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Department of Medicine, University of California, San Diego, La Jolla, California 92093-0623
Submitted 19 February 2003 ; accepted in final form 28 April 2003
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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O2 max), a
thermal dilution technique was used in conjunction with arterial and venous
femoral blood sampling in six sedentary young (19.8 ± 1.3 yr) and six
sedentary old (66.5 ± 2.1 yr) males during incremental knee extensor
exercise (KE). Young and old attained a similar maximal KE work rate
(WRmax) (young: 25.2 ± 2.1 and old: 24.1 ± 4 W) and
QO2 max
(young: 0.52 ± 0.03 and old: 0.42 ± 0.05 l/min). QMBF during KE
was lower in old subjects by 
500 ml/min across all work rates, with old
subjects demonstrating a significantly lower QMBF/W (old: 174 ± 20 and
young: 239 ± 46 ml · min–1 ·
W–1). Although the vasodilatory response to
incremental KE was 142% greater in the old (young: 0.0019 and old: 0.0046
mmHg · min · ml–1 ·
W–1), consistently elevated leg vascular
resistance (LVR) in the old, 80% higher LVR in the old at 50% WR and
40% higher LVR in the old at WRmax (young: 44.1 ± 3.6
and old: 31.0 ± 1.7 mmHg · min ·
ml–1), dictated that during incremental
KE the LVR of the old subjects was never less than that of the young subjects.
Pulse pressures, indicative of arterial vessel compliance, were 36%
higher in the old subjects across all work rates. In conclusion, well-matched
sedentary young and old subjects with similar quadriceps muscle mass achieved
a similar WRmax and
QO2 max during
incremental KE. The old subjects, despite a reduced QMBF, had a greater
vasodilatory response to incremental KE. Given that small muscle mass
exercise, such as KE, utilizes only a fraction of maximal cardiac output,
peripheral mechanisms such as consistently elevated leg vascular resistance
and greater pulse pressures appear to be responsible for reduced blood flow
persisting throughout graded KE in the old subjects.
vascular resistance; quadriceps; pulse pressures; O2 conductance
Studies (3,
35,
49) of whole body exercise
have documented 20–30% lower blood flow during cycle exercise in
elderly males (55–74 yr). Poole et al.
(33) recently reported that
old sedentary subjects (69.3 ± 2.0 yr) had an increasing blood flow
deficit in comparison with young control subjects during cycle exercise from
50% of the maximal work rate (WRmax). Conversely, small muscle
mass experiments have shown preserved perfusion in recreationally active older
males. Specifically, similar blood flows were recorded in active young and a
wide range of active middle-aged to old (44–69 yr) males during
one-legged exercise (26), and
similar perfusion and vasodilatory capacity were reported in older
(60–74 yr) subjects immediately after dynamic handgrip exercise
(21). Together, these findings
suggest that in aging populations, blood flow to skeletal muscle is limited by
central factors and is therefore preserved during small muscle mass exercise.
Casting doubt on these interpretations are data indicating that many
peripheral vascular and metabolic factors decline with age, such as decreased
reactivity to infused vasodilatory stimuli
(9) and increased pulse
pressures indicative of arterial vessel stiffening
(8). Given that blood flow
regulation has been reported to match oxygen demand and local metabolic
requirements of skeletal muscle
(2), others have implicated
factors such as attenuated muscle mass that leads to reduced metabolic demand
from chronically inactive muscle
(13), decreased mitochondrial
density, reduced oxidative capacity
(7), and reduced citrate
synthase activity (6) for the
attenuated skeletal muscle blood flow with age.
The relative contributions of central versus peripheral factors in
modulating blood flow are still contested, and both systems are known to
decline with age. Therefore, the purpose of this study was to use the knee
extensor exercise (KE) modality to study isolated dynamically exercising
skeletal muscle in both young and old subjects, thereby investigating the
consequences of aging on quadriceps muscle blood flow (QMBF) without the
contribution of central factors. Specifically, we had several hypotheses.
First, old subjects will demonstrate attenuated skeletal muscle blood flow,
increased leg vascular resistance, and decreased vasodilatory capacity due to
an age-related decline in vascular function. Second, for any given submaximal
WR, maximum quadriceps O2 consumption
(QO2 max) will
be similar for young and old subjects. Third, the reduced peripheral blood
flow will result in either a compensatory increase in arterialvenous (A-V)
O2 difference or a reduction in WRmax and muscle
QO2 max in the
old.
