|
Aging and ultimate death seem characteristic of all living organisms. Atherosclerosis and arteriosclerosis progressively decrease the tissue oxygen supply, and in some organs such as the brain, cells that die are not replaced. In other tissues, the cell constituents change with aging; for example, cross-linkages develop between adjacent collagen fibrils, decreasing their elasticity and facilitating mechanical injury. In consequence, most biological functions show a progressive, age-related deterioration (8).
The mechanisms underlying the aging process are not well understood. Possible hypotheses (2, 8) include a "wear and tear" which exceeds the reparative capacity of the tissues, a development of immunity to the individual's own protein constituents, and errors in cell division, associated with exposure to external radiation or endogenous mitogens such as peroxidases. Some biologists have even argued that aging has been "programmed" by evolution to avoid the hazard of overpopulation.
Young adulthood typically covers the period from 20-35 years of age, when both biological function and physical performance reach their peak. During young middle-age (35-45 years), physical activity usually wanes, with a 5-10 kg accumulation of body fat. Active pursuits may be shared with a growing family, but it becomes less important to impress either an employer or persons of the opposite sex with physical appearance and performance. During later middle-age (45-65 years), women reach the menopause, and men also substantially reduce their output of sex hormones. Career opportunities have commonly peaked, and a larger disposable income often allows energy demanding domestic tasks to be deputed to service contractors. The decline in physical condition thus continues and may accelerate.
In early old age (65-75 years), there may be a modest increase of physical activity, in an attempt to fill free time resulting from retirement (8). By middle old age (75-85 years), many people have developed some physical disability, and in the final stage (very old age, over 85 years) they become totally dependent. A typical expectation is of 8-10 years of partial disability, and a year of total dependency (5).
There are nevertheless wide inter-individual differences in functional status at any given chronological age. In terms of maximal oxygen intake, muscle strength and flexibility, the best preserved 65-year-old may out-perform a sedentary 25-year-old. Whether assessing fitness for continuing employment or recommending an exercise prescription, decisions should thus be based upon biological rather than chronological age. Unfortunately, there is no very satisfactory method of determining a person's biological age, because the different biological systems age at differing rates. Attempts to combine such measurements as graying of the hair, loss of skin elasticity, a decrease of vital capacity, and a decrease of reaction time into a global index seem to provide no more than a complicated and inaccurate method of assessing the individual's chronological age.
A major fraction of total daily energy demand arises from resting metabolism, and it is thus important to note that resting metabolism decreases with aging, by about 10% from early adulthood to the age of retirement, and a further 10% subsequently. One reason is the loss of metabolically active muscle mass and parallel increase in metabolically inert depot fat. In later old age, there may also be some overall reduction in cellular metabolism. Food intake must be correspondingly adjusted if body fat is not to increase further. A low total intake of food may fail to satisfy daily requirements of protein and other key nutrients, particularly calcium. One important by-product of a physical activity program for the older senior is thus an increased intake of key nutrients without recourse to the provision of synthetic dietary supplements.
The maximal oxygen intake declines by about 5 ml.kg-1.min-1 per decade from 25 to 65 years of age, with some possible acceleration thereafter (8). It is difficult to be certain how much of this loss is inevitable, and the extent to which the decline results from a progressive decrease of habitual physical activity; ordinary people certainly become more sedentary as they age and even older athletes usually reduce the rigor of their training. There have been occasional claims that individuals who become vigorously physically active can sustain an unchanged maximal oxygen intake for many years (6), but a critical review of the data suggests that once such subjects have realized any immediate training response, they resume a relatively normal rate of aging. Even in athletes who maintain their daily training volume, the rate of decrease of maximal oxygen intake is only a little slower than in the general population. Potential causes of the age-related loss in aerobic power include decreases in maximal heart rate, stroke volume and arterio-venous oxygen difference.
Heart Rate
Maximal heart rate decreases mainly because of a decreased responsiveness to circulating catecholamines. The classical equation [peak rate = (220 - age in years)] implies a maximum of about 155 beats.min-1 at age 65 years (1). More recent research suggests that a well-motivated 65-year-old can attain a rate of 170 beats. min-1 or more during uphill treadmill running, although muscle weakness may lead to somewhat lower maxima during cycle ergometry (10). Peak values are further reduced if the subject experiences breathlessness (in chronic pulmonary disease) or develops myocardial ischemia (in the sick sinus syndrome).
