Aging, Respiratory Function, and Exercise: Roy J. Shephard

Journal of Aging and Physical Activity, 1993, 1, 59-83
O 1993 Human Kinetics Publishers, Inc.
Aging, Respiratory Function, and Exercise
Roy J. Shephard
Aging leads to a progressive deterioration of lung function, including a
decrease of vital capacity, an increase of residual volume, a tendency for
the airways to collapse during expiration, enlargement of all components of
the respiratory dead space, a poor mixing of inspired gas, poor matching of
ventilation with perfusion, a decrease of pulmonary diffusing capacity, and a
substantial increase in the work of breathing. Ventilatory demand is increased
during most physical tasks, but arterial blood homeostasis is surprisingly
well maintained when elderly persons undertake vigorous exercise because
peak cardiac output declines in parallel with the loss of ventilatory function.
However, dyspneaprogressively restricts peak effort as one ages. The exercise
specialist cannot restore aged or damaged pulmonary tissue but can attempt
to reduce the rate of future functional loss by encouraging smoking cessation,
avoiding air pollution, and controlling acute infections. Enhanced fitness,
stronger skeletal muscles, and better coordination can reduce ventilatory
demand. Resisted breathing exercises may also strengthen the chest muscles
and allow a mechanically more efficient pattern of breathing.
Key Words: arterial oxygen saturation, breathing exercises, dyspnea, lung
volumes, respiratory dead space
In the young adult, sustained physical activity is typically limited by the
cardiovascular component of the oxygen transport chain (Shephard, 1971, 1977;
Shephard & Wstrand, 1992). As one ages, a combination of increased ventilatory
demand, an increased oxygen cost of breathing, and weaker ventilatory muscles
may cause dyspnea to become the primary constraint (Killian, 1987; Shephard,
1987a), although in the absence of respiratory disease, arterial blood homeostasis
is surprisingly well maintained through 70 years of age or older (Johnson &
Dempsey, 1991). After considering some of the technical problems that hamper
an evaluation of the aging of respiratory function, this review will examine the
structural and physiological changes that occur during normal aging and will
attempt to assess whether any of the respiratory elements in the oxygen transport
chain become major determinants of aerobic performance in a healthy elderly
person. Finally, the review will consider how far the usually observed age related
deterioration of ventilatory function may be minimized by programs of general-
ized physical activity or localized training of the respiratory muscles.
Roy J. Shephard, School of Physical & Health Education, and Faculty of Medicine,
University of Toronto, 320 Huron St., Toronto, Ontario, Canada M5S 1Al.
60 Shephard
The Evaluation of Aging

TECHNICAL PROBLEMS
Evidence concerning the aging of respiratory function is taken from a variety of
sources, including an examination of analogous changes that occur in other
parts of the body, animal experiments, studies of isolated tissue or postmortem
specimens, and in vivo human studies, usually cross-sectional rather than longitu-
dinal in type. Unfortunately, much of the in vivo human data have been collected
under resting conditions, often with the subject supine, and there is little informa-
tion on any age differences in the respiratory responses to maximal exercise.
Evidence by Analogy. There is now a substantial amount of literature de-
scribing age related changes in skin, muscle, cartilage, and bone in other parts
of the body. However, such information cannot necessarily be applied to aging
of the respiratory system. For example, collagen cross-linkages seem much less
readily reversible in the lungs than in other tissues (Last, Summers, & Reiser,
1989; Schofield, 1979). Moreover, the muscles, joints, and bones involved in
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normal, resting ventilation have inevitably escaped the disuse atrophy that is a
common problem of aging in other parts of the musculoskeletal system.
Animal Experiments. Animal experiments allow random assignment to
exercise or control regimes, with the possibility of extensive biopsy or postmortem
study at the conclusion of the experiment. Nevertheless, it is difficult to extrapolate
such data to human aging. The experimental conditions of enforced exercise andl
or restrictive caging with a controlled laboratory diet are not typical of normal life,
and even if such technical problems could be overcome, interspecies differences of
lifespan make it very difficult to compare training durations or observed rates
of aging between animals and humans (Reiser, Hennessy, & Last, 1987).
Human Experiments. In human subjects, aging is confounded with the
responses to such variables as declining habitual physical activity, a decreased
motivation for maximal effort, chronic chest disease, cigarette smoking, and
exposure to urban and environmental air pollutants. Postmortem studies are
supposedly drawn from those free of respiratory disease, but the lungs are particu-
larly vulnerable to terminal pathological changes. Often the subjects who are
recruited to in vivo studies also are atypical of the general population; some have
been health-conscious volunteers or fit survivors, and the pulmonary function of
others has been subnormal because of admission to the hospital for conditions
that supposedly did not affect respiratory function.
There are substantial differences in the apparent rate of aging of lung
volumes between longitudinal and cross-sectional studies (Glindmeyer, Diem,
Jones, & Weill, 1982; Vollmer, Johnson, McCamant, & Buist, 1988). The longitu-
dinal studies cited were of relatively short duration; thus, the findings were
characteristic of the immediate rather than the long-term environment. In contrast,
the findings from cross-sectional studies are affected by secular trends in exposure
to cigarettes, air pollutants, and respiratory infections (Vollmer et al., 1988).
Sometimes (e.g., Johnson & Dempsey, 1991) the young and the elderly have
been matched in terms of maximal oxygen intake, but a preferable basis of
matching is to choose individuals at a similar percentage of age-specific fit-
ness norms.
Other possible factors include the recruitment of health-conscious individu-
als to a longitudinal survey, the progressive learning of respiratory function test
Aging and Respiratory Function 61
techniques by subjects (although Glindmeyer et al., 1982, found their data were
affected little by ignoring the first of five tests), and technical problems of
spirometry that may have yielded less accurate measurements of dynamic lung
volumes 30-40 years ago (Shephard, 1956a). The secular trend to an increase
of adult stature (about 0.1 cmtyear) could cause an apparent aging of absolute
lung volumes amounting to about 9 mlfyr, but unless there is an associated and
major change in the ratio of trunk to limb lengths, it is unlikely to have distorted
the aging coefficients in the usual multiple regression equations based on standing
height and age.
A number of technical problems, particularly the effects of air pollution
and smoking, are cumulative and thus become progressively more important in
older populations. For instance, Milne and Williamson (1972) made a potentially
valuable cross-sectional study of respiratory function in 487 subjects 62 to 90
years of age. However, it is difficult to view their findings as normative, since
92% of the men who were recruited were either smokers or ex-smokers and 33%
of their group had a chronic cough.
The Implications of Aging

