Longitudinal studies of aging in 37 men

Robinson, Sarah; Dill, D. B.; Tzankoff, S. P.; Wagner, J. A.; Robinson, Richard D.

doi:10.1152/jappl.1975.38.2.263

Cited by 65 publications

(25 citation statements)

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“…Subjects with high exercise tolerance achieved higher maximal heart rates (r = 0.42, p = 0.008), had lower submaximal heart rates (r -0.52,p = 0.001 for phase 1; r = 0.55, p = 0.0007 for phase 2; r = 0.72, p = 0.0001 for phase 3; r = 0.65,p = 0.0006 for phase 4; r = 0.76, p = 0.0002 for phase 5 of the exercise protocol) and had a smaller rate of change of heart rate witn exercise (r = -O.68,p = 0.0001) ( fig. 3).…”

Section: Maximal Exercise Treadmill Testmentioning

confidence: 95%

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

Kostis¹,

Moreyra²,

Amendo³

et al. 1982

Circulation

151

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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

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Section: Maximal Exercise Treadmill Testmentioning

confidence: 95%

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

Kostis¹,

Moreyra²,

Amendo³

et al. 1982

Circulation

151

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“…From several studies it is well known that resting metabolic rate (RMR) declines with advancing age (Keys et al, 1973;Robinson et al, 1975;Tzankoff & Norris, 1978). Aging is also associated with a decrease in fat-free mass (FFM), which is the main determinant of RMR (Steen et al, 1979;Reed et al, 1991;Baumgartner et al, 1995;Suominen, 1997).…”

Section: Introductionmentioning

confidence: 99%

Lower resting metabolic rate in the elderly may not be entirely due to changes in body composition

et al. 2004

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Objective: To investigate whether or not the lower resting metabolic rate (RMR) in the elderly is entirely due to changes in body composition. Design: Cross-sectional data of 132 female (age 69.975.5 y, body mass index (BMI) 26.574.0 kg/m 2 ) and 84 male (age 68.975.1 y, BMI 26.172.8 kg/m 2 ) participants of the longitudinal study on nutrition and health status in an aging population of Giessen, Germany, as well as that of 159 young women (age 24.873.0 y, BMI 21.172.5 kg/m 2 ) and 67 young men (age 26.873.4 y, BMI 23.372.4 kg/m 2 ) were analysed. RMR was measured by indirect calorimetry after an overnight fast and body composition was estimated by bioelectrical impedance analysis and predictive equations from the literature. Analysis of covariance was used to adjust RMR for body composition, body fat distribution and smoking habits. Additionally, RMR that is to be expected theoretically, was calculated on the basis of the subjects' body composition and the specific metabolic rate of the different organs and was compared to measured RMR. Results: Compared to young subjects adjusted RMR was significantly lower in elderly women (5432782 vs 5809770 kJ/day, Po0.01) and men (6971799 vs 75587121 kJ/day, Po0.001). In both elderly women and men, measured RMR was markedly lower than calculated RMR (À6257404, À5157570 kJ/day). By contrast, measured and calculated RMR were nearly the same in young men (1597612 kJ/day); in young women the difference between measured and calculated RMR was only À3007457 kJ/day. In both sexes, these differences are significantly larger in the elderly when compared to young adults. Conclusion: These results support the point of view that the decline in RMR with advancing age cannot be totally due to changes in body composition.

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“…The decline in mHR proceeds at approximately the same rate for all individuals, without regard for lifestyle or physical fitness (4)(5)(6)(7)(8). For many otherwise healthy elderly people, it is the factor that ultimately restricts the ability to live independently (9,10).…”

mentioning

confidence: 99%

Depressed pacemaker activity of sinoatrial node myocytes contributes to the age-dependent decline in maximum heart rate

Larson

Clair

Sumner

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

111

163

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An inexorable decline in maximum heart rate (mHR) progressively limits human aerobic capacity with advancing age. This decrease in mHR results from an age-dependent reduction in "intrinsic heart rate" (iHR), which is measured during autonomic blockade. The reduced iHR indicates, by definition, that pacemaker function of the sinoatrial node is compromised during aging. However, little is known about the properties of pacemaker myocytes in the aged sinoatrial node. Here, we show that depressed excitability of individual sinoatrial node myocytes (SAMs) contributes to reductions in heart rate with advancing age. We found that agedependent declines in mHR and iHR in ECG recordings from mice were paralleled by declines in spontaneous action potential (AP) firing rates (FRs) in patch-clamp recordings from acutely isolated SAMs. The slower FR of aged SAMs resulted from changes in the AP waveform that were limited to hyperpolarization of the maximum diastolic potential and slowing of the early part of the diastolic depolarization. These AP waveform changes were associated with cellular hypertrophy, reduced current densities for L-and T-type Ca 2+ currents and the "funny current" (I f ), and a hyperpolarizing shift in the voltage dependence of I f . The agedependent reduction in sinoatrial node function was not associated with changes in β-adrenergic responsiveness, which was preserved during aging for heart rate, SAM FR, L-and T-type Ca 2+ currents, and I f . Our results indicate that depressed excitability of individual SAMs due to altered ion channel activity contributes to the decline in mHR, and thus aerobic capacity, during normal aging. O ne of the most insidious aspects of growing older is an inevitable decline in maximum heart rate (mHR), which limits maximum aerobic capacity with advancing age (1-3). The decline in mHR proceeds at approximately the same rate for all individuals, without regard for lifestyle or physical fitness (4-8). For many otherwise healthy elderly people, it is the factor that ultimately restricts the ability to live independently (9, 10).The decrease in mHR with age results primarily from a parallel age-dependent decline in "intrinsic heart rate" (iHR) (11-13), which is measured during autonomic blockade, and thus reflects the spontaneous pacemaker activity of the sinoatrial node of the heart. Although it is known that the intact sinoatrial node from aged animals contracts more slowly (14, 15) and contains fewer pacemaker myocytes (16), little is known about the functional properties of individual myocytes from the sinoatrial node of the aged heart.Sinoatrial myocytes (SAMs) are highly specialized cells that serve a primarily electrical function as cardiac pacemakers via their production of spontaneous action potentials (APs). Sinoatrial APs are characterized by a spontaneous depolarization during diastole that drives the membrane potential to threshold, thereby triggering the subsequent AP. This "diastolic depolarization" (DD) phase of the sinoatrial AP results from the coordinated activit...

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Longitudinal studies of aging in 37 men

Cited by 65 publications

References 0 publications

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

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

Lower resting metabolic rate in the elderly may not be entirely due to changes in body composition

Depressed pacemaker activity of sinoatrial node myocytes contributes to the age-dependent decline in maximum heart rate

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