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Department of Sports Medicine, Research Center on Aging and Adaptation, Shinshu University School of Medicine, Matsumoto 390-8621, Japan
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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We assessed the effects of aerobic
and/or resistance training on thermoregulatory responses in older men
and analyzed the results in relation to the changes in peak oxygen
consumption rate (
O2 peak) and
blood volume (BV). Twenty-three older men [age, 64 ± 1 (SE) yr; O2 peak, 32.7 ± 1.1 ml · kg
1 · min1] were
divided into three training regimens for 18 wk: control (C;
n = 7), aerobic training (AT; n = 8),
and resistance training (RT; n = 8). Subjects in C were
allowed to perform walking of ~10,000 steps/day, 6-7 days/wk.
Subjects in AT exercised on a cycle ergometer at 50-80%
O2 peak for 60 min/day, 3 days/wk, in addition to the walking. Subjects in RT performed a resistance exercise, including knee extension and flexion at 60-80% of one repetition maximum, two to three sets of eight repetitions per day, 3 days/wk, in addition to the walking. After 18 wk of training, O2 peak increased by 5.2 ± 3.4% in C (P > 0.07), 20.0 ± 2.5% in AT
(P < 0.0001), and 9.7 ± 5.1% in RT
(P < 0.003), but BV remained unchanged in all trials.
In addition, the esophageal temperature (Tes) thresholds
for forearm skin vasodilation and sweating, determined during 30-min
exercise of 60% O2 peak at 30°C,
decreased in AT (P < 0.02) and RT (P < 0.02) but not in C (P > 0.2). In contrast,
the slopes of forearm skin vascular conductance/Tes and
sweat rate/Tes remained unchanged in all trials, but both
increased in subjects with increased BV irrespective of trials with
significant correlations between the changes in the slopes and BV
(P < 0.005 and P < 0.0005, respectively). Thus aerobic and/or resistance training in older
men increased O2 peak and lowered
Tes thresholds for forearm skin vasodilation and sweating but did not increase BV. Furthermore, the sensitivity of the increase in skin vasodilation and sweating at a given increase in
Tes was more associated with BV than with
O2 peak.
aerobic training; resistance training; skin blood flow; sweating
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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THERMOREGULATORY
RESPONSES have been known to deteriorate with aging, which is
likely associated with the decrease in peak oxygen consumption rate
(O2 peak). Tankersley et al. (32) suggested that 50-60% of the reduction in
forearm skin blood flow (FBF) response to increased esophageal
temperature (Tes) in older subjects was caused by a
decrease in O2 peak by performing a
study that compared the FBF response with that in younger subjects
whose O2 peak was matched.
Moreover, Havenith et al. (12) reconfirmed the results in
a greater number of subjects, providing a regression equation to
estimate the highest FBF during exercise at 65-70%
O2 peak from
O2 peak and age. In
addition to these cross-sectional studies, Thomas et al.
(33) reported a 16-wk aerobic training for older men increased the FBF response in addition to the
O2 peak. Although these results
suggest a close association between enhanced FBF response and increased
O2 peak after exercise training in
older subjects, the precise mechanisms remain unknown.
Aerobic training increases blood volume (BV) in younger subjects, and the increased BV is considered to be one of the mechanisms involved in training-associated enhancement of FBF response by increasing the venous return to the heart (26, 31). Indeed, the maneuvers to increase the venous return to the heart, such as by intravenous saline infusion (22), head-out water immersion (21), and continuous negative pressure breathing (20), have been reported to enhance FBF response by stretching baroreceptors in addition to by increasing cardiac stroke volume during exercise in a hot environment. Hagberg et al. (9) suggested that in older subjects those who were aerobic trained showed greater BV than their sedentary counterparts, leading to higher cardiac stroke volume and cardiac output at a given relative intensity of exercise. Ho et al. (13) suggested that hypervolemia is the lone mechanism for the increased FBF response because splanchnic and renal vasoconstriction during exercise was not increased after aerobic training in older men, unlike in younger men. These results suggest that hypervolemia after aerobic training improves FBF response by increasing the venous return to the heart in older subjects.