AFFECTED STRUCTURES
The chest muscles, rib cage, lungs, and air passages are somewhat less accessible
to investigation than the muscles, cartilage, and bones of the limbs, and thus
inferences regarding age related alterations of cellular characteristics have often
been made by reference to the characteristics of aging as seen in other organs
and tissues (Shephard, 1987b).
Respiratory Muscles. The skeletal muscles in the body as a whole undergo
a progressive wasting as a person becomes older. The diminution of lean mass
begins at the age of 35 to 40 years. There is commonly a 20 to 25% decrease
of lean mass by the age of 65 years, with a tendency to an accelerating loss of
lean tissue with further aging (Forbes & Reina, 1970). Much of the loss of muscle
protein is due to a progressive decline in habitual physical activity, and it can
be restored by an appropriate training program (Fiatarone et al., 1990). It is
unclear how far the respiratory muscles share in the general wasting phenomenon.
A reasonable inference might be that there is a parallel loss of contractile protein
from the accessory muscles, but that because of constant recruitment, the muscles
involved in normal resting ventilation largely escape such changes.
In part because of mechanically imposed changes in the shape of the thorax,
the chest muscles become progressively shorter in an older individual. This
adversely affects both their lengthttension relationships and their ability to under-
take the mechanical work of breathing (Green, Mead, & Sears, 1978; Road,
Newman, Derenne, & Grassino, 1986; Zadai, 1985).
Biopsies of the limb muscles show a selective, age related decrease in the
average cross-sectional surface (but probably not in the total number) of fast-
twitch, Type I1 skeletal muscle fibers (Aniansson, Grimby, Hedberg, & Krotkiew-
ski, 1981; Aoyagi & Shephard, 1992; Larsson, 1978). Myosin ATPase levels are
reduced, the time to development of peak tension is prolonged, peak tension is
reduced, and the half-relaxation time is extended (Davies & White, 1983). A
deterioration of neural coordination, a change in the electrical properties of both
62 Shephard
fast- and slow-twitch motor units, and a degenerative denervation with subsequent
reinnervation of individual fibers may all contribute to the observed functional
changes (see Aoyagi & Shephard, 1992, for references).
The number of capillaries supplying a single muscle fiber tends to decrease
with aging, but because the average fiber cross-section also diminishes, the
mitochondria1 oxygen supply is not necessarily diminished (Aoyagi & Shephard,
1992; Celli, 1986). The diaphragm seems spared many of these changes, at least
in relatively old (24 month) experimental rats (Gosselin, Bohlmann, & Thomas,
1988). It would seem important to extend such observations to human subjects,
examining the structure and functional characteristics not only of the aging
diaphragm but also of the various accessory muscles of respiration. Particularly
in women, aging is usually associated with a loss of tone and a weakening of
muscles in the abdominal wall; this increases the descent of the diaphragm and
reduces its mechanical advantage.
Rib Cage. One dominant change in the musculoskeletal system is an alter-
ation in the structure of collagen (Boucek, Noble, & Marcks, 1961; Eyre, Paz, &
Gallop, 1984; Hall, 1978; Prockop, Kivirikko, & Tuderman, 1979). Trifunctional
3-hydroxypridinium cross-linkages are formed between adjacent collagen fibrils,
and these bonds seem very resistant to any attempts at remodeling (Last et al.,
1989; Reiser et al., 1987). There is thus a progressive loss of resilience in bone
and cartilage. The major bones also undergo a progressive loss of both matrix
and calcium (Smith, Smith, & Gilligan, 1990). Structural and articular cartilage
show a decrease in the content and aggregation of proteins with chondroitin and
keratin-sulphate side-chains (Grahame, 1978; Hass, 1943a), probably related to
an activation of the enzymes that degrade collagen (cathepsin, hyaluronidase,
and collagenase). There is also a progressive loss of function in the chondrocytes
that would synthesize replacement collagen in a younger person.
The tendinous parts of joints are adversely affected by the aging of elastic
tissue. The synovial linings also deteriorate, with an increase in the number of
villi, a decrease in the vascularity of the joint capsule, and the appearance of
patches where cartilage formation is initiated (Chung, 1966).
The rib cage apparently does not escape these problems. The most striking
effects of aging are a loss of elasticity and an increase in density, these changes
ultimately progressing to complete calcification of the costal cartilages (Edge,
Millard, Reid, & Simon, 1964; Liebow, 1964; Mittman, Edelman, Norris, &
Shock, 1965; Stanescu, 1979). The costovertebral joints also become progres-
sively stiffer, and eventually they ankylose (Edge et al., 1964).
The spine is affected by the age related deterioration in the structure of bone
and cartilage. Osteoporotic collapse of the vertebrae and a flattening of intervertebral
discs that have become less resilient (Edge et al., 1964) lead to a progressive
kyphosis (Semine & Damon, 1975), sometimes characterized as the "dowager's
hump." The anterior-posterior diameter of the chest is increased. The tendency to
a mechanically inefficient barrel-shaped deformity of the thoracic cage (Edge et
al., 1964) is exacerbated by a decrease in the elasticity of the lungs; this in turn is
related to a decrease in the amount or an alteration in the mechanical properties of
alveolar elastic fibers (D'Errico et al., 1989; Pierce & Ebert, 1965).
Airways. Aging does not necessarily change the intrinsic dimensions of
the larger airways at any given alveolar volume. There may be some increase
in the number andlor size of mucous glands (Reid, 1967), although it is hard to
draw a clear line between the effects of aging and effects attributable to chronic
bronchitis. There is also a progressive decrease of ciliary function (Puchelle,
Zohm, & Bertrand, 1977),even in nonsmokers (Wanner, 1977), sometimes with a
deterioration of immune responses (Goodwin, Searles, & Tung, 1982; Roghmann,
1987) that leaves the elderly person more vulnerable to both bacterial and vi-
ral infections.
Postmortem specimens from cases of sudden death show a progressive
increase in the volume/weight ratio of the lungs at a standard inflation pressure
(Andreotti, Bussotti, Cammelli, Aiello, & Sarnpognaro, 1983). A progressive
loss of cartilaginous and fibrous support leaves the larger air passages more
vulnerable to collapse during a forceful expiration. However, this component of
the aging response is not clearly delineated from the impact of moderate emphy-
sema (Shephard, 1987b). Early gross analyses revealed little overall change in
the amount of collagen or fibrous protein in the lungs of older individuals
(Pierce & Ebert, 1965), but changes in the elasticity of the lungs suggest a
dramatic change in the location and/or mechanical properties of the supporting

