The effect of age on heart rate in subjects free of heart disease. Studies by ambulatory electrocardiography and maximal exercise stress test.

Abstract

SUMMARY To delineate the effects of true aging, undetected heart disease and deconditioning on heart rate, we performed 24-hour ambulatory electrocardiography and maximal exercise stress test on 101 subjects with normal hearts. The maximal heart rate recorded was 180 beats/min; the minimum was 35 beats/min. A distinct diurnal pattern was observed.With increasing age, a decrease of the maximal heart rate achieved during exercise stress test (r = 0.27,p = 0.05) or spontaneously recorded during the day (r = 0.41, p = 0.0005) or night (r = 0.24, p = 0.03) was observed. The resting and average heart rates were not affected by age. Older subjects had lower exercise tolerance (r = 0.41, p = 0.0001). Low exercise tolerance was associated with higher increments of heart rate for submaximal exercise levels (r = 0.53, p = 0.001), steeper increase of heart rate with increasing intensity of exercise (r = 0.68, p = 0.0001) and lower maximal heart rates (r = 0.43, p = 0.008).These changes of heart rate with age are not due to undetected cardiac disease, because the subjects included in the study were meticulously screened by noninvasive and invasive means.MANY STUDIES have shown that the maximal exercise heart rate declines with age.18 The intrinsic heart rate after autonomic blockade with atropine and propranolol also decreases with age with a slope similar to that of the maximal exercise heart rate.9 However, the average daily heart rate is not influenced by age,'0 and contradictory or few data are available on the effect of age on resting heart rate, on the increment of heart rate induced by standardized exercise and on the diurnal variation of heart rate." 64,[10][11][12][13][14][15][16][17][18] A common problem in studying the effect of age on the heart is the difficulty in separating the true effects of aging from those due to deconditioning or unrecognized diseases. Deconditioning due to sedentary lifestyle is a common accompaniment of aging, and undetected significant coronary artery disease may be present in more than one-fourth of persons older than 45 years of age.9-22In the studies mentioned above, the effect of age cannot be clearly distinguished from the effects of subclinical coronary artery disease or deconditioning. To further define the effect of age on the heart rate, we performed 24-hour ambulatory electrocardiography and maximal exercise stress testing on 101 subjects free of detectable heart disease verified by extensive noninvasive and invasive testing. Materials and Methods PopulationOne hundred one subjects with normal hearts were identified among 1500 patients referred for cardiac From

Longitudinal Age-Related Changes in 24-Hour Total Heart Beats and Premature Beats and Their Relationship in Healthy Elderly Subjects

“…Previous cross-sectional HR studies in healthy adults showed that maximal HR on exercise, maximal and mean HR during Holter monitoring, and intrinsic HR after pharmacological autonomic block all decreased with age. [1][2][3][4] On the con- trary, our longitudinal study of 15 healthy elderly subjects at the mean age of 70 showed that the number of THBs was significantly increased 15 years later in most of the subjects (13 of 15 subjects). The increase in THB with age in healthy elderly subjects may derive from the decrease in cardiac output and total blood volume and respiratory dysfunction with aging, as well as from age-related changes in norepinephrine metabolism at the neuroeffector gaps in the sinus node and norepinephrine spillover from the synapses in heart and other organs to circulatory blood with age, 6,16,19,20) or from a decline in vagal activity due to a decrease in nitric oxide and muscarinic receptors with age.…”

TGF-β 1 -Mediated Fibrosis and Ion Channel Remodeling Are Key Mechanisms in Producing the Sinus Node Dysfunction Associated With SCN5A Deficiency and Aging

“…Aging did not exert effects in such in vivo recordings in intact animals, which could be due to autonomic alterations known to increase sympathetic activation with age as has been observed in humans. 23,24 Interacting effects of aging and Scn5a disruption were observed in Poincaré plots representing HRV (Figure 2). Such HRV alterations are considered critically predictive of cardiac arrhythmic events in the form of ventricular tachycardia and sudden cardiac death.…”

Differing circadian patterns of symptom onset in subgroups of patients with acute myocardial infarction.

“…Also, the late-evening and early-morning onset could be linked to dilation of the left ventricle at lower heart rates in the supine position with elevation of filling pressure, which has been reported to be associated with nocturnal ischemia. 32 It is now established that persistently increased sympathetic activity causes desensitization and receptor down-regulation.33 This has been described in patients with heart failure34 and appears to occur with increasing age.35 Such down-regulation also may be present in smokers because normal subjects consuming 24 cigarettes during a 12-hour period have been reported to have a 45% rise in urinary excretion of norepinephrine and a higher heart rate during the day and night.36 Modulation of receptor sensitivity occurs quite rapidly37 and may be one explanation for the blunted morning peak and increased late peak of onset observed in this study among smokers compared with nonsmokers and for the absent morning peak among patients with a history of congestive heart failure and for those with previous myocardial infarction.…”