Entropy rules. The degree of disorder of a system—organic or inorganic—increases with time. Organization becomes disorganization. In the end, everything runs down. From the jar of mayonnaise on the second shelf, to the 1968 Buick, to the stars of the most distant galaxies. They all disintegrate with the passage of the days, years, or centuries. Indeed, the existence of things is bracketed, is defined, by time. After the hands of the clock have advanced just so far, the mayonnaise is no longer mayonnaise, the Buick is no longer an automobile, the giant red star is no longer a luminary body. It is obvious, then, that time, existence, and entropy are all intimately linked.
Humans run down, too. Our presence on earth as ourselves is dictated by the inexorable course of the years, which, at least physically, will define a lifetime. Like T.S. Eliot’s women, we “come and go, talking of Michelangelo.” Or, for those preferring the sports vernacular, at the moment of your conception, the shot clock starts up. You’ve got about 80 years to get a shot off before the buzzer sounds.
But not all is gloom and doom. There are, without doubt, certain advantages to be gained in the aging process (although the list is disappointingly short). Like acquiring wisdom. And lower prices at the movies. Cheaper lift tickets. No more 2:00 a.m. feedings. The time could even be ripe for mature romance. In Gilbert and Sullivan’s The Mikado, Ko-Ko proposes marriage (albeit reluctantly) to the aged spinster Katisha, singing the following:
Are you old enough to marry, do you think?
Won’t you wait until you’re 80 in the shade?
There’s a fascination frantic
In a ruin that’s romantic;
Do you think you are sufficiently decayed?
Athletes, of course, hear the same clock ticking. After a heady couple of decades of steady improvement, personal bests, promises of athletic stardom, and hopes for Olympic gold, it all inevitably starts to deteriorate. Passes fall short, 10K times drift upward, doubles replace singles, knee braces become standard apparel. There is, in fact, probably no area of human endeavor in which biological deterioration with increasing age is so clearly and disappointingly obvious than to those who are trying to push back barriers of motor performance.
So, it is fitting that this book concludes by considering the grandest clock of all, the one that marks off our moments of existence, and just how it influences athletic performance. This chapter discusses what we know about why performance universally declines as we get older and, importantly, if and how such deterioration might be avoided, or at least slowed. As the human life span has increased, this topic has captured an extraordinary degree of both lay and scientific attention. We will thus be limited to but a brief survey of the subject in these few pages. This chapter provides references to more comprehensive works as we move along.
Before launching into our topic, the discerning reader should be aware of certain important concepts and cautions. To start with, it should be recognized that two kinds of aging exist. Primary aging is an intrinsic process of all human tissues, independent of disease and environmental factors, in which progressive deterioration of cellular integrity and function over time eventually leads to death. This inexorable decline in function, which generally starts by the beginning of one’s fourth decade, is universally evident in all physiological processes.
We’re all aware of those extraordinary athletes who have performed at the top of their sport well beyond normal age expectations. These are the competitors who have pushed the envelope on the performance clock in a remarkable way. People like football’s George Blanda, who was thought by Houston to be washed up. After being let go at age 39, he reemerged as a star in Oakland. He played his final game at age 48. Satchel Paige, the first black pitcher in the American League, pitched his last game in 1966. Paige’s actual age was always in dispute, but the discovery of his birth certificate in the county health department of Mobile, Alabama, finally confirmed that he was 59 years old when he quit. His autobiography is titled Maybe I’ll Pitch Forever.
Equally impressive were Gordie Howe, who finally hung up his skates at age 52; Arnold Palmer, who golfed in the 2004 Masters at age 75; and Willie Shoemaker, who at age 54, became the oldest jockey to win the Kentucky Derby (with a little help from his horse Ferdinand). We shouldn’t forget, too, Aladàr Gerevich, who holds a record for having won an Olympic gold medal in the same event (fencing) six times. He garnered his last in 1960 when he was 50 years old.
Contemporary tennis fans are awed by Martina Navratilova, who after 18 career singles titles went on to gain further success on the doubles court before retiring at age 49. What fans may not know is that she also coauthored an intriguing 2007 book titled Art Grand Slam de Paris, in which she created abstract pieces of art by firing paint-laden tennis balls at a canvas.