tissues (Davies, 1991).
Pierce and Ebert (1965) noted age related increases of elastin in the pleura
and around the pulmonary vessels and bronchi, but not in the lung parenchyma.
Likewise, Andreotti et al. (1983) reported that the elastin content of the lung
parenchyma remained unchanged between 10 and 75 years of age, although the
collagen/elastin ratio decreased in older lungs. The content of stable, Type I11
collagen increases relative to younger adults, but the elastic tissue of the respira-
tory bronchioles appears to remain unchanged through the eighth decade of life
(D'Emco et al., 1989). The number and thickness of the radial alveolar elastic
fibers that maintain the patency of the smaller air passages decreases (D'Emco
et al., 1989), and the diameter of the small airways is progressively narrowed
(GuCnard, in press). However, tissue destruction may enlarge the terminal alveolar
ducts as one ages, thereby expanding one substantial segment of the ventilatory
dead space (Weibel, 1964).
Alveoli. Microscopic examination of the fine structure of the aging lung
shows a lighter and fluffier tissue than in a young adult, with a progressive
deterioration and disintegration of supporting structures. Studies using polyclonal
antibodies suggest some thickening of the alveolar basement membrane, due to
an accumulation of Type IV collagen and laminin (D'Errico et al., 1989). On
the other hand, the overall thickness of the alveolar wall is decreased; both animal
(Shimura, Boatman, & Martin, 1986) and human (Pump, 1976) studies show a
progressive increase in the number and size of the window-like communications
("Pores of Kohn") between adjacent alveoli, with an increase in the average
size of the alveoli. These changes seem to be a consequence of collagen cross-
linkage and a resulting reduction of elastic forces (Reid, 1967; Reiser et al.,
1987; Weibel, 1964).
There seems little change in alveolar surfactant production. Despite some
decrease of lamellar bodies in the Type I1 alveolar cells of older monkeys (Shimura
et al., 1986), observations on rat lung tissue show no significant age related
decrease in the incorporation of 3[H]-palmitic acid into lecithins (Yasuoka,
Manabe, Oaki, & Tsubura, 1977).
The total alveolar surface area of a 20-year-old is about 80 mZ.Some 90%
of this interface is served by capillaries, so the effective gas exchanging surface
64 Shephard
is around 70 m2.With aging, the lung often shows some disintegrationof interalve-
olar septae (Pump, 1976) and a reduction in the total number of pulmonary
capillaries, both changes shading imperceptibly into the pathology of emphysema
(Shephard, 1976). Because of such changes, the functional area decreases by an
average of 0.27 m2 (4%) per year of adult life, to 50-60 m2 at 80 years of age
(Mauderly, 1978; Thurlbeck & Angus, 1975).
Pulmonary Vessels. Aging of the pulmonary arteries is marked by alter-
ations in the structure of the vessel walls, as in other parts of the circulation
(Hass, 1943b). There is a thickening of the media and increasing intimal fibrosis
(Wagenvoort & Wagenvoort, 1965), leading to a loss of vessel elasticity. The
smaller pulmonary vessels may also show collagen deposition and hyalinization
(Simons & Reid, 1969), although because pressures are low in the pulmonary
circuit of a young adult, age related increases of pulmonary arterial pressures
are less marked than in the systemic circulation (Masoro, 1981).
lMFERENCES FROM STRUCTURAL CHANGES
We may infer from the structural changes described above that aging challenges
the bellows function of the chest through weakness of the accessory respiratory
muscles and alterations in the elasticity of the rib cage and lungs. The alterations
of pulmonary mechanics may also disturb the distribution of inspired gas within
the alveoli, and the matching of ventilation with perfusion in individual alveoli.
Finally, the decrease of gas-exchanging surface hampers the equilibration of
alveolar gas with pulmonary capillary blood. However, much of the available
information is qualitative rather than quantitative. Thus it remains difficult either
to estimate the likely physiological impact of the various changes or to determine
which, if any, threaten the process of oxygen transport.
PHYSIOLOGICAL CHANGES
Respiratory Muscle Function. The potential consequences of an age related

decrease in strength of the respiratory muscles and an increased impedance to
ventilation might include (a) an increase of respiratory sensations for a given
ventilation, and thus an earlier onset of dyspnea during vigorous exercise; (b) a
reduction of peak respiratory forces, and thus a diminution of the peak effort-
dependent component of ventilation; and (c) the earlier onset of fatigue with
sustained ventilatory demand.
Complaints of dyspnea suggest that respiratory sensations become a signifi-
cant determinant of peak oxygen transport in sedentary older adults. The impact
of muscle aging upon the mechanical functioning of the chest bellows has typically
been examined in terms of peak inspiratory and expiratory pressures, the maximal
voluntary ventilation, or peak flow rates over the effort-dependent fraction of
expiration (Shephard, 1982, 1987b). A linear or an accelerating age related
decrease of mechanical performance has generally been described (Momis,
Mosk, & Johnson, 1971; Schoenberg, Beck, & Bouhuys, 1978). Nevertheless,
there is much interindividual and interstudy variation, in part because the reported
values depend on success in obtaining an equivalent maximal effort from subjects
of differing ages.
Peak inspiratory and expiratory pressures are critically dependent upon
muscle length and thus initial lung volumes (Otis, Fenn, & Rahn, 1949150; Road
et al., 1986). Furthermore, the observed values depend as much on the condition
of the accessory muscles of respiration as on the muscles used during relaxed
breathing. Early studies suggested a small decrease of peak expiratory pressures
in men and of inspiratory and expiratory pressures in women >55 years (Black &
Hyatt, 1969). A more recent study also found a trend to lower peak ventilatory
pressures in those >70 years, although because of interindividual variability and a
fairly small sample size, the overall effect of aging was not statistically significant
(McElvaney et al., 1989).
Respiratory muscle fatigue has been inferred in young adults from a decline
of maximal eucapnic hyperventilation with time (Freedman, 1970; Shephard,
1967), an increase of blood lactate with maximal voluntary hyperventilation
(Cobley, Cooke, Freedman, & Moxham, 1981), a decline in maximal voluntary
ventilation and peak pressures following a marathon race (Loke, Mahler, &
Virgulto, 1982; Maron, Hamilton, & Maksud, 1979), a decrease in the glycogen
content of the rat diaphragm with prolonged exercise (Gorski, Namiot, & Giedrojc,
1978; Moore & Gollnick, 1982), and a decreased electromyographic response to
phrenic nerve stimulation after performing a maximal treadmill test against added
respiratory resistance (Levine & Henson, 1988).
One might anticipate that as subjects became older they would find it more
difficult to sustain a high level of ventilation during prolonged exercise. One
study of very fit 69-year-old subjects (a maximal oxygen intake averaging 204%
of age-predicted norms!) found no decrease of peak inspiratory pressures over
3 min of all-out exercise (Johnson, Reddan, Seow, & Dempsey, 1991a; Johnson,
Reddan, Pegelow, Seow, & Dempsey, 1991b). However, there is a need to repeat
these observations on more typical old people during longer periods of exercise.
Compliance and Static Pulmonary Gas Volumes. Static pulmonary gas vol-
umes are determined by the compliance of the respiratory system (the change
of volume per unit of applied pressure). The overall compliance of the respiratory
system C (and thus the functional residual capacity, FRC, observed when the
chest muscles are relaxed at the end of a normal expiration) is found by reciprocal
summation of respective compliance values for the rib cage (Cc) &d the-lungs
(C,):
The greater stiffness of the chest wall, discussed above, doubles its elastic resis-
tance to ventilation in those over the age of 60 years (Mittman et al., 1965).
Viscous resistance is also probably increased, although precise figures are needed.
These two factors together place an additionalmechanical load upon chest muscles
that may have already been weakened by aging (Rochester & Braun, 1976).
Rigidity of the rib cage encourages and eventually requires a much more complete
reliance upon use of the diaphragm during vigorous breathing, particularly at
lung volumes below the functional residual capacity. In the eighth decade, changes
of chest circumference account for only about a quarter of the resting tidal volume
(Rizzato & Marazzini, 1970).
The loss of elastic tissue from the aging lung leads to an increase of
pulmonary compliance in both men (Martin, Chihara, & Chang, 1977; Murray,
1981) and women (Gibson, Pride, O'Cain, & Quaglioto, 1976). However, the
66 Shephard
increase in stiffness of the rib cage tends to offset the increase of CL.Thus there
is only a small age related increase in total lung compliance.
The resulting pattern of age related changes in static lung volumes is well
accepted. There is an increase of residual gas volume (RV), whether expressed as
an absolute volume or as a fraction of total lung capacity, and a corresponding
decrease in the expiratory reserve volume (the difference between the FRC and
the RV), but little change of FRC (Cotes, 1979; Culver & Butler, 1985; Murray,
1981; Shephard, 1987b). A decrease of vital capacity roughly matches the increase
of RV, without much change of total lung capacity (TLC) (Burrows, Lebowitz,
Camilli, & Knudson, 1986; Morris et al., 1971), whether the TLC be measured in
vitro (Berend, Skoog, Waszkiewicz, & Thurlbeck, 1980) or in vivo (Cotes, 1979;
Jones, Overton, Hammerlindel, & Sproule, 1978; Niinimaa & Shephard, 1978a).
There remains some disagreement on the magnitude of aging effects in
healthy adults. Part of the difficulty lies in the definition of normality, since there
is a subtle shading from normality into emphysematous disease (Pump, 1976;
Shephard, 1976). Other possible factors increasing the apparent rate of aging are
cigarette smoking (Wilson, Meador, Jay, & Higgins, 1960), previous respiratory
disease (Anderson,Brown, Hall, & Shephard, 1968), and exposure to air pollutants
(Rokaw et al., 1980, but not Buist et al., 1979). The cumulative loss of function
seems to be much smaller in healthy, physically active nonsmokers who have
held white collar jobs than in sedentary hourly workers who have been exposed
to pollutants through their occupation, their area of residence, and cigarette
smoking (Morris et al., 1971; Niinimaa & Shephard, 1978a). Changes are also
larger in cross-sectional than in longitudinal studies (above).
Residual Volume. The direct impact of the enlarged residual volume upon
the steady-state gas exchange of a "young-old" person (age range 65-75 years)
is quite small, even during vigorous exercise. To the extent that the expansion
occurs in the terminal alveolar ducts rather than in the alveoli proper, there is
an enlargement of series dead space and thus a slowing of diffusional gas mixing
between inspired air and alveolar gas (Shephard, 1956b).
One possible disadvantage of a larger resting alveolar volume is that its
gas composition responds more slowly to an increase of ventilation. Thus the
increase of alveolar oxygen pressure normally seen at the beginning of vigorous
exercise develops more slowly, with a potentially negative influence upon the
oxygen consumption on-transient. From the viewpoint of gas exchange, greater
importance attaches to the indirect effects of the enlarged residual volume (a
decrease in mechanical efficiency of the chest muscles, a restriction of vital
capacity, and a resulting tendency to dyspnea).
Vital Capacity. Many of the commonly used equations for the prediction
of lung volumes at various ages have assumed a linear loss of function over the
span of adult life, continuing steadily from 20 to 60,65, or even 70 years of age
(Cotes, 1979). But in practice, vital capacity and many related volumes continue
to increase until about the age of 24 years (Anderson et al., 1968). There is then
a relatively linear loss of function through middle age and an accelerating loss
of function in the final years of life (Schoenberg et al., 1978). The cross-sectional
survey by Morris and associates (1971) found that in successive decades from
25 to-75-years of age the vital capacity of nonsmoking men decreased by 19,
33, 17, 68, and 82 mllyr. Such data would not be well represented by assuming
a linear loss of 44 mllyr throughout the period of observation.
Anderson and associates (1968) found that whereas smoking influenced

