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-adrenergic-receptor system
on human lymphocytes
Institute of Sports Medicine, University of Paderborn, 33098 Paderborn, Germany
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The influence of increased training on the sympathoadrenergic
system was investigated. Moderately trained male subjects
(n = 15) increased their training
within 10 wk by 60%; eight of the subjects increased their training
volume, and seven increased their training intensity. Before and after
the training, an exhaustive treadmill exercise was carried out. Acute
treadmill exercise increased 
-adrenergic receptor number on
mononuclear lymphocytes, isoproternol-stimulated cAMP production, and
plasma catecholamine concentration. The increase of receptor number can
at least partially be explained by a changed lymphocyte composition at
rest and after exercise. After training, the exercise-induced increase
of -adrenergic receptor number was significantly blunted, and the
exercise-induced increase of the isoproternol-stimulated cAMP
production per -receptor was enhanced. Subjects who experienced
increased symptoms of physical discomfort and/or mood changes showed an
enhanced cAMP production after training. These findings point to an
altered regulation of the receptor and postreceptor mechanisms as an
effect of a 10-wk period of hard training.
catecholamines; adenosine 3',5'-cyclic monophosphate; lymphocyte subsets; exercise; overtraining
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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IT HAS BEEN WELL DOCUMENTED that short-term exhaustive
exercise (4, 6, 7, 11, 16, 32) and short-term infusion of adrenergic
agonists (26, 29) upregulate the -adrenergic-receptor number on
mononuclear lymphocytes (MNL) and intracellular isoproterenol (Iso)-stimulated production of cAMP of MNL. Less is known
about the effects of long-term training on the sympathoadrenergic
system. Endurance training as well as long-term infusion of adrenergic agonists seem to downregulate the -adrenergic-receptor density on
MNL with a concomitant reduced cAMP production (11, 12, 20).
The regulation of the sympathoadrenergic system seems to play an
important role in training effects and in the development of
overtraining (5, 18, 28). Both increased and decreased basal
catecholamine concentrations have been shown in overtrained athletes
(9, 17), pointing to a dysregulation of the sympathoadrenergic system,
possibly depending on the stage of overtraining (9). In different
periods of endurance training or high-intensity training in several
sports disciplines (11), receptor density and responsiveness may be
changed in a different manner. Consequently, receptor regulation and
postreceptor mechanisms may be involved in adaptation to increasing training or, on the other hand, may be responsible for symptoms of
overload, overreaching, or early phases of overtraining. Therefore, we
studied the effect of an acute bout of exercise on -adrenoceptor density on MNL, Iso-stimulated cAMP-production of MNL, and the plasma
concentration of catecholamines before and after 10 wk of increased
volume of training as well as increased intensity of training.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Training Groups and Training Program
Healthy, drug-free, moderately trained male students (n = 15) participated in the study after having given their informed written consent.The subjects were allowed, depending on their personal preferences, to
choose one of two training groups to ensure that they would achieve
their training program. The two groups had to complete a training
program of progressively increasing training load during 10 wk. The
high-volume group (HV group; n = 8 subjects, age 26 ± 3 yr, height 182 ± 3 cm, weight 76.6 ± 5.1 kg) increased their training volume by increasing the
number of sessions per week as well as by increasing the distance from
30.7 ± 18.3 to 48.2 ± 19.3 km/wk (see Table 1
for details). The intensive group (I group;
n = 7 subjects, age 24 ± 2 yr,
height 183 ± 8 cm, weight 77.3 ± 8.3 kg) increased their
training intensity by introducing more interval training into their
training program and adding high-speed races. At the beginning of the
training period they ran 22.2 ± 7.5 km/wk below the speed at the
anaerobic threshold and 8.9 ± 5.5 km/wk above the speed at the
anaerobic threshold; after training they ran 10.7 ± 7.9 km/wk below
and 18.7 ± 12.3 km/wk above the speed at the anaerobic threshold
(see Table 1 for details).
