I am going to assume that the reader is taking my advice and reading the easily available reference articles that are provided. So to begin again with Dr. Herbert J Levine’s Editorial, pp1105…
“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 10^20-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, 10^-8 O2 molecules/heart beat.
“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 through- out 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…”
 Azbel MY. Universal biological scaling and mortality. Proc Natl Acad Sci USA 1994;91:12453–7.
 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