the age related loss of vital capacity significantly, this effect disappeared if
subjects with a history of chronic respiratory disease were excluded. Their data
support the view that although smoking has adverse effects on the elastic tissue
of the lungs, its impact is concentrated in a genetically vulnerable segment of the
population who lack alpha,-antitrypsins and thus develop chronic chest disease.
Having excluded the group with respiratory disease, Anderson et al. (1968) found
an annual loss of 17.4 ml/yr in the men and 10.5 mllyr in the women.
Most studies on the aging of vital capacity have been cross-sectional, with
resulting complications from cohort effects and secular trends (Vollmer et al.,
1988). The older portion of a typical cross-sectional sample differs in smoking
history (the proportion of smokers, the age at which each began and/or ceased
smoking, and the types of cigarettes consumed, e.g., high vs. low tar). Those
born 60, 70, and 80 years ago also lived a substantial part of their lives before
the introduction of modern antibiotics and thus had a much greater chance of
adverse effects from acute respiratory disease.
Keeping in mind these limitations of cross-sectional results, in six studies

of urban men the average rate of aging of vital capacity was 24.4 ml/yr. In 13
assorted ethnic groups living in remote regions with little exposure to air pollution,
the loss was rather similar, at 25.4 ml/yr (Shephard, 1978). The rate of loss was
generally smaller in women, averaging 18.3 mllyr in five studies of urban females
and 12.7 ml/yr in three female groups living in remote areas (Shephard, 1978).
Vital capacity is a cubic function of stature (Von Dobeln, 1966), so a 32%
difference in both the absolute capacity at any given age and in the annual loss
of vital capacity would be anticipated between men and women. The difference
is indeed of this order in many urban samples, but the gap is wider than 32%
both in the prediction equation of Anderson et al. (1968) and in the rural ethnic
groups. Possible explanations of larger discrepancies include a selective exposure
of some groups of urban men to occupational and urban pollution, and the fact
that smoking has been less widespread among women until recently.
How significant is the decline in vital capacity from the viewpoint of
oxygen transport? As vital capacity decreases, attempts to sustain tidal volume
must draw upon the mechanically inefficient extremes of chest movement, in-
creasing the tendency to dyspnea, and in general there is at least an equal
proportional decline in the 1-sec forced expiratory volume. Nevertheless, even
if we assume the relatively large loss of 25 mllyr indicated by some cross-
sectional surveys, the cumulative impact at 65 years of age would amount to
only about 20%, rather less than the overall decline in oxygen transport with age.
An acceleration of the rate of loss in later old age could have more serious
consequences. Depending on motivation and experience, a young adult develops
unpleasant dyspnea when the tidal volume reaches 33 to 75% of vital capacity
(Gilbert & Auchincloss, 1969; Killian, 1987; Killian & Jones, 1988; Shephard,
1987a). The dyspnea threshold seems just as variable in fit 70-year-old men (43
to 86% of vital capacity, Johnson et al., 1991a, 1991b). Muscle weakness and a
large functional residual capacity (Jones, 1984) undoubtedly reduce the threshold
for a typical senior citizen, but even if utilization of 50% of vital capacity were
to remain acceptable, a healthy 65-year-old man with a vital capacity as large
as 4.4 liters (Niinimaa & Shephard, 1978a) would tolerate a tidal volume of no
more than 2.2 liters. If the peak respiratory rate also remained at 40 breathslmin,
68 Shephard
as in a young adult (Shephard, 1982), a respiratory minute volume of 88 Llmin

