The mitochondria in our cells take in food and oxygen and use it to produce ATP, a chemical used as fuel to power the rest of the cell. This is known as mitochondrial respiration, or cellular respiration. In the process, oxygen radicals - also generally known as free radicals or reactive oxygen species (ROS) - are produced. These damaging byproducts go on to wreck other molecules and cellular mechanisms in a drawn-out process that is one part of degenerative aging. This is the essence of the mitochondrial free radical theory of aging - that we are slowly slain by the accumulated toxic byproducts of essential metabolic processes. Evolution cares not, because we've long passed the test of reproductive fitness by the time our bodies are choked with metabolic pollutants.
One might think that the faster metabolism runs, the worse the situation becomes: more oxygen consumed means more ROS unleashed to cause harm. This is not in fact the case, as the relationship between the metabolic rate - the rate at which oxygen is consumed - and the rate at which ROS are created is not linear. Rather like cars, levels of fuel efficiency and average time to next breakdown for the engine vary widely depending on speed and circumstance - and cars can neither repair themselves nor change significantly to adapt to new circumstances, both of which complicate the picture for human metabolism.
For humans, most of the simple things that reduce the rate at which ROS are generated also speed metabolism. Exercise and calorie restriction with optimal nutrition, for example, raise metabolic rate and are demonstrably good for healthy longevity - better for most folk in the long term than anything yet produced by medical science. Here's a paper that provides a succinct overview of the situtation:
Various recent investigations relevant to the study of aging mechanisms have recently found that increases in longevity during dietary restriction can occur together with lack of decreases or even increases in [oxygen, or O(2)] consumption. This is frequently interpreted as contradictory with the mitochondrial free radical theory of aging. But this is based on the erroneous assumption that increasing O(2) consumption must increase the rate of mitochondrial oxygen radical generation. Here it is shown that the opposite occurs in many important situations. Strong decreases in absolute and relative (per unit of O(2) consumed) mitochondrial oxygen radical production occur during aerobic exercise bouts, chronic exercise training, and hyperthyroidism, and notably, during dietary restriction. Mitochondrial oxygen radical generation is also lower in long-lived birds than in short-lived mammals of similar body size and metabolic rate. Total rates of reactive oxygen species generation can also vary between tissues in a way not linked to their differences in oxygen consumption. All this indicates that mitochondrial reactive oxygen species (ROS) production is not a simple byproduct of mitochondrial respiration. Instead, it is regulated independently of O(2) consumption in many different physiologic situations, tissues, and animal species. Thus, the apparently paradoxical increases in O(2) consumption observed in some models of dietary restriction do not discredit the mitochondrial free radical theory of aging, and they can further strengthen it.