Constant work increases the amount the heart beats and like any work shortens life expectancy through heart and work rate
From the Royal Society of Biology https://www.rsb.org.uk/images/pdf/Heart_Facts_QA.pdf
And
Rest Heart Rate and Life Expectancy
HERBERT J. LEVINE, MD, FACC Boston, Massachusetts
Website with graphs
https://www.jacc.org/doi/pdf/10.1016/S0735-1097%2897%2900246-5
Among mammals, there is an inverse semilogarithmic relation between heart rate and life expectancy. The product of these variables, namely, the number of heart beats/lifetime, should provide a mathematical expression that defines for each species a predetermined number of heart beats in a lifetime. Plots of the calculated number of heart beats/lifetime among mammals against life expectancy and body weight (allometric scale of 0.5 3 106 ) are, within an order of magnitude, remarkably constant and average 7.3 6 5.6 3 108 heart beats/lifetime. A study of universal biologic scaling and mortality suggests that the basal energy consumption/body atom per heart beat is the same in all animals (;1028 O2 molecules/heart beat). These data yield a mean value of 10 3 108 heart beats/lifetime and suggest that life span is predetermined by basic energetics of living cells and that the apparent inverse relation between life span and heart rate reflects an epiphenomenon in which heart rate is a marker of metabolic rate. Thus, the question of whether human life can be extended by cardiac slowing remains moot and most likely will only be resolved by retrospective analyses of large populations, future animal studies and clinical trials using bradycardic therapy. (J Am Coll Cardiol 1997;30:1104–6) ©1997
by the American College of Cardiology . . . the fundamental object of contention in the life struggle, in the evolution of the organic world, is available energy.
Ludwig Boltzmann (1886)
It is common knowledge that smaller mammals have higher heart rates and shorter life spans than larger members of their class. The explanation of the former is a biophysical imperative in which the ratio of heat loss (a function of body surface area) to heat production (a function of body mass) increases as body size is reduced. Prevention of a fall in body temperature in homeotherms necessitates an increased metabolic rate, which in turn is correlated with, and is perhaps responsible for, an increased heart rate. Indeed, regression analysis on logarithmic coordinates between body mass and metabolic rate among mammals yields a straight line that has exactly the same slope as a plot between body mass and heart rate (1). In addition to the role of metabolic rate, other allometric biophysical principles may be operative in determining the optimal heart rate in animals of differing size (2). The explanation of a shorter life span in smaller mammals, however, is less apparent.
According to Sohal and Weindruch (3), there are only three regimens that reliably extend the maximal life span of animals: 1) lowered ambient temperature in cold-blooded animals and hibernating mammals; 2) a decrease in physical activity in cold-blooded animals; and 3) caloric restriction. Although associated decreases in heart rate generally accompany all three of these regimens, a primary reduction in heart rate has not been established as etiologic in extending life span. The following represents an effort to examine the variations in life span in mammals, with particular reference to their relation to heart rate.
Among mammals, with the exception of the human species, there is a linear, inverse semilogarithmic relation between heart rate and life expectancy. As illustrated in Figure 1, this relation, excluding humans, spans a 35-fold difference in heart rate and a 20-fold difference in the life span of these mammals. Although some minor differences exist among the four major orders of mammals (Life span/unit weight of primates . Carnivores 5 Rodents . Ungulates) (7), this overall inverse relation between heart rate and life span appears valid. The one conspicuous exception to this observation is humans. One might speculate as to the reasons why, or more specifically how, modern humans have stretched the boundaries of biology to achieve a life expectancy of 80 years. Perhaps the most obvious explanations would credit advances in science, medicine and sociology. Although there are moments and events in our present civilization that seem to threaten this achievement, it is clear that at least for now the human species is, among mammals, the front runner in life expectancy.
If we accept the observation that there is indeed an inverse relation between heart rate and life span, then the product of these variables, namely, the number of heart beats/lifetime, should provide a mathematical expression that defines for each species a predetermined number of heart beats in a lifetime.
In Figure 2A, the calculated number of heart beats/lifetime among mammals is plotted against life expectancy. It will be seen that despite a 40-fold difference in life expectancy, the number of heart beats/lifetime is, within an order of magnitude, remarkably constant. When the calculated number of heart beats/lifetime of mammals is plotted against body mass (Fig. 2B), the constancy of heart beats/lifetime is even more striking, particularly when it is appreciated that the allometric range spans almost 0.5 million-fold in body weight (from hamster to whale). Because heart weight and body weight are almost linearly related in large and small mammals (8) (heart weight is 0.5% to 0.6% of body weight), this allometric relation would be the same between heart weight and heart beats/ lifetime.
