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ski1,ska1,1 Department of Sport Medicine, Academy of Physical Education, 61-871 Poznan; 2 Department of Applied Physiology, Medical Research Centre, Polish Academy of Sciences, 02-106 Warsaw, Poland; and 3 Laboratory for Human Environmental Physiology, National Aeronautics and Space Administration Ames Research Center, Moffett Field, California 94035-1000
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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To test the hypotheses that
short-term bed-rest (BR) deconditioning influences metabolic,
cardiorespiratory, and neurohormonal responses to exercise and that
these effects depend on the subjects' training status, 12 sedentary
men and 10 endurance- and 10 strength-trained athletes were submitted
to 3-day BR. Before and after BR they performed incremental
exercise test until volitional exhaustion. Respiratory gas exchange and
heart rate (HR) were recorded continuously, and stroke volume (SV) was
measured at submaximal loads. Blood was taken for lactate concentration
([LA]), epinephrine concentration ([Epi]), norepinephrine
concentration ([NE]), plasma renin activity (PRA), human growth
hormone concentration ([hGH]), testosterone, and cortisol
determination. Reduction of peak oxygen uptake
(
O2 peak) after BR was greater in the
endurance athletes than in the remaining groups (17 vs. 10%).
Decrements in O2 peak correlated positively with the initial values (r = 0.73, P < 0.001). Resting and exercise respiratory exchange
ratios were increased in athletes. Cardiac output was unchanged by BR
in all groups, but exercise HR was increased and SV diminished in the
sedentary subjects. The submaximal [LA] and [LA] thresholds were
decreased in the endurance athletes from 71 to 60%
O2 peak (P < 0.001); they also had an earlier increase in [NE], an attenuated increase in
[hGH], and accentuated PRA and cortisol elevations during exercise. These effects were insignificant in the remaining subjects. In conclusion, reduction of exercise performance and modifications in
neurohormonal response to exercise after BR depend on the previous level and mode of physical training, being the most pronounced in the
endurance athletes.
exercise tolerance; blood lactate threshold; catecholamines; hormones; plasma renin activity
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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PROLONGED BED REST (BR) causes reduction of exercise performance as a result of impairment of oxygen transport (7, 16, 17) and thermoregulation (15, 22), disturbances in intermediary metabolism (3, 30), and adverse changes in musculoskeletal structure and function (4).
Both cardiovascular and metabolic adjustments to exercise are controlled by the autonomic nervous and endocrine systems. In addition, enhanced secretion of growth hormone and testosterone exert a prolonged effect by stimulating anabolic processes in skeletal muscles and other tissues after exercise. Thus, for better understanding of the BR deconditioning mechanisms, it is necessary to elucidate functioning of the neural and hormonal regulatory systems.
Importance of the sympathetic nervous system (SNS) for determining work
tolerance and aerobic capacity during deconditioning was emphasized by
Sullivan et al. (34), who showed that administration of
dobutamine (a synthetic adrenomimetic drug) to BR subjects prevented
the decline in peak oxygen uptake
(O2 peak) and attenuated the increase
in blood lactate concentration ([LA]) during exercise. However, there
are few data on the influence of BR deconditioning on the sympathetic
nervous system response to exercise. Engelke and Convertino
(14) demonstrated a marked increase in the
post-maximal-exercise plasma norepinephrine concentration ([NE])
after 16 days of BR without change in plasma epinephrine ([Epi]),
whereas Sullivan et al. (34) found, after 21 days of BR,
higher arterial [Epi] during submaximal exercise without significant change in [NE] at both submaximal and maximal exercise.
Microneurography data during forearm isometric exercise indicated that
forearm muscle sympathetic nerve activity (MSNA) during isometric
exercise after 14 days of BR was similar to that before BR, but the
MSNA response to muscle ischemia, induced by circulatory arrest
after exercise, was attenuated (24). These findings
indicate that the metaboreflex from skeletal muscles, which activates
SNS, can be attenuated by BR deconditioning.