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METHODS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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O2 max in both
groups (Table 1). Health
histories and physical examinations were completed. Subjects were not allowed
to participate if they were found to be taking any medications that would
alter blood flow responsiveness. Informed consent was obtained according to
the University of California-San Diego Human Subjects Protection Program
requirements.
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Exercise modality and exercise protocol. Single-leg KE was performed that limited work to the quadriceps muscle group, as originally described by Andersen and Saltin (1), and more recently documented by Richardson et al. (38). The ergometer was adjusted so that contraction of the quadriceps muscles turned a flywheel producing a 90°-170° arc of the lower leg. To provide progressive levels of resistance to the quadriceps muscle, tension was incremented by increasing friction on a belt surrounding the flywheel as a percentage of WRmax until the subject could no longer maintain a contraction frequency of 1 Hz. Subjects were allowed sufficient practice during preliminary testing to familiarize with the exercise equipment, ensuring that maximal effort was achieved during the catheter study day. At each WR, data collection proceeded as follows: 1) the subjects were allowed to attain an equilibrium at the given WR, 2) blood samples (3 ml each) were taken from the arterial and venous catheters, 3) blood flow measurements were made, 4) blood sampling and blood flow measurements were repeated, 5) blood pressure readings were taken, and 6) the subject was challenged with the next WR.
Surgical procedures. Several days after the familiarization and
preliminary testing, subjects returned to undergo the catheter-based study.
Two catheters (model DSA 400L, Cook; Bloomington, IN) were inserted: one in
the femoral artery and the second in the femoral vein. In addition, a
thermocouple (model IT-18, Physitemp Instruments; Clifton, NJ) was placed in
the femoral vein 10 cm proximal to the tip of the venous catheter. All
were inserted with the use of a sterile technique as previously described
(40) to facilitate blood
sampling and the thermodilution blood flow measurement technique.
Leg blood flow, heart rate, and blood pressure. QMBF was measured
by the thermodilution technique during KE as previously described
(2,
16). Measured blood flow
during KE is accepted as a close approximation of QMBF by reason that blood is
directed toward working muscle, and the quadriceps muscles are the sole
working muscle mass of the leg during KE
(36,
40). Thermistors connected to
two digital thermometers (model IT-18, Physitemp Instruments) interfaced to a
personal computer (Biopac Systems; Santa Barbara, CA) measured both venous and
infusate temperatures during 15-s saline infusions. QMBF data were
collected after a metabolic steady state was achieved at each WR (2–4
min depending on the exercise intensity) and was calculated using a
heat-balance equation (1).
Heart rate was obtained from a three-lead electrocardiogram signal (Lifepak
9A, Lifeline; Santa Barbara, CA). Femoral arterial and venous blood pressures
in the inguinal region were continuously monitored with the use of pressure
transducers raised to the level of the heart (model PX-MK099, Baxter). Mean
arterial pressure (MAP) and mean venous blood pressures (MVP) were computed by
integration of each pressure curve. Leg vascular resistance was calculated as
(MAP – MVP)/QMBF. Pulse pressures were calculated as systolic –
diastolic pressure.
Blood analyses. Total hemoglobin ([Hb]) and blood O2
saturation were determined spectrophotometrically with a CO-oximeter (model
IL-682, Clayton). Hematocrit, PO2,
PCO2, and pH were determined with a blood gas analyzer
(IL-Synthesis, Clayton), and the data were temperature corrected to match each
subject's body temperature at each WR. Blood lactate concentration was
measured with the use of a lactate analyzer (YSI 2300 Stat Plus, Yellow
Springs). Concentration of arterial oxygen (in ml/dl)
(CaO2) was calculated as 1.39 x [Hb] x
O2 saturation + 0.003 x PO2.
QO2 max was
calculated as the product of the mean QMBF and the O2 difference
between the femoral artery and vein (CaO2 –
CvO2). Muscle O2 delivery was calculated as
the product of QMBF and CaO2. P50 was
calculated as the PO2 at which Hb saturation was equal
to 50% using the equation from Perego et al.
(32). Net venous lactate
outflow, representative of the lactate efflux from the quadriceps muscle, was
calculated as the product of QMBF and [arterial lactate] – [venous
lactate].