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Each subject received an individual training plan referring to his personal ventilatory anaerobic threshold. Every week the subjects had to perform a control test (50-m sprint, 300-m sprint, 45-min run with measurement of the distance covered). Training plans were adapted every 2 wk according to the personal daily training protocol and the results of the weekly control test. After 10 wk of training, the subjects had increased their training by ~60% (see Table 1 for details).
To monitor their physical and mood status, subjects had to answer a
questionnaire based on the one described by Lehmann et al. (18): they
rated weekly their physical complaints in general, complaints directly
after training, and complaints in the morning after the training. In
detail, "score A" asked for the
following: well behavior (very well to bad = 0-2 points), illness
[no symptoms = 0 points or points = number of symptoms like
headache, cold, arthralgia, myalgia, fever below (1 point) or above (2 points) 38.5°C multiplied by number of days the symptoms
lasted], illness-induced training pause (points = number of
failing training sessions), signs of musculoskeletal overload like
tendopathia, muscle soreness, complaints concerning joints (points = number of symptoms multiplied by number of days the symptoms lasted).
In "score B," subjects rated in
comparison with the week before (0-2 points for unchanged, decrease, or increase) their appetite, resting heart rate in the morning, weight, sleep, performance in general or in test results (50-m
sprint, 300-m sprint, 45-min run), and accomplishing daily activities
(easier, unchanged, harder). In a similar three-point scale, we asked
for the feeling after the end of each training session (well to very
exhausted) and in the morning after the training (regenerated to worn
out) and the time to recovery after the training (0.5, 1, >2 h) on
the average that week. Furthermore, the subjects rated their mood in
general and mood in life besides training in a four-point scale index:
1) good,
2) balanced,
3) changing,
4) bad. Table
2 shows the score indexes in the course of
the 10-wk period. In this way, by an increasing index of
score A and/or score
B we were able to judge in a qualitative
experience-based manner whether or not particular subjects tolerated
increasing training load.
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Treadmill Excercise Bout and Blood Sampling
At the beginning and the end of the study, the subject's ventilatory anaerobic threshold was determined according to Wasserman et al. (30) by increasing exhaustive treadmill exercise (Woodway treadmill). The test was performed between 8:00 and 10:00 AM after a day without training to exclude effects of short-term fatigue. The subjects were allowed to have a small breakfast without coffee or tea. Running speed started at 8 km/h at a constant slope of 1%, increasing every 3 min by 2 km/h until subjective exhaustion (leveling-off phenomenon of oxygen uptake). Minute ventilation, oxygen uptake, and carbon dioxide production were measured with EOS-Sprint (Jaeger). Venous blood samples were taken before the treadmill exercise (after a 30-min rest in a supine position) and immediately after exhaustion. Within seconds after puncture of an antecubital vein with a Venofix winged infusion set (Braun), blood was collected in vacutainers containing ice-cold EGTA and reduced glutathione (Amersham) for determination of catecholamines and was immediately centrifuged at 4°C (1,000 g, 10 min). An additional 45 ml of blood were collected in a 50-ml Falcon tube (Becton Dickinson) containing 5 ml of 1% Na-EDTA for cell preparation (receptor and cAMP assay), and a further 5 ml were collected in evacuated monoject blood collection tubes with K-EDTA (Sherwood Medical) for the cell counting and fluoresence-activated cell sorter analysis.-Adrenergic Receptors
-Adrenergic receptors were determined on MNL by radioligand assay.
Cell separation. The venous blood anticoagulated with EDTA was diluted 1:1 with NaCl (0.9%), and lymphocytes were isolated by density-gradient centrifugation (Lymphoprep, Nycomed Pharma, Oslo, Norway). After the centrifugation (800 g, 20 min, 25°C), the separated lymphocytes were washed twice (250 g, 10 min, 25°C) with NaCl (0.9%) and resuspended in PBS at a fixed number of 5 × 106 cells/ml.
-Adrenergic-receptor radioligand assay.
Aliquots of 400 µl lymphocytes (5 × 106 cells/ml) were incubated with
100 µl 3[H]CGP-12177
(5 final concentrations in the range 0.8-17 nM) and 100 µl PBS.