However, it has been controversial whether aerobic training increases BV in older subjects, and if it does, it is yet unknown how the increased BV enhances the FBF response. Some studies have reported that aerobic training increased BV in older subjects (4, 24), but others did not (29, 30, 35). In addition, few of these studies reported change in the FBF response after training. One study by Ho et al. (13) suggested that the enhanced FBF response was caused by increased cardiac output due to increased plasma volume (PV) after a 4-wk aerobic training, but they found no significant increase in PV because of too small number of subjects.
In the present study, we examined the effect of 8- and 18-wk aerobic or
resistance training on BV and FBF response in older subjects to
elucidate the involvement of increased BV in the exercise training-induced enhancement of FBF response in older men. The reason
for adding a resistance training trial was that the training enabled us
to distinguish the mere effect of increased
O2 peak on FBF response from other
effects induced by aerobic training, such as more prolonged
cardiovascular and/or heat loading. In addition, we measured the
changes in sweat rate (SR) response to increased Tes after
exercise training because, to our knowledge, there have been no studies
on the effects of exercise training on this factor in older men. In
addition, we assessed Tes thresholds for forearm skin
vascular conductance (FVC) and SR responses and slopes of the
response-Tes relationships to examine how
O2 peak and/or BV modify the
responses to increased Tes.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects and Procedures
The procedures in this study were approved by the Review Board on Human Experiments, Shinshu University School of Medicine. After the experimental protocols were fully explained, 23 older (58-72 yr) healthy men gave their written informed consent before participating in this study. The subjects were relatively active but did not participate in any regular exercise training program. All subjects were nonsmokers and had no overt history of cardiovascular or pulmonary diseases or any orthopedic limitations to the exercising test and training. During the experiment, no subject was taking medication that had a potential to impact cardiovascular and thermoregulatory function or BV and constituents.Subjects were randomly divided into the three training trials for 18 wk
[control (C; n = 7), resistance training (RT;
n = 8), and aerobic training (AT; n = 8); Table 1] to avoid differences in
physical characteristics among the trials before training. In the C
trial, subjects were not engaged in a specific training program except
for walking of 9,465 ± 1,954 steps/day, 6.7 ± 0.2 days/wk.
Subjects in the RT and AT trials trained under our supervision in
addition to the walking of 10,353 ± 2,336 and 8,749 ± 490 steps/day, respectively. The training was performed between September
and April to avoid any effect of heat acclimatization during the summer season. Averaged ambient temperature (Ta) in the city was
19°C in September, 
1°C in January, and 4°C in April.
Relative humidity (RH) was ~70% throughout the period.
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O2 peak, ventilation threshold
(VT), BV and constituents, and muscle strength for isometric knee
extension were measured in all subjects before and after 8-wk and 18-wk
training. FBF and SR were also measured during exercise in a hot environment.
Measurements
O2 peak and VT.
O2 peak was measured while the
subjects were in an upright position with the use of a cycle ergometer
at Ta of 25.0 ± 0.1°C and RH of 46 ± 1%
(means ± range). After baseline measurements at rest were taken
for 3 min, the subjects started pedaling bicycles at 60 cycles/min
without loading. Exercise intensity was increased by 30 W
every 3 min until 120 W, and, above this intensity, it was increased by
15 W every 2 min until subjects could not maintain the rhythm. Oxygen
consumption rate (O2) was determined
every 15 s from the oxygen and carbon dioxide fractions in expired
gas and the expired ventilatory volume (Aeromonitor AE260, Minato, Tokyo, Japan). Heart rate (HR) was recorded every 1 min from the trace
of an electrocardiogram (Life Scope 8, Nihon Kohden, Tokyo, Japan).
O2 peak was determined after the
three largest consecutive values at the end of exercise were averaged.
The criteria for determining
O2 peak were that the respiratory
exchange ratio was >1.1, O2 leveled
off despite increasing workload, and HR reached the age-predicted
maximal value. VT was determined by the V-slope method and presented as
O2 at VT (2).