Estimate of mean capillary PO2 and diffusional
conductance. A Bohr integration technique was used to calculate an
estimate of mean capillary PO2
(PcaPO2) and diffusional conductance
(DmO2) at WRmax. PcaPO2
was calculated as described previously
(47) as the numerical average
of all PO2 values computed equally spaced in time along
the capillary as it traverses the muscle bed from the arterial to venous end.
This technique has been discussed in detail elsewhere
(17,
41) based on a proposal by
Wagner (48) with the
assumption of a homogeneously perfused muscle. Briefly, the drop in
PO2 along a capillary is calculated using Fick's law of
diffusion (Eq. 1)
 | (1) |
Thigh volume measurement. With the use of thigh length, circumference, and skinfold measurements, thigh volume was calculated to allow an estimate of quadriceps femoris muscle mass, as suggested by Jones and Pearson (22), and utilized originally by Andersen and Saltin (2).
Statistical analysis. Data were analyzed post hoc with the use of
regression analysis with paired and unpaired t-tests. Statistics were
performed with the use of commercially available software (GraphPad, San
Diego, CA, and SPSS Software, version 10.1). The data were subjected to a
power analysis resulting in a 
-value 
0.8 in the majority of
variables (e.g., QO2
max, = 0.74). All data are expressed as means ± SE.
Significance was established at a 
-level of P 
0.05.
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RESULTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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O2 max (young:
31.6 ± 2.3 and old: 20.3 ± 1.8 ml ·
min–1 · kg–1).
In contrast, during small muscle mass KE, the young and old subjects were
equally matched in terms of quadriceps WRmax (young: 27.0 ±
2.5 W and old: 24.1 ± 4.0 W; Table
2).
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QMBF and vascular pressures. QMBF was initially lower in the old
subjects, yet the aging subjects showed a greater vasodilatory response to
incremental KE (Fig.
1A and
2C). Specifically, at
the initial WR (3.6 W), QMBF was attenuated in the old (old: 958 ±
52 ml/min and young: 1,711 ± 143 ml/min). While the quadriceps muscles
were challenged by progressive increases in KE WR, the corresponding increase
in QMBF per watt (115 ml · min–1
· W–1) was not different between young and
old subjects (Fig.
1A). Although the vasodilatory response to incremental KE
(change in vascular resistance per watt) was 142% greater in the old
(Fig. 2C), at no point
was this response sufficient to overcome the elevated initial LVR in the old,
as LVR remained 80% higher in the old at WR-50%, and 40% higher at
WRmax (young: 30.1 ± 1.7 mmHg/ml and old: 44.1 ± 3.6
mmHg/ml; Fig. 2C). MAP
was not different between young and old subjects at maximal KE. The driving
force on blood across the muscle bed (MAP–MVP) was not different between
young and old subjects throughout incremental KE, and both groups showed a
similar and gradual increase in A-V pressure with increasing work
(Fig. 2A). Pulse
pressures, a measure of arterial vessel compliance, were 36% higher in
the old subjects, and the rate of increase throughout incremental KE was
similar in both groups (Fig.
2B).
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Leg oxygen consumption. At each incremental WR,
QO2 max was
slightly reduced in the old subjects, which did not achieve statistical
significance, and was more apparent at WRs <50% of WRmax.
Although not statistically significant, the old subjects tended toward a lower
y-intercept (young: 0.13 ± 0.02 l/min and old: 0.05 ±
0.01 l/min; Fig. 1B).
Both groups revealed a similar rise in
QO2 max per
watt (slope: young, 0.014 ± 0.001; and old, 0.018 ± 0.002 l
· min–1 ·
W–1, Fig.
1B). Finally, both groups achieved similar
QO2 max values
(young: 0.52 ± 0.03 l/min and old: 0.42 ± 0.05 l/min;
Table 2).
A-V O2 difference. Elevated A-V O2 difference was recorded in the old subjects at 3.6 W (young: 11.1 ± 0.8 ml/dl and old: 12.8 ± 1.0 ml/dl), more clearly illustrated by the increased y-intercept (young: 10.7 ± 0.73 ml/dl and old: 12.9 ± 0.68 ml/dl; Fig. 1C). Similar to the increasing A-V O2 seen in trained athletes, younger subjects increased O2 extraction as the wattage was incremented during KE. Although not statistically different from that of the young, the old subjects revealed a more constant A-V O2 difference (slope: young, 0.045 ± 0.01; old, 0.046 ± 0.02 ml · dl–1 · W–1; Fig. 1C).
