Physical Activity and Longevity
It is now well recognized that those who are physically active, on the average, survive longer than those living sedentary lives. The research data clearly indicate that this is specifically an expression of the favorable effect of habitual energy expenditure on secondary aging. Regular exercise reduces health risk factors (dyslipidemia, hypertension, obesity, reduced bone density). In addition, it may have direct protective effects against the atherosclerotic vascular process. Athletes who maintain high levels of sport activity through their adult years can expect to benefit from limited secondary aging.
Whether high levels of physical activity can extend the natural, or primary, aging process is not known, but at present, no evidence supports that idea. The question, of course, would be extraordinarily difficult to address in the experimental setting for human beings. The best we can do is look at animals, who don’t live as long and can be coerced to participate as long-term research subjects more easily. Too, in animals, we can expect to more distinctly examine the effects of exercise on the primary aging process.
In a particularly pertinent study (at least for rodents), John Holloszy and Bill Kohrt described the influence of regular running on the longevity of healthy rats who experienced no associated decline in food intake or growth retardation. Beginning at 4 months of age, 62 rats were housed in cages with running wheels. They started out exercising spontaneously an average of 9,173 meters per day. Running distances gradually decreased, falling to 965 meters daily at 34 months of age. Compared with nonexercising control rats, the running rats demonstrated an average life span that was 9% greater (1009 ± 132 days versus 924 days ± 155 days). There was, however, no significant difference between the two groups in maximal duration of life. The age of death of the two oldest rats was 1239 ± 14 days and 1199 ± 44 days in the runners and nonrunners, respectively.
What Factors Delay Primary Aging?
At the present time, only two documented means exist of extending the duration of primary aging—calorie-restricted diets and genetic manipulation. Both of these lines of evidence have been established in animals. As of this moment, their potential application to humans is a tantalizing idea that has not been well explored.
Although the science of aging is generally clouded in mystery, one piece of experimental data has been repeatedly established: In animals, a low-calorie diet that is sufficient in specific nutrients (does not lead to malnutrition) will extend life span. This was first documented in 1917 in rats, and the effect has since been replicated in a wide variety of animals, ranging from fleas to monkeys. The usual experimental technique is to reduce caloric input to about 60% of ad libitum, which can be expected to prolong animal life by 25 to 40%. Just how this works is uncertain. Some have suggested that caloric restriction protects mitochondrial function, preserves activity of the electron transport chain, or blocks the deleterious actions of reactive oxygen species. Certain biochemical actions associated with caloric restriction in animals have been observed in humans as well, leading to speculation that H. sapiens might similarly benefit from extension of the life span.
If you happen to be a nematode worm—or are closely related to one—there is hope for you. More than 20 years ago, investigators reported that a single gene mutation in C. elegans significantly lengthened the worm’s life span, as much as sixfold in some cases. Since that time, antiaging gene mutants have been described in a large number of organisms. The most advanced in terms of evolution is the mouse (with increases that are much more conservative, at 50 to 60%). How these genetic changes act to extend life remains problematic, but it is interesting that most of these gene loci share some connection with alterations in insulin signaling pathways.
It’s almost needless to say that the explosive growth in techniques to manipulate gene loci in humans has fueled speculation that someday such fountain-of-youth interventions might extend human life, maybe (gasp!) indefinitely. (This, I believe, should be differentiated from the ideas of Friedrich Nietzsche, who claimed that we will forever relive our lives, just as the time before. The alert reader is, of course, conscious of the similarity of this concept of eternal return to Bill Murray’s plight in the film Groundhog Day.)
What About Secondary Aging?
We all know that the increase in average life span over the past century is linked to reduced risks of infectious diseases and avoidance of health risk factors such as high-calorie diets, smoking, physical inactivity, and high blood pressure. Dr. Alexander Leaf wanted to look at this more closely. So, he left the safe confines of Massachusetts General Hospital one day and set out to visit remote populations reputed for their longevity in places like Hunza, a kingdom in the Hindu Kush mountains on the China-Afghanistan border; Georgia; and Vilcabamba, in the Andes mountains of Ecuador. (It turned out that the actual longevity of these people was in some doubt. In the latter village, for instance, the oldest citizen was supposedly 134 years old, but turned out at his death to be actually 93.)
Dr. Leaf describes his observations as “a monotonous litany of similar lifestyles.”1 He witnessed the following in all three locations:
- Poor, agrarian culture in which daily hard labor was the norm
- Vigorous daily physical activity beginning in childhood and persisting throughout life
- A vegetarian diet
- Strong support for the elderly
“No one retired or was put on the shelf to feel redundant and useless,” he observed. “Chores changed, but the elderly continued to do tasks that, although less vigorous, continued a useful role for them in the community and supported their self-esteem. Old age was greeted with respect rather than derision, and the elders were valued for their wisdom.”1
Food for thought!