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1 Centre for Activity and Aging, School of Kinesiology and 3 Department of Physiology, The University of Western Ontario, London, Ontario, Canada N6A 3K7; and 2 Department of Kinesiology, Kansas State University, Manhattan, Kansas 66506-0302
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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This study examined the effect of
heavy-intensity warm-up exercise on O2 uptake
(
O2) kinetics at the onset of
moderate-intensity (80% ventilation threshold), constant-work rate
exercise in eight older (65 ± 2 yr) and seven younger adults
(26 ± 1 yr). Step increases in work rate from loadless cycling to
moderate exercise (Mod1), heavy exercise, and moderate
exercise (Mod2) were performed. Each exercise bout was 6 min in duration and separated by 6 min of loadless cycling.
O2 kinetics were modeled from the onset
of exercise by use of a two-component exponential model. Heart rate (HR) kinetics were modeled from the onset of exercise using a single
exponential model. During Mod1, the time constant (
) for the predominant rise in O2
(O2) was slower (P < 0.05) in the older adults (50 ± 10 s) than in young adults
(19 ± 5 s). The older adults demonstrated a speeding
(P < 0.05) of O2
kinetics when moderate-intensity exercise (Mod2) was
preceded by high-intensity warm-up exercise
(O2, 27 ± 3 s), whereas
young adults showed no speeding of O2
kinetics (O2, 17 ± 3 s).
In the older and younger adults, baseline HR preceding Mod2
was elevated compared with Mod1, but the for HR
kinetics was slowed (P < 0.05) in Mod2
only for the older adults. Prior heavy-intensity exercise in old, but
not young, adults speeded O2 kinetics
during Mod2. Despite slowed HR kinetics in Mod2
in the older adults, an elevated baseline HR before the onset of
Mod2 may have led to sufficient muscle perfusion and
O2 delivery. These results suggest that, when muscle blood
flow and O2 delivery are adequate, muscle O2 consumption in both old and young adults is limited by intracellular processes within the exercising muscle.
aging; heart rate; oxygen transport; oxygen utilization
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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AGING IS
ASSOCIATED WITH a slowing of pulmonary O2 uptake
(O2) kinetics during the on-transition
to a step increase in work rate (WR) of moderate intensity (2, 7,
25), implying that the rate of O2 utilized at the
muscle is also slowed with increasing age. Although it has been
demonstrated that, for older adults, O2
kinetics responses due to exercise in muscles that are chronically active remain similar to those of young adults (8) or
speed toward values seen in young adults as a consequence of chronic exercise training (1), it is unclear whether these
adaptations are a consequence of improved blood flow and/or
O2 delivery or of a faster activation of the biochemical
reactions in muscle, factors that have been implicated as limiting
muscle O2 consumption in young adults (20,
34).
Recently, it was shown in young adults that
O2 kinetics after the start of
heavy-intensity exercise became faster as a consequence of a prior
"warm-up" bout of heavy-intensity exercise, whereas, in contrast,
O2 kinetics during moderate-intensity
exercise were not affected by a warm-up bout of exercise (18,
23). Gerbino et al. (18) argued that the prior bout
of heavy-intensity exercise acted to improve muscle perfusion (rather
than activate muscle biochemical processes), which suggested that
O2 kinetics during moderate-intensity
exercise were not limited by muscle perfusion or muscle O2
delivery in young adults.
The purpose of this study was to examine the effect of heavy-intensity
warm-up exercise on O2 at the onset of a
moderate-intensity, constant-work-rate exercise in older adults. A
group of young adults was also studied for comparison with previous
publications (5, 18, 23). We hypothesized that performing
prior heavy-intensity exercise would speed
O2 kinetics during a subsequent bout of moderate-intensity exercise in the old but not the young adults. This
hypothesis is consistent with the view that
O2 kinetics in older adults are limited
by a slower rate of blood flow redistribution and O2
delivery to the exercising muscle rather than by the rate set by the
oxidative phosphorylation potential.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects.
