Circulation. 2005;112:624-626
doi: 10.1161/CIRCULATIONAHA.105.553321
(Circulation. 2005;112:624-626.)
© 2005 American Heart Association, Inc.
Accelerated Decline of Aerobic Fitness With Healthy Aging
What Is the Good News?
Philip A. Ades, MD;
Michael J. Toth, PhD
From the University of Vermont College of Medicine, Burlington.
Correspondence to Philip A. Ades, MD, McClure 1, Cardiology, University of Vermont College of Medicine, Fletcher-Allen Health Care, Burlington, VT 05401. E-mail Philip.Ades{at}vtmednet.org
Key Words: Editorials • exercise • aging • physiology
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Introduction
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As we get older, even if we are healthy, we become less fit.
At the extreme, we become disabled and eventually die. Although
this deterioration in physical work capacity is widely accepted,
few studies have characterized changes in aerobic capacity across
the age span. Instead, the majority of studies have utilized
cross-sectional designs. These studies are limited, however,
by selective survival—ie, older participants, as a group,
are inherently healthier than younger individuals, as evidenced
by their survival. Thus, the 5% to 10% drop in aerobic fitness
per decade, defined from cross-sectional studies, may well be
an underestimate.
1–6
See p 674
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The Baltimore Longitudinal Study of Aging
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The Baltimore Longitudinal Study of Aging began recruiting healthy
individuals into a long-term descriptive study in 1978.
7 Subjects
were screened at baseline for clinical heart disease. Screening
included a symptom-limited exercise test supplemented by nuclear
perfusion imaging in men >40 and women >50 years of age.
The participants were predominantly white and college educated
and lived in the Baltimore-Washington metropolitan area. Every
2 years they spent 2 full days at the Gerontology Research Center
in Baltimore, Md, where they underwent medical, physiological,
and psychological testing. Individuals without onset of clinical
heart disease underwent maximal treadmill exercise testing on
alternate visits. It should be noted that although elimination
of individuals who developed clinical heart disease allowed
the researchers to examine the effects of aging per se on exercise
capacity without the confounding effects of disease, this approach
almost certainly removed less-fit individuals from the analysis
because poor fitness is a well-known cardiac risk factor. A
total of 3379 exercise tests were performed in this study, all
consistently supervised by the same cardiologist (Dr Fleg).
Another 10% of tests were excluded because of failure to attain
85% of the maximal predicted heart rate or because the tester
deemed a test to be nonmaximal on the basis of direct observation.
Finally, another 3% were excluded for individuals who were taking
a ß-adrenergic–blocking medication. One could
question whether the individuals with chronotropic incompetence
or inability to attain 85% of the maximal age-predicted heart
rate should have been excluded if they otherwise performed a
maximal test, verified by the attainment of a respiratory exchange
ratio >1.00, as these simply may have reflected the tail
of the bell-shaped maximal heart rate curve. It is possible
that this factor, again, excluded the least fit individuals.
The resulting dataset represents the most comprehensive examination of longitudinal changes in aerobic fitness throughout the aging spectrum in healthy individuals. By clustering repeated exercise test data within 6 age decades, a rate of decline within successive decades is calculated. Thus, the selection biases inherent in cross-sectional studies—in particular, the fact that older participants, by dint of their survival, are generally healthier than younger participants overall—are avoided. Fleg and coworkers7 show that the previously defined linear decline of aerobic capacity of 5% to 10% per decade is indeed incorrect, particularly in the later decades of life. Most importantly, these data suggest that the age-related decrease in aerobic capacity is nonlinear, increasing progressively each decade. For example, whereas the decline in peak 
O2 was 3% to 6% in the third and fourth decades, it was far greater, >20% per decade, after age 70. The accelerated decline persisted even when the data were adjusted by fat-free mass, which also declines with age. Although it is possible that the effect of fat-free mass on peak O2 was not entirely corrected for by calculating a simple ratio of peak O2 (mL/min) divided by fat-free mass,8 it is unlikely that loss of muscle mass alone accounts for the accelerated decline in fitness given the pattern of age-related changes in fat-free mass. Reduced peak O2 was found in all physical activity quartiles. It should not be overlooked, however, that more physically active individuals had higher peak O2 measures than less active individuals at all ages. From a physiological perspective, these results suggest that the loss of aerobic fitness with age is not attributable to the erosion of muscle mass or to physical inactivity. Instead, changes that alter the delivery of oxygen to exercising muscles or the ability of muscles to utilize oxygen are more likely determinants of declining aerobic fitness. If this is the case, age-related changes in muscle perfusion or oxidative capacity may lie at the root of diminished aerobic exercise capacity in the elderly. In support of an effect of age on muscle oxidative capacity, recent findings show that aging is associated with impaired skeletal muscle mitochondrial function secondary to mitochondrial DNA oxidative damage and loss.9
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Fitness Declines Precipitously in Late Middle Age: Bad News?
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Because the logical end point of declining exercise capacity,
at its extreme, is death, one can question whether these data
are also relevant to overall mortality. Similarly, one can also
question if, as Fleg et al
7 suggest, the presented data are
relevant to an accelerated development of functional disability.
