in response to test situations, but the elevations in plasma corticosteroids were substantially greater for Saimiri than for Callicebus. The results indicate that the species differ with respect to organization of physiological regulatory systems in a manner consistent with behavioral contrasts between them.

Experimental investigations on the antidotal treatment of nifedipine overdosage.

Rats anesthetized with pentobarbital and ventilated artificially were infused with 0.5 mg/kg X min nifedipine. They exhibited a sharp decline of blood pressure, heart rate, cardiac output and peripheral resistance and died after 62.3 +/- 5.3 min of infusion. In the ECG, sinus bradycardia followed by AV-dissociation and an escape rhythm originating from the AV-node or the bundle of His occurred. The survival time of nifedipine-infused rats increased by 100% and more upon additional infusion with calcium chloride, calcium gluconate, isoproterenol or dopamine and by 50% after prenalterol. Epinephrine, norepinephrine, angiotensin amide and the plasma expander polygeline were ineffective in this respect. All drugs prolonging the survival time elevated the cardiac output. Ca++ and dopamine also increased the blood pressure whereas isoproterenol accelerated the escape rhythm. Similar cardiovascular changes as in rats occurred in rabbits infused with 0.2 mg/kg X min nifedipine, the survival time without antidotal treatment amounting to 46.3 +/- 7.9 min. Calcium chloride more than doubled the survival time in rabbits, too, but isoproterenol and dopamine proved to be ineffective. Excess calcium did not overcome the inhibitory effects of nifedipine on pacemaker activity, atrioventricular conduction and peripheral resistance. The antidotal efficacy of calcium appears to be attributable to a reversal of the negative inotropic activity of nifedipine. In conclusion, Ca++ seems to be the drug of choice for the antidotal treatment of nifedipine intoxication.

Effects of exhaustive submaximal exercise on cardiovascular function during sleep.

The influence of an afternoon bout of exhaustive submaximal exercise on cardiovascular function and catecholamine excretion during sleep was examined in five female and four male subjects. Subjects walked on a treadmill for successive 50-min periods at 50, 60, and 70% maximal O2 consumption, separated by 10-min rest periods. Exercise terminated with volitional exhaustion. Following an adaptation night, electroencephalographic and impedance cardiographic measures were obtained during three successive nights of sleep, with exercise preceding night 3. Relative to the base-line night (night 2), exhaustive exercise resulted in a sustained elevation of heart rate and cardiac output throughout the entire night's sleep. The magnitude of these elevations was unaffected by sleep stage but decreased over the night. The typical pattern of circadian decline in cardiac output was unaltered. However, the decline in heart rate with sleep onset was greater on the exercise night. Changes in impedance dZ/dt and R-Z interval suggested an enhanced myocardial contractility during the first 3 h of sleep postexercise. Analysis of morning urine samples revealed that in seven of nine subjects norepinephrine excretion increased, epinephrine excretion decreased, and dopamine excretion was unchanged during sleep on the exercise night. It is suggested that these cardiac changes reflect a sustained increase in myocardial beta-receptor activity.

Acute deletion of arterial baroreceptor input in the conscious rabbit.

We describe the use of a snare to denervate the carotid sinus in conscious rabbits whose other arterial baroreceptors had been denervated 8-14 days previously by surgical operation. Within 2 min of tightening the snare arterial blood pressure had risen from 81 +/- 2 to 119 +/- 5 mmHg, and heart rate had risen from 214 +/- 9 to 280 +/- 9 beats min-1. They remained at these high levels for 15 min but then fell, so that after 30 min blood pressure and heart rate were 103 +/- 9 mmHg and 265 +/- 8 beats min-1 respectively. They declined somewhat further, but irregularly, over the succeeding 7 days. The previously brisk baroreceptor-heart rate and carotid sinus reflexes were abolished by ensnaring the carotid sinus nerve, and remained absent over the succeeding 7 days. This method of deleting input from the arterial baroreceptors is not confounded by general anaesthesia or surgical injury, and allows observations to be made within minutes. The rapid decline in blood pressure and heart rate after 15 min, and the subsequent slow downward trend, are unexplained. They are of potential importance in experiments designed to quantitate the effects of baroreceptor input on the circulation. We also noted that, whereas spontaneous activities of the baroreceptor-intact rabbit were usually associated with transient rises of blood pressure and heart rate, after deletion of baroreceptor input the same activities were usually associated with transient falls.

Beneficial effect of diltiazem on ischemia-reperfusion injury in the dog.