Little is known about the effects of BR on endocrine responses to exercise. McCall et al. (27) utilized a series of isometric plantar flexions after BR and found that an increase in plasma bioassayable growth hormone concentration was inhibited, suggesting that lack of activity and/or unloading of skeletal muscles causes disruption of the muscle afferent-pituitary axis, modulating growth hormone release. They did not find any influence of BR on either resting or postexercise levels of plasma immunoassayable growth hormone ([hGH]), testosterone, cortisol, or thyroid hormones. There appear to be no data on the effect of BR on the renin-angiotensin system response to exercise, although an increase in resting plasma renin activity (PRA) during BR has been reported consistently (18).
Physiological responses to exercise depend on the subjects' level of
physical fitness; however, except for maximal oxygen uptake
(O2 max), few data are available on the
impact of subjects' fitness status (initial
O2 max) on neuroendocrine responses to
exercise after BR. Some data indicate that the magnitude of the
O2 max decline during BR is greater in
highly fit subjects than in those with lower working capacity (9, 10, 31, 35). However, a positive correlation between the initial
O2 max per kilogram body mass and its
percent decrease was not confirmed (21) unless the
subjects exercised in the supine position, which minimized the
influence of orthostatic factors on cardiovascular adjustments
(10).
The present study was designed to test the following hypotheses: 1) short-term BR influences neurohormonal responses to exercise, and 2) metabolic, cardiorespiratory, and neurohormonal responses to exercise after BR depend on the level and mode of the subjects' habitual physical activity and their working capacity. Thus cardiorespiratory parameters, blood lactate [LA], plasma [Epi], [NE], [hGH], testosterone, cortisol, and PRA responses to graded incremental exercise were compared among sedentary men and endurance-trained and strength-trained athletes after 3 days of BR deconditioning.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects.
Twelve healthy, untrained male students, 10 endurance-trained athletes
(cyclists), and 10 bodybuilders volunteered for this study after giving
written informed consent (Table 1). The
study protocol was approved by the Ethics Committee of Academy of
Physical Education in Pozna, Poland. The
endurance-trained athletes were amateur cyclists who had been training
regularly for 5.5 ± 2.7 (SD) yr, and their average training
distance was 100 km/wk. The bodybuilders' resistance training
experience was 3.6 ± 1.8 (SD) yr, and they were currently
training for at least 3 h/wk with a program that included bench press
and leg press and squat exercise.
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Procedure.
The BR was conducted in the students' hospital in Pozna where
the subjects reported 2-3 days after their last training
session. Three days of BR were selected because exposure to a
few days of inactivity is sufficient to attenuate exercise performance (18). Also, such a short period of confinement is often
prescribed for treatment of injury and mild diseases. During BR the
subjects were allowed to ambulate no more than 20 min/day (to shower
and toilet); for the rest of the day they read books, listened to the
radio, and watched television in the supine position. A nursing staff
provided 24-h care. The subjects had mineral water ad libitum, and
their diet consisted of three meals per day freshly prepared in the
hospital kitchen with a total energy intake of 12,000 kJ/day (carbohydrates 50%, fat 35%, protein 15%).
E BTPS) and
respiratory gas exchange were measured continuously using the
Cardiopulmonary Exercise System (MedGraphics, St. Paul, MN), and heart
rate (HR) was recorded by the Sport Tester (PE 3000, Polar Electro,
Kempele, Finland). Stroke volume (SV) and cardiac output were measured during submaximal loads up to 100-150 W by impedance cardiography (26) using a monitoring device designed in this laboratory
(11). Validity of SV measurements was determined at rest
by using echocardiography (r = 0.90, n = 21, P < 0.001) (12) and during exercise by
using the CO2-rebreathing method (r = 0.72, n = 10, P < 0.01).
Immediately after each exercise load, 3-ml blood samples were taken
through an indwelling catheter inserted 30 min before exercise into the
antecubital vein for blood [LA] and plasma [Epi] and [NE]
determinations. Additional 5-ml blood samples were taken before and
after exercise for determination of PRA, [hGH], and testosterone and
cortisol concentrations.