Major blood-related variables. Arterial PO2, O2 saturation, [Hb], and therefore, arterial O2 content were not different between young and old. O2 delivery was not different between young and old, as the lower blood flow in the old was compensated for by a tendency toward elevated CaO2. Net venous lactate outflow, a marker of relative stress, rose exponentially with increasing work and was not different between young and old across all WRs and at WRmax (Table 2). PcapO2 and DmO2 were similar between the young and old.
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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500 ml/min) in
old sedentary subjects when compared with young sedentary subjects of similar
quadriceps muscle mass. Second, LVR was elevated in the old throughout KE,
and, as the driving force on blood across the muscle bed (A-V pressure) was
similar for both groups, elevated LVR was responsible for reduced QMBF in the
old subjects. Third, the vasodilatory response to incremental KE (fall in LVR
W–1) was elevated in the old subjects, indicating
that the vasodilatory pathways activated in response to incremental KE are
capable of producing a greater change in LVR from the initial WR of 3 W to
WRmax. These changes, however, were insufficient to overcome the
initially elevated LVR in the old subjects, who therefore always had a greater
absolute LVR than the young subjects. Finally, old and young sedentary
subjects of equal quadriceps muscle mass achieved similar WRmax and
QO2 max during
small muscle mass KE. During cycle exercise, the old subjects revealed lower
WRmax and pulmonary
O2 max,
indicating an age-related central limitation to maximal whole body exercise.
When taken together, these findings indicate that when central limitations are
minimized during small muscle mass KE, peripheral factors usually associated
with declining vascular function, including elevated LVR, elevated pulse
pressures, and reduced QMBF persist in the old subjects throughout KE. Perhaps
in compensation for the initially reduced QMBF and elevated LVR, the old
subjects revealed a greater vasodilatory response to incremental KE, which,
when coupled with the elevated A-V O2 difference documented in the
old subjects, facilitate the attainment of equal O2 uptake and
power output to the young subjects during maximal isolated skeletal muscle
exercise.
Attenuated QMBF in old subjects throughout KE. QMBF was
consistently lower (500 ml/min) in the old subjects during KE. These data
differ from previous findings obtained with a similar KE model that revealed
similar perfusion between young and middleaged to older subjects
(26). This disparity in
findings is perhaps explained by the difference in age range and activity
levels between the subjects in Magnusson's study compared with the present
research. Whereas Magnusson studied a wide range (44–69 yr) of
middleaged to old men who were regularly physically active, the current study
focused on sedentary old subjects (66 ± 2.5 yr).
Findings from the current study also revealed that at maximal KE, older subjects have attenuated QMBF. This is not in agreement with the data presented by Jasperse et al. (21), who reported similar perfusion between young and old subjects immediately after submaximal and maximal dynamic handgrip exercise. The subjects in the Jasperse study were reported to be "chronically physically active" possibly increasing forearm vascular conductance and accounting for the similarities in conductance and the equalization of blood flow. On the basis of mounting evidence implicating endurance exercise in modifying certain aspects of vascular function, such as improved vessel compliance (46) and improved vascular reactivity to infused pharmacological agents (9), one should use caution when comparing data from trained subjects and sedentary subjects. In addition, blood flow measurements presented by Jasperse et al. (21) were made directly after each level of exercise and may not be representative of the pathways controlling blood flow that are activated during dynamic exercise. It is also possible that the vasculature in the upper and lower extremities respond differently to the aging process.
The current data, however, are in accordance with previous studies
(23,
49) that have documented
reductions in skeletal muscle blood flow in aging subjects during exercise. In
a related study from our laboratory, Poole et al.