The grand title of the world’s oldest athlete, however, has to be presented posthumously to John Whittemore, track competitor whose career began at Santa Barbara High School in 1915 and ended in the fall of 2004 when he threw the javelin and discus at the Senior Olympics just before his 105th birthday. At that time, he had established age-group records for the discus, hammer throw, javelin, shot put, and decathlon. During his final competition, he was reported to have remarked, javelin in hand, “If I don’t drop it on my foot, I set a world record.” Whittemore passed away in April of 2005.
No one knows exactly how long the primary aging process occurs—that is, how long we would live if we could somehow escape the ravages of chronic disease in our older years. But, based on extrapolation of survival curves, it has been suggested that the maximal natural life span of humans could be as high as 120 or 130 years. That’s consistent with the oldest recorded human, a French woman named Jeanne Louise Calment who died in 1997 after reaching her 122nd birthday.
Secondary aging refers to a similar deterioration and loss of cellular function that occurs as the aging human is affected by extrinsic factors: disease, malnutrition, and deleterious environmental insults. Myocardial cells fail from the chronic anoxic effect of coronary artery disease. Inadequate levels of exercise and calcium intake lead to bone fractures from osteoporosis. Cigarette smoking may lead to lung cancer.
The progressive rise in longevity in developed nations—doubling in the United States from an average of about 40 years in the mid-1800s to around 80 years at present—is due entirely to a delay in secondary aging. The obvious explanation is the dramatic improvements in health care, sanitation, and nutrition that have occurred over the past 150 years. It is probable, however, that the natural course of primary aging in human beings has not changed over time. We’ll discuss this a bit more later on.
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.
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.)
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!
The reason for human aging and its relentless deterioration of physiological function can be sought at two different levels. The first asks for an explanation on an evolutionary basis, seeking an answer in the realm of the order and efficiency of biological processes. The second is mechanistic—just what goes wrong that causes cells, tissues, organs, and entire beings to progressively fail, ultimately extinguishing the life process itself?
Scientists are used to—indeed, they usually only feel comfortable—regarding biological processes as satisfying some manner of order, something that makes sense, a function that satisfies a higher benefit for the organism or its social context. Just what that higher order is, of course, is open to all sorts of individual interpretations and topics of debate (Fortunately, for the author, these are not appropriate for these pages.) The generally accepted paradigm for most biologists involves some sense of Darwinian forces, which hold that biological processes should ultimately serve reproductive fitness to maintain survival of the species.
But what good is the aging process? How can it possibly be adaptive? Is aging logical? August Weismann, writing in the early 1900s, proposed that, in fact, this was the case. In a kind of neodarwinism, he suggested that for the survival of populations, older people—who cannot reproduce and drain the resources of a society—are best gotten rid of. Thus, this selective force weeds out unnecessary older persons through the aging process. (One can only hope that Professor Weismann was more fun at dinner parties.)
Well, pretty much no one believes this any more. In fact, most now view the logic of aging in the opposite way: Because older people are past the age of reproduction, they are no longer subject to the controls of natural selection as envisaged by Darwin. Thus, when adverse changes naturally take place in body systems (as outlined in the following section), there is nothing to act (positively or negatively) on these alterations. That is, no force limits functional deterioration.
It sometimes seems that the more basic a human function is, the more difficult it is to explain. And, in direct proportion, it engenders more proposed explanations. Why do we sleep? How do we reason? Why do fools fall in love? Who knows? Aging, here, is no exception. Closer looks at genetic, biochemical, and stress determinants of cellular deterioration with time have drawn us closer to new insights, but clear explanations remain elusive. Consequently, proposed mechanisms abound. It has been estimated that more than 300 theories have been put forward for the basis of the aging process, leading Vijg to comment that “there is probably no subspecialty in science in which formulation of theories has been as pervasive as in the science of aging.”2
You will recall that this chapter starts with an allusion to the role of entropy—a thermodynamic explanation—in the aging process. It sounded good at the time, but now it must be admitted that this only indicates how far behind this author is in his reading. In fact, the last person to truly embrace this idea was Hippocrates, who claimed, 300 years before the birth of Christ, that the aging process reflected a progressive and irreversible loss of heat from the body. (This is only one step above a common idea in the late 1800s that aging was an outcome of intestinal putrefaction.)