Stroke Volume
Weisfeldt et al. (12) argued that if care was taken to exclude subjects with myocardial ischemia, the heart of a typical 65-year-old subject could compensate for a low maximal beating rate by increasing the end-diastolic volume and thus cardiac stroke volume. However, their view has not been confirmed by subsequent research (10). During submaximal exercise, the stroke volume may be greater than in a younger adult, but an elderly person has difficulty in sustaining stroke volume as maximal effort is approached (7).
There are many constraints upon peak ventricular function in the elderly. Venous filling is impaired by poor peripheral venous tone, varicosities, and a slow relaxation of the ventricular wall. Reduced sensitivity to catecholamines blunts the inotropic increase of myocardial contractility during vigorous exercise. After-loading of the ventricle also rises more than in a younger individual, in part because of hypertension and a loss of arterial elasticity, and in part because weakened skeletal muscles must contract at a larger fraction of their peak voluntary force. Finally, ventricular contractility may be impaired by the development of silent myocardial ischemia.
Arterio-Venous Oxygen Difference
The maximal arterio-venous oxygen difference decreases from perhaps 140-150 ml.dL-1 in a young adult to 120-130 ml.dL-1 in a senior citizen. This change reflects the direction of a larger fraction of the total cardiac output of the exerciser to regions (the skin and the viscera) where oxygen extraction is quite limited (10).
Functional Consequences
Depending on the nature of the task and the working environment, sustained exercise is fatiguing if it demands more than 33-50% of the person's maximal oxygen intake. Thus, the aging of oxygen transport progressively restricts the ability of the senior citizen to undertake the normal activities of daily living such as walking up a slight rise (9). Full independence probably requires a peak oxygen transport of 12-14 ml/[kg.min]. The maximal oxygen intake of many seniors drops below this threshold around 80 years of age, the final precipitant of dependence being the added loss of function caused by a period of bed rest for some inter-current illness.
An appropriately graded aerobic training program can augment the aerobic power of 65 year old subjects by as much as 10 ml.kg-1.min-1 over a 3 month period, effectively reducing the biological age of the oxygen transporting system by 20 years. A lack of aerobic power thus should not limit the independence of a well-trained, active individual unless she or he survives to the unlikely age of 100 years. Aerobic training eliminates premature disability, but has little influence on survival beyond the age of 80 years. Rather, it induces a "squaring" of morbidity and mortality curves, so that good health is preserved until shortly before death (4). Activity patterns in late middle age are quite strong predictors of the likelihood of dependency as a senior (11).
Because initial fitness is quite low, the aerobic condition of a senior can be improved by low intensity of training. Gains are greatest if a heart rate of 130-140 beats.min-1 can be sustained, but useful if slower progress is seen with regular training at heart rates of 110-120 beats.min-1 . In the frail elderly, heart rates rarely exceed 85 beats.min-1, and some training response may then be anticipated even with activities inducing a heart rate of only 100 beats.min-1.
Aging and Musculo-Skeletal Function
Aging leads to a progressive decrease of muscle strength and flexibility.
Muscles
Strength peaks around 25 years of age, plateaus through 35 or 40 years of age, and then shows an accelerating decline, with 25% loss of peak force by the age of 65 years. Muscle mass decreases, apparently with a selective loss in the cross-section if not the numbers of type II fibers. It is unclear whether there is a general hypotrophy of skeletal muscle, or a selective hypoplasia and degeneration of Type II fibers, associated with a loss of nerve terminal sprouting.
Other possible causes of functional loss include a deterioration of end-plate structures, impaired excitation-contraction coupling, and decreased fiber recruitment. Both contraction time and half-relaxation time are prolonged, and maximal contraction velocity is decreased. Changes are greater in the legs than in the arms, possibly because there is a greater decrease in use of the legs with aging. Muscular endurance at a given fraction of maximal voluntary force apparently improves with age, in part because the muscles now contain a larger proportion of type I fibers and in part because weaker muscle contractions restrict perfusion less than in a younger person.
Loss of strength progressively impedes every day living. It becomes difficult to carry a 5 kg bag of groceries, to open a vial of medicine, and even to lift the body mass from a toilet seat (9). The male/female strength ratio is unchanged, so that women are limited by a loss of strength at an earlier age than men.
Muscle strength can be greatly improved by as little as 8 weeks of resisted training, even in 90 year old subjects (3). Protein synthesis proceeds more slowly than in a younger adult, but cross-sectional comparisons between active and inactive individuals suggest that much of the wasting of lean tissue can be avoided by regular resisted exercise. Stronger muscles further enhance function by stabilizing osteo-arthritic joints, reducing the risk of falls, and lessening the extent of dyspnea.
