Actually, there is a physical mechanism in cellular life that sets a lifespan limit, by roughly constraining the number of replications most differentiated cell lines in a body can support. Thus the correlation between slower metabolism and longer lifespan. The 'number of heartbeats' observation is a consequence of that correlation.<p>The mechanism is a little too complicated to describe accurately here. You can find a great deal on it with google search terms "telomere fraying" or "telomere fuse".<p>Very roughly, every chromosome has a 'telomere' structure at each end that acts to prevent the DNA double helix strands from 'fraying'. In the single cell embryo these structures are several thousand bases long. In every cell division after that, some random number of the telomere bases fail to be replicated. So the telomeres get shorter and shorter with each replication. In a cell where the telomere is all gone on a chromosome, genes at the end of that chromosome get progressively destroyed - thus (depending whether it's an active gene) wrecking some aspect of the cell's metabolism. With many different chromosomes (eg 26 in humans), 2 ends per chromosome, shifting gene arrangements, huge statistical populations of cells with individual telomere failures, and multiple lines of differentiated cells all replicating at differing rates, it's no wonder 'aging' shows such complex and variable symptoms.<p>I suspect if someone did a study of multiple species examining embryonic telomere lengths, average telomere loss per cell replication, replication (metabolic) rate, and average lifespan, there'd be a function of those factors giving a much more precise connection than 'number of heartbeats'.