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1 Human Cardiovascular Research Laboratory, Department of Kinesiology and Applied Physiology, University of Colorado, Boulder 80309; and 2 Divisions of Cardiology and Geriatric Medicine, Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado 80262
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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To determine the
relation between habitual endurance exercise status and the
age-associated decline in maximal aerobic capacity [i.e., maximal
O2 consumption
(
O2 max)] in men, we performed a
well-controlled cross-sectional laboratory study on 153 healthy men
aged 20-75 yr: 64 sedentary and 89 endurance trained.
O2 max (ml · kg
1 · min1),
measured by maximal treadmill exercise, was inversely related to age in
the endurance-trained (r = 
0.80) and sedentary
(r = 0.74) men but was higher in the
endurance-trained men at any age. The rate of decline in
O2 max with age
(ml · kg1 · min1)
was greater (P < 0.001) in the endurance-trained than
in the sedentary men. Whereas the relative rate of decline in
O2 max (percent decrease per decade
from baseline levels in young adulthood) was similar in the two groups,
the absolute rate of decline in O2 max was 5.4 and 3.9
ml · kg1 · min · decade1
in the endurance-trained and sedentary men, respectively.
O2 max declined linearly across the
age range in the sedentary men but was maintained in the
endurance-trained men until ~50 yr of age. The accelerated decline in
O2 max after 50 yr of age in the
endurance-trained men was related to a decline in training volume
(r = 0.46, P < 0.0001) and was
associated with an increase in 10-km running time (r = 0.84, P < 0.0001). We conclude that the rate of
decline in maximal aerobic capacity during middle and older age is
greater in endurance-trained men than in their sedentary peers and is
associated with a marked decline in O2 pulse.
maximal oxygen consumption; aging; functional capacity
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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MAXIMAL AEROBIC
CAPACITY, as measured by maximal O2 consumption
(O2 max), declines progressively
with adult aging (10, 12, 14, 15, 35, 47). Although
O2 max may not provide an optimal
measure of functional capacity (27), the decline in
O2 max with age contributes
importantly to the age-associated reduction in physical functional
capacity (11, 22, 39). Because a
O2 max of 15-18
ml · kg1 · min1
must be maintained for independent function (11, 30),
maintaining maximal aerobic capacity is an important component of
successful aging. The age-related reduction in maximal aerobic capacity
is also associated with increased prevalence of cardiovascular disease (2, 5, 18, 38), the number-one cause of death in the United States (1). Specifically, higher
O2 max values are associated with
more favorable coronary heart disease risk profiles (18),
as well as lower cardiovascular mortality and morbidity (2, 5,
38). Because reduced maximal aerobic capacity is linked to
elevated cardiovascular disease risk and mortality, as well as reduced
physical functional capacity, it is important to understand the
modulatory influences of the decline in
O2 max with age.
O2 max has been studied extensively
in endurance-trained and sedentary men (4, 13, 20, 29, 34, 36,
37, 43, 46, 48). Although it is quite clear that
O2 max is higher in
endurance-trained than in sedentary men of similar age
(41), whether or not the rate of decline differs between the two groups is still unclear. Rates of decline have been reported to
be attenuated (4, 19, 20, 29, 36, 46), similar (37,
43, 48), or slightly greater (13) in
endurance-trained than in sedentary men. Discrepant results among
studies may be attributed to an incomplete age range (29,
46), small group numbers (43), inclusion of
diseased populations (20, 43), different measurement
procedures (19, 36, 46), poorly defined training status
criteria (4, 29, 37, 43, 46), and/or absence of an
appropriate sedentary control group (13, 19, 48). This is
the first well-controlled study employing a wide age range, selective
inclusion criteria, large group numbers, and standardized measurement procedures.
Recently, we used meta-analysis, as well as cross-sectional and
longitudinal laboratory-based experimental approaches, to establish
that O2 max actually declines at a
greater absolute rate
(ml · kg1 · min1 · decade1)
in endurance-trained than in sedentary women (6, 8, 44), whereas the relative rates of decline (percent decrease from baseline in young adulthood) were not different. In contrast to these findings in women, however, our meta-analysis of the literature in men indicated
no significant difference in the absolute rate of decline in
O2 max between endurance-trained
and sedentary men (47).