Analytic methods Blood [LA] was measured enzymatically by using commercial kits (Boehringer, Mannheim, Germany), whereas plasma [Epi] and [NE] were measured by the radioenzymatic method of DaPrada and Zurcher (13) using the Catechola tests produced by Immunotech (Prague, Czech Republic). Plasma [hGH] was determined by radioimmunoassay using the HGH-IRMA MI-131 kits (Polatom, Swierk, Poland), plasma cortisol and testosterone concentrations with the radioimmunoassay kits of Orion Diagnostica (Espoo, Finland), and PRA by radioimmunoassay using Immunotech Angiotensin I kits (Prague, Czech Republic). The intra-assay analytic errors (coefficients of variation) for Epi, NE, hGH, PRA, cortisol, and testosterone were 10.8, 8.7, 4.2, 4.4, 7.2, and 3.5%, respectively.
Calculations. The exercise loads associated with a rapid increase in blood LA, Epi, and NE concentrations were defined as thresholds of these variables and calculated by using the two-segmental linear regression (log exercise load vs. log [LA], [Epi], or [NE]) according to Beaver et al. (2).
Statistics.
Statistical evaluation of differences between pre- and post-BR data was
made using a two-way analysis of variance for repeated measures. The
two factors were the testing condition and repeated measures of
cardiorespiratory parameters, blood LA, and hormone concentrations
during exercise. When a significant F value was achieved, a
paired Student's t-test was used to locate the pairwise differences between means. The same test was used for evaluation of
differences between the pre- and post-BR maximal exercise load, O2 peak, blood LA, and plasma
catecholamine thresholds. A comparison between groups was made using a
nonparametric Whitney-Mann test. Linear regression was used to evaluate
a relationship between the initial
O2 peak and its decrease during BR. As
a level of significance P < 0.05 was accepted. All
results are presented as means ± SE unless otherwise stated.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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BR reduced the maximal exercise load and
O2 peak in all groups (Table
2) without a change in the subjects'
body mass (data not presented). The decreases in
O2 peak were more pronounced in the
endurance-trained subjects (by 17%; P < 0.01) than in
strength-trained or sedentary subjects (by 10%; P < 0.01). However, the post-BR O2 peak in
the endurance athletes was still higher (P < 0.001)
than the initial value in the sedentary subjects. The individual values
of BR-induced decreases in O2 peak
(l/min) correlated positively with the initial O2 peak expressed in liters per minute
(Fig. 1; r = 0.73, P < 0.001). Significant correlations were also present
when the decreases in O2 peak were
expressed as percentages of the initial values (r = 0.64, P < 0.001), when
O2 peak and its decreases were
calculated per kilogram body mass (r = 0.52, P < 0.01), and when the decreases of
O2 peak per kilogram body mass were
expressed as percentages of the initial values (r = 0.40, P < 0.01).
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The resting and submaximal E values were similar
before and after BR in all groups. Maximal E was
lowered significantly by BR (94.7 ± 6.9 vs 74.5 ± 3.8. l/min; P < 0.05) in the endurance athletes, but the
ratio of E to oxygen uptake
(O2) was unchanged. Before BR the
respiratory exchange ratio (RER) at rest was significantly higher
(P < 0.01) in the endurance-trained than in sedentary
or strength-trained subjects. After BR the RER values at rest and during submaximal loads were higher than before BR in both groups of
athletes but not in the sedentary subjects (Fig.
2).
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Before BR the preexercise HR and SV did not differ significantly
between the groups. Resting HR was increased and SV was decreased after
BR in the sedentary and endurance-trained subjects. During submaximal
exercise the HR were increased and SV decreased by BR only in the
untrained subjects (Fig. 3). In no group
did BR modified cardiac output during exercise.
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Maximal [LA] was unchanged in all groups by BR (Table 2, Fig.