Eight older adults (Table 1) participated
in this study. Seven young subjects (Table 1) were also studied to
confirm that prior heavy exercise does not speed
O2 kinetics in healthy young subjects,
which has been previously reported (18). Each subject was
informed of all risks associated with participation in the experimental
protocol and provided written consent. This study was approved by The
University of Western Ontario Review Board for Health Sciences Research
Involving Human Subjects.
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Exercise protocol.
Subjects were studied on seven separate occasions at approximately the
same time of the day for each subject. Subjects reported to the
laboratory after consuming only a light meal and abstaining from heavy
exercise and beverages containing caffeine for at least 12 h
preceding the test. Preliminary testing consisted of a ramp exercise
test (10-25 W/min) to volitional fatigue on a electromagnetically braked cycle ergometer (model H-300-R, Lode) for the determination of
the ventilatory threshold (Tvent) and peak
O2
(O2 peak). The highest mean
O2 calculated over a 20-s duration was
taken as O2 peak. The Tvent
was determined by visual inspection and defined as the
O2 at which the ventilatory equivalent
for O2 and end-tidal
PO2 increased systematically with no
concomitant increase in the ventilatory equivalent for CO2
output or decrease in end-tidal PCO2
(12).
O2 equivalent to 80% of the
O2 at the Tvent, and a
heavy-intensity WR was selected to elicit a
O2 corresponding to ~50% of the
difference between the O2 at
Tvent and O2 peak, i.e.,
50% = Tvent + [(O2 peak 
Tvent) × 0.50]. An appropriate lag time
(~30-60 s) between the onset of the ramp forcing function and a
discernable increase in O2 was allowed
for each subject when determining the
O2-WR relationship (13).
During each visit to the laboratory, subjects performed two step
transitions in WR of moderate intensity (Mod1 and
Mod2), which were separated by a step increase in WR of
heavy intensity (i.e., moderate-heavy-moderate-intensity exercise
bouts). Exercise was performed continuously; the duration of each step transition was 6 min, with 6 min of loadless cycling between each exercise transition. The exercise protocol was performed during six
visits to the laboratory, resulting in six repetitions for each subject
and condition (Mod1 and Mod2). In five of the
older subjects, the above protocol was modified so that the
high-intensity exercise bout was preceded by two moderate-intensity
exercise bouts and followed by a single bout of moderate-intensity
exercise. This exercise protocol was performed to establish whether
successive bouts of moderate-intensity exercise would affect
O2 kinetics in older adults.
Materials.
Inspired and expired airflows were measured by using a low-resistance,
low-dead-space (90 ml) bidirectional turbine and volume transducer
(Alpha Technologies, VMM-110). The turbine and volume transducer signal
was calibrated with a syringe of known volume (990 ml) before each
test. Respired gases were sampled continuously at the mouth (1 ml/s)
and analyzed for fractional concentrations of O2,
CO2, and N2 by mass spectrometry (Perkin-Elmer
MGA-1100). The mass spectrometer was calibrated with precision-analyzed
gas mixtures before each test. Analog signals from the mass
spectrometer and turbine transducer were sampled at 50 Hz and stored on
computer for off-line breath-by-breath computations of
O2, CO2 output, ventilation,
and end-tidal PO2 and
PCO2. Gas concentrations were time aligned with
inspired and expired volumes by measuring the time delay for a
square-wave bolus of gas to pass from the turbine to the analysis
system (i.e., mass spectrometer and sampling capillary time delays).
Corrections for breath-by-breath fluctuations in lung gas stores were
made in the computer algorithms (3). Temperature and water
vapor corrections were made for conditions measured near the mouth.
Heart rate (HR) was monitored by use of an electrocardiogram with the
electrodes placed in a modified V-5 configuration.
Data analysis: curve fitting.