One particularly intriguing observation seems to reside over many of the theories about the mechanism of aging. The introduction to this book mentions this briefly: The resting metabolic rate of animals is inversely related to both their body size and their life span. Smaller animals have a higher metabolic rate per kilogram of body mass and a shorter life span than larger ones. Metabolic rate and life span across the animal kingdom generally both relate to body mass0.20. That is, all animals turn out to have the same number of metabolic events in their lives, regardless of their size. It’s like there is a bank in which a particular number of heartbeats, for instance, are on deposit. All animals, regardless of size, have the same absolute amount in their bank account at birth. The small animals, like mice, make withdrawals rapidly, exhausting their supply and dying in bankruptcy at an earlier age than the big ones, like whales, who withdraw their events over a greater period of time. By this observation, the mechanism for aging must somehow be connected with the rate of metabolic function of the cell.
A number of mechanistic theories for aging are consistent with this concept. In fact, any process that is linked to metabolic rate might fit. So, inevitable adverse DNA mutations within the mitochondria that go unrepaired would work. So would progressive telomere shortening with repetitive cell divisions. Damage from free radicals (reactive oxygen species), altered protein synthesis, or accumulation of metabolic waste (lipofuscin) would be expected to be associated with metabolic activity.
Some have viewed aging as a failure of repair mechanisms to respond to environmentally induced cell damage (heat, ionization, radiation, infection). Others see progressive imbalances in immune function or neuroendocrine regulation as playing a critical role.2
Characteristic changes in both body composition and level of habitual physical activity are observed as humans age. Since they can affect physical fitness and its measurement, such factors need to be put into the equation when considering patterns of motor performance associated with senescence.
The hallmark changes in body composition during aging are a progressive loss of lean body mass (skeletal muscle) and an increase in body fat. Percentage of body fat more than doubles between ages 25 and 75, while muscle mass decreases by 3 to 6% per decade. This shift in body composition needs to be taken into account when adjusting physiological variables for body size in studies of aging individuals. Maximal oxygen uptake, for instance, should be expressed relative to lean body mass, not to total body mass (which would provide spuriously lower values as subjects become older).
The course of human aging is also marked by a progressive decline in the level of daily physical activity. Although it is certain that this decline partially reflects the effects of environment, chronic disease, and loss of muscle mass, it has a central biological basis as well. In fact, a progressive decrease in daily energy expenditure (related to body size) is a lifelong feature that begins in early childhood. This phenomenon is observed throughout the animal kingdom and is paralleled by declines in basal metabolic rate and caloric intake. Decreased physical activity in the elderly may adversely accelerate muscle loss and accelerate declines in motor performance while increasing risks for chronic disease.
Now we’re ready to think about just how the time clock of aging acts to slow motor performance. But first, it’s worthwhile to point out the challenges facing investigators who have been trying to answer just this question. The difficulties are many. It’s important to keep these in mind as we examine this literature in order to realize how investigators have sought to minimize these obstacles.3
Consider, for instance, how you might examine performance on a 1-mile (1.6 km) run during the course of human aging. You could do it by cross section, taking a group of 40-, 60-, and 80-year-olds and creating a nifty graph of age versus running times. But that doesn’t really work very well because the 80-year-olds are a selective group—they’ve survived this far and have lost more than a few of their colleagues along the way. Too, the three groups might differ in determinant factors, such as diet, health, occupation, and habitual physical activity. And, of course, you’d be comparing three groups of genetically different people.
A longitudinal study in which you make repeated measurements of the same subjects as they age makes a lot more sense. But, how daunting is a 40-year follow-up study? You’ll have to keep it funded for four decades and you can bet on a serious dropout rate. Sadly, it is likely that many of the subjects will outlive the investigators. The subjects could alter their lifestyle habits simply because they’re in the study. If the investigators make frequent measurements during the four decades, there could be a practice effect of performing the test itself.
A major obstacle to these kinds of aging studies is separating out the processes of primary and secondary aging. In any longitudinal study starting with a cohort of 40-year-olds, for example, a certain number will eventually experience a decrement in performance due to coronary artery disease (covert or overt), arthritis, or peripheral vascular disease from diabetes. And each subject will be affected differently (the curve of secondary aging will be unique to each person).