4); however, the submaximal [LA] values
were higher after BR and the blood [LA] threshold was shifted to
lower workloads in the endurance athletes (Table 2).
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Similar to blood [LA], the plasma [Epi] and [NE] increased
exponentially during exercise (Figs. 5
and 6). Before BR the calculated NE
threshold was higher (P < 0.01) in both groups of
athletes compared with sedentary subjects, with no significant
difference between the endurance and strength athletes. The plasma Epi
thresholds were similar in all groups. Neither preexercise nor exercise
plasma [Epi] and [NE] was affected significantly by BR, but the
plasma NE threshold was lowered by BR (P < 0.05) in
the endurance athletes. The post-BR NE thresholds in athletes were
still higher (P < 0.01) than in sedentary subjects.
There was a significant correlation (r = 0.48, P < 0.01) between the BR-induced changes in [LA] and [NE] thresholds for all subjects. The correlation coefficient in the
endurance athletes was 0.78 (P < 0.01). The plasma Epi thresholds were not affected by BR.
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Resting and postexercise plasma hormone concentrations before and after
BR are presented in Table 3. Before BR
there were no differences between groups in either resting or
postexercise concentrations of cortisol and testosterone as well as
PRA, whereas the postexercise plasma hGH levels were significantly
higher (P < 0.05) in the athletes than in the
sedentary subjects. In all groups the exercise caused significant
increases in plasma [hGH]. BR did not affect [hGH] at rest, whereas
the postexercise values were significantly lower in both groups of
athletes. Also, the exercise-induced increases in [hGH] were lowered
by BR in the endurance athletes (P < 0.01), whereas a
tendency (P = 0.07) toward lower increases occurred in
the bodybuilders. Thus the differences between groups in the
postexercise [hGH] values were not significant after BR.
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Exercise before BR did not cause significant increases in plasma cortisol in any group, whereas after BR there was a significant (P < 0.05) exercise-induced increase in cortisol concentration in the endurance athletes.
Exercise both before and after BR caused significant elevation (P < 0.01) in the plasma testosterone concentration in all groups, but BR did not change either resting or postexercise testosterone concentration levels. In all groups, BR elevated significantly (P < 0.01) resting PRA; the highest values occurred in the sedentary subjects and differed significantly (P < 0.01) from those in both groups of athletes. In the endurance- and strength-trained athletes, the exercise-induced increases in PRA were greater after than before BR (P < 0.01 and P < 0.05, respectively).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The present data clearly showed that only 3 days of BR can cause
marked reduction in exercise tolerance manifested by a decrease in
maximal exercise load and corresponding
O2 peak that occurred during
incremental exercise. The most pronounced effect of BR deconditioning
was found in the endurance-trained athletes with the highest aerobic
capacity. The strength-trained athletes, who did not differ
significantly from sedentary subjects in their ambulatory
O2 peak, also had similar post-BR
decreases in exercise tolerance. The percent decline in
O2 peak in the latter two groups (by
~10%) is comparable to that reported after short-term BR
deconditioning in highly fit but not regularly training subjects,
whereas the nearly 17% reduction in
O2 peak in the endurance-trained
athletes in the present study corresponds with levels obtained after
2-3 wk of BR (7). The significant correlation
coefficients confirmed a relationship between the ambulatory exercise
capacity and the decrease in post-BR
O2 peak in a relatively large group of
32 subjects.
BR deconditioning involves effects of changes in body position and usually a decrease in physical activity. The contribution of postural changes to the effect of BR was probably similar in all three groups of subjects. However, the degree of reduction in physical activity was certainly greater in the endurance athletes than in the sedentary subjects. With the bodybuilders, training was directed mainly to enhance their muscle mass and strength but not their aerobic capacity; thus their habitual physical activity was also reduced by BR more than in the sedentary subjects, but the test applied in this study was not specific for their training regime. Thus the more pronounced decrease of aerobic exercise performance in endurance athletes than in strength-trained or sedentary subjects, as well as lack of a major difference between the two latter groups, was expected.