The breath-by-breath data obtained during each step increase in WR were
linearly interpolated at 1-s intervals. Each transition was time
aligned and ensemble averaged to provide a single response for each
subject. O2 kinetics were determined by
use of a two-component exponential model
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O2
above loadless cycling (baseline; BSL) at time t, Amp is
amplitude, TD is the time delay, and is the time constant. The
overall time course of the response (i.e., mean response time, MRT) was
calculated from a weighted sum of TD and for each component
![MRT<IT>=</IT>[Amp<SUB>1</SUB><IT>/</IT>(Amp<SUB>1</SUB><IT>+</IT>Amp<SUB>2</SUB>)]<IT>·</IT>(<IT>&tgr;</IT><SUB>1</SUB><IT>+</IT>TD<SUB>1</SUB>)](/content/vol92/issue2/fulltext/609/img002.gif)
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![<IT>+</IT>[Amp<SUB>2</SUB><IT>/</IT>(Amp<SUB>1</SUB><IT>+</IT>Amp<SUB>2</SUB>)]<IT>·</IT>(<IT>&tgr;</IT><SUB>2</SUB><IT>+</IT>TD<SUB>2</SUB>)](/content/vol92/issue2/fulltext/609/img003.gif)
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. The model
parameters were determined by least-squares nonlinear regression in
which the best fit was defined by minimization of the residual sum of squares.
Studies that have used prior heavy-intensity exercise to speed
O2 kinetics have done so when the
subsequent bout of exercise was also high intensity (i.e., above the
Tvent) (18, 23). Because the purpose of the
present study was to examine the effect of prior heavy exercise on
O2 kinetics during a subsequent bout of
moderate-intensity exercise, linear regression analysis was used to
ensure that a steady-state O2 was
achieved during 3-6 min of exercise in each subject consistent
with the exercise being moderate-intensity (i.e., below the
Tvent).
Statistics.
The kinetic parameter estimates for O2
and HR during moderate-intensity exercise were analyzed by using a
two-way ANOVA with one repeated measure (i.e., the moderate-intensity
exercise bouts) and age as the main effect. A significant
F-ratio was further analyzed by using Student-Newman-Keuls
post hoc analysis. Statistical significance was accepted at
P < 0.05. All values are reported as means ± SE.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The physical characteristics and results of the ramp exercise test
for the young and old subjects are presented in Table 1. Although the
exercise protocol could only be repeated four times in one older
subject because of technical difficulties, the exercise response was
not appreciably different from those of the other older subjects. In
the present study, O2 and HR kinetics
were compared during moderate-intensity exercise. The steady-state O2 in this moderate domain of exercise
represented 79 ± 4 and 77 ± 3% Tvent for the
old and young groups, respectively, or as a
%O2 peak corresponded to 46 ± 3 (old) and 42 ± 3% (young). In addition, the slope of the
O2 response between 3 and 6 min of
Mod1 and Mod2 was calculated to confirm that a
steady-state O2 had been achieved and
that a slow component of O2 that is seen
during heavy exercise performed above the Tvent did not exist; the O2 slope (3-6 min) was
not different from 0 for either the old or young subjects during
Mod1 (old, 2 ± 1 ml/min; young, 7 ± 4 ml/min)
or Mod2 (old, 0.1 ± 2 ml/min; young, 4 ± 5 ml/min).
O2 on-kinetics.
The parameter estimates of the kinetic analysis of the
O2 response to prior warm-up exercise
are summarized in Table 2. The
O2 responses for an individual young and
old subject for Mod1 and Mod2 are presented in
Fig. 1. The increase in
O2 above loadless cycling values (i.e.,
Amp1 + Amp2) was lower in the old group
during both Mod1 and Mod2, consistent with the
lower absolute WR. The phase 2 O2
on-transient kinetics (2) and overall on-transient kinetics (MRT) were slower in the old compared with young subjects in
Mod1. In young subjects, the
O2 on-transient kinetics (i.e., 2 or MRT) were similar in Mod1 and
Mod2. In old subjects, however, a prior bout of
heavy-intensity exercise resulted in a significant speeding
(P < 0.05) of O2
on-transient kinetics (both 2 and MRT) during
Mod2 compared with Mod1 to values similar to
those observed in the young group during the on-transitions to
Mod1 and Mod2.