would be accepted. This is plainly an upper limit for the average senior; often
a weakening of the chest muscles and a reduction of their mechanical advantage
make it difficult to reach the postulated 50% ceiling.
The corresponding limitation of oxygen transport depends also upon the
ventilatory equivalent (the ventilation required to transport one liter of oxygen).
In a young adult the ventilatory equivalent is about 25 L/L during submaximal
exercise, rising to 35 L/L during maximal effort. Since many aspects of oxygen
transfer become less efficient with aging, some increase of ventilatory equivalent
might be anticipated. Johnson et al. (1991a) found an average of 38 L/L in very
fit 70-year-old men, but changes are not always this large. Sidney and Shephard
(1977) found peak readings of 25 to 27 L/L when moderately fit 65-year-old
men and women performed treadmill exercise, and their values rose to 34 L/L
during maximal exercise on a cycle ergometer.
If we were to assume a ventilatory equivalent of 30 L/L during maximal
effort, then a ventilation of 88 Llmin would permit a peak oxygen uptake of
2.93 Llmin, or about 38 ml/(kg.min) in a man weighing 77 kg, a little above the
peak oxygen intake of 25 to 30 ml/(kg.min) usually observed at 65 years of age
(Shephard, 1978). A ventilatory equivalent larger than 30 L/L might be anticipated
in the frail elderly because of weakness of the skeletal muscles, an early accumula-
tion of hydrogen ions (Kay & Shephard, 1969), a poor distribution of inspired
gas, and an enlargement of physiological dead space. Let us assume that by the
age of 85 years the ventilatory equivalent becomes at least 35 L/L.
According to the cross-sectional data of Morris and associates (1971), the
loss of vital capacity from 65 to 85 years of age might average 70 mllyr; this
would reduce the vital capacity of a healthy 85-year-old to 3.0 liters. Even in
the unlikely circumstance that such a person could still utilize 50% of his or her
vital capacity, the peak respiratory minute volume would probably be no more
than 60 Llmin, and a sensation of dyspnea would restrict oxygen transport to a
peak of about 1.71 Llmin, or 22 ml(kg.min). At this stage of life dyspnea seems
very likely to become the primary factor limiting physical performance.
In practice, shortness of breath may limit function before a person reaches
the age of 85 years (Shephard, 1987b), particularly if the individual uses a large
fraction of his or her maximal inspiratory pressure (Johnson & Dempsey, 1991).
Factors that would be likely to increase the tendency to dyspnea at any given
oxygen intake include an increase of ventilatory equivalent, alterations in respira-
tory perceptions associated with a lack of recent experience of vigorous ventila-
tion, weakness of the thoracic muscles, a poor mechanical advantage associated
with the barrel-shaped chest, collapse of the airways during vigorous expiratory
efforts, and an alteration of sensory input or central neuronal processing linked
to stiffening of the rib cage and an overall increase in the impedance to breathing.
Pulmonary Dynamics. The thickening of the mucosal lining in the smaller
air passages and the decrease of thoracic compliance tend to narrow the small
air passages, increasing resistance to both inspiratory and expiratory airflow
(Johnson et al., 1991a) and augmenting the pressure gradient from the lungs to
the extra-thoracic portion of the airway for any given flow rate. Collapse of the
airway occurs if the alveolar/intrabronchial pressure gradient substantially ex-
ceeds the opposing force of elastic recoil (Davis, Campbell, Openshaw, Pride, &
Woodruff, 1980; Shephard, 1982). This situation does not arise in a young adult
at sea level, even with maximal exercise. However, it becomes a likely scenario
in the elderly patient, since an increased pressure gradient along the length of
the airway is coupled with the loss of elastic tissue and thus a reduction of the
recoil force that maintains patency in a younger individual (Davis et al., 1980;
Shephard, 1982).
Aging progressively increases the likelihood that an exerciser will reach
the effort-independentportion of the expiratory flow-volume curve, where more
forceful expiratory efforts merely increase collapse of the small airways without
augmenting airflow (Johnson & Dempsey, 1991). The end-expiratory lung volume
is increased in an attempt to minimize this effect, at the cost of a diminished
mechanical efficiency of the inspiratory muscles. Dynamic compliance also de-
creases, as the subject uses the unfavorable segment of the pressure volume
diagram (extreme inspiration).
Under resting conditions, narrowed airways and expiratory collapse of the
air passages lead to a progressive decrease in various indices of dynamic function
such as the maximal voluntary ventilation, the peak expiratory flow rate, and the
1-sec forced expiratory volume (Moms et al., 1971; Shephard, 1987b). Data for
the forced 1-sec volume show a faster age related rate of deterioration than that
usually reported for vital capacity (Burr, Phillips, & Hurst, 1985; Coe, Watson,
Joyce, & Pride, 1989). Thus, cross-sectional surveys show that the proportion
of the vital capacity expired in 1 sec drops from about 82% to perhaps 75% in
65-year-old men, and from 86% to about 79% in women of the same age
(Anderson et al., 1968; Shephard, 1978).
As with forced vital capacity, the apparent rate of aging of the forced
expiratory volume depends on the extent of the cumulative insults the lungs have
received, but even in nonsmokers living in an area with little air pollution the
annual loss over the span of working life is about 32 ml in men and 25 ml in
women. Likewise, the decrease in peak expiratory flow rate amounts to about
25% over the span of working life, the annual rate being 4 Llmin in men and
2.5 L/min in women (Gregg & Nunn, 1989).
The magnitude of these changes is no greater than the age related decrease
in maximal oxygen intake. It is thus unlikely that bellows function is imposing
a major direct limitation upon oxygen transport in the healthy "young-old"
person. Nevertheless, Johnson and Dempsey (1991) noted that a limiting expir-
atory flow was reached over 40 to 90% of the tidal range in fit 70-year-olds,
and that many of these individuals were unable to increase their ventilation
further if carbon dioxide was inhaled during maximal exercise. Other negative
consequences are a heavy increase in the oxygen cost of breathing, dyspnea
associated with an overloading of the inspiratory muscles, and an increase in the
lung volume at which airway collapse becomes inevitable during expiration (the
"closing volume").
Gas Distribution. By the age of 65 years, at least the final quarter of the vital
capacity range is affected by airway closure (Anthonisen, Danson, Robertson, &
Ross, 1970; Frank, Mead, & Fenis, 1957; Gibson et al., 1976; LeBlanc, Ruff, &
Milic-Emili, 1970). For hydrostatic reasons, ventilation becomes restricted mainly
in the dependent parts of the lungs (Davis et al., 1980; Kronenberg, Drage, Ponto, &
Williams, 1973). Unfortunately, a large fraction of the pulmonary blood flow is
distributed to the lower third of the lungs; thus, airway collapse leads to a progressive
worsening in the matching of ventilation with perfusion.
70 Shephard
In part because of premature airway closure, and in part because of patchy