Alterations in cardiac and vascular functions induced by prolonged BR
deconditioning have been reported to be the main factors responsible
for diminution of exercise performance (7, 16, 17), but
the mechanisms of the reduction of exercise performance after 3 days of
BR are not clear. In the present study, the maximal cardiac output was
not measured; however, in the sedentary subjects, the submaximal SV
values were diminished and HR was elevated after BR. If it is assumed
that SV during graded exercise reaches the maximum level at submaximal
loads, it might be expected that the maximal cardiac output was reduced
in this group. On the other hand, in neither group of athletes was the
exercise HR or SV up to 150 W altered by BR. This suggests that
reduction of maximal cardiac output is not the main factor responsible
for the decline in O2 peak. However, SV
in the athletes can increase progressively during incremental exercise
with no plateau (20). Thus, on the basis of the submaximal
SV values, the maximal cardiac output cannot be predicted and the
contribution of reduced maximal cardiac output to limitation of
performance after BR cannot be excluded.
The reduced exercise performance cannot be attributed to decreased
pulmonary gas exchange because the maximal exercise
E did not differ significantly from the pre-BR
values in the sedentary subjects and strength athletes. In the
endurance-trained subjects, the maximal E was
reduced proportionally to the decrease in O2 because
E/O2 was not
affected. Lack of influence of BR deconditioning on the maximal
E was reported previously (8, 9, 31).
It seems likely that inadequate adjustment of the peripheral circulation to exercise or an impairment of muscle aerobic capacity contributes to the limitation of working capacity after short-term BR. This hypothesis is supported by the enhanced blood [LA] during submaximal exercise and lowered blood LA threshold after BR in the endurance athletes. This is in agreement with previous data (9, 25) that showed greater increases in blood [LA] at submaximal loads after BR lasting 5-10 days. Moreover, Convertino et al. (9) reported that the anaerobic threshold, detected on the basis of pulmonary ventilation during graded exercise, is shifted toward lower exercise intensity after 10 days of BR. Sullivan et al. (34) also found a decrease of anaerobic threshold after 3 wk of BR unless the subjects were treated with dobutamine.
Greater LA production and shifting of its threshold may also result from an increased contribution of carbohydrates to the energy-yielding processes, as occurs after a high-carbohydrate diet (36). After BR, both at rest and during submaximal exercise, the RER was elevated in both groups of athletes. However, despite similar elevation of RER after BR in endurance- and strength-trained subjects, only in the former was the blood [LA] threshold markedly lowered. An increased RER after prolonged BR was reported previously (3, 8, 30), but the mechanism of this effect is still unclear. The diet during BR in the present study did not contain excessive amounts of carbohydrates compared with the subjects' habitual diet, but avoidance of exercise for 2 days preceding and during the next 3 days of BR could result in muscle glycogen accumulation and/or reduction in activities of muscle enzymes involved in fatty acid oxidation.
BR did not affect the preexercise plasma [Epi] and [NE] in any group, indicating that the previously reported inhibition of basal sympathetic activity after deconditioning (32, 33) is blunted in subjects sitting on a cycle ergometer anticipating exercise. The maximal postexercise plasma catecholamine concentrations were similar before and after 3 days of BR, contrary to results of Engelke and Convertino (14), who found plasma [NE] at volitional exhaustion higher by 64% after BR, but the duration of their BR was longer (16 days) than in the present investigation. In agreement with previous reports (6, 29), our data demonstrated an exponential pattern of changes in the plasma catecholamine concentrations during progressive graded exercise with thresholds similar to that of [LA]. In the sedentary and strength-trained subjects, the plasma catecholamine concentrations at submaximal loads and the catecholamine thresholds were similar before and after BR; however, in the endurance athletes the plasma [NE] at submaximal loads tended to be higher after BR and the NE threshold was significantly lower. Thus the deconditioning effect of 3 day-BR on the SNS response to exercise became evident only in the endurance-trained subjects.