(33) reported an attenuated
increase in blood flow to leg muscles in sedentary aging subjects during whole
body cycle exercise from 50% of WRmax to WRmax,
suggestive of a progressive maldistribution of blood flow with increasing
exercise intensity, which was responsible for the attenuated leg blood flow in
the old subjects. If central limitations were solely responsible for reduced
muscle perfusion during cycle exercise in the old, it would be expected that
when these central limitations are minimized (as in KE) perfusion in the old
subjects should reach equal values to young subjects at the same WR. The
finding of a lower QMBF suggests that in the old subjects, peripheral vascular
limitations during isolated small muscle mass exercise persist and are
responsible for the attenuated blood flow in the old subjects. Possible
mechanistic explanations for these observations may be the previously
documented augmentation of -adrenergic vasoconstriction
(11) and/or the decreased
ability of insulin to alter blood flow to skeletal muscle
(30). Although resting QMBF
data were not collected in the current study, we cannot discount the
possibility that low resting QMBF resulting from attenuated vasodilatory
factors at rest in the old subjects (e.g., nitric oxide via an endothelial
nitric oxide synthase mechanism) may persist during exercise and may be
responsible for the consistently attenuated QMBF recorded throughout
incremental KE (12,
15,
50).
Elevated LVR and pulse pressures in old subjects. The driving
force on blood through the muscle bed (MAP – MVP) was not different in
the old subjects. Similarly, MAP at WRmax was not different between
young and old. LVR was elevated in the old subjects throughout incremental KE
and is therefore responsible for decreased QMBF in the old subjects. LVR is
largely determined by two age-dependent factors, arteriolar cross-sectional
area, and compliance of the arterial wall. Previous studies have documented
multiple factors that contribute to elevated vascular resistance in aging
populations, including decreased arterial and arteriolar diameter as a result
of arterial wall thickening
(10), arterial stiffening
(25), insulin resistance
(30), age-related reductions
in tonic nitric oxide-mediated vasodilation
(31,
44), and increases in
endothelin-1-mediated vasoconstriction
(4). Offering further
mechanistic insight into elevated LVR in the old are the elevated pulse
pressures seen throughout KE. Elevated pulse pressures are indicative of large
artery stiffness (8,
25) and decreased vessel
conductance both leading to reduced QMBF. These findings of elevated pulse
pressures in the old are supported by research presented by Dinenno et al.
(10), who concluded that
age-associated femoral arterial wall thickening was due to increased
-adrenergic vasoconstriction. In addition, Kass et al.
(24) implicated glycation end
products and their interference with long-lived arterial collagen and elastin
fibers as a mechanism underlying age-associated vessel wall stiffening.
Greater reduction in LVR to graded KE in old subjects. Our findings of increased vasodilatory response to KE in the old subjects are in accordance with studies conducted by Jasperse et al. (21), which revealed greater peak increases in forearm vascular conductance in the old subjects. Because the vasodilatory pathways are responding more dramatically in old subjects, it appears that a basal limitation to QMBF is continually and equally dampening the vasodilatory efforts of the smooth muscle reactive pathways across all WRs (Fig. 2C). Because the old subjects begin with a high LVR, it is perhaps simply by necessity that they have a greater reduction in LVR than the young subjects, permitting the required blood flow response to achieve an equal WRmax.
The present data, documenting an increased vasodilatory response to incremental KE (Fig. 2C), may at first appear to conflict with the findings of several other research groups who have reported age related declines in endothelium-dependent vasodilation (5, 9, 45). However, it must be remembered that much of this research has been performed at rest when the role of the endothelium in mediating vasodilation may be most significant. During exercise, as in the current study, diminished endothelial function may be overcome by other vasodilatory mechanisms such as metabolite concentrations. In addition, when data presented by DeSouza et al. (9) are examined more closely, it appears that from baseline to the intra-arterial infusion of 1 µg ACh/100 ml tissue that there is a difference between the vasodilatory response in young and old. However, from this point on, the slopes of the two lines (change in conductance per microgram of ACh infusion) are remarkably similar for young and old subjects suggestive of similar vasodilatory capabilities in young and old subjects. This result was not recognized in the study by DeSouza et al. (9). Although resting pharmacological intervention studies have contributed significantly to the current understanding of blood flow regulation by offering a specific insight into select pathways, they may produce different results from the current study because they are designed to evoke responses from a specific pathway from the many regulatory mechanisms that may govern blood flow during exercise and cannot account for the complex combination of mechanical and metabolic changes that influence vascular resistance during exercise. Finally, studies involving dynamic muscle contraction reveal how muscle blood flow is affected by the combination of naturally occurring stimuli in a situation much more akin to those occurring in everyday life, and, in such a scenario, the older subjects do not reveal a diminished vasodilatory response to incremental KE (Fig. 2C).