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O2 kinetics after high-intensity
exercise that was observed in the older adults, the change in MRT
(i.e., MRT) from Mod1 to Mod2 was examined
by use of linear regression analysis. As shown in Fig.
2, MRT was significantly correlated
(r = 0.68, P < 0.05) with fitness (as
O2 peak) in the old but not young
subjects. Significance was lost when the older subject who exhibited
the least improvement in MRT was included in the analysis.
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O2 on-transient kinetics were affected
by a prior warm-up bout of moderate-intensity exercise, five older
adults performed two consecutive bouts of moderate-intensity exercise.
No differences were observed in either the Amp (i.e.,
Amp1 + Amp2) or on-transient kinetic
responses for O2 between the initial
(Amp, 205 ± 29 ml/min; 2, 43.1 ± 7.3 s;
MRT, 58.1 ± 4.4 s) and subsequent moderate-intensity exercise bouts (Amp, 211 ± 30 ml/min; 2, 52.5 ± 7.8 s; MRT, 57.6 ± 5.1 s).
HR on-kinetics.
The parameter estimates for the kinetic analysis of the HR response are
presented in Table 3. The individual HR
responses for a young and old subject to a step increase in
moderate-intensity exercise before and after a bout of heavy-intensity
exercise are presented in Fig. 3. During
loadless cycling before Mod1, HR was similar in the old and
young subjects. The baseline HR before the start of Mod2
was elevated in the old (P = 0.06) and young subjects
(P < 0.05) compared with the baseline preceding
Mod1. In the older adults, the HR Amp was similar for both
moderate-intensity exercise trials; the HR Amp was reduced
(P < 0.05) in young adults during Mod2
compared with Mod1. The HR (and MRT) was similar in the
old and young groups during Mod1. However, after
heavy-intensity exercise, the HR (and MRT) for Mod2 was
slowed (P < 0.05) in the old, but not young, adults.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The major new finding of the present study was that in old, but
not young, adults the adaptation of pulmonary
O2 during the on-transition to
moderate-intensity exercise (as determined by the
O2 phase 2 time constant,
2, and the MRT) became significantly faster when
preceded by a bout of heavy-intensity exercise. To our knowledge, this
is the first demonstration of speeding of O2 kinetics at the onset of
moderate-intensity exercise in healthy subjects after an acute
intervention. On the basis of the data from the present study, we
speculate that in healthy, older adults muscle O2
consumption may be limited by inadequate muscle perfusion and/or
O2 delivery, at least initially with no prior warm-up
(i.e., Mod1). However, after a bout of heavy-intensity
exercise, which may improve muscle perfusion and thus provide
sufficient blood flow and O2 delivery (i.e.,
Mod2), activation of biochemical reactions governing
mitochondrial respiration determines the rate for muscle O2
consumption in old adults. In healthy, young adults with relatively fast O2 kinetics (i.e., ~20 s), no
effect was seen with prior heavy-intensity exercise (and presumably
improved muscle perfusion and O2 delivery), suggesting that
in this group the limitation to muscle O2 consumption may
be intrinsic to the muscle.
Aging and O2 kinetics with no prior
warm-up.