To define the unspecific binding, 100 µl propanolol (final
concentration 60 × 10
5 M) were used instead of
the buffer. The incubation of 30 min at 37°C was stopped by the
addition of 5 ml ice-cold NaCl (0.9%) and rapid filtration over
Whatman GF/C fiberglass filters. The filters were washed
with 10 ml NaCl. The specific activities of wet-cell-containing filters
were determined after adding 3 ml of a scintillation cocktail
(Rotiscint Eco Plus, Carl Roth, Karlsruhe, Germany) in a scintillation
counter [Packard Tri-Carb 4530 (35634) United Technologies
Packard].
Data analysis. Data were analyzed according to the method of Scatchard (22).
cAMP
As an indicator for responsiveness of the-adrenergic receptors, the
basal production of cAMP by MNL as well as the cAMP production after
the stimulation by Iso were determined. The cAMP assay was performed in
duplicate, following the protocol as described previously (25). The
venous blood was prepared in the same way as for the
-adrenergic-receptor assay. After centrifugation (800 g, 20 min) and washing twice (250 g, 10 min, 25°C) in NaCl (0.9%), the cells were resuspended in theophylline buffer (120 mM NaCl, 5 mM
KCl, 1.2 mM
MgSO4 · 7H2O,
15 mM
NaCOOCH3 · 3H2O,
1 mM Na2-EDTA, 10 mM glucose, 10 mM HEPES, 1 mM ascorbic acid, 0.1% human serum albumin, and 1.6 µg/ml theophylline) at a fixed number of 2 × 106 cells/ml. Aliquots (500 ± l) of isolated mononuclear cells were stimulated by addition of 50 µl
Iso (1 and 10 µM final concentrations) and incubated for 2 min. The
basal cAMP production was determined by incubation without Iso. The
incubation was stopped by centrifugation (7 min, 400 g, 25 °C). For complete
destruction of the cells, the pellet was resuspended in 500 µl
of lysing solution (50 mmol/l Na acetate + 1.6 µg/ml
theopylline), incubated 15 min at 8°C, and finally boiled in a
water bath for 15 min. After centrifugation (20 min, 1,000 g) the cAMP-containing supernatant
was collected and frozen at 
20°C until detection with a
commercially available radioimmunoassay (NEN-DuPont, Dreieich, Germany).
The results for the stimulation of the two concentrations of Iso were
similar. Therefore, results are only shown for the final concentration
of 1 µl Iso. The cAMP production was calculated by substracting the
cAMP concentration of nonstimulated cells (basal production) from the
concentration of stimulated cells. To get information about the
receptor function, we also calculated the cAMP production per
-adrenergic receptor as follows: cAMP production per
106 cells/-receptor number per
cell resulting in cAMP production per -receptor × 106.
Catecholamines
Free and sulfoconjugated catecholamines (epinephrine, norepinephrine) in plasma were determined by high-performance liquid chromatography separation as described elsewhere (31).Flow-Cytometric Analysis of Lymphocytes
White blood cells were counted by a blood analyzer (Sysmex CC180, TOA Medical Electronics). Lymphocytes were analyzed in whole blood by monoclonal antibodies (Becton Dickinson, Heidelberg, Germany) conjugated with FITC or phycoerythrin (PE). One hundred microliters of venous blood were incubated with 10 µl antibody solution for 15 min at room temperature in the dark, and then 500 µl lysing solution (Becton Dickinson) were added. After 10 min the incubation was stopped by addition of 2 ml PBS and centrifugation (250 g, 5 min, 25°C); the cells were washed with 2 ml PBS. The pellet was resuspended in sheath fluid (Becton Dickinson), and the immunofluorescence was measured with a flow cytometer (FACScan, Becton Dickinson). An analysis of the relative proportion of each subset was obtained by electronic gating of lymphocytes based on forward and sideward scatter parameters and on simultaneous staining of leukocytes (CD45+, FITC labeled) and monocytes (CD14+, PE labeled), resulting in a nonlymphocyte contamination of <5% in the gate. The gate contained at least 95% of all lymphocytes. The absolute cell number in each subset was calculated on the basis of total lymphocytes. The lymphocyte subsets were identified by the following antibodies: CD3+ (FITC) for T cells, CD4+ (FITC) for helper/inducer T cells, CD3/CD16+/CD56+
(PE) for natural killer (NK) cells.