Given the limitations of meta-analysis, the equivocal data in the
literature on men, and our contradictory findings in women, we sought
to confirm the findings of the meta-analysis in men with a
well-controlled, cross-sectional, laboratory-based investigation. On
the basis of the meta-analysis in men, we hypothesized that there would
be no difference between sedentary and endurance-trained men in
absolute or relative rates of decline in
O2 max with advancing age.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects. We studied 153 men: 89 endurance-trained (age range 21-74 yr) and 64 sedentary (age range 20-75 yr). All subjects were healthy and free of overt cardiovascular disease as assessed by medical history. Irrespective of training status, men >40 yr of age were further evaluated by physical examination and by resting and maximal exercise electrocardiograms. None of the subjects were smokers or were taking medications that could affect circulatory function. To eliminate the confounding influence of severe obesity, only subjects with a body mass index <35 kg/m2 were included in the study. To ensure that the endurance-trained men were highly competitive runners, we recruited men who finished among the top 10 finishers from their age group in the Bolder Boulder road race (the second-largest 10-km road race in the United States). The men in the sedentary group were interviewed thoroughly to ensure that they performed no regular aerobic physical exercise. Before participation, verbal and written explanations of the procedures and potential risks were provided. In turn, the subjects gave their written informed consent to participate in the study. The study was approved by the Human Research Committee of the University of Colorado at Boulder.
Measurements.
O2 max was determined by a
continuous incremental treadmill protocol by using on-line
computer-assisted open-circuit spirometry, as described in detail
previously (7, 42). Gas fractions were analyzed with a
mass spectrometer (model MGA-1100, Perkin-Elmer, Ponoma, CA) previously
calibrated with standard gases of known concentrations. Expired air
volume was measured with a turbine (model VMN-2, Interface Associates,
Laguna Niguel, CA) or a pneumotachometer (Hans Rudolph, Kansas City,
MO). There were no differences between these two systems when
ventilation, O2 uptake, and CO2 production were
analyzed simultaneously. Before each trial, these analyzers were
calibrated with standard gases of known concentrations. Heart rates
were continuously monitored with an electrocardiogram.
O2 max, at least three of the
following four criteria were met by each subject: 1) a
plateau in O2 uptake with increasing exercise intensity, 2) respiratory exchange ratio 
1.10, 3)
achievement of age-predicted maximal heart rate (±10 beats/min), and
4) a rating of perceived exertion 18 units (9,
16).
Body mass was measured with a physician's balance scale (Detecto, Webb
City, MO) to the nearest 0.1 kg. Percent body fat and fat-free mass
(FFM) were estimated using dual-energy X-ray absorptiometry (DXA-IQ,
Lunar Radiation, Madison, WI; software version 4.1), as previously
described (45).
Information was obtained from each subject regarding his training
records. Endurance-trained men reported average frequency (days/wk),
duration (min/session), and volume (min/wk) of training over the past
year. Subjects also reported a recent 10-km race time.
Statistics.
One-way analysis of variance was used to determine differences in the
dependent variables among age groups. Univariate correlations and
regression analyses were performed to determine the relations among the
dependent variables and the proportion of variance in O2 max explained by selected
predictor variables, respectively. Parallelism of regression lines was
used to determine differences between slopes. Stepwise
multiple-regression analyses were used to identify significant,
independent determinants for the age-related decline in
O2 max. Values are means ± SE. Statistical significance was set a priori at P < 0.05.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subject characteristics.
Table 1 displays the mean values for the
subject characteristics. FFM was negatively correlated with age in the
endurance-trained men, whereas no relation was observed in the
sedentary men. Conversely, body mass was unchanged in the
endurance-trained men but increased with age in the sedentary men.
Percent body fat increased throughout the age range in sedentary and
endurance-trained men; the rate of increase did not differ between
groups.
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Responses to maximal exercise.
All subjects attained O2 max on the
basis of the criteria described above.
O2 max, maximal heart rate, and maximal O2 pulse declined with age in both groups
(P < 0.0001; Table 2).
Maximal pulmonary minute ventilation and respiratory exchange ratio
declined with age in the endurance-trained men (P < 0.05) only. Maximal ratings of perceived exertion did not differ with
age in either group.
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Age-related changes in O2 max.
On the basis of linear regression analysis,
O2 max
(ml · kg1 · min1)
was inversely related to age in sedentary (r = 0.74)
and endurance-trained (r = 0.80) men (Fig.
1). By testing for parallelism of the
regression lines, we found that the slope of the change in
O2 max (ml · kg1 · min1)
with advancing age was greater in the endurance-trained than in the
sedentary men (P < 0.001). Specifically, the change in O2 max was greater in the
endurance-trained than in the sedentary men (5.4 vs. 3.9
ml · kg1 · min1 · decade1;
Fig. 2A). Similar differences
between endurance-trained and sedentary men existed when
O2 max was expressed in liters per
minute and when normalized per kilogram of FFM. Conversely, the
relative (%/decade) rate of change in
O2 max was similar in
endurance-trained (10.8%) and sedentary (11.2%) men (Fig.