It has been pointed out that assessment of cardiorespiratory function during aging should be conducted by exercise testing, which discloses limitations of functional reserve that may not be quite so apparent during rest. Yet the process of performing a cycling or treadmill test in the elderly may itself be influenced by psychological and noncardiac physiological features that could confound an accurate assessment of true cardiorespiratory function.
Trained athletes, people who are physically active, and those who adopt sedentary lifestyles all experience a progressive deterioration in performance of motor tasks as they reach the elderly adult years. A great deal of interest surrounds the potential for regular physical activity and sports participation to counteract this decay of function, thereby delaying secondary aging and improving the well-being of the elderly. Veteran athletes who continue to participate at highly competitive levels wish to know, as well, by what means training might postpone declines in their performance as they age. As noted previously, the volume of information regarding the role of improved physical activity and sports participation in slowing declines in physical function and performance for the aged has grown tremendously. For the purpose of this short chapter, here are perhaps the four most salient points.
1. Among the general population, aging is eventually associated with a universal, progressive decline in all forms of motor performance.4 The first two decades of life witness a progressive improvement in all types of motor performance. The extent of this rise in physical capabilities is impressive—the average 15-year-old boy can run a mile in almost half the time it takes for a 5-year-old to do it. These dramatic improvements are all pretty much due to increases in body size. That is, children become stronger as they grow, mainly because of muscle enlargement. Improvements in aerobic endurance fitness and exercise economy happen mainly due to increases in leg length and stride frequency. Age-related increases in 
O2max parallel the larger stroke volumes of bigger heart ventricles. In this age group, then, increases in performance and markers of physiological fitness over time generally reflect the action of hormonal agents that are responsible for promoting body growth.
By the third decade, physical performance measures in healthy, untrained individuals are pretty much at their peak. After this apogee, it all begins to get turned around at age 30. After this, a progressive decline in these same motor measures is observed that persists to the end of the life span. Some of the most commonly reported are outlined in the following list:
• Grip strength
• Dynamic flexor and extensor strength
• Stride length and frequency during locomotion
• Reaction time
• Speed of repetitive movement
• Muscular coordination
• Aiming movements
• Grip precision
• Aerobic endurance performance
• Time of single-foot balance
Although some variation certainly exists, it is generally considered that beyond age 40, the decline of such performance is about 1% per year (10% per decade). It is possible, then, to draw what one might dare to call a lifetime motor performance curve, as in figure 7.1, that would apply to most measures of physical performance measures.
2. The etiology of decline with aging in any particular form of motor performance rests in deterioration of the anatomical and physiological determinants of that measure.5 We’ve said that the ascending limb of the lifetime motor performance curve is a manifestation of somatic growth (bigger skeletal muscle, heart, lungs). But its descent in the second half of life, quite differently, can be attributed to a universal deterioration of physiological function. The body parts just don’t work as well. We need to go no further than the changes in key physiological processes that account for physical performance to see why.
Take maximal oxygen uptake (O2max), for instance. As an indicator of the limits of muscle to utilize oxygen during exercise, O2max is a critical determinant of performance in aerobic endurance events (running, cycling, swimming). As measured on a maximal treadmill or cycling test, it’s a numerical value that reflects the combined function of a chain of variables of multiple oxygen delivery and utilization. And all of these factors decline during the aging process.
It is no surprise, then, that O2max falls in the older years. As one might expect, the decline parallels that of aerobic endurance performance (about 10% per decade). All of the physiological determinants of O2max contribute to this change, including declines in maximal heart rate, stroke volume, arterial-venous oxygen difference, muscle capillarization, muscle oxidative capacity (mitochondrial density), and blood flow to muscles. Other features share in the age-related decline of cardiorespiratory function during exercise. The heart muscles’ ability to contract and relax are compromised, arterial blood pressure rises, the arteries become stiffer, the enzyme content and cell metabolic efficiency declines, and the function of the lungs decreases. It’s not a pretty picture.