changes in compliance and resistance (Kitamura, Sawa, & Ikezono, 1972), the
distribution of inspired gas is less uniform in the elderly than in younger subjects
(Holland, Milic-Emili, Macklem, & Bates, 1968). Following inspiration of a
single 500-ml breath of oxygen under resting conditions, the slope of the nitrogen
plateau seen during a slow and steady expiration increases from about 1.3%
nitrogen per 1,000 ml in a young adult to around 2.3%/1,000 ml at the age of
retirement (Cohn & Donoso, 1963; Shephard, 1956b).
Resting observations on the distribution of oxygen (Shephard, 1956b), *'Kr
(Harf & Hughes, 1978), or '33Xenon(Holland et al., 1968) do not necessarily
apply to vigorous exercise, wherein the tidal volume occupies a much larger
fraction of the vital capacity range. With maximal inspiration, ventilation is
directed to the lower, well-perfused parts of the lungs, and under such conditions
aging does not increase the nonuniformity of ventilation (Kronenberg et al.,
1973). However, the rapid respiratory rate of vigorous exercise may not allow
adequate time for the equilibration of inspired gas between the terminal alveolar
ducts and the alveoli, or from one alveolus to another (Shephard, 1956b); this
is particularly important in older adults, in which a loss of elastic tissue leads
to an expansion of the terminal alveolar ducts and an inhomogeneity of time
constants (Kitamura et al., 1972). Thus, whereas vigorous exercise usually de-
creases the vertical nonuniformity of ventilation (Gledhill, Forese, Buick, &
Bryan, 1978; West, 1962), it may increase nonuniformity in the horizontal axis
(Shephard, 1982; West, 1962).
Alveolar Ventilation. The dead space of the respiratory system comprises
an anatomical component corresponding to the volume of the conducting airways,
plus a physiological component due to diffusion across the alveolarlairway inter-
face (the series element) and a parallel element (due to a poor distribution of
gas and a poor matching of ventilation with perfusion).
There is inevitably some increase of the total respiratory dead space with
aging. The dimensions of the major airways vary in direct proportion to alveolar
volume (Shephard, 1982), so the average volume of the anatomical dead space
increases with the development of an expanded, barrel-shaped chest; Cotes (1979)
has estimated the change at 10 mlldecade. Nevertheless, the main cause of the
increase in dead space probably lies in the finer structures of the lung. The age
related expansion of the terminal alveolar ducts and alveoli leads to a less complete
diffusional mixing between inspired gas and alveolar gas, increasing the series
element of the physiological dead space (Shephard, 1956b).
Airway closure and any bronchial disease causes a selective impairment
of ventilation of alveoli at the base of the lungs, and unfortunately these alveoli
typically receive a large fraction of the total pulmonary blood flow (Davis et al.,
1980). The reduction of the pulmonary capillary bed also leaves a large number
of alveolar spaces that are ventilated but poorly perfused. A small increase of
pulmonary arterial pressure may facilitate perfusion of the upper parts of the
lungs, and thus improve ventilation/perfusion ratios (Holland et al., 1968). How-
ever, marked pulmonary hypertension has a negative effect on cardiorespiratory
function, restricting peak blood flow and eventually progressing to cardiac failure
(as in the emphysematous patients known as "blue-bloaters").
Some researchers have argued that aging should lead to a substantial wors-
ening of the matching of ventilation to perfusion (Davies, 1991; Wagner, Lara-
vuso, Uhl, & West, 1974), augmenting the so-called parallel component of the
physiological dead space. Nevertheless, experimental data in elderly, healthy
nonsmokers show surprisingly normal resting ventilation/perfusion ratios (Hol-
land et d., 1968; Kronenberg et al., 1973). To the extent that exercise leads to
a greater uniformity of both ventilation and perfusion of the lungs (Shephard,
1982), the problems of the elderly person are likely to be even less severe during
vigorous exercise than under resting conditions.
The overall impact of the various dead space elements can be assessed in
terms of the dead spaceltidal volume ratio. Johnson and Dempsey (1991) noted
that although the overall dead spaceltidal volume ratio was 15 to 20% larger in
elderly than in younger subjects, the importance of this handicap decreased
progressively during exercise.
Pulmonary Diffusion. The efficiency of gas exchange between the alveoli
and the pulmonary capillaries can be examined in terms of diffusing capacity or
alveolar-arterial pressure gradients. The diffusing capacity of the lungs (DL)is
usually measured in terms of carbon monoxide uptake and comprises iwo compo-
nents: the diffusing capacity of the alveolar capillary membrane (Dm)and the
rate of reaction between carbon monoxide and pulmonary capillary blood (OV,):
Resting values for D, decrease in subjects older than 40 years, and there
also seems to be a decrease of pulmonary capillary blood volume, particularly
after the age of 60 years. Expressing diffusing capacity in the traditional units
of mllmin per mm Hg partial pressure gradient, the annual loss of resting function
has been estimated at about 0.15 ml/min/mmHg (Georges, Saumon, & Loiseau,
1978; Horvath & Borgia, 1984). As with many other body functions, there is
thus about a 25% loss of resting function over the span of normal working life,
corresponding roughly with changes in the functional area of the gas exchange
surface (Mauderly, 1978). Nevertheless, the score for the standard test of diffusing
capacity is based on an averaging of the driving pressure of CO across well and
poorly ventilated alveoli. The observed value is thus not a pure measure of
diffusional exchange, and much of the age related loss reflects a worsening of
gas distribution rather than a loss of actual diffusing surface.
Vigorous exercise increases the uniformity of gas distribution and also
increases the number of perfused alveoli. The effect of aging on diffusing capacity
thus tends to diminish during vigorous physical activity. Indeed, Niinimaa and
Shephard (1978a) found that healthy and relatively fit 65-year-old subjects had
almost as large a maximal diffusing capacity as young adults. More data are
needed on the maximal diffusing capacity of the elderly, but it seems unlikely
that pulmonary diffusion limits oxygen transport in healthy seniors.
Alveolar-Arterial Gas Pressure Gradients. The alveolar-arterial oxygen pres-
sure gradient reflects mainly the effects of incomplete equilibration of alveolar
gas with pulmonary capillary blood, poor matching of ventilation and perfusion,
and frank venous-arterial pulmonary shunts.
Young adults show almost no gradient of oxygen partial pressure between
alveolar gas and the blood leaving the lungs in the pulmonary veins. This suggests
that neither the pulmonary diffusing capacity nor its interactions with ventilation
and blood flow offers any appreciable barrier to oxygen transport (Shephard,
72 Shephard
1977, 1982). Endurance athletes are one exception to this generalization. When
such individuals engage in maximal exercise, a large cardiac output leads to a
very rapid passage of red cells through the pulmonary capillary bed, and the
transit time in some of the shorter pathways may be insufficient for a complete
equilibration of alveolar and blood gas pressures. Dempsey, Powers, and Gledhill
(1990) argued that an alveolar-arterial oxygen pressure gradient of 20-30 Torr
could develop, causing the oxygen saturation of pulmonary venous blood to drop
below 90%, although this interpretation has since been questioned (Warren,
Cureton, Middendorf, Ray, & Warren, 1991).
It might be anticipated that the age related decrease of the pulmonary
capillary bed would exacerbate any problems of transit time and thus equilibration
between alveolar gas and pulmonary capillary blood, particularly during vigorous
exercise. In practice, any effect from the decrease of pulmonary vascular bed
seems to be offset by a smaller peak cardiac output (Niinimaa & Shephard,
1978b; Shephard, 1987b), thus the time available for gas equilibration is no
shorter than in younger people.
The classical view has been that even under resting conditions aging is
associated with a 6 to 25 Ton decrease in the partial pressure of oxygen in
arterial blood and a significant widening of the alveolar-arterial gradient (Kanber,
King, Eshcar, & Sharp, 1968; Kitamuraet al., 1972; Monis et al., 1971; Needham,
Hogan, & McDonald, 1954; Sorbini, Grassi, Solinas, & Muiesan, 1968; Ward,
Tolas, Benviste, Hansen, & Bonica, 1966). However, this is not invariably the
case; Johnson and Dempsey (1991) found that the alveolar-arterial gradient of
fit 70-year-old subjects was only 2 to 5 Torr greater than in young adults, and
this small gradient was thought due to poor matching of ventilation with perfusion
rather than to problems of gas transfer in ventilated alveoli. Even during maximal
exercise, alveolar-arterial gradients had a negligible impact on oxygen transport;
in only 4 of 19 subjects was the arterial oxygen pressure less than 75 Torr and
the arterial oxygen saturation less than 92%.
WORK OF BREATHING
The magnitude of the work of breathing depends on the ventilation associated