Figure 1. Semilogarithmic relation between rest heart rate and life expectancy in mammals. Most coordinates represent average values (4–6). See website https://www.jacc.org/doi/pdf/10.1016/S0735-1097%2897%2900246-5
From the Department of Medicine, Division of Cardiology, Tufts University School of Medicine and New England Medical Center, Boston, Massachusetts. Address for correspondence: Dr. Herbert J. Levine, New England Medical Center, 750 Washington Street, Box 315, Boston, Massachusetts 02111. E-mail: herbert.levine@es.nemc.org.
These observations suggest that despite wide variations in body size and heart rate, the total number of heart beats/ lifetime among mammals is remarkably constant. Although this analysis has not been examined among nonmammalian vertebrates, there is reason to believe that the relative constancy of heart beats/lifetime is widely distributed in the animal kingdom. For example, a Galapagos tortoise with a life expectancy of 177 years and a heart rate of 6 beats/min (4) has 5.6 3 108 beats/lifetime, quite similar to the mean value of 7.3 3 108 calculated from the mammals shown in Figure 2. Among fish, the average number of heart beats/lifetime tends to be an order of magnitude less than that in mammals (i.e., 3.5 3 107 for haddock and 6.7 3 107 for brown trout), whereas the tiny arthropod Daphnia uses up to 1.3 3 107 heart beats (at 25°C) in a brief life span of 30 days (9).
However, it does appear clear that there is little variation in the total number of heart beats/lifetime among mammals, and perhaps this observation can be extended to many species of animals. This finding suggests that a basic characteristic of the energetics of living matter drives this phenomenon. Some insight into this mechanism is provided by the intriguing report by Azbel (10) on universal biologic scaling and mortality. Drawing from a wide allometric scale of 1020-fold among living organisms, Azbel concludes that the energy consumption/body atom per heart beat is the same (within an order of magnitude) in all animals. Indeed, he calculates that the basal O2 consumption/body atom of all animals is ;10 O2 molecules/lifetime and in those animals with a heart, ;1028 O2 molecules/heart beat. It is therefore not surprising that the number of heart beats/ lifetime calculated from these data (10 3 108 ) is strikingly similar to the mean value observed among the mammals shown in Figure 2 (7.3 3 108 ). That Azbel extends his analysis to include protozoa and bacteria with oxygen metabolism (unit time replacing a heart beat) further suggests that life span is predetermined by basic energetics of living cells and that the apparent inverse relation between life span and heart rate reflects an epiphenomenon in which heart rate is a marker of metabolic rate.
These considerations do not exclude the possibility that rest heart rate may prove to be a determinant of life span, and perhaps the obvious extension of these observations is to ask whether there is the potential to prolong life by measures that reduce average heart rate. If humans are predetermined to have ;3 billion heart beats/lifetime, would a reduction in average heart rate extend life? If so, one might estimate that a reduction in mean heart rate from 70 to 60 beats/min throughout life would increase life span from 80 to 93.3 years. Although this experiment has never been performed in humans, Coburn et al. (11) have made an effort to examine this question in an animal study. Several hundred A/J mice, on weaning, were fed normal feed or feed containing ;0.05 mg digoxin/day. Although equivalent doses of digoxin would promptly kill a human (.100 mg/day), the treated mice lived longer than control mice (50% survival of 850 vs. 700 days, p , 0.001) and had slower heart rates (266 vs. 563 beats/min, p , 0.001). However, the conclusion that prolongation of life in these mice was the consequence of a slower heart rate was seriously confounded by the fact that the mice treated with digoxin had a lower body weight than control mice, and starvation has been shown to extend the life of rodents (3). Interestingly, the digoxin-treated mice were found to have caloric intake comparable to the control mice, and therefore the explanation for weight loss in the treated mice is unex plained. Thus, a specific role for cardiac slowing in the prolongation of life in digoxin-treated A/J mice remains at best uncertain.
Figure 2. Relation between life expectancy and total heart beats/ lifetime (A) and allometry of total heart beats/lifetime (B) among mammals (see text). see website.
Together, the above observations suggest that a primary reduction in myocardial metabolic rate, with associated cardiac slowing, may have the potential to prolong human life. However, because myocardial O2 consumption/unit weight is the same in normal, hypertrophied and failing human hearts (12), the demonstration that a primary reduction in heart rate prolongs life would have to invoke a mechanism other than a reduction in myocardial metabolic rate. Nonetheless, clinical studies abound with the suggestion that cardiac slowing may improve survival. Beta-adrenergic blockade improves survival in patients after myocardial infarction (13) and possibly in patients with dilated cardiomyopathy (14,15), and the bradycardic effects of regular exercise are considered by many to extend life in those with or at risk for coronary disease. Although it is acknowledged that the malefic effects of sustained beta-adrenergic stimulation in cardiac disease are far greater than that of positive chronotropism, the provocative observation that heart rate and life expectancy among mammals are inversely related and that their product is a near constant begs the question, “Can human life be extended by cardiac slowing?”