We determined the effect of the calcium antagonistic agent, diltiazem hydrochloride upon ischemia-reperfusion injury in the dog. Ischemia was produced by occluding the left anterior descending artery for 40 min. Subsequent reperfusion was accomplished for 120 min by virtue of removal of the occlusion. Sixteen of the dogs studied were randomly assigned to diltiazem (D)-treated group (n = 8) and saline (S)-treated group (n = 8). D in saline was intravenously infused at a concentration of 3 mcq/kg/min starting 15 min after the occlusion. Myocardial blood flow (MBF) was measured using hydrogen gas clearance method. Infarct size was quantified as percent myocardium at risk by triphenyltetrazolium chloride staining. D administration caused a slight decline in mean aortic pressure, heart rate, and heart rate X systolic blood pressure throughout the periods of occlusion and reperfusion. However, there was no significant difference observed in both groups of dogs. MBF to ischemic myocardium was not significantly enhanced by D during ischemia. After 5 min of reperfusion subepicardial MBF was increased in group S, indicating a tendency towards reactive hyperemia. After 120 min of reperfusion there was a significant reduction in subendocardial MBF in group S and the transmural blood flow ratio was 1.23 +/- 0.59 in group D as compared with 0.53 +/- 0.39 in group S (p less than 0.05). The infarcted area as a percentage of the risk area was considerably smaller in group D than in group S (27.5 +/- 3.0 vs 47.0 +/- 6.5%, p less than 0.05). D markedly reduced the elevation of tissue calcium especially in the subendocardium. These findings suggest that D reduces the ultimate infarct size through the beneficial effect on ischemia-reperfusion injury.

A new pacemaker for monitoring asystole and prevention of Adams-Stokes syndrome and sudden cardiac death.

Patients with suspected Adams-Stokes syndrome are examined by Holter monitoring. During the monitoring, there is the danger of syncopes occurring and there are even reports of sudden cardiac death. We therefore developed a pacemaker for cardiac arrest monitoring and the prevention of Adams-Stokes syndrome and sudden cardiac death, which has the following functions: (1) the longest escape interval of the pacemaker not exceeding the value at which syncope is induced is determined by the decline of the mean heart rate including the asystole to a certain threshold rate; (2) once the pacemaker escapes from the interval it continues pacing for a while at a physiological rate to allow recover from ischemias in organs or tissues; and (3) to prevent overdrive suppression to the heart, the pacing rate gradually declines and stops pacing until the next asystole. This pacemaker is useful not only in the diagnosis of Adams-Stokes syndrome but also in pharmacological and pathophysiological studies and in determining when pacing should cease.

Autonomic contribution to heart rate recovery from exercise in humans.

To assess the contribution of the autonomic nervous system to heart rate recovery following exertion, heart rate was observed after peak treadmill exercise in six men following parasympathetic blockade (PB) with atropine sulfate (0.03 mg/kg), sympathetic blockade (SB) with propranolol hydrochloride (0.20 mg/kg), double blockade (DB) with both drugs, and no drugs (ND). Least-squares analysis of each subject's heart rate (HR) as an exponential function of recovery time (t) was computed for each treatment giving an equation of the form HR = aebt. HRs at rest, peak exercise, and 10 min of recovery, the coefficients a and b, and the least-squares correlation coefficient (r) were compared among treatments by nonparametric analysis of variance and rank-sum multiple comparisons. HR recovered in an exponential manner after dynamic exercise in each subject with each of the treatment modes (P less than 0.01 for each r, mean across all treatments r = 0.94). Coefficients a and b differed the most between PB and SB. At the cessation of exercise the decreases in venous return and the systemic need for cardiac output are accompanied by an exponential HR decline. The exponential character of the cardiodeceleration seen after peak exercise appears to be an intrinsic property of the circulation because it occurred under each experimental condition.

Hemodynamic effects of captopril in chronic heart failure: Efficacy of low-dose treatment and comparison with prazosin

