///// A G I N G ///// A G I N G \\\\\ A G I N G \\\\\ Part I /////

Aging-1







The Phenomenon of Aging

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.

Age Classification

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.



Aging and Energy Consumption

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.

Aging and Aerobic Performance

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