Declines in muscle strength in the elderly can be attributed to a progressive loss of skeletal muscle mass, or sarcopenia, which in turn reflects decreases in both cross-sectional area and number of fibers. Here, there is also some contribution of both shrinking size and declining function. This process of muscle atrophy, which is most obvious in fast-twitch (Type II) fibers, causes a decrease in the size of the muscles which amounts to—here’s that number again—10% per decade. That means that by age 80, the typical person has lost 40% of the muscle mass he had in his prime at age 40.
Neurological degeneration adds to the decline in muscle strength with aging. The motor nerve cells that are responsible for activating muscle fibers are lost at the now predictable rate of 1% yearly. Similar loss of neurons in the central nervous system explains deterioration of reaction times and motor coordination.
Such decays in performance-related physiologies are, in turn, manifestations of some combination of those 300 possible aging mechanisms we talked about before. Certain of these are probably more likely candidates: low-grade inflammation with damaging effects of circulating cytokines, mitochondrial aging (mutations and deletions, diminished protein synthesis), uncoupling of excitation and contraction caused by denervation, nuclear apoptosis, and accumulated oxidative stress.
It has not been lost on those who care about such things that the features of physiological decline of aging closely resemble those observed when subjects adopt a sedentary lifestyle or are forced into prolonged periods of bed rest. Given the significant decline in daily energy expenditure with aging, then, reductions in habitual activity might be expected to contribute to falls in physiological and motor performance. Just how much, though, remains uncertain. Studies comparing the decline of O2max with age in athletes with that of sedentary subjects suggest that physical inactivity itself might account for as much as 50% of physiological decline. And, of course, we could argue that the arrow can go in the other direction: Loss of physical fitness might cause the elderly to reduce their levels of physical activity. In any event, it’s a circular effect that calls for an argument to keep elderly persons physically active.
3. The anatomical and physiological effects of exercise training directly counter those of the aging process.6 Reflecting on this statement, you can’t help but be struck with a rather remarkable idea. The beneficial effects of regular exercise, of physical training, are just those that would be expected to counter this deterioration in function that occurs with aging. If an elderly person keeps physically active, wouldn’t that delay the aging process? We know that regular aerobic endurance exercise increases O2max and improves the heart’s pumping capacity, develops growth of muscle capillaries, and stimulates the metabolic machinery in the mitochondria. Resistance training augments strength, fiber size, and neurological activation of our skeletal muscles. These are, in fact, just those items on the list of deterioration we see with senescence. In exercise, then, we should have a powerful antiaging agent. If not a fountain of youth, at least a very useful way of reducing and delaying the functional deterioration of getting old. This would be true, that is, if the responses of the body to exercise training are the same for the 65-year-old retiree as for the 22-year-old cross country runner. Is this so?
No person has probably thought about this more than Bill Evans. In the 1980s, when he was the head of the physiology lab at the Human Nutrition Research Center on Aging at Tufts University, he set out to answer that question. Professor Evans noted that past research on exercise efforts in aged persons had simply been based on animal studies and extrapolations from results of younger subjects. This didn’t make much sense. His idea was to take elderly subjects themselves, put them in the testing laboratory, submit them to exercise training programs, and see what happened.
He and his colleagues started by looking at the effects of periods of weight training. They went out to a local nursing home and found 87- to 96-year-old women who would be willing to break away from their TV sets and perform a prescribed regular resistance program for 8 weeks. The results? Their average muscle strength tripled and their muscle size increased by 10%. Then came a 12-week strength training program in 60- to 70-year-old men that resulted in a mean increase in their lifting ability from 44 to 85 pounds (20 to 40 kg). Subsequent studies found the same thing. So, there you have it. Good evidence has it that elderly persons are just as capable of increasing muscle strength with regular weight training as younger ones.
The same thing is observed with aerobic endurance training. If you put sexagenarians into a regular walking or running program, their maximal oxygen uptake increases by 20 to 30%. You’ll also see the same magnitude of increases in muscle oxidative capacity that young adults experience under the same regimen. Concluded Evans, “Advanced age is not a static, irreversible biological condition of unwavering decreptitude. Rather, it’s a dynamic state that, in most people, can be changed for the better no matter how many years they’ve lived or neglected their body in the past.”6
Think about that for a moment. If a program of aerobic endurance or resistance training can improve function in the elderly by even 30%, that’s the same thing as reversing the aging process by roughly three decades. Here’s a way in which one can truly make the clock of physiological time move backward.