At one time, it was feared that resisted exercise might cause a dangerous rise of blood pressure, provoking a heart attack. However, if the subject avoids performing a Valsalva maneuver and individual contractions are held for no more than a few seconds at 60% of peak voluntary force, the rise of blood pressure is no greater than would be anticipated during a typical bout of cycle ergometer exercise.
Flexibility
The elasticity of tendons, ligaments and joint capsules is decreased as cross-linkages develop between adjacent fibrils of collagen. Over the span of working life, adults lose some 8-10 cm of lower-back and hip flexibility, as measured by the "sit-and- reach" test. The restriction in the range of movement at the major joints becomes yet more pronounced during retirement, and eventually, independence is threatened because the subject cannot climb into a car or a normal bath, ascend a small step, or complete the movements required for dressing and combing the hair.
Flexibility is thought to be conserved or improved by gently taking the main joints through their full range of motion each day. If muscle weakness and arthritis are already advanced, such activities are best attempted in warm water. Buoyancy then supports body-weight, and warmth increases the immediate flexibility of the joints.
Bone Structure
There is a progressive decrease in the calcium content and a deterioration in the organic matrix of the bones with aging. However, the dividing line between normality and pathology is unclear, and it is also uncertain how far a decrease of habitual physical activity contributes to the age-related calcium loss. Changes are more marked in women than in men, due in part to sex differences in the hormone profile and in part to a lower intake of calcium and good quality protein in women.
The calcium loss can begin as early as 30 years, and in women the process accelerates for some 5 years around the menopause. In later old age, the bones become so weak that a mild fall, a bout of coughing, or even a vigorous muscle contraction can cause a "pathological" fracture. A fracture of the hip quite commonly initiates irreversible bed rest and death. A deterioration of the vertebrae also contributes to senile kyphosis.
Regular load-bearing exercise can halt and sometimes even reverse bone mineral loss through the eighth decade of life. Such a regimen is particularly effective when accompanied by a high calcium diet (1500 mg/day). In women, many authorities also recommend the administration of estrogens, although the risks of such therapy require further assessment.
Many hormonal control mechanisms work less efficiently in an older person. For example, the pancreas and the thyroid are affected by damage to and/or a decrease in the number of secreting cells, and the ventricular muscle has a decrease in the number or the affinity of catecholamine receptors. Clinical consequences of these hormonal changes include the development of maturity-onset diabetes, and myxedema, with resulting obesity, poor cold tolerance and depression.
Diabetes mellitus presents immediate risks of ketosis, hyperglycemia and hypoglycemia. Long-term complications (skin infections, ulcers, peripheral vascular arteriosclerosis, myocardial ischemia, peripheral neuropathy, retinopathies and cataract formation) can also limit the subject's exercise tolerance. However, moderate exercise with some restriction of energy intake is an effective treatment for maturity-onset diabetes mellitus; many patients are thus spared the complication of long-term insulin therapy and rigid control of food intake. Exercise may also correct both obesity and depression in the patient with hypothyroidism.
The age of peak athletic performance depends upon the key functional element required of the successful competitor. In events where flexibility is paramount (for example, gymnastics and brief swimming events) the top competitors are commonly adolescents. In aerobic events, performance usually peaks in the mid-twenties, as gains from prolonged training, improved mechanical skills and competitive experience are negated by decreases in maximal oxygen intake and flexibility. Because of a longer plateauing of muscle strength, performance in anaerobic events declines less steeply, and in pursuits such as golf and equitation, where experience is paramount, the best competitors are aged 30-40 years.
Caution is needed in drawing physiological inferences from athletic records, since the pool of potential competitors decreases with age. Moreover, the motives of older participants often change from competitive success (winning at all costs) to social interaction, and some participants in Masters events lack cumulated skills, since they did not begin competing until they reached their late thirties.
The risk of a cardiac emergency is increased substantially when a person is actually exercising. Some physicians have thus argued that older people who intend to exercise should undergo exhaustive preliminary screening, including an exercise electrocardiogram. This may be desirable if the person intends to embark on very strenuous competitive training, but it is undesirable if an older individual merely wishes to make a small increase in their habitual daily physical activity.