Muscle strength for isometric knee extension. Muscle strength for isometric extension was measured in each side of the knee with a dynamometer (Biodex 3, Biodex Medical System, Shirley, NY). After regular warming-up and familiarization protocols, the anatomic axis of the knee joint was aligned with the mechanical axis of the dynamometer arm to adjust the angle between the lower and upper legs to 105°. Then, three 3-s maximum voluntary contractions, intermitted by a 30-s recovery, were conducted. The peak torque averaged for three trials was adopted for the value for one side of the knee, and it is given as an averaged value of both sides of the knee in Table 1.
BV and constituents. On the day of the measurement, subjects reported to the laboratory at 7:00 AM normally hydrated but without having taken any food for 8 h before the experiment. PV was determined by the Evans blue dye-dilution method (7). The background absorbance due to turbidity was corrected by using a regression equation on the relationship between 620 and 740 nm, previously determined on 64 control plasma samples in 22 subjects according to the method reported elsewhere (5, 30). BV was calculated from PV and hematocrit (Hct) values after correction for plasma trapped among the red blood cells in the Hct tube (0.96) and an F-cell ratio (0.91) (8). The measurement error of BV was 2.1 ± 1.8% (means ± SD) (n = 4), which was obtained by measuring BV twice in the same subjects with a BV of 64.9-93.5 ml/kg after 2- to 3-wk intervals. The residues of blood samples drawn before the injection of the dye were used to determine the Hct (microcentrifuge method) and plasma albumin concentrations ([Alb]p; colorimetry). Total albumin content in plasma (Albtot) was determined as a product of PV and [Alb]p. The BV measurement was not performed in one of eight subjects in the AT trial who showed an allergic reaction to the patch test of the dye performed 24 h before the measurement on every subject.
FBF and SR measurements.
Subjects reported to the laboratory normally hydrated but having fasted
for at least 2 h before the measurement, at the same time of day
before and after the training regimens to avoid any effect of circadian
rhythm. Clad in shorts and shoes, subjects emptied their bladders,
entered the chamber controlled at 30.0 ± 0.1°C of
Ta and 50 ± 1% of RH (means ± range), and sat
in the contour chair of the cycle ergometer in a semirecumbent position for 45 min while all measurement devices were applied. After baseline measurements were taken at rest for 10 min, the subjects exercised in a
semirecumbent position at 60% of their pretraining
O2 peak for 20 min without fan cooling.
sk) was determined as
sk = 0.25 · Tfa + 0.43 · Tch + 0.32 · Tth
(25), where Tfa, Tch, and
Tth are skin surface temperature at the forearm, chest, and
thigh measured with the thermocouples, respectively. SR was determined by capacitance hygrometry, calculated from the relative humidity and
temperature of the air (THP-B3T, Shinei, Tokyo, Japan) flowing out of a
12.56-cm2 capsule at the rate of 1.5 l/min on the chest at
5 cm below the left clavicle. FBF was measured by venous
occlusion plethysmography with a mercury-in-Silastic tube strain gauge
placed around the upper side of the subject's left forearm positioned
above the heart level, with the hand eliminated from the circulation by inflation of an occlusion cuff to a supra-arterial pressure (~280 mmHg) (34). HR was recorded every 1 min as described in
O2 peak and VT.
Systolic (SAP) and diastolic arterial blood pressures (DAP) were
measured every 1 min from the right upper arm at the heart level by
inflation of the cuff with a sonometric pickup of Korotkoff's sound
(STPB-780, Colin, Komaki, Japan). Mean arterial blood pressure (MAP)
was calculated as DAP + (SAP DAP)/3. FVC was calculated as
FBF/MAP (reported in units of ml · 100 ml1 · min1 · 100 mmHg1). Tes,
Exercise Training Regimen
Subjects in the RT and AT trials trained for 18 wk according to the protocol recommended by the American College of Sports Medicine (1). As warming-up and cooling-down protocols, subjects in the AT and RT trials performed a 5-min stretch exercise and a 5-min cycle ergometer exercise at 50%O2 peak before and after the main exercise.
Subjects in the RT trial performed an exercise protocol, consisting of a knee extension and flexion, chest press, pull-dip and arm curl with weight resistance machines (Athlete, Mizuno, Tokyo, Japan) at 60-80% of one repetition maximum (1 RM), two to three sets of eight repetitions per day, 3 days/wk. The exercise intensity was increased with the training days: two sets of each exercise at 60, 70, and 75% 1 RM in the 1st, 2nd, and 3rd wk, respectively, and three sets at 80% 1 RM after the 4th wk. In addition to the exercise, supportive upper back extension, pelvic rise, and crunch without weight loading were performed throughout the training period.