I once heard Bill Evans deliver a presentation on this, his favorite subject at a sports medicine meeting up in Lake Placid. And, you know, by the end, his findings were just so persuasive that I suspect half the audience was thinking that they just couldn’t wait to get old. His slides of smiling 90-year-old people lifting weights are memorable. Along with his coworker Irwin Rosenberg, Evans went on to publish a book called Biomarkers, which imparts not only enthusiasm but also practical exercise advice for the elderly. It’s a classic. Why this is not included in the “Medicare and You” information packet one receives from the government at age 65 is a mystery to me.
So, when you get to that age “when you get winded playing chess, when you’re still chasing women but can’t remember why, when you stoop down to tie your shoelaces and ask yourself, ‘What else can I do while I’m down here?’”7 don’t forget Evans’ advice. “The markers of biological aging can be more than altered: In the case of specific physiological functions, they can actually be reversed.” 6
4. Veteran athletes who continue training exhibit superior fitness in the elderly years compared to nonathletes. The rate of decline of physiological performance, however, is similar in the two groups.8 What does all this mean for senior athletes? Will continued sports training prevent the functional declines that come with aging? Specifically, as David Proctor and Michael Joyner posed the question “Exercise and aging: Can the biological clock be stopped?” The answer is probably not. The senior athlete demonstrates superior physical fitness and physiological capacities compared to the nonathletic elderly person. This gap will be maintained as long as the athlete continues training. But the rate of decay in these features over time appears to be the same, whether you’re a superb master athlete or not.
In addressing this question, the most frequent variable studied has been O2max. Values of O2max in highly trained male aerobic endurance athletes aged 60 to 70 are often around 50 to 60 ml/kg/min, or almost double that of their sedentary peers. O2max is lower for females than for males, but the magnitude of differences between the elderly trained and sedentary are similar.
Some early studies indicated that this superior level of aerobic fitness would also delay the decline of O2max over time by as much as 50% of that of nonathletes. However, two subsequent meta-analyses of multiple studies that provided a broader assessment—one in men, the other in women—have failed to bear out this optimism. Margaret Fitzgerald and colleagues reviewed data on the decline of O2max with aging from 109 cross-sectional studies in female subjects. The women were divided into three groups: those who were training in aerobic endurance, active, and sedentary. The rate of decline of O2max with age was found to be directly related to exercise status, with decreases of 6.2, 4.4, and 3.5 ml/kg/min per decade in the three groups, respectively (figure 7.2a). However, no differences in reduction rate of aerobic fitness were found between groups when values were expressed as percentage change from O2max at age 25 (losses of 10.0-10.9% per decade).
A similar metaanalysis of 242 studies in males by Teresa Wilson and Hirofumi Tanaka revealed similar findings. (It is not surprising that training mileage in the endurance runners decreased in direct proportion to age, but it is rather astonishing to note that they were still putting in an average of 50 kilometers a week at age 65.) Rates of both absolute declines in O2max with age and percentage change from age 25 were not significantly different among the three groups (figure 7.2b). These authors concluded that “the age-related rate of decline in O2max is not associated with habitual exercise status in healthy men.”8 And the same appears to be true in women as well.
Patterns of decline in different forms of athletic performance have typically been examined by plotting graphs of age-related world records or performances in certain championship events. This approach, of course, suffers from several of the methodological problems outlined earlier in this chapter. Most particularly, in almost all cases, there is no means by which comparisons can be made with changes in performance of nonathletes. But these graphs do give us some general insights on what happens to highly trained seniors as they age.
Fall off in 10K race times typically begins around age 35, with a steady decline until the late 50s, and then more precipitous decline after that. An examination of world-record holders at the U.S. Masters National Championships in 2002 demonstrates a 40% decrement in velocity in the 100-meter, 800-meter, and 10K running events between ages 35 and 75. This is pretty much what Hirofumi Tanaka and Doug Seals found when they plotted world-record times and top freestyle performances in the U.S. masters swimming championships from 1991 to 1995. Between age 40 and 70, the decrement in 1.5K times was approximately 44%, or about 15% per decade. Declines in men and women were about the same until age 80, when females dropped off more.
