The Elements of Evolution (51-4) Rate of Living

Rate of Living

Live fast, die young…. ~ American novelist Willard Motley in the novel Knock on Any Door (1947)

Some plants last mere months, while others stand sentry for millennia. Fruit flies have a fleeting existence of 40 days, while an ocean quahog – a mollusk native to the North Atlantic – may live 400 years or more. One quahog – Ming the Clam (~1498–) – is over 500 years old. Despite such disparity, it has long been pondered whether there is an approximate constant among life-history variables: relative lifespan related to the rate of living.

Different flora and fauna live at different paces. For animals, basal metabolic rate – energy consumption at rest – has been used as a proxy. Heart rate has also been considered another rough measure.

German physiologist Max Rubner studied metabolism and energy physiology. In 1883 he introduced the surface hypothesis: that the metabolic rate of endotherms is roughly proportional to body surface area.

Subsequent work led to the broader concept of life’s pace dictating longevity. In 1908 Rubner proposed the rate-of-living hypothesis: that the faster an animal’s metabolism the shorter its lifespan. Rubner observed that the lifespan of large animals exceeds small ones and that larger animals had slower metabolisms.

In the mid-1920s American biologist Raymond Pearl expanded on Rubner’s work by studying the life histories of fruit flies and cantaloupe seeds. Pearl corroborated Rubner’s observation that slower metabolism increased lifespan.

Across species a gram of tissue on average expends about the same amount of energy before it dies regardless of whether that tissue is located in a shrew, a cow, an elephant or a whale. This fact led to the notion that aging and lifespan are processes regulated by energy metabolism rates, and that elevating metabolism will be associated with premature mortality – the rate-of-living theory. ~ Scottish biologist John Speakman

The rate-of-living hypothesis was later popularized as the heartbeat hypothesis: that every endotherm has a lifespan of a billion heartbeats. Hummingbirds and humans are commonly analogized, though hummingbirds last 1.26 billion heartbeats, while humans may make 2.45 billion.

One study noted that athletically fit people tend to a lower resting heart rate and are prone to a longer life than the unhealthy. This is, at best, tepid support for the heartbeat hypothesis, as it ignores many factors associated with physical fitness.

Anecdotal evidence upholds a relation between longevity and the pace of living. Life in the slow lane lets giant tortoises live 150 years. Even houseflies live longer if they take it easy.

While larger animals tend to live longer than smaller ones, there are consistent exceptions. Some species live far longer than expected based on their size. A crucial factor for this seems to be flight. Birds and bats tend to live longer than other animals of similar size. This is especially true of those active during the day (diurnal) or night (nocturnal). Those in action at dusk or dawn suffer somewhat from greater predation.

Max Kleiber’s allometric power law succored the notion that rate-of-living was a life-history variable. Various cellular mechanics were proposed as attributive to longevity for both plants and animals.

In 1954, free OH radicals in cells provoking reactive oxygen species (ROS) stress were cited by American biogerontologist Denham Harman as causing aging.

In 2003, Australian biologist A.J. Hulbert pointed to the fatty acid composition of cellular membranes as seminal in lifespan determination.

Life requires membranes. The rate-of-living theory cannot alone explain all of the variation in longevity of animals. Many of the exceptions can be explained by knowledge of membrane fatty acid composition in each particular case. ~ A.J. Hulbert

Exceptions which violate straightforward rate-of-living correlation suggest a complex relationship between energy expenditure and longevity.

The rate-of-living theory (RLT) faces 4 types of challenges. 1st, the predicted correlation between energy expenditure and lifespan does not hold when comparisons are made across taxons. A typical example is that birds have higher metabolic rate than mammals with the same body mass yet live much longer. 2nd, RLT also fails to explain why within a species, such as domestic dogs, the larger breeds with lower mass-specific metabolic rates usually have shorter lifespans. 3rd, a few lifespan extending interventions, such as diet restriction (DR) and genetic modification of growth hormone, generally do not alter, or only slightly reduce, mass-specific metabolic rate. Moreover, a few studies even showed that when metabolic rate is altered by DR, it is positively correlated with lifespan. The 4th challenge comes from experimental manipulations that increase metabolic rate but do not shorten lifespan. For example, long-term cold exposure largely increases energy expenditures in mice, rats, and voles, but has no effects on lifespan. Moreover, voluntary exercises increased food intake in female rats while increasing lifespan.

Oxidative metabolism can affect cellular damage and longevity in different ways in animals with different life histories and under different conditions. Qualitative data and the linearity between energy expenditure, cellular damage, and lifespan assumed in previous studies are not sufficient to understand the complexity of the relationships.

The oxidative stress theory of aging (OST), another theory that links energy metabolism and longevity, suggests that the deleterious productions of oxidative metabolism (e.g., reactive oxygen species, ROS) cause various forms of molecular and cellular damage, and the accumulation of the damage is associated with the process of aging. Widely considered by many as a modern version of the RLT at the molecular and cellular level, this theory shares all the supports and challenges of the RLT, as well as a few of its own. New sources of supports include the evidence that (1) external oxidative insults shorten lifespan, (2) the level of oxidative damage to macromolecules increases with age, and (3) genetic interventions and diet restriction, while extending lifespan, reduce the oxidative damage. New challenges to OST mainly come from the studies in which adding antioxidants to diet or genetically altering the expression of antioxidant enzymes, which were assumed to change the oxidative damage, failed to affect longevity. In some cases these interventions even yielded results that opposed the theory’s predictions. ~ Chinese zoologist Chen Hou & Indian molecular biologist Kaushalya Amunugama in 2015

Hou and Amunugama proposed that rate-of-living is more complicated than mere energy expenditure, as cells have mechanisms to repair the effects of stress which incur aging – activities which take energy but extend life.

Energy trade-offs and protective efficiency affect animal lifespan. Biosynthesis plays a role in oxidative damage accumulation and the process of aging. The detailed energy trade-offs between life-history traits and the efficiency of energy utilization are the keys to understanding the complex nature of the energy-longevity correlation. ~ Chen Hou and Kaushalya Amunugama

Energy used during growth is the key to understanding longevity. ~ Chen Hou

It is unsurprising that the molecular biomechanics of energy use as they relate to lifespan are too complex to model, even as there appears to be some connection between metabolism and longevity. Then there is luck.