Subjects in the AT trial performed a cycle ergometer exercise at
50-80% of O2 peak for 60 min/day, consisting of four sets of 15-min exercise followed by a 5-min
rest. The exercise intensity was increased with the training days: 50, 60, and 65% O2 peak for the 1st,
2nd, and 3rd wk, respectively; 70% O2 peak for the 4th to 8th wk, 75%
O2 peak for the 9th to 10th wk; and
80% O2 peak after the 11th wk. HR
was continuously monitored and recorded every 5 min during exercise.
The exercise intensity was readjusted every 1 wk so that HR at 5 min of
exercise was equivalent to the target exercise intensity.
The environmental condition for the training room was controlled at Ta of ~20°C and RH of ~50% without any significant differences between the RT and AT trials. During exercise, the subjects were allowed access to water ad libitum, and the amount was monitored. Subjects were weighed before and after the training regimen each day to estimate sweat loss. Body weight loss after training per day was 4-6 ml/kg body wt for the RT trial and 8-10 ml/kg body wt for the AT trial.
Statistics
The effects of training on physical characteristics, BV, blood constituents, THSR, THFVC, SR/Tes, and FVC/Tes within each trial were tested by a 3 (C, RT, AT) × 3 (before, 8 wk, and 18 wk) ANOVA for repeated measures (Table 1 and see Table 3). The effects of training on cardiovascular and thermoregulatory responses in a hot environment within each trial were tested by three-way ANOVA for repeated measures (Table 2). Subsequent post hoc tests to determine significant differences in the various pairwise comparisons were performed by using Scheffé's test. The null hypothesis was rejected when there were values of P < 0.05. Regression analyses were performed by Brace's methods (3). Because two of eight subjects in the RT trial quit the last 10-wk training regimen, the comparison between 8- and 18-wk training was performed on only six subjects. Values are expressed as means ± SE for seven subjects in the C trial and for eight subjects in the RT and AT trials, except as noted.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Table 1 shows the physical characteristics, BV, and PV before and
after training. After 8-wk training,
O2 peak increased by 8.4 ± 2.9% (P < 0.01) in the RT trial and by 13.2 ± 2.4% in the AT trial (P < 0.0001) with respect to the
pretraining values. After 18-wk training, it further increased by
9.7 ± 5.1% in the RT trial (P < 0.003) and by
20.0 ± 2.5% in the AT trial (P < 0.0001), whereas it remained unchanged in the C trial. There were no significant changes in body weight, maximal heart rate (HRmax), BV, PV,
and [Alb]p after 8- and 18-wk training.
Table 2 shows HR, MAP, Tes, and sk
during exercise in a hot environment before and after 8- and 18-wk
training in three trials. Only the values at rest and at 5 and 20 min
after the start of exercise are presented in the table to simplify.
After 8- and 18-wk training, HR at rest decreased in the RT and AT
trials but not in the C trial. The increase in HR during exercise was reduced in the AT trial but was enhanced in the RT and C trials. MAP at
rest decreased significantly in all trials. The increase in MAP during
exercise was reduced at 5 and 20 min in the AT trial, at 5 min in the
RT trial, and at 20 min in the C trial, but it was enhanced at 20 min
in the RT trial. Tes at rest decreased significantly in all
trials. The increase in Tes during exercise was attenuated
at 5 and 20 min in the RT and AT trials and at 5 min in the C trial.
sk at rest was not altered in any trials. The
increase in sk during exercise was reduced at 5 and
20 min in the AT trial and at 20 min in the C trial, but it increased at 5 min in the C trial.
The SR and FVC responses to increased Tes during
exercise in a hot environment are shown in Fig.