2B). Figure 3 portrays the
greater slope of the O2 max vs. age
regression line in endurance-trained men after 50 yr of age compared
with before 50 yr of age.
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Age-related changes in maximal heart rate.
Maximal heart rate was inversely related to age in both groups
(P < 0.0001; Fig. 4).
The absolute rates of change were similar in endurance-trained and
sedentary men (6.3 vs. 8.8 beats · min1 · decade1).
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Changes in training factors with age in the endurance-trained men.
Table 3 presents the exercise training
data for the endurance-trained men (n = 67). Frequency
of training was negatively correlated with age (r = 0.25, P < 0.05). The 10-km race time increased
(r = 0.76, P < 0.0001), whereas
training volume decreased (r = 0.36,
P < 0.001) with advancing age. Moreover,
O2 max was correlated with 10-km
race time (r = 0.84, P < 0.0001) and training volume (r = 0.46, P < 0.0001).
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Correlates of the age-related decline in
O2 max.
Stepwise regression analysis was used to identify the significant
predictor variables of the age-associated changes in
O2 max (Table
4). In endurance-trained and sedentary
men, age was the primary predictor of
O2 max, describing 65 and 55% of the variance, respectively. For both groups, percent body fat was the
secondary predictor of O2 max,
accounting for an additional 9 and 21% of the variance in the
endurance-trained and sedentary men, respectively. When the groups were
combined, percent body fat was the primary predictor of
O2 max, whereas age was the
secondary predictor, accounting for 69 and 75% of the variance,
respectively. In the endurance-trained men, reductions in the frequency
(r = 0.31, P < 0.005) and volume
(r = 0.46, P < 0.001) of average
weekly training with age correlated with the corresponding decrease in
O2 max. The age-associated increase
in 10-km running time was strongly related to the corresponding decrease in O2 max
(r = 0.84, P < 0.0001).
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Changes in O2 pulse with age.
Figure 5 illustrates the reduction in
O2 pulse with age in endurance-trained and sedentary men.
As with O2 max, the slope of change
in O2 pulse with age was greater in the endurance-trained than in the sedentary men (P < 0.001). At any age,
however, O2 pulse was higher in the endurance-trained than
in the sedentary men.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The primary findings of the present study are as follows.
1) The absolute, but not relative, rate of decline in
O2 max with increasing age was
greater in endurance-trained than in sedentary men. 2) In
the endurance-trained men, O2 max
declined minimally before 50 yr of age but at an enhanced rate
thereafter; in the sedentary men, there was a linear relation between
O2 max and age. 3) The
greater rate of decline in O2 max
with age in the endurance-trained men was not due to a greater rate of
change in maximal heart rate or body composition but, rather, was
associated with a decrease in weekly training volume.
The decline in O2 max with age can
be partially attributed to a reduction in maximal cardiac output, which
is mediated in part by a reduction in maximal heart rate (10, 14,
15, 29). Hence, differences in the rate of reduction in maximal heart rate with age could lead to corresponding differences in the rate
of decline in maximal aerobic capacity. In the present study, the
reduction in maximal heart rate with age was strongly correlated with
the age-related reduction in O2 max
among individual subjects. However, we found no difference in the
age-related rate of decline in maximal heart rate between
endurance-trained and sedentary men, consistent with previous
observations (32, 47). As such, age-related changes in
maximal heart rate do not explain the accelerated rate of decline in
O2 max in our endurance-trained men.
Differential changes in body composition could also explain the greater
rate of decline in O2 max with age
in the endurance-trained men. Because we expressed
O2 max relative to body weight
(ml · kg1 · min1),
increases in body mass would directly reduce
O2 max. In addition, increases in
percent body fat and reductions in lean body mass may also be related
to the diminished O2 max (17,
26, 37). However, the age-related increases in percent body fat
and body mass, as well as decreases in FFM, did not differ between our
two groups, nor did the rates of decline in
O2 max differ between the groups
when normalized for FFM. Therefore, we cannot attribute the greater
rate of decline in O2 max with age
in endurance-trained men to differences in age-related changes in body
composition or mass.
