Why do animals vary so much in life span?

It seems larger animals live longer than smaller ones generally (whale vs. house fly).

I remember hearing once that if you measure lifespan in heartbeats instead of years, most animals (or was it just mammals?) come in at about the same number, about 2*10^6 or something.

I was curious, why is it that dogs will live somewhere in the 10-20 year range, but humans make it to 80, and animals vary so much?

Heart beats represent energy expenditure. Life span is not determined by the number of heart beats, but the number of heart beats represents the amount of energy expended by mammals; it is a marker of our energy expenditure of cells, which still makes it useful.

This has come up before. And as someone mentioned, there seems to be a correlation with heart rate and life span. I can't find the refernce i used last time, but this has a table. Scroll down to Lifetime Heartbeats and Animal Size.

http://www.sjsu.edu/faculty/watkins/longevity.htm

It has a table, but I would not trust the graphs or mathematics there. It looks like a homework project with the target "we have to find some relations to get a good grade".

The life expectancy of humans is a bit special anyway.

Abstract

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 x 10(6)) are, within an order of magnitude, remarkably constant and average 7.3 +/- 5.6 x 10(8) 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 (approximately 10(-8) O2 molecules/heart beat). These data yield a mean value of 10 x 10(8) 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.

The transgenic manipulation studies are confounded by the problem that transgenic manipulations often also affect body size. This raises issues about how metabolic rate should be normalised (see discussions in Ramsey et al., 2000; Speakman et al., 2002) that are not yet resolved. How this normalisation is performed dramatically alters the conclusions that are drawn about the effects of metabolism. Some researchers therefore claim that the transgenic effects act via metabolism; others suggest there is an independence of the effects from metabolism. In other species, particularly mice, the measurements have simply not yet been made to indicate what is going on. This problem of normalising for effects of body size also besets the whole area of whether caloric restriction acts via a decrease in metabolism or not (reviewed in Ramsey, 2000). Comparisons across different strains of dogs and mice are much clearer in suggesting a positive association of metabolism and longevity, and this effect was also found in the single comparison made to date of individual variability within a strain of mice