1. THSR, THFVC,
SR/Tes, and FVC/Tes, are summarized in Table
3. THSR decreased by 0.22 and 0.28°C in the RT trial and by 0.15 and 0.17°C in the AT trial, after 8-wk and 18-wk training, respectively, but it did not change significantly in the C trial. Similarly, THFVC decreased by
0.27 and 0.32°C in the RT trial and by 0.15 and 0.29°C in the AT
trial, after 8- and 18-wk training, respectively, but it did not change significantly in the C trial. There were no significant changes in
SR/Tes and FVC/Tes before and after training in
any trials.
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When the data from all the trials were pooled, the change in
O2 peak after training was weakly
but significantly correlated with those in THSR
(
THSR; r = 0.30, P < 0.05) and THFVC (THFVC; r = 0.34, P < 0.03) but not with those in
SR/Tes [(SR/Tes); P > 0.05] or FVC/Tes [(FVC/Tes);
P > 0.4]. In contrast, the change in BV (BV) after
training was significantly correlated with (SR/Tes)
(r = 0.51, P < 0.0005) and
(FVC/Tes) (r = 0.45, P < 0.005) (Fig. 2, A and
B) but not with THSR (P > 0.1) or THFVC (P > 0.3). As shown in
Fig. 3 (A and B),
THSR was significantly correlated with
THFVC (r = 0.79, P < 0.0001), and (SR/Tes) was significantly correlated with
(FVC/Tes) (r = 0.63, P < 0.0001). As shown in Fig. 4, the
change in Albtot after 8- and 18-wk training was
significantly correlated with that in PV (r = 0.68, P < 0.0001).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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In the present study, we verified the results previously reported
in older men that BV did not increase after aerobic training (29,
30, 35) and that THFVC and THSR
decreased with the increase in
O2 peak, whereas
FVC/Tes and SR/Tes remained unchanged
(33). Moreover, we confirmed the results not only after
aerobic but also after resistance training. In addition, we clarified
that the reductions in THFVC and THSR were more
associated with increased O2 peak
than with increased BV, whereas changes in FVC/Tes and
SR/Tes were more associated with that in BV than
O2 peak.
THFVC and THSR After Training
As shown in Table 1,O2 peak
in the RT and AT trials increased after 8- or 18-wk training. The
reductions in THFVC and THSR in the RT and AT
trials were weakly but significantly correlated with the increase in
O2 peak. THFVC or
THSR at a given absolute exercise intensity has been
reported to decrease after aerobic training not only in younger
(18, 25) but also in older subjects (33).
Smolander et al. (28) demonstrated that THFVC
increased with relative exercise intensity in individual younger
subjects. Thomas et al. (33) reported that 16-wk aerobic training decreased THFVC in subjects who increased
O2 peak by >5%. Moreover, Ho et
al. (13) suggested that, in older subjects, THFVC was not altered after a 4-wk training even when
absolute exercise intensity was increased from 60 to 70% of
pretraining O2 peak, equivalent to
60% of posttraining
O2 peak. These results
suggest that the reduction in THFVC and/or THSR after training was associated with reduced relative exercise intensity due to increased O2 peak.
O2 peak and BV After Training
O2 peak per day for 6 days at
36°C of Ta and RH of 40%) and compared the results
between older and younger men. They suggested that BV remained
unchanged in older subjects, whereas it increased by ~5% in younger
men. They also suggested that recovery from body fluid loss during 2-h
rehydration was twofold higher in younger men than that in older
subjects and that the recovery was augmented after heat acclimatization
in younger men but not in older men. They ascribed the results to the
attenuated water intake and the reduced release of body fluid-retention
hormones during rehydration in older men. Although in the present
study, aerobic training was performed in a cooler environment and body
fluid loss was less than in previous studies (30), the
blunted body fluid conservation mechanisms in older men may be involved
in no increase in BV for the AT trial.
Another possible explanation for no increase in BV for the AT trial may be associated with no increase in Albtot for older men (Table 1 and Fig. 4). The exercise training-induced hypervolemia has been suggested to be dependent on an increase in Albtot, causing a fluid shift from the interstitial to intravascular fluid space according to the colloid osmotic pressure gradient between the spaces (10, 19, 27). In younger subjects, exercise training-induced hypervolemia has been reported to be typically accompanied by an increase in Albtot (10, 19, 27). On the other hand, Zappe et al. (35) reported that, in older men, PV did not increase after 4 days of repeated exercise with a cycle ergometer because of attenuated increases in Albtot. They suggested that the failure to increase Albtot in older men after exercise was caused by the lower ability to synthesize (19) or translocate protein into the intravascular space than that reported in younger men (11). The interindividual variation in the increase in Albtot for the present study may be related to factors other than the active exercise training regimens, protein in diet (14), or heat acclimatization (27).
