The rate of living view of aging is one of the discarded historical hypotheses that occurred along the way to the modern competing ideas about why aging occurs, and why there are differences in longevity between species. Roughly, the rate of living hypothesis says that a faster metabolism means a shorter life, that underlying processes (such as accumulation of molecular damage) depend strongly on metabolic rate. This doesn't appear to be the case, however; setting aside more detailed considerations, there are enough exceptions to the rule, species with high metabolism and exceptional longevity, to sink the argument. It isn't just metabolic rate that determines species longevity.
In today's single author paper, rate of living sidles back into the picture via a more complicated relationship between energy metabolism, body mass, temperature, heart rate, and respiratory rate. Species across a wide range of sizes and metabolic rates all come decently close to conforming. So perhaps this scientist is on to something, and one will find that these aspect of physiology correlate quite well to the pace of creation of important forms of molecular damage in aging, or, alternatively, exceptions will be found and this will go the way of the original rate of living theory. Either way, the data is the data, and it is an interesting read.
It is natural to try to associate the process of aging with metabolism, since all living organisms obtain the energy required to stay alive from such a process. In 1908 researchers compared the energy metabolisms and lifespans of five domestic animals (guinea pig, cat, dog, cow and horse) and humans and found that the lifespan (total) energy expenditure per gram for the five species is approximately constant, suggesting that the total metabolic energy consumption per lifespan is fixed, which later became known as the 'rate of living' theory.
Decades later, a mechanism was found by which the idea behind a fixed energy consumption per lifespan might operate, the 'free-radical damage' hypothesis of aging, in which the macromolecular components of the cell are under perpetual attack from toxic byproducts of metabolism, such as free radicals and oxidants. However, the 'free-radical' theory has lost support in recent years, with evidence that a reduction in free radicals by antioxidant supplementation in the diets of laboratory animals does not significantly increase their life expectancy.
The rate of living relation was partially confirmed for approximately one hundred mammals and was extended to birds, ectotherms, and even unicellular organisms such as protozoa and bacteria, totaling almost three hundred different species in a range of 20 orders of magnitude in body mass. Although the total metabolic energy exhausted per lifespan per body mass of a given species appears to be a relatively constant parameter - approximately a million Joules per gram of body weight for mammals - variations of more than an order of magnitude have been found among different animal classes; this result is considered the most persuasive evidence against the 'rate of living' theory.
Here, we present a universal relation that relates lifespan energy consumption to several physiological variables, such as body mass, temperature, and the ratio of heart rate to respiratory rate, which have been shown to be valid for ∼300 species representing different classes of living organisms, from unicellular organisms to the largest mammals. This relation has an average scattered pattern restricted to factors of 2, with 95% of the organisms having departures of less than a factor of π from the relation, despite the difference of ∼20 orders of magnitude in body mass.
This result can be interpreted as supporting evidence for the existence of an approximately constant total number (10^8) of respiration cycles per lifetime for all organisms studied, effectively predetermining the extension of life through the basic energetics of respiration. This is an incentive to conduct future studies on the relation of such a constant number of cycles per lifetime due to the production rates of free radicals and oxidants, or alternative mechanisms, which may yield definite constraints on the origin of aging.