Statistics
All values are shown as means ± SD. Statistical calculations were performed by using the statistical software package SPSSwin (SPSS Software, Munich, Germany). The statistical analysis was carried out by ANOVA. When appropriate, matched pairs were compared post hoc by using the nonparametric Wilcoxon test. Differences between the two groups were determined post hoc by the Mann-Whitney U-test. The significance levels were set at P < 0.05.| |
RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The training had no effects on maximal oxygen uptake [HV group:
55.8 ± 5.1 ml · min1 · kg1
before training (BT) compared with 57.0 ± 3.3 ml · min1 · kg1
after training (AT); I group: 59.5 ± 6.0 ml · min1 · kg1
BT compared with 59.6 ± 6.8 ml · min1 · kg1
AT] and on respiratory minute ventilation (HV group l/min: 141.2 ± 18.6 l/min BT compared with 144.1 ± 13.7 AT, I group: 156.5 ± 14.3 BT compared with 154.9 ± 13.6 l/min AT).
The type of training (HV group: pure endurance training; I group:
high-intensity training) had no effects on the results of the weekly
test for the evaluation of performance (50-m sprint time, 300-m sprint
time, 45-min running distance), nor did test results change
significantly within the 10-wk period (data not shown). Furthermore, we
did not find a significant influence of the training type on the other
determined parameters. Therefore, the results were pooled and are shown
for the whole training group. Compared with the whole group, four subjects of HV group and three subjects of I group showed a higher incidence of infections as well as longer lasting exhaustion, mood and
sleep disturbances, increased anger, and reduced force for a duration
of >1 wk, especially at the end of the 10-wk period; their index for
psychophysiological scores increased above the median values of the
whole group in the last 2 wk of training (mean ± SD of whole group;
see Table 2). Two persons did not answer their questionnaire. The
remaining six subjects had no or only small changes in their indexes.
Nevertheless, we found statistically significant differences between
these subgroups of seven vs. six subjects only in the behavior of the
Iso-stimulated cAMP production. Thus first the results are shown for
the whole training group.
Effects of Acute Exercise
The treadmill exercise increased significantly the-adrenergic-receptor density (P < 0.01 BT, P < 0.05 AT) (Fig.
1), the plasma catecholamine concentration
(P < 0.001 BT and AT)
(Fig. 2), and the cAMP production
(P < 0.05 BT,
P < 0.01 AT) (Fig.
3). As an index of the -adrenergic
receptor function, we calculated the Iso-stimulated cAMP production per
receptor. Before training, the Iso-stimulated cAMP production per
-adrenergic receptor remained unchanged by exercise. After training,
the Iso-stimulated cAMP production per -adrenergic receptor
increased significantly by exercise
(P < 0.05) (Fig. 3).
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Exhaustive treadmill exercise caused a significant leukocytosis
(P < 0.01 BT and AT) and
lymphocytosis (P < 0.01 BT
and AT) (Table 3).
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Because lymphocyte subsets differ in their -adrenergic-receptor
density, we also had to consider the lymphocyte subset composition. Acute physical stress increased significantly the absolute numbers of
lymphocytes (P < 0.01 BT and AT) and
lymphocyte subsets (P < 0.01 BT and
AT) (Table 3). The relative numbers of
CD3/CD16+/CD56+
(NK) cells were significantly increased by treadmill exercise (P < 0.01 BT,
P < 0.05 AT), whereas the relative
numbers of CD3+ cells
(P < 0.01 BT and AT) and
CD4+ cells
(P < 0.01 BT and AT) decreased after
stress (Table 3).
Influence of Training on the Effects of Exhaustive Treadmill Exercise
After the training phase the exercise-induced increase of-adrenergic-receptor number was significantly lower
(P < 0.05) compared with pretraining
values (Fig. 1), and the exercise-induced increase of catecholamines
(Fig. 2) was slightly blunted after training (no significance). After
training, we observed a slightly enhanced increase of the cAMP
production (Fig. 3). Before training, we did not determine an
exercise-induced increase in cAMP production per -adrenergic
receptor; after training we observed a significant (P < 0.01) increase (Fig. 3).