Same thing for cyclists. Records from the 2002 U.S. Cycling Federation 20K races show a 30% decline between age 40 and 80. The difference in age-group first-place finish times for the 40-year-olds and 70-year-olds in the Masters National Rowing Regatta in 2000 was approximately 26%. In these aerobic endurance sports, then, the rates of decline in performance are similar (10% per decade). They generally match those of physiological markers (O2max), which, as we’ve seen, are comparable in athletes and nonathletes.
The same performance decline of 10% per decade is described in national records of weightlifting and powerlifting. From these data, Professors Proctor and Joyner concluded that “the average rates of change for weightlifting records, as a function of age, are not much less than the rates of strength loss in the general sedentary population. However, strength-trained athletes are stronger and more powerful at any given age, providing higher functional reserve.”8
This statement seems to pretty much sum up, based on current data, our understanding of how aging affects elite-level veteran athletes. Their performance is superior—and will continue to be as long as training is maintained—but the disappointing effects of the aging process take the same toll.
1. Leaf, A. 1988. “The aging process: Lessons from observations in man.” Nutrition Review 46: 40-44.
2. Read more about what makes us age in the following sources: Austad, S.N. 1998. “Theories of aging: An overview.” Aging 10: 146-147. Hepple, R.T. 2009. “Why eating less keeps mitochondria working in aged skeletal muscle.” Exercise Sport Science Review 37: 23-28. Van Remmen, H., M.L. Hamilton, and A. Richardson. 2003. “Oxidative damage to DNA and aging.” Exercise Sport Science Review 31: 149-153. Vijg, J. 2007. Aging of the genome. The dual role of DNA in life and death. Oxford: Oxford University Press.
3. The difficulties in figuring out how aging affects physical performance are described in detail here: Groeller, H. 2008. “The physiology of aging in active and sedentary humans.” In Physiological bases of human performance during work and exercise, ed. N.A.S. Taylor and H. Groeller, 289-306. Philadelphia: Elsevier.
4. See the following articles: Spiroduso, W.W., K.L. Francis, and P.G. Mac Rae. 2005. Physical dimensions of aging. 2nd ed. Champaign, IL: Human Kinetics. Stones, M.J., and A. Kozma. 1985. “Physical performance.” In Aging and human performance, ed. N. Charness, 261-292. London: Wiley.
5. For further reading: Tanaka, H., and D.R. Seals. 2008. “Endurance exercise performance in Masters athletes: Age-associated changes and underlying mechanisms.” Journal of Physiology 586: 55-63.
6. See the following: Evans, W., and I.H. Rosenberg. 1991. Biomarkers. New York: Simon and Schuster. Rogers, M.A., and W.J. Evans. 1993. “Changes in skeletal muscle with aging: Effects of exercise training.” Exercise Sport Science Review 21: 65-102.
7. Burns, George. 1983. How to live to be one hundred or more. New York: G.P. Putnam’s Sons.
8. More information on the effects of training by veteran athletes can be found in the following articles: Fitzgerald, M.D., H. Tanaka, Z.V. Tran, and D.R. Seals. 1997. “Age-related declines in maximal aerobic capacity in regularly exercising vs. sedentary women: A meta-analysis.” Journal of Applied Physiology 83: 160-165. Proctor, D.N., and M.J. Joyner. 2008. “Exercise and aging: Can the biological clock be stopped?” In Physiological bases of human performance during work and exercise, ed. N.A.S. Taylor and H. Groeller, 313-319. Philadelphia: Elsevier. Wilson, T.M., and H. Tanaka. 2000. “Meta-analysis of the age-associated decline in maximal aerobic capacity in men: Relation to training status.” American Journal of Physiology 278: H829-H834.
1. Beyond age 40, all athletes, despite highly intensive training regimens, inevitably experience a progressive fall in performance. This decline largely reflects anatomical and physiological deterioration that is part of the body’s general aging process. Changes in other determinants, such as body composition, physical activity, and training volume, also contribute.
2. Continued training in the elderly years will keep the athlete’s performance superior to that of nonathletes.
3. Persistent training will not, however, lessen the rate of fall in performance, which is similar (a loss of about 10% per decade) to that of those who don’t train.
4. These patterns are evident in all forms of sport and are not dramatically different in males and females.