As shown in Table 1, the increased
O2 peak in the RT and AT trials was
not accompanied by hypervolemia in older subjects. However, in younger
subjects, it has been suggested that hypervolemia after aerobic
training increased O2 peak by
increasing venous return to the heart and maximal cardiac stroke volume
(26, 31). Frontera et al. (6) reported that,
in older subjects, 12-wk strength training induced a 6% increase in
O2 peak and a 107% increase in 1 RM of the knee extensor, but they found no increase in BV. Recently,
Jubrius et al. (15) studied the cellular energetic
adaptation to 6-mo aerobic or resistance training in older subjects and
reported that oxidative capacity increased by 31 and 57% after aerobic
and resistance training, respectively. Because muscle strength for knee
extensor in the AT trial increased by the same degree as that in the RT
trial (Table 1), the increase in
O2 peak for the AT trial was caused
by the increased oxidative capacity or oxygen extraction rate in the
lower leg muscles.
FVC/Tes and SR/Tes and BV
As shown in Fig. 2,BV was positively correlated with
(FVC/Tes) and (SR/Tes). To our knowledge,
there have been no studies showing the effects of exercise
training-induced hypervolemia on the slopes in older subjects. In
younger subjects, the maneuvers to increase the venous return to the
heart [saline infusion (22), head-out water immersion
(21), or continuous negative pressure breathing
(20)] increase FVC/Tes during exercise. These
results suggest that increased BV enhances the FBF response by
increasing cardiac output and/or by suppressing baroreflex-induced
attenuation of skin vasodilation by increasing venous return to the
heart in older subjects. Ho et al. (13) reported that a
4-wk aerobic training enhanced the FBF response during exercise of 60%
of O2 peak in a hot environment.
They ascribed this to increased cardiac output by PV expansion,
although they found no significant increase in PV before and after
training as a result of the small number of subjects. Coupled with the
results of the present study, it is suggested that the slopes were
increased by hypervolemia, irrespective of the increase in
O2 peak in older men.
The significant correlations between THFVC and
THSR (Fig. 3A) and between
(FVC/Tes) and (SR/Tes) (Fig.
3B) suggested the close association of the active
vasodilator and sudomotor systems (16). Mack et al.
(16) demonstrated in young subjects that reduction of
central venous pressure by lower body negative pressure decreased not
only FVC/Tes but also SR/Tes during exercise,
suggesting that the reductions were caused by suppression of the
sudomotor and active vasodilator systems by unloading cardiopulmonary
baroreceptors. Thus the sudomotor and active vasodilator
systems are closely associated during dynamic exercise. We confirmed
this in older men after exercise training.
Summarizing these results, aerobic and/or resistance training in older
men improved FVC and SR responses by the downward shift of
THFVC and THSR rather than by their increased
slopes of FVC/Tes and SR/Tes, which was
associated more with the increased
O2 peak than with BV regardless of
trials. In contrast, the change in the slopes was associated more with
the change in BV, which was not necessarily accompanied by increased
O2 peak after training in older men.
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ACKNOWLEDGEMENTS |
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We thank the volunteer subjects for participating in this study. We also thank Drs. A. Takamata, Y. Yanagidaira, A. Sakai, and H. Endoh for helpful comments and discussion on this study.
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FOOTNOTES |
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This study was supported in part by grants from the Ministry of Education, Science, Sports and Culture of Japan and Japan Space Forum.
Address for reprint requests and other correspondence: H. Nose, Dept. of Sports Medicine, Research Center on Aging and Adaptation, Shinshu Univ. School of Medicine, 3-1-1 Asahi Matsumoto 390-8621, Japan (E-mail: nosehir{at}sch.md.shinshu-u.ac.jp).
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.
July 12, 2002;10.1152/japplphysiol.00222.2002
Received 14 March 2002; accepted in final form 6 July 2002.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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