The slower O2 on-transient kinetics seen
in old compared with young adults during the initial bout of
moderate-intensity exercise (i.e., Mod1) confirms previous
observations of slowed O2 kinetics in
older adults performing moderate-intensity exercise without adequate
warm-up (2, 4, 7, 8, 11, 25). Although this slower kinetic
response in the elderly may be related to slower activation of key
regulatory enzymes and/or slower provision of substrate to mitochondria
within the active muscle units, we suggest that inadequate muscle
perfusion and/or O2 delivery may limit
O2 at exercise onset under these
conditions. In the present study, although baseline HR before the onset
of Mod1 was similar in young and old adults, the adaptation
of HR during Mod1 tended to be slower in the old (HR,
33 s; MRT, 36 s) than in the young (HR, 22 s; MRT,
18 s) adults, in agreement with others (2, 7, 14)
showing significantly slower HR kinetics during cycling exercise in old
compared with young adults. Although absolute HR and HR kinetics may
not reflect the time course of blood flow changes to or within
exercising muscle, a slower adaptation of HR may contribute to a slowed
rate of increase of cardiac output [because stroke volume probably
changes little from that seen during baseline cycling (~15 W)],
which in turn could result in a slower adaptation of blood flow to the
muscle at exercise onset in the elderly. In addition, it has been shown
recently that aging is associated with a greater femoral vascular
resistance and reduced femoral vascular conductance (15,
16), lower leg blood flow during dynamic exercise
(28), increased sympathetic vasoconstrictor activity
(15), and a reduced ability to shunt blood away from the
splanchnic and renal circulations to muscle during exercise (19). Although it is not known whether the kinetics of
blood flow redistribution within muscle at exercise onset are slowed with aging, these results suggest that the ability to redistribute blood flow to the active muscle units may be impaired in older adults.
O2 kinetics at the onset of
moderate-intensity exercise in both the old and young adults may be
limited by enzyme activation and/or substrate provision within muscle.
In this case, activation of biochemical reactions governing
mitochondrial O2 utilization would be slower in the older
adults, and this slower time course of activation would be speeded by
prior heavy-intensity exercise in the older, but not young, adults as
reflected by faster O2 kinetics during Mod2 compared with Mod1. Whipp and Mahler
(34) proposed that O2
kinetics are determined by intrinsic metabolic factors governing the
utilization of O2 in exercising muscle. Recently, Rossiter et al. (29a) demonstrated a close relationship
between phase 2 pulmonary O2 kinetics
and the kinetics of intramuscular phosphocreatine (PCr) breakdown after
the onset of moderate-intensity exercise in young adults and suggested
that the use of intramuscular PCr concentration changes could serve as
a proxy variable for the kinetics of muscle O2 consumption.
Chilibeck et al. (6) also reported a correspondence
between PCr and pulmonary O2 kinetics in
older adults, although in their study of moderate-intensity plantar-flexion exercise there was no difference comparing old and
young adults in the exercise on-transient kinetics of PCr breakdown or
O2 kinetics. Also, the kinetics of PCr
concentration recovery after exercise have been shown to be either
similar as a function of age (6, 21) or slower in old
compared with young adults (9, 24). With regard to enzyme
activation and substrate provision, Timmons et al. (32)
demonstrated in young adults that activation of the mitochondrial
pyruvate dehydrogenase complex before the start of exercise by
administration of dichloroacetate reduced PCr breakdown and lactate
accumulation, implying that the O2 deficit was reduced and
that muscle O2 consumption was activated more rapidly.
However, a comparison of pyruvate dehydrogenase activation and
O2 kinetics during exercise onset, to
our knowledge, has not been established experimentally for any age
group. In the present study, if muscle enzyme activation and/or
provision of substrate were the primary limitation for muscle
O2 consumption in older adults during the initial bout of
moderate-intensity exercise, then faster
O2 kinetics might have been expected
when moderate exercise was preceded by a bout of either moderate- or heavy-intensity exercise. As shown in this study, repeated bouts of
moderate-intensity exercise did not speed
O2 kinetics in the older subjects, nor
was this seen after a bout of moderate-intensity exercise in young
subjects (18). Thus, although it is possible that a
delayed activation of metabolic events in muscle may contribute to the
slower O2 kinetic response in the old
compared with young adults of this and other studies, data from this
study and from those showing that blood flow redistribution in muscle
may be impaired in the elderly suggest that adaptation of muscle blood flow and/or O2 transport may limit muscle O2
utilization during moderate-intensity exercise in old adults, at least
when exercise is initiated without adequate warm-up.