The acute hemodynamic effects and long-term therapeutic actions of low doses of the oral angiotensin-converting enzyme (ACE) inhibitor captopril (CPT) were evaluated in 18 patients with severe chronic congestive heart failure (CHF). Increasing doses of 1, 2.5, 6.25, 12.5, and 25 mg of CPT were given at 2-hour intervals. Increased stroke volume index (SVI) and reduced mean pulmonary capillary wedge (PCW) pressure occurred at 1 hour ( p < 0.05) with an associated decline of blood pressure. Maximal hemodynamic improvement for the group was seen at 6 and 7 hours following the 6.25 and 12.5 mg doses when SVI was elevated 35% and mean PCW pressure decreased 40% from control. CPT in doses of 12.5 to 50 mg every 8 hours was continued long term in these 18 CHF patients. Four patients died, and one was noncompliant; drug therapy was withdrawn in two patients with symptomatic hypertension and in one patient who experienced an alteration in taste. The remaining 10 patients showed significant improvement in symptoms and treadmill exercise duration at 3 months after CPT therapy was started. Moreover, repeat hemodynamic measurements were similar to optimal measurements obtained during the initial study. In a further study, the acute hemodynamic and hormonal effects of sequentially randomized 5 mg prazosin and 25 mg CPT were compared in 10 CHF patients. While both drugs reduced PCW pressure and vascular resistance, CPT effects were greater. Further, CPT alone effected a small rise in cardiac index and minor decline in heart rate, and CPT diminished aldosterone levels and increased plasma renin activity while prazosin did not.

Heart rate decrease: a comparison of feedback modalities and biofeedback with other procedures

Sixty subjects were divided into six groups in a comparison of heart rate (HR) decreases obtained with (1) visual feedback, (2) auditory biofeedback, (3) combined visual and auditory biofeedback, (4) instructions to decrease HR without biofeedback, (5) sitting quietly, (6) abbreviated relaxation training, and, as a comparison, a group of 10 experienced meditators were also studied. Biofeedback stimuli were pulsed signals generated by the R-wave of the heartbeat. The results indicated that (a) there was no differential advantage on a HR decrease task to subjects receiving visual, auditory or combined biofeedback; and (b) all groups showed evidence of some decline in HR over the testing session. The meditation group showed the greatest overall decline.

Concentration effect relationships of infused histamine in normal volunteers.

Histamine was infused in six normal volunteers at rates of 16, 32, 64 and 96 ng/kg/min increasing at 5-min intervals followed by 128 ng/kg/min for 45 min. Heart rate increased, diastolic blood pressure decreased and skin temperature increased in a dose-dependent fashion. Mean heart rate increased by 15.6 +/- 5.7 beats/min, mean diastolic pressure fell by 8.8 +/- e.2 mmHg and mean skin temperature increased by 1.2 +/- 0.3 degrees C at the highest infusion rate. Mean plasma histamine rose from a basal level of 0.20 +/- 0.03 ng/ml to 1.97 +/- 0.25 ng/ml at the end of the highest infusion rate. The threshold infusion rate for physiological effects was 64-96 ng/kg/min corresponding to 0.77-0.97 ng/ml. Salivary flow was stimulated by 21% after 30 min at the highest dose infusion (P = 0.05). Plasma adrenaline increased 132% but plasma noradrenaline was unchanged. There was a linear decline in heart rate after terminating the histamine infusion with a half time of 82 sec. The half life of infused histamine in the plasma was 102 sec. The clearance of histamine from the plasma was 6.1 %/- 0.2 l/min or 83 ml/kg/min. These concentration effect relationships in normals throw doubt on some of the high endogenous plasma histamine values in the literature.

Effects of tyrosine infusion in normotensive and hypertensive rats.

To clarify further the action of acute administration of L-tyrosine in lowering blood pressure, L-tyrosine ethylester was infused intravenously into awake [deoxycorticosterone acetate (DOCA)-salt] hypertensive rats, two-kidney Goldblatt hypertensive rats, and normotensive rats. The effects of tyrosine were measured on arterial pressure, heart rate, plasma catecholamine levels, and plasma renin activity. Blood pressure and heart rate were lowered in all groups despite significant elevation of plasma dopamine in all groups and epinephrine in the hypertensive groups, norepinephrine did not rise significantly, and plasma renin activity was always found to be within the ranges expected for each model. It was concluded that tyrosine produced the progressive decline in blood pressure and heart rate by bringing about a sustained state of parasympathetic dominance, as effective sympathetic compensation did not occcur. This could be attributed to increased alpha-adrenergic activity in certain sites in brain secondary to increased catecholaminergic activity in these areas.

Fetal oxygen consumption and mechanisms of heart rate response during artificially produced late decelerations of fetal heart rate in sheep

Delayed decelerations of fetal heart rate were produced by abruptly decreasing uterine blood flow to zero for 20 seconds in chronically instrumented, normoxic sheep. Fetal O2 content, and O2 tension in umbilical blood decreased significantly before the decline in heart rate. Fetal arterial blood pressure did not change significantly. Complete vagal blockade abolished the late deceleration and uncovered a late acceleration, which in turn was eliminated by total β-adrenergic blockade. We conclude that these late decelerations in normoxic sheep are vagally mediated and due to chemoreceptor rather than baroreceptor activity.