It is usually difficult to motivate older people to exercise regularly. Insistence on extensive screening suggests that physical activity is dangerous, and creates additional barriers of cost and time which reduce the likelihood that an intention to exercise will result in active exercise behavior. In fact, the interpretation of exercise ECGs is very difficult in many elderly persons, and there is little evidence that either a clinical evaluation or a stress electrocardiogram can detect those who will have an adverse exercise outcome. Moreover, the person who begins an exercise program is at a lower overall risk of sudden death than a sedentary peer, and perhaps because of a less ambitious attitude toward exercise, the relative risks of physical activity (deaths when exercising vs deaths when sedentary) decrease rather than increase as a person becomes older. Finally, if a well-loved form of exercise does provoke sudden death in an 80-year-old, this is a more pleasant end than many alternative ways of dying.
Nevertheless, certain precautions can increase the safety of exercise for the older individual. The recommended dose of exercise should do no more than leave the participant pleasantly tired on the following day. Recovery processes proceed slowly, and vigorous training should thus be pursued on alternate days. In individuals with pre-existing articular disease, walking should be substituted for jogging or running; fast walking offers an adequate training stimulus, with less risk of slipping, and a much smaller impact stress on the knees. Weight-supported activities such as swimming and aquabics are particularly helpful for those with joint problems. Vision, hearing and balance are all poorer than in a younger person. The senior should thus avoid sports where there is a risk of collision with opponents or stationary objects. If there is a history of falls, special care is needed in pursuing activities that require a good sense of balance (whether climbing, skiing and cycling, or merely walking on a slippery pool deck). In older people taking hypotensive medication, there is a danger of a sudden loss of consciousness when standing at the end of a bout of exercise, particularly if the room is hot, or the veins are relaxed by a period in a pool. Environmental extremes are poorly tolerated, and if the weather is extremely hot or cold, activity should be taken inside an air-conditioned facility (for example, rapid walking in an indoor shopping mall). For those who are extremely frail, some physical conditioning can be achieved using exercises taken from a sitting position.
Exercise training cannot restore tissue that has already been destroyed, but it can protect the individual against a number of the chronic diseases of old age. More importantly, it maximizes residual function. In some instances, biological age is reduced by as much as 20 years. Life expectancy is increased, partial and total disability are delayed, and there are major gains in quality-adjusted life expectancy. Exercise is thus a very important component of healthy living for the senior citizen.
References
1. Asmussen, E. &
Molbech, S.V. Methods and standards for evaluation of the
physiological working capacity of patients. Hellerup, Denmark:
Communications of the Testing and Observation Institute, 4, 1-16,
1959.
2. Comfort, A.
Aging. The Biology of Senescence. 2nd Ed. New York:
Holt, Rinehart, Winston, 1979.
3. Fiatarone, M.A., Marks,
E.C., Ryan, N.D., Meredith, C.N., Lipsitz, L.A. & Evans,
W.J. High intensity strength training in nonagenerians.
Effects on skeletal muscle. Journal of the American Medical
Association, 263, 3029-3034, 1990.
4. Fries, J.F. Aging
Well. Reading, Mass.: Addison-Wesley, 1989.
5. Health & Welfare
Canada. Health Promotion Survey: Ottawa: Health & Welfare,
Canada.
6. Kasch, F.W., Wallace, J.P.,
Van Camp, S.P. & Verity, L. A longitudinal study of
cardiovascular stability in active men aged 45 to 65 years.
Physician and Sportsmed, 16 (1), 117-126, 1988.
7. Niinimaa, V. &
Shephard, R.J. Training and exercise conductance in the elderly. (2).
The cardiovascular system. J. Gerontology, 35, 672-682,
1978.
8. Shephard, R.J. Physical
Activity and Aging. 2nd Ed. London: Croom Helm
Publishing, 1987.
9. Shephard, R.J.
Fitness and aging. In: Aging into the Twenty First Century. C.
Blais (ed.). Downsview, Ont.: Captus University Publications, 1991,
pp. 22-35.
10. Shephard, R.J.
Health and Aerobic Fitness. Champaign, IL.: Human Kinetics
Publishers, 1993.
11. Shephard, R.J. &
Montelpare, W. Geriatric benefits of exercise as an
adult. J. Gerontology (Med. Sci.), 43, M86-M90,
1988.
12. Weisfeldt, M.L.,
Gerstenblith, M.L. & Lakatta, E.G. Alterations in
circulatory function. In: Principles of Geriatric Medicine. R.
Andres, E.L. Bierman & W.R. Hazzard (eds.). New York:
McGraw Hill, 1985, pp. 248-279.