Aging and O2 kinetics after prior
heavy-intensity warm-up.
The O2 on-transient kinetics during
moderate-intensity exercise (i.e., Mod2) became faster
after a bout of heavy-intensity exercise in old, but not young, adults.
That O2 kinetics in young adults were
not affected by a prior bout of heavy exercise has been demonstrated
previously (5, 18). However, the speeding of pulmonary
O2 on-transient kinetics after a prior
bout of heavy-intensity warm-up exercise, to our knowledge, has not
been previously seen in apparently healthy, older adults, although speeding of pulmonary O2 kinetics was
seen in cardiac transplant recipients performing two bouts of
moderate-intensity exercise (26), and in sedentary older
adults with resting left ventricular diastolic dysfunction performing
moderate-intensity exercise after a 4-h treatment with the
Ca2+-channel blocker verapamil (27). If, as
suggested by Gerbino et al. (18), muscle perfusion and/or
muscle O2 delivery is improved after a prior bout of
heavy-intensity exercise, then the speeding of
O2 kinetics during the second bout of
moderate exercise (i.e., Mod2) may be related to improved
perfusion within muscle before the start of Mod2 but
independent of the adaptation of blood flow and O2 delivery
during the exercise transient. The higher baseline HR immediately
before the onset of Mod2 (HR of 94 beats/min) compared with
Mod1 (HR of 84 beats/min) in this study suggests that
cardiac output (and perhaps muscle blood flow) was elevated before the start of the second moderate-intensity exercise bout. Thus, after the
onset of Mod2, compared with conditions existing before
Mod1, an already elevated muscle blood flow and
O2 transport may have been adequate to support the
requirements for the exercise-induced increase in mitochondrial
respiration and would not be influenced by the additional but slower 10 beats/min increase in HR. In this instance, with adequate blood flow
and O2 transport before the start of Mod2,
activation of muscle O2 consumption at the onset of
moderate-intensity exercise in old (and young) subjects may then be
limited by activation of biochemical reactions governing mitochondrial
O2 utilization. If HR kinetics reflect O2
delivery to the working muscle, independent of the absolute cardiac
output, then the slower HR kinetics seen in Mod2 in the
older adults might predict a further slowing of
O2 kinetics in the older adults. Despite
the slowed HR kinetics, pulmonary O2
kinetics were speeded during Mod2 (relative to
Mod1) in the older adults, consistent with the view that
biochemical processes within the muscle limits the rate of
O2 utilization at the onset of exercise. In support of this
view, Yoshida et al. (35) reported a speeding of
O2 kinetics during repeated bouts of
single-leg cycle ergometer exercise that was independent of cardiac
output and HR kinetics. However, baseline values for both cardiac
output and HR preceding each subsequent bout of exercise appeared to be
higher, thereby allowing for adequate muscle perfusion before the onset
of each subsequent exercise bout. Determination of the actual limiting
factor for muscle O2 consumption during the two bouts of
moderate-intensity exercise in old and young adults requires additional testing.
Effect of fitness on the speeding of
O2 kinetics.
Babcock et al. (1) demonstrated that endurance training in
old adults can lead to faster O2
kinetics at the onset of moderate-intensity exercise that approach
values seen in healthy young adults. Also, Chilibeck et al.
(7) reported that cardiorespiratory fitness was the most
significant predictor of O2 kinetics
(followed by age) in a large group of elderly subjects. Together, these data suggest that cardiorespiratory fitness rather than age per se may
determine O2 kinetics. As shown in Fig.