Limitations to maximal exercise. A hallmark of the aging process
appears to be a fall in maximal exercise capacity
(3,
33,
35). Although this attenuation
of maximal exercise was apparent in the current subjects during the
prescreening bicycle exercise testing
(Table 1), when exercise was
isolated to a relatively small muscle mass in the form of KE, the difference
between young and old was lost. In support of these findings, variables
reflecting relative stress, such as venous lactate outflow and pH, were nearly
identical between young and old subjects during submaximal and maximal KE
(Table 2). These findings are
in agreement with Jasperse et al.
(21), who documented a similar
WRmax in young and old physically active males during small muscle
mass dynamic handgrip exercise. However, it should be recognized that a
statistical analysis of
QO2 max
revealed marginally acceptable power = 0.74 and a P value of
0.14 (two-tailed paired t-test). Thus the potential of a type II
error as a consequence of the limited sample size cannot be ruled out.
In terms of convective O2 transport, the old subjects
demonstrated a consistently reduced QMBF, but the tendency toward an elevated
CaO2 resulted in a similar O2 delivery in the
young and old subjects. Thus both the young and old achieved the same
WRmax, A-V O2 difference, and
QO2 max. These
findings are starkly different from the 30% reduction in both WRmax
and pulmonary O2
max exhibited by the same old subjects during the bicycle exercise
test. These data suggest a central limitation in aging persons resulting in
disparities between young and old subjects during centrally taxing exercise
(e.g., maldistribution of cardiac output), which are resolved during a small
dynamic muscle mass exercise such as KE.
When the diffusional component of O2 transport is assessed by
the calculation of a normoxic DmO2, the young and old
subjects appear similar in terms of the movement of O2 from blood
to muscle cell (Fig. 3).
Recently published data (33)
collected in our laboratory during maximal cycle exercise in nine sedentary
young and nine sedentary old subjects revealed a significantly lower maximal
quadriceps muscle DmO2, pulmonary
O2 max, and
QO2 max in the
old subjects. It is possible that the decreased DmO2 and
QO2 max
reported during cycle exercise results from central limitations (e.g.,
inappropriate distribution of a finite cardiac output) that are not present
when the quadriceps muscle bed is now the sole muscle with high metabolic
demand. It is noteworthy that both the young and old subjects show a greatly
reduced DmO2 compared with data collected from young
endurance trained subjects performing KE in our laboratory (37;
Fig. 3). These findings suggest
that both DmO2 and
QO2 max are
much more strongly associated with a sedentary lifestyle rather than simply
age.
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The finding of similar quadriceps mass, WRmax, and
QO2 max
appears to disagree with reports that normal aging brings about a general
reduction in muscle mass of up to 25–30% by age 70
(6,
13,
42) and a concomitant
30–40% reduction in muscle strength
(34). In addition, others have
shown 50% lower oxidative capacity per unit volume resulting from
decreased ATP per mitochondria recorded during MRI twitch studies
(7) and decreased muscle
metabolic capacity, as represented by an age-related decline in pulmonary
O2 max,
citrate synthase, and phosphocreatine
(28). On the basis of these
latter findings, it would be expected that for a similar muscle mass, aging
subjects should have 50% lower WRmax and
QO2 max.
Perhaps resolving this disparity are studies showing that typically persons
>50 years of age remain the most sedentary segment of the population, with
persons >70 years of age being extreme examples of this inactive group
(43), and that this
progressive decline in activity level causes the concomitant fall in strength,
blood flow, metabolic capacity, etc. Typically, young sedentary volunteers are
most likely more active than their older counterparts due to daily routine and
leisure activities, tending to magnify the apparent aging effect. The subject
selection criteria for this study were strict and many young subjects were
rejected for participation in any exercise, even if only on an occasional
recreational basis.
In summary, six equally matched sedentary young and old subjects who
differed significantly in terms of maximal cycle exercise capacity achieved
similar QO2
max and WRmax when tested during KE. Submaximally, the
old subjects revealed an elevated A-V O2 difference, and attenuated
QMBF, yielding a similar
QO2 max to the
young subjects across all WRs. Elevated LVR is likely responsible for the
attenuation in QMBF in the old subjects and may be the result of factors
present at rest, which persist during incremental KE, such as decreased
arterial cross-sectional area, decreased vasodilatory stimuli, such as
endothelial nitric oxide, increased -adrenergic vasoconstriction, and
decreased arterial compliance resulting in increased pulse pressures that
contribute to the obstruction of blood flow in the old subjects. However,
these differences did not hinder the vasodilatory response to incremental KE
(measured as a change in LVR per watt), which was greater in the older
subjects. In addition, diffusional O2 transport in this small
muscle mass condition appeared to be uncompromised in the old subjects.