A reduction in peripheral O2 uptake with age could also
explain the age-related reduction in
O2 max. McGuire et al. (24) reported that, in men followed over a 30-yr period,
the decrease in O2 max was
associated with a reduction in peripheral O2 extraction,
rather than a decrease in maximal cardiac output. In the same
population, a 6-mo endurance exercise training program restored
O2 max via peripheral mechanisms
(25, 40). In the present study, we found that
O2 pulse, a commonly used index determined in part by
peripheral O2 extraction, was attenuated with advancing age
in sedentary and endurance-trained men. O2 pulse was,
however, maintained at a higher absolute level in the endurance-trained
men at any age. The reduction in peripheral O2 uptake with
age can be attributed to reductions in muscle volume and oxidative
capacity per muscle volume (3). Indeed, Neder et al.
(28) reported a relation between the reductions in
O2 max and leg strength and leg
muscle mass with age.
Within individuals, habitual exercise behavior modulates
O2 max (17, 33).
Consistent with our meta-analysis in men (47), we found
that frequency of training decreased with advancing age and correlated
with the decline in O2 max in the
endurance-trained men. These results suggest that the reduction in
O2 max with age in the
endurance-trained men can be partially attributed to a decline in
training volume. Our findings are consistent with longitudinal data
showing preserved O2 max when
exercise training volume is maintained over periods of 10-20 yr
(21, 23, 31). We should emphasize that a reduction in training intensity also may contribute to the accelerated decline in
O2 max after 50 yr of age. We are
unable to elucidate, however, whether the decrease in training volume
and intensity with age causes
O2 max to be reduced or,
alternatively, with the age-related reduction in
O2 max, perception of exercise
difficulty is increased and training volume and intensity are
consequently decreased. The accelerated decline in
O2 max after 50 yr of age in our
endurance-trained runners likely had a functionally significant impact
on performance, in that 10-km race time increased with age and
correlated with the decrease in
O2 max. Figure
6 illustrates the enhanced rate of increase in 10-km race time after 50 yr of age in the endurance-trained men.
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We previously suggested that the greater rate of decline in
O2 max with age in
endurance-trained than in sedentary women may be mediated in part by
"a law of initial baseline" effect (8, 44). That is,
because endurance-trained women had higher absolute levels of
O2 max than sedentary women during young adulthood, trained women experienced greater absolute rates of
decline in O2 max with advancing
age. This is supported by the observation that the relative rate of
decline in O2 max (i.e., percent
change from young adulthood) did not differ between sedentary and
endurance-trained women. In the present study, we also found that the
absolute, but not the relative, rate of decline in
O2 max was greater in
endurance-trained than in sedentary men. Therefore, the greater
absolute rate of decline in O2 max with age in the endurance-trained men may be mediated in part by their
higher initial baseline levels.
A limitation of our study is its cross-sectional design. We realize
that the rate of decline in O2 max
with age cannot be definitively determined using a cross-sectional
study design. However, when Jackson et al. (17) employed
cross-sectional and longitudinal analyses in a single study, the
average rate of decline in O2 max
was similar with both types of analyses. Moreover, our cross-sectional
and longitudinal studies in women provided similar results (6,
44). Still, we recognize that genetic and constitutional factors
may have influenced our cross-sectional findings. Longitudinal studies
are required to confirm the present cross-sectional observations.
Additionally, we acknowledge that self-reported physical activity is a
crude measure of habitual exercise behavior. To ensure that our
subjects were categorized appropriately, we thoroughly screened our
sedentary and trained subjects. All our endurance-trained subjects were
elite athletes who finished among the top 10 finishers in the
second-largest 10-km road race in the United States, whereas our
sedentary subjects abstained from regular aerobic physical activity.
Furthermore, we understand that our measures of training volume also
were relatively crude. However, despite this limitation, training
volume strongly correlated with measures of
O2 max (ml · kg1 · min1;
r = 0.46, P < 0.001) and 10-km race
time (r = 0.84, P < 0.001).
In conclusion, despite their greater rate of decline in
O2 max
(ml · kg1 · min1)
across age, endurance-trained men demonstrated a similar relative rate
of decline (%/decade) and much higher mean levels of
O2 max at any age than their
sedentary peers. The greater rate of decline in absolute
O2 max with age in the
endurance-trained men may be mediated by their higher baseline levels
of O2 max than in sedentary men and
a reduction in exercise training stimulus after 50 yr of age.
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ACKNOWLEDGEMENTS |
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This study was supported by National Institutes of Health Grants AG-00847, AG-13038, and HL-07851.
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FOOTNOTES |
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Address for reprint requests and other correspondence: P. E. Gates, Dept. of Kinesiology and Applied Physiology, University of Colorado at Boulder, Boulder, CO 80309-0354 (E-mail: phillip{at}spot.colorado.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
First published January 17, 2003;10.1152/japplphysiol.00774.2002
Received 23 August 2002; accepted in final form 14 January 2003.
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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