with a given effort and the mechanical efficiency of the chest bellows. The work
of breathing comprises elastic and resistive components, with a minimal influence
of tissue inertance.
Ventilatory Demand. The resting respiratory minute volume and its compo-
nents (tidal volume and respiratory rate) remain largely unchanged with advancing
age (Shephard, 1987b), but the ventilation associated with the performance of
any given external task is progressively increased, perhaps by as much as 3 to
5% per year. Many factors contribute to the greater ventilatory demand, including
a lesser efficiency of the chest bellows and an increased oxygen cost of activity.
However, there does not seem to be any increase in the sensitivity of the respiratory
centers; indeed, Dill, Hillyard, and Miller (1980) found that the whole body
response to hypoxia and hypercapnia was apparently diminished, perhaps by as
much as 50% relative to a younger person.
A given respiratory minute volume may be developed less efficiently in
the elderly patient, because of an increase in airflow and tissue resistance, adoption
of a smaller tidal volume and a more rapid respiratory rate (Shephard, 1982),
airway collapse, distortion of the rib cage, or a shift of ventilation to an unfavorable

portion of the pressure/volume curve (Johnson & Dempsey, 1991). Ventilation
may also be augmented to compensate for increases in anatomical, series, and
parallel components of the respiratory dead space. In general, the size of each
breath is augmented by at least the volume of any added dead space (Shep-
hard, 1982).
Other factors that increase ventilation during submaximal work include a
greater accumulation of lactate (due to a slow oxygen consumption on-transient,
a poorer myocardial contractility, weaker skeletal muscles, and an impaired
peripheral circulation). One measure of ventilatory response is the ventilatory
equivalent. During treadmill exercise, Sidney and Shephard (1977) found values
that were quite similar to the average 25 L/L value observed in young adults,
but Johnson and Dempsey (1991) found values as high as 38 L/L.
Oxygen Cost. The oxygen cost of the primary task is increased by a loss
of mechanical efficiency. Joint stiffness, poor motor coordination, increased body
sway, and a lack of recent familiarity with most types of heavy exercise increase
the oxygen cost of all forms of effort. For instance, the net mechanical efficiency
of cycle ergometry drops from 23% in a young adult to about 21.5% in the
average 65-year-old person (Shephard, 1987b; Sidney & Shephard, 1977). There
is also an increased oxygen cost associated with an augmentation of respiratory
work, to be discussed below; and the age related rise of systemic blood pressure
and heart rate at any given intensity of exercise increase the oxygen consumption
of the heart.
The decrease in elastic recoil of the lungs, measured at a fixed 60% of
total lung capacity, averages about 0.25 mm H,O per year (Murray, 1981). One
might thus anticipate that an older person could sustain a given ventilation by
applying smaller forces to the thoracic cage, with a corresponding reduction in
the elastic work of breathing. However, this potential advantage is offset by an
increase in the rigidity of the chest wall. With the increased tidal volume of
exercise, a substantial amount of elastic energy is stored in the chest wall during
inspiration, and much of this energy can be recouped during expiration (Shephard,
1982). Thus, during vigorous exercise some of the theoretical disadvantage of
increased elastic work against the rib cage disappears.
Airway collapse and a stiffening of the rib cage both augment resistive
work, so that the total work of breathing is likely to be much greater in an old
person than in a younger person. Unfortunately, measurements of the oxygen
consumed by the chest muscles are extremely difficult to make during vigorous
exercise, since they are greatly overshadowed by the oxygen demands of the
skeletal muscles. A young adult may well divert as much as 5 to 10% of the
total maximal oxygen intake to the mechanics of ventilation (Shephard, 1966).
Johnson and Dempsey (1991) estimated that the respiratory cost increased from
an average of 6% in young adults to 13% in fit 70-year-old men.
Many elderly people have some emphysema, and Chemiack (1956) noted
that in this condition the respiratory muscles consume 10 to 20 times more
oxygen than in a healthy young adult. The magnitude of the respiratory oxygen
consumption is in no way revealed by the individual's maximal oxygen intake
score, since the observed total maximal oxygen intake includes not only the
oxygen that is available to the skeletal muscles but also the oxygen that is
consumed by the respiratory and cardiac muscles, together with the oxygen
74 Shephard
consumption of the viscera. It is thus possible for an elderly person to retain a

maximal oxygen intake that would be adequate to sustain the activities of daily
living in a younger person, and yet exhaust much of this apparent reserve in the
work of breathing.
Effects of General and Localized Training

Perhaps the most important practical question for the health professional is
whether the functional changes that normally occur during aging can be prevented
or corrected either by a program of general physical activity or by a more specific
local training of the respiratory muscles.
Plainly, there is no mechanism that can rebuild areas of lung that have
been damaged by a loss of elastic tissue, emphysematous change, or a destruction
of the pulmonary capillary bed. The prime emphases must therefore be on the
prevention of further tissue loss and the containment of ventilatory demand.
PREVENTIVE MEASURES
Preventive measures, unfortunately, have no impact on the normal aging of the