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DISCLOSURES |
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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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.
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  D. W. Trott, F. Gunduz, M. H. Laughlin, and C. R. Woodman Exercise training reverses age-related decrements in endothelium-dependent dilation in skeletal muscle feed arteries J Appl Physiol, June 1, 2009; 106(6): 1925 - 1934. [Abstract] [Full Text] [PDF]
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 B. S. Kirby, W. F. Voyles, C. B. Simpson, R. E. Carlson, W. G. Schrage, and F. A. Dinenno Endothelium-dependent vasodilatation and exercise hyperaemia in ageing humans: impact of acute ascorbic acid administration J. Physiol., May 1, 2009; 587(9): 1989 - 2003. [Abstract] [Full Text] [PDF]
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 D. W. Wray, S. K. Nishiyama, A. Monnet, C. Wary, S. Duteil, P. G. Carlier, and R. S. Richardson Multiparametric NMR-Based Assessment of Skeletal Muscle Perfusion and Metabolism During Exercise in Elderly Persons: Preliminary Findings J Gerontol A Biol Sci Med Sci, April 17, 2009; (2009) glp044v1. [Abstract] [Full Text] [PDF]
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 D. W. Wray, S. K. Nishiyama, and R. S. Richardson Role of {alpha}1-adrenergic vasoconstriction in the regulation of skeletal muscle blood flow with advancing age Am J Physiol Heart Circ Physiol, February 1, 2009; 296(2): H497 - H504. [Abstract] [Full Text] [PDF]
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K. F. Herspring, L. F. Ferreira, S. W. Copp, B. S. Snyder, D. C. Poole, and T. I. Musch Effects of antioxidants on contracting spinotrapezius muscle microvascular oxygenation and blood flow in aged rats J Appl Physiol, December 1, 2008; 105(6): 1889 - 1896. [Abstract] [Full Text] [PDF]
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S. K. Nishiyama, D. W. Wray, and R. S. Richardson Aging affects vascular structure and function in a limb-specific manner J Appl Physiol, November 1, 2008; 105(5): 1661 - 1670. [Abstract] [Full Text] [PDF]
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 D. W. Wray, S. K. Nishiyama, R. A. Harris, and R. S. Richardson Angiotensin II in the Elderly: Impact of Angiotensin II Type 1 Receptor Sensitivity on Peripheral Hemodynamics Hypertension, June 1, 2008; 51(6): 1611 - 1616. [Abstract] [Full Text] [PDF]
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R. E. Carlson, B. S. Kirby, W. F. Voyles, and F. A. Dinenno Evidence for impaired skeletal muscle contraction-induced rapid vasodilation in aging humans Am J Physiol Heart Circ Physiol, April 1, 2008; 294(4): H1963 - H1970. [Abstract] [Full Text] [PDF]
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B. A. Parker, S. L. Smithmyer, J. A. Pelberg, A. D. Mishkin, and D. N. Proctor Sex-specific influence of aging on exercising leg blood flow J Appl Physiol, March 1, 2008; 104(3): 655 - 664. [Abstract] [Full Text] [PDF]
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M. D. Delp, B. J. Behnke, S. A. Spier, G. Wu, and J. M. Muller-Delp Ageing diminishes endothelium-dependent vasodilatation and tetrahydrobiopterin content in rat skeletal muscle arterioles J. Physiol., February 15, 2008; 586(4): 1161 - 1168. [Abstract] [Full Text] [PDF]
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L. H. Chung, D. M. Callahan, and J. A. Kent-Braun Age-related resistance to skeletal muscle fatigue is preserved during ischemia J Appl Physiol, November 1, 2007; 103(5): 1628 - 1635. [Abstract] [Full Text] [PDF]
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D. W. Wray, S. K. Nishiyama, A. J. Donato, M. Sander, P. D. Wagner, and R. S. Richardson Endothelin-1-mediated vasoconstriction at rest and during dynamic exercise in healthy humans Am J Physiol Heart Circ Physiol, October 1, 2007; 293(4): H2550 - H2556. [Abstract] [Full Text] [PDF]