The training period did not modify the effects of an acute bout of exercise on the absolute lymphocyte subset counts and the lymphocyte composition (Table 3).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Although within an increasing number of weekly training sessions I group dramatically reduced the percentage of moderate-training intensity and HV group performed exclusively long-distance training sessions with an intensity below the ventilatory anaerobic threshold, ANOVA revealed no training-induced differences between the two groups in any determined parameter. Therefore, only results of all subjects as a whole group are discussed.
Effects of Acute Exhaustive Treadmill Exercise
In agreement with earlier investigations (2, 4, 7, 16, 32), we determined a significant increase in-adrenergic-receptor number,
plasma catecholamine concentration, and cAMP production after acute
exhaustive treadmill exercise. Werle et al. (32) observed an increase
of receptor density on isolated
CD4+ and
CD8+ cells after strenuous
short-term exercise. More recent investigations suggest that the
increased receptor number after exercise may be at least partially an
effect of the different redistribution of lymphocyte subsets after
exercise. Maisel and co-workers (19) explain the exercise-induced
increase of -adrenergic-receptor density of mixed lymphocytes by the
redistribution of lymphocyte subsets in the circulation that differ in
their receptor number. Fujii et al. (6) reported that dynamic exercise
induces the translocation of -adrenergic receptors from the inside
of lymphocytes to the outside, resulting in a higher receptor number
and function determined by Iso-stimulated cAMP production. With respect
to the redistribution of lymphocytes, they concluded that
redistribution effects can only partially explain the increase in
receptor number. According to Van Tits et al. (29), who reported a
recruitment of younger cells with a different receptor density after
acute exercise, both redistribution effects and changes in receptor number are involved in the upregulation of -adrenergic-receptor density after a single bout of exercise.
Because of the very large amount of blood necessary for the assay, we did not determine receptors on separated lymphocyte subpopulations in our investigation. NK cells, which are known to have a very high receptor density (14), increase in the most remarkable way after exercise. CD8+ cells and B cells are also known to possess a high receptor number (15, 29, 19). CD8+ and NK cells increase during exercise (14, 15, 29, 19), whereas B cells are mainly unaffected by acute exercise (24) and thus will not contribute in a major way to shifts in receptor number due to acute exercise. The CD8+ marker is coexpressed on some NK cells (23). Schedlowski and co-workers (23) found an increase of NK (CD16+, CD56+) and CD8+ cells after 20-min infusion of epinephrine; the increase of the CD8+ cells could be explained by the increase of NK cells coexpressing the CD8+ marker (23). In our investigation the percentage of CD3+ and CD4+ decreased by acute exercise; thus there could have been only a minor increase in CD8+ cells. Such a small increase can be explained by the pronounced increase of NK cells that we observed, part of which coexpressing the CD8+ marker. Thus the increased receptor number after acute exercise in our study could have been an effect of the differential lymphocyte mobilization. It remains to be elucidated whether this cell mobilization is an effect of simple redistribution or, according to Van Tits et al. (29), depends on the appearance of younger cells with a different receptor number.
Effects of the Training Period
The plasma catecholamine concentration was not significantly affected by training in our investigation. We only observed a slightly blunted exercise-induced increase of catecholamines after training. Previous investigations reported an increased norepinephrine excretion in stale swimmers (9), or a reduced catecholamine excretion of resting subjects after intensified training, that was considered as an effect of hypothalamic dysfunction (18). Hooper and co-workers (9) assumed a dual catecholamine response to overtraining depending on the stage of overtraining, and Urhausen and co-workers (27) suggested that the type of overtraining (addisonoid/basedowoian) might influence the catecholamine reaction. Our results reporting only a minor change in plasma catecholamine concentration after 10 wk of intensified training suggest that there is no clear border between the catecholamine reaction to training and the catecholamine reaction to an early stage of overreaching.We observed a blunted -adrenergic-receptor upregulation after
exercise as an effect of the 10 wk of increasing training load. In
agreement with investigations on endurance-trained athletes (3, 11) and
long-term infusion of adrenergic agonists (1), this downregulation of
-adrenergic receptors seems to be an adaptation to training as a
consequence of the frequently enhanced catecholamine concentration
during the training sessions. In contrast to the reaction to acute
exercise, there is a real change in receptor number as an effect of
long-term training: The composition of lymphocytes remained unchanged
after training, but the increase of receptor number after strenuous
exercise was lower after training.