Thus, although there are considerable constraints on the likelihood of demonstrating a life-prolonging effect of cardiac slowing in humans, efforts to do so should not be discouraged. Perhaps a first attempt in this direction would be an actuarial analysis of life insurance data because a purely bradycardic agent for use in animal studies and clinical trials is not yet available to us.
References
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2. Levine HJ. Optimum heart rate of large failing hearts. Am J Cardiol 1988;61:633–8.
3. Sohal RS, Weindruch R. Oxidative stress, caloric restriction, and aging. Science 1996;273:59–63.
4. Spector WS. Handbook of Biological Data. Philadelphia: WB Saunders, 1956.
5. Encyclopedia Brittannica. Chicago: W Benton, 1971.
6. White PD, Jenks JL, Benedict FG. The electrocardiogram of the elephant. Am Heart J 1938;16:744–50.
7. Economos AC. Taxonomic differences in the mammalian life span–body weight relationship and the problem of brain weight. Gerontology 1980;26: 90–8.
8. Stahl WR. Organ weights in primates and other mammals. Science 1965; 150:1039–42.
9. Ingle L, Wood TR, Banta AM. A study of longevity, growth, reproduction and heart rate in Daphnia longispina as influenced by limitations in quantity of food. J Exp Zool 1937;76:325–52.
10. Azbel MY. Universal biological scaling and mortality. Proc Natl Acad Sci USA 1994;91:12453–7.
11. Coburn AF, Grey RM, Rivera SM. Observations on the relation of heart rate, life span, weight and mineralization in the digoxin-treated A/J mouse. Johns Hopkins Med J 1971;128:169–93.
12. Levine HJ, Wagman RJ. Energetics of the human heart. Am J Cardiol 1962;9:372–83.
13. Hennekens CH, Albert CM, Godfried SL, Gaziano JM, Buring JE. Adjunctive drug therapy of acute myocardial infarction—evidence from clinical trials. N Engl J Med 1996;335:1660–7.
14. Eichorn EJ, Bristow MR. Medical therapy can improve the biological properties of the chronically failing heart. Circulation 1996;94:22850–96.
15. Packer M, Colucci WS, Sackner-Bernstein JD, et al. Double-blind, placebocontrolled study of the effects of carvedilol in patients with moderate to severe heart failure. Circulation 1996;94:2793–9.
From the Department of Medicine, Division of Cardiology, Tufts University School of Medicine and New England Medical Center, Boston, Massachusetts. Address for correspondence: Dr. Herbert J. Levine, New England Medical Center, 750 Washington Street, Box 315, Boston, Massachusetts 02111. E-mail: herbert.levine@es.nemc.org.
Does every species get a billion heartbeats per lifetime?
posted by Jason Kottke Feb 08, 2013 https://kottke.org/13/02/does-every-species-get-a-billion-heartbeats-per-lifetime
There’s an assumption that because of the relationship between metabolic rates, volume, and surface area, animals get an average of one billion heartbeats out of their bodies before they expire. Turns out there’s some truth to it.
As animals get bigger, from tiny shrew to huge blue whale, pulse rates slow down and life spans stretch out longer, conspiring so that the number of heartbeats during an average stay on Earth tends to be roughly the same, around a billion.
Mysteriously, these and a large variety of other phenomena change with body size according to a precise mathematical principle called “quarter-power scaling”.
It might seem that because a cat is a hundred times more massive than a mouse, its metabolic rate, the intensity with which it burns energy, would be a hundred times greater. After all, the cat has a hundred times more cells to feed.
But if this were so, the animal would quickly be consumed by a fit of spontaneous feline combustion, or at least a very bad fever. The reason: the surface area a creature uses to dissipate the heat of the metabolic fires does not grow as fast as its body mass.
To see this, consider a mouse as an approximation of a small sphere. As the sphere grows larger, to cat size, the surface area increases along two dimensions but the volume increases along three dimensions. The size of the biological radiator cannot possibly keep up with the size of the metabolic engine.
Humans and chickens are both outliers in this respect…they both live more than twice as long as their heart rates would indicate. Small dogs live about half as long.
Pembroke Corgis by Balletcor 