2, the decrease in MRT from Mod1 to Mod2 was
significantly correlated with fitness (as
O2 peak) in the older adults. Those
older adults having the higher O2 peak
values 1) had O2 kinetics for
the initial exercise bout (i.e., Mod1) that approached
values seen in the young adults and 2) did not demonstrate a
marked speeding of O2 kinetics after the
bout of high-intensity exercise. Also, those subjects who had slowest
O2 kinetics during the initial exercise
bout demonstrated the greatest improvement (i.e., speeding) in
O2 kinetics as a consequence of the
prior bout of heavy-intensity exercise. These observations are
consistent with poor cardiorespiratory fitness, rather than
chronological age per se, being a contributing factor to the slowing of
O2 kinetics in the elderly. The role of
cardiorespiratory fitness vs. aging in the speeding of
O2 kinetics after a bout of
heavy-intensity exercise awaits further investigation in a
significantly larger group of subjects with a wider range of ages and
fitness levels.
HR kinetics.
Baseline HR before the start of Mod1 was similar in old and
young adults. After the onset of Mod1, the increase in HR
above baseline was lower in old compared with young subjects, whereas the time constant () for heart kinetics tended to be slower in old
compared with young adults. HR kinetics in old adults have been shown
to be either slower (8, 11) or similar to (2, 7,
14) those of young adults. Although statistical significance for
HR kinetics was not achieved in the present study, perhaps explained by
the large intersubject variability observed in this and other studies
(e.g., Ref. 7), the tendency for slower HR kinetics in the
older group during Mod1 (, ~10 beats/min; MRT, ~20
beats/min) may be physiologically significant with respect to the time
course of blood flow adaptation in the older adults. The smaller
increase in HR observed in the old compared with the young adults
performing the same relative exercise intensity was expected during
dynamic exercise (8, 22, 30) and may reflect an
age-related reduction in either resting cardiac vagal tone (31) or 
-adrenergic-receptor sensitivity (10,
33).
O2 after the onset of
moderate-intensity exercise became faster in old, but not young, adults
after a prior bout of heavy-intensity exercise. The results of the
present study indicate that, in the absence of adequate warm-up
exercise, pulmonary O2 kinetics are
slower in old compared with young adults, which may be a consequence of
a slower rate of muscle blood flow redistribution and/or O2
delivery within the exercising muscle of the older adult, although the
alternate possibility of a slower rate of activation of metabolic
enzymes and substrate provision cannot be discounted. After a warm-up
bout of heavy-intensity exercise in old, but not young, adults,
pulmonary O2 kinetics were speeded and
were similar to values seen in young adults. In this instance, with
adequate muscle perfusion and O2 delivery (as reflected by
the elevated baseline HR), the limitation to muscle O2
consumption in both old and young adults may reside within the muscle
at the level of biochemical processes controlling O2 utilization.
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ACKNOWLEDGEMENTS |
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We thank the participants who took part in this study. The technical support offered by Brad Hansen and Timothy Wilson was greatly appreciated.
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FOOTNOTES |
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Financial support was provided to J. M. Kowalchuk by an operating grant from the Natural Sciences and Engineering Research Council of Canada (NSERC). B. W. Scheuermann was supported by a NSERC Doctoral Fellowship. This research was carried out at The Centre for Activity and Aging (affiliated with the Faculty of Health Sciences, School of Kinesiology and the Faculty of Medicine at The University of Western Ontario and The Lawson Research Institute at the St. Joseph's Health Centre).
Present address of B. W. Scheuermann: Dept. of Kinesiology, 8 Natatorium, Kansas State University, Manhattan, KS 66506-0302.
Address for reprint requests and other correspondence: J. M. Kowalchuk, Centre for Activity and Aging, School of Kinesiology, Univ. of Western Ontario, London, ON, Canada N6A 3K7 (E-mail: jkowalch{at}uwo.ca).
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.
10.1152.japplphysiol.00186.2001
Received 23 February 2001; accepted in final form 5 October 2001.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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) and younger (
) adults. Dashed
line line represents results for linear regression analysis for all
older subjects. When the older subject that showed the smallest change
in MRT from Mod1 to Mod2 was excluded from the
analysis, the relationship between the decrease in MRT was inversely
related to fitness in the older adults.