In contrast to the downregulation of -adrenergic receptors, the
cells showed a sensitized reaction to adrenergic stimulation. The
exercise-induced increase of the cAMP production was slightly enhanced
after the training period. This may be due to the fact that after the
training period the seven subjects with higher psychophysiological
indexes, who experienced increased signs of discomfort, delayed
recovery, susceptibility to infections, and other symptoms of overload,
had a significantly increased Iso-stimulated cAMP production compared
with pretraining values. Figure 4
differentiates between the above-mentioned seven subjects with
("maladapted") and the six subjects without changes in their
physical and mood state ("well adapted"). The latter subjects
showed identical values and reactions to exercise before and after the
training period. Previous investigations describe a downregulation of
-adrenergic receptors of MNL, stimulatory G protein
(Gs), and cAMP production of
lymphocytes after endurance training (11, 20, 21) or after long-term
infusion of adrenergic agonists (12).
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In contrast to the above-mentioned authors, at the end of the training
period, we observed in the group as a whole a higher cAMP production
and cAMP production per receptor, whereas receptors were
downregulated. Because NK cells and
CD8+ cells have a high receptor
number, this might have been an effect of increased percentage of NK or
CD8+ cells (14, 29). Nevertheless,
relative and absolute lymphocyte numbers remained unchanged by
training. Moreover, the cAMP production per receptor, a parameter
including the decreased receptor number and the increased cAMP
production, was also higher after training. Consequently, the enhanced
exercise-induced increase of cAMP production can be considered as
enhanced receptor function. Hammond et al. (8) observed in pigs after
7-9 wk of running training a decreased receptor density with a
concomitant increase of Gs,
indicating an increased receptor function. Similarily, in our
investigation we too found a reduced -adrenergic receptor
upregulation with sensitized postreceptor mechanisms but only in those
seven athletes with increased score indexes of illness and vegetative
and mood changes.
In conclusion, we found that 10 wk of increased training sensitize the
postreceptor system in MNL, which might affect the cell
function. Because NK cells possess a high receptor
density (14) and play an important role in antiviral defense, and
because -adrenergic stimulation seems to suppress immune function
(33), altered sensitivity to adrenergic stimuli might partially explain the increased susceptibility to infections described for overtraining (5, 17).
In summary, after acute exercise we observed an increase of plasma
catecholamine concentration, -adrenergic-receptor density and cAMP
production. The increased receptor number after a single bout of
exercise could at least partially be explained by redistribution effects of lymphocyte subsets. In contrast, the 10 wk of a high training load led to a blunted receptor reaction to acute exercise with
a concomitant increased receptor sensitivity and cell function during
acute exercise; these effects were independent of the type of training.
Our results point to a central role of the sympathetic regulation in
the physiological reaction to acute exercise and training. Cellular
mechanisms show the most sensitive reaction. Further investigations on
overtraining should include the -adrenoreceptor system and the
postreceptor function.
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ACKNOWLEDGEMENTS |
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The authors acknowledge the expert technical assistance of Gabriele Busse, Ulrike Münster, and Michaela Linnenbrock.
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FOOTNOTES |
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This study was supported by Bundesinstitut für Sportwissenschaften KZ Grant VF 0407/01/41/94.
Address for reprint requests and other correspondence: M. Weiss, Institut of Sports Medicine, Univ. of Paderborn, Warburger Str. 100, 33098 Paderborn, Germany (E-mail: weiss{at}sportmed.unipaderborn.de).
Received 17 October 1997; accepted in final form 12 March 1999.
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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