Do individuals have no ability to alter structure, function,
or clinical outcome by exercise or other lifestyle habits? Should
all who pass the age of 40 passively resign themselves to a
fast track to physical disability?
With regard to the implications of these data on mortality, I am reminded of the treatise of baseball statistician Bill James relating the peak of a player’s hitting ability to the length of his career in the Major Leagues.10 The higher the peak of the parabolic curve of hitting ability versus age, the broader the parabola as it crosses the x-axis (in years), the longer the stay in the Major Leagues. Although the data of Fleg et al7 support the concept that whatever the aerobic fitness level, whatever the physical activity level, there is a sharper decline over time after age 60 or 70 than before, they do not deny data from several sources that relate peak aerobic capacity and physical activity in middle-aged adults to increased longevity11–13 and delayed disability.14,15 Again, a higher peak yields a broader parabola with increased longevity. Furthermore, if you accept the concept that some physical dysfunction will generally precede death (absent a sudden death), it is in fact preferable for the graph of the decline to have a shelf with maintained aerobic capacity, until an accelerating late drop, as opposed to a more protracted, linear deterioration.
A separate though relatively minor concern with these fitness data from the Baltimore Longitudinal Study of Aging is that of the healthy cohort effect.16 This suggests that individuals who volunteer for health-related research studies are often more fit and health oriented than the population as a whole. In the study of Vita et al,14 several lifestyle factors, including exercise patterns, body mass index, and smoking, were closely related to end-of-life disability patterns. Not only was the onset of disability delayed by up to 5 years in the lowest-risk group (those who were thin, did not smoke, and exercised), but it was also noted that these same factors led to a compacting of end-of-life disability. If indeed the data of Fleg et al7 are skewed by such healthier volunteers, along with the elimination of individuals who did not attain 85% of their maximal predicted heart rate and individuals who developed heart disease, we may be observing such an effect. Rebutting this, at least in part, would be their finding that even their least fit individuals also saw a decline in fitness in their 70s.
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Fitness Versus Disability
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Whether this decline in aerobic fitness leads to functional
disability is not as clear as implied. Disability is a complex
construct that includes not only aerobic capacity, which in
practical terms is reflected by walking capacity, but also strength,
balance, coordination, and psychological factors.
17,18 Perhaps
the best-studied biological correlate of physical function outside
of aerobic fitness is muscle strength. Muscle strength has been
shown to be at least as important a determinant of functional
capacity as endurance in healthy and diseased elderly persons,
19–21 and strength training can improve performance of walking, climbing
stairs, carrying groceries, and other household activities without
altering aerobic capacity.
22–24 This implies that the
very activity of lifting the leg while walking, a trivial detail
in the young, is a limiting factor to walking endurance in the
elderly. Caution should be taken, however, in imparting too
much importance to biological factors alone. As much as functional
capacity is limited by physiological capacity, it is undoubtedly
dependent on psychological factors. For instance, recent work
from our laboratory showed that mental depression was an equally
important determinant of self-reported disability as was aerobic
fitness in older patients with heart disease.
17 These findings
do not, of course, deny the findings of Fleg et al,
7 but raise
the question of whether the drop in aerobic capacity translates
into a proportional drop in physical functional performance.
For instance, Posner et al
25 showed that the ability to perform
activities of daily living was not dependent on aerobic fitness
until peak
O2 dropped below
750 mL/min. Thus, although erosion
of peak
O2 with age undoubtedly accompanies the development
of disability, its overall contribution to the reduced capacity
to perform normal daily activities is unclear.
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Conclusions
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The important article by Fleg and colleagues presents a comprehensive
examination of longitudinal changes in aerobic fitness through
the aging spectrum in healthy individuals. The foresight and
energy of the investigators are laudable, as such a dataset
could not have been assembled without persistence and focus.
A particular strength is the collection of repeated-measures
longitudinal data, which avoids the biases of cross-sectional
studies. A decline in aerobic fitness was noted after age 40,
which accelerates as individuals enter their sixth and seventh
decades. This decline is independent of muscle mass and physical
activity levels. Thus, the bad news is that your aerobic fitness
will decline with age no matter what you do. The good news is
that individuals who start with higher aerobic capacity and
continue their activity habits throughout life maintain a greater
fitness level at all points in the aging spectrum. In light
of the relationship between aerobic fitness and mortality,
11–13 this suggests that performance of regular exercise throughout
the lifespan will both lengthen life and postpone and compact
end-of-life disability.
13,14
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Acknowledgments
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Dr Ades is supported in part by grants NHLBI 9 RO1-HL72851-04A1,
R01 HL73351-01A1, and MO1RR00109. Dr Toth is supported by grants
AR-02125 and AG-021602. The authors thank Patrick Savage, MS,
for reviewing this manuscript.
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Footnotes
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The opinions expressed in this article are not necessarily those
of the editors or of the American Heart Association.
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References
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Introduction
The Baltimore Longitudinal Study...