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F. Pinaud, A. Bocquet, O. Dumont, K. Retailleau, C. Baufreton, R. Andriantsitohaina, L. Loufrani, and D. Henrion Paradoxical Role of Angiotensin II Type 2 Receptors in Resistance Arteries of Old Rats Hypertension, July 1, 2007; 50(1): 96 - 102. [Abstract] [Full Text] [PDF]
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 D. C. Poole and L. F. Ferreira Muscle-energetic and cardio-pulmonary determinants of exercise tolerance in humans: Oxygen exchange in muscle of young and old rats: muscle-vascular-pulmonary coupling Exp Physiol, March 1, 2007; 92(2): 341 - 346. [Abstract] [Full Text] [PDF]
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A. J. Donato, L. A. Lesniewski, and M. D. Delp Ageing and exercise training alter adrenergic vasomotor responses of rat skeletal muscle arterioles J. Physiol., February 15, 2007; 579(1): 115 - 125. [Abstract] [Full Text] [PDF]
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B. J. Behnke, R. D. Prisby, L. A. Lesniewski, A. J. Donato, H. M. Olin, and M. D. Delp Influence of ageing and physical activity on vascular morphology in rat skeletal muscle J. Physiol., September 1, 2006; 575(2): 617 - 626. [Abstract] [Full Text] [PDF]
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A. J. Donato, A. Uberoi, D. W. Wray, S. Nishiyama, L. Lawrenson, and R. S. Richardson Differential effects of aging on limb blood flow in humans Am J Physiol Heart Circ Physiol, January 1, 2006; 290(1): H272 - H278. [Abstract] [Full Text] [PDF]
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F. A Dinenno, S. Masuki, and M. J Joyner Impaired modulation of sympathetic {alpha}-adrenergic vasoconstriction in contracting forearm muscle of ageing men J. Physiol., August 15, 2005; 567(1): 311 - 321. [Abstract] [Full Text] [PDF]
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K. E. Eklund, K. S. Hageman, D. C. Poole, and T. I. Musch Impact of aging on muscle blood flow in chronic heart failure J Appl Physiol, August 1, 2005; 99(2): 505 - 514. [Abstract] [Full Text] [PDF]
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D. S. DeLorey, J. M. Kowalchuk, and D. H. Paterson Adaptation of pulmonary O2 uptake kinetics and muscle deoxygenation at the onset of heavy-intensity exercise in young and older adults J Appl Physiol, May 1, 2005; 98(5): 1697 - 1704. [Abstract] [Full Text] [PDF]
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D. N. Proctor, K. U. Le, and S. J. Ridout Age and regional specificity of peak limb vascular conductance in men J Appl Physiol, January 1, 2005; 98(1): 193 - 202. [Abstract] [Full Text] [PDF]
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S. E Bearden, G. W Payne, A. Chisty, and S. S Segal Arteriolar network architecture and vasomotor function with ageing in mouse gluteus maximus muscle J. Physiol., December 1, 2004; 561(2): 535 - 545. [Abstract] [Full Text] [PDF]
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D. R. Seals and F. A. Dinenno Collateral damage: cardiovascular consequences of chronic sympathetic activation with human aging Am J Physiol Heart Circ Physiol, November 1, 2004; 287(5): H1895 - H1905. [Abstract] [Full Text] [PDF]
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S. A. Spier, M. D. Delp, C. J. Meininger, A. J. Donato, M. W. Ramsey, and J. M. Muller-Delp Effects of ageing and exercise training on endothelium-dependent vasodilatation and structure of rat skeletal muscle arterioles J. Physiol., May 1, 2004; 556(3): 947 - 958. [Abstract] [Full Text] [PDF]
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F. A. Dinenno Ageing, exercise training, and resistance vessels: more than just no NO? J. Physiol., May 1, 2004; 556(3): 673 - 673. [Full Text] [PDF]
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L. Lawrenson, J. Hoff, and R. S. Richardson Aging attenuates vascular and metabolic plasticity but does not limit improvement in muscle VO2 max Am J Physiol Heart Circ Physiol, April 1, 2004; 286(4): H1565 - H1572. [Abstract] [Full Text] [PDF]
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