healthy lungs, but they can have a major effect when aging would otherwise be
accelerated by the cumulative insults of occupational and urban air pollution,
smoking, and respiratory disease.
All health professionals should be strong advocates of measures to reduce
pollution at the work site and in the urban environment. One of the most important
of urban contaminants is ozone, arising from auto exhaust (Folinsbee, 1990;
Godlee, 1991). The exercise specialist can make a useful contribution to solving
the problem of auto exhaust by encouraging people to walk or cycle rather than
drive as a part of any exercise prescription; too often, their advice is to drive 20
miles to a central gymnasium!
Cigarette smoking is perhaps the most important cause of an accelerated
loss of lung function (Boss6 & Rose, 1984), and because of the close and frequent
contacts involved in supervised exercise sessions, practitioners are in a valuable
position to offer specific advice to their clients who still smoke. There is also
some possibility that general programs to increase habitual activity may encourage
the interest of the patients in health, thus initiating smoking withdrawal and/or
avoiding recidivism once they have stopped smoking (Shephard, 1989). Plainly,
teaching by example is especially important, and it is vital that all members of
the health care team be health exemplars,convinced nonsmokers with a vigorously
active personal lifestyle.
Finally, we have noted the adverse impact of chronic respiratory infection
upon lung volumes (Anderson et al., 1968). Measures for the prevention of
viral infections and the early containment of secondary infections of the upper
respiratory tract (such as the use of appropriate broad-spectrum antibiotics) are
thus important facets of treatment, particularly in the patient with a tendency to
chronic bronchitis. If sputum does accumulate, then measures such as postural
drainage should be instituted promptly and pursued energetically, before a vicious
cycle of chronic infection and worsening pulmonary function is established. In
theory, vigorous exercise might be expected to facilitate mucus clearance by
opening up collapsed areas of lung. However, in practice such effects seem slight
(Wolff, Dolovich, Obminsky, & Newhouse, 1977) or nonexistent (OlsCni &
Wollmer, 1990) in normal subjects, and equally controversial in patients with
bronchial hypersecretion (Oldenburg, Dolovich, Montgomery, & Newhouse,
1979; OlsCni, Midgren, & Wollmer, 1992). If indeed there is any benefit, the
increase of mucus clearance seems less than could have been achieved by encour-
aging bouts of deliberate coughing (Camner, Mossberg, & Philipson, 1973;
Oldenburg et al., 1979).
GENERAL PHYSICAL CONDITION
Cross-sectional studies have shown that very fit elderly (maximal oxygen intake
50 ml/[kg.min] at an age of 65 years) have vital capacity and dynamic lung
volumes up to 20% larger than their sedentary peers, with smaller advantages
of maximal pulmonary diffusing capacity and a comparable alveolar-arterial
oxygen partial pressure gradient despite a much greater peak oxygen intake
(Hagberg, Yerg, & Seals, 1988; Johnson & Dempsey, 1991).
Aerobic conditioning may also yield small increases of dynamic lung
volumes in healthy elderly subjects; for example, Williams et al. (1984) noted
a 7% increase of 1-sec forced expiratory volume over a 12-week, thrice-weekly
program. However, once lung function has deteriorated, even rigorous general
conditioning can make only a marginal difference to either static or dynamic
lung volumes (Mertens, Kavanagh, & Shephard, 1978). The best method of
reducing disability at this stage is to decrease the overall oxygen cost of a given
activity and the ventilatory demand associated with this oxygen consumption.
A combination of specific exercises to strengthen the main skeletal muscles
(Lake, Henderson, Briffa, Openshaw, & Musk, 1990; Mertens et al., 1978; Schols,
Mostert, Soeters, & Wouters, 1991; Simpson, Killian, McCartney, Stubbing, &
Jones, 1992) and an improvement of general physical condition may improve
the patient's coordination, so that the energy cost of a given task is reduced
(Paez, Phillipson, Masangkay, & Sproule, 1967; Vyas, Banister, Morton, &
Grzybowski, 1971). As confidence improves, even a simple task such as treadmill
walking may be performed more efficiently (e.g., by increasing stride length).
Strengthening of the skeletal muscles may facilitate their perfusion during vigor-
ous exercise (Kay & Shephard, 1969) and increase local capillarity, mitochondria1
density, and the concentration of aerobic enzymes (Saltin & Gollnick, 1983),
thus reducing the accumulation of lactate and the resultant drive to the ventilatory
centers (Casaburi et al., 1991).
Some researchers have argued that breathing exercises can teach the patient
to adopt a more relaxed usti tin-& Ausubel, 1992) and/or a more efficient pattern
of breathing, although this hypothesis needs critical evaluation. For instance,
because of rigidity of the chest cage, maximal use of the diaphragm will probably
reduce the respiratory work rate. If premature airway collapse is occurring, the
adoption of a slower expiration or expiration against closed lips may reduce such
a tendency. This will not only be helpful in its own right but will also reduce
the work of breathing and thus ventilatory demand (Shephard, 1976).
Finally, it is important that the patient accept the sensations of vigorous
breathing. Much of the functional limitation observed in the young-old or middle-
old individual is related to anxiety and fear of dyspnea rather than to a true
76 Shephard
physiological limitation. It is thus very important that rehabilitation break any

cycle of anxiety, decreasing activity, further loss of general condition, and increas-
ing dyspnea (Mertens et al., 1978).
SPECmC TRAINING
Given recent demonstrationsof the dramatic response to skeletal muscle strength-

ening programs in nonagenarians (Fiatarone et al., 1990), it seems reasonable to
anticipate that the chest muscles of senior citizens would benefit from a compara-
ble program. Specific exercises such as vigorous isocapnic hyperpnea or repeated
expirations against an external resistance can indeed strengthen the respiratory
muscles, both in young adults (Leith & Bradley, 1976; Morgan, Kohrt, Bates, &
Skinner, 1987) and in patients with chronic obstructive lung disease (Belman &
Mittman. 1980).
A greater reserve of force in the chest muscles would not in itself correct
an expiratory collapse of the airways, but it might allow the patient to take a
faster inspiration; this in turn would permit a slower expiration, reducing the
likelihood of airway collapse. However, there is a need to evaluate such a tactic
carefully, particularly with respect to any negative impact on gas distribution. If
the chest muscles were strengthened,they would also contract at a smaller fraction
of their maximal voluntary-force. This would reduce the perceived respiratory
effort (Redline, Gottfried, & Altose, 1991) and might also facilitate perfusion of
the chest muscles (Kay & Shephard, 1969; Royce, 1958), reducing the tendency
to local muscle fatigue. There have been suggestions that such fatigue can contrib-
ute to dyspnea (Killian & Jones, 1988), although there remains a need to evaluate
the adequacy of local perfusion and the tolerance of sustained effort by both the
diaphragm and the accessory muscles of breathing.
Conclusions
Aging is associated with a progressive loss of respiratory function. The bellows
function diminishes, the respiratory dead space is increased, and pulmonary
diffusing capacity is reduced, but arterial homeostasis is generally well maintained
even during vigorous exercise. The main limitation of performance, and thus of
peak oxygen transport, commonly arises in the link between ventilatory mechanics
and respiratory sensation. A substantial component of the observed oxygen trans-
port may be consumed by the muscles of respiration. An exercise training program
cannot reverse structural changes in the chest and lungs, but it can reduce the
oxygen cost of a given task and may also allow development of a larger peak
oxygen intake by desensitizing an old person to dyspnea.
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Journal of Aging and Physical Activity, 1993, 1, 59-83

O 1993 Human Kinetics Publishers, Inc.

Aging, Respiratory Function, and Exercise

The Evaluation of Aging

The Implications of Aging

dramatic change in the location and/or mechanical properties of the supporting

lMFERENCES FROM STRUCTURAL CHANGES

Respiratory Muscle Function. The potential consequences of an age related

Anderson and associates (1968) found that whereas smoking influenced

Keeping in mind these limitations of cross-sectional results, in six studies

as in a young adult (Shephard, 1982), a respiratory minute volume of 88 Llmin

In part because of premature airway closure, and in part because of patchy

The magnitude of the work of breathing depends on the ventilation associated

airway collapse, distortion of the rib cage, or a shift of ventilation to an unfavorable

consumption of the viscera. It is thus possible for an elderly person to retain a

Effects of General and Localized Training

Preventive measures, unfortunately, have no impact on the normal aging of the

GENERAL PHYSICAL CONDITION

physiological limitation. It is thus very important that rehabilitation break any

Given recent demonstrationsof the dramatic response to skeletal muscle strength-

older athletes. Journal of Applied Physiology, 65, 101-105.

Biochimica et Biophysica Acta, 990, 182-189.

muscle endurance training on ventilatory and endurance performance of moderately

in patients with bronchial hypersecretion. Scandinavian Journal of Rehabilitation

populations. Human Biology, 47, 101-1 16.

controlled trial of weightlifting exercise in patients with chronic airflow limitation.

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