It seems likely that the shift of the [NE] threshold toward lower exercise loads, reflecting earlier activation of the SNS, contributed to the increased lactate production because the BR-induced changes in the [NE] and [LA] thresholds were significantly correlated. There is an apparent discrepancy between this observation and the findings of Sullivan et al. (34), who reported that dobutamine administration during BR prevented the fall in exercise performance and lowering of the anaerobic threshold. However, application of daily infusions of dobutamine throughout 3 wk of BR probably simulated effects of aerobic exercise training on the cardiovascular system and on oxidative enzymes in skeletal muscle cells.
The decrease in hGH response to exercise after BR is consistent with data reported by McCall et al. (27); they used isometric exercise performed with a small group of muscles, which, before BR, induced an increase in the bioassayable, but not in immunoassayable, form of hGH. The exercise-induced increases in hGH were much greater in both groups of our athletes than in the sedentary subjects. However, in the group of strength-trained athletes there were three subjects with very high levels of hGH both before and after BR. If these subjects were excluded from the calculations, the mean exercise induced increments in this group would have been lower than in the endurance athletes but still higher than in the sedentary subjects. The decrease in the hormone responses to exercise after BR occurred in both athletic groups, but it was more pronounced in the endurance-trained subjects. These data suggest that the magnitude of the hGH response to maximal cycle exercise depends on the absolute exercise intensity, and the BR-induced reduction of this response may be the result of earlier exhaustion. However, disruption of the reflex mechanism activating hGH release, as suggested by McCall et al. (27), cannot be excluded.
Although activation of the renin-angiotensin system after BR is well
documented (19), there are no data on the effect of BR
deconditioning on the PRA response to exercise. The present results
indicated that, apart from elevation of resting and postexercise PRA
values in all groups of subjects, BR caused an enhanced PRA response to
exercise in the athletes despite their reduced maximal exercise load.
-Adrenergic stimulation of the juxtaglomerular apparatus of the
kidney is probably the main mechanism responsible for an increase in
renin release during exercise (23). Thus it appears that
the increased PRA response to exercise after BR can be attributed to
the -adrenergic-receptor sensitization, as was suggested previously
from experiments with -adrenergic-agonist infusion at rest (1,
28). Earlier activation of the SNS, as indicated by lowering of
the [NE] threshold after BR in the endurance athletes, may also have
facilitated their greater PRA response to exercise.
In none of the subjects did BR modify resting or postexercise plasma testosterone concentration, in confirmation of results of McCall et al. (27). In contrast, however, our postexercise cortisol levels were significantly elevated in the endurance athletes despite lower workloads after BR.
In summary, these data show that work tolerance, aerobic capacity, and the anaerobic threshold are diminished in endurance-trained men after only 3 days of BR, whereas less pronounced changes occur in sedentary subjects and strength-trained athletes. Three-day BR increased resting PRA in all three groups of subjects. In endurance athletes it modified neuroendocrine responses to graded exercise by an earlier increase in plasma [NE], attenuation of the increase in plasma [hGH], and accentuated elevation of PRA and cortisol. The effect of 3-day BR on the hormonal responses to exercise was negligible in strength-trained athletes and sedentary subjects. It appeared that the initial aerobic capacity determines the magnitude of these exercise effects. Further studies are needed to elucidate whether they depend on the level of activity specific for endurance training preceding BR or the genetic factors associated with aerobic capacity.
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ACKNOWLEDGEMENTS |
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The study was partly supported by Polish State Committee for Scientific Research Grant 4 PO5D040 12.
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FOOTNOTES |
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Address for reprint requests and other correspondence: H. Kaciuba-Uscilko, Dept. of Applied Physiology, Medical Research Centre, Pol. Acad. Sci., 5 Pawinskiego str., 02-106 Warsaw, Poland (E-mail: kaciuba{at}cmdik.pan.pl).
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.
Received 9 May 2000; accepted in final form 5 February 2001.
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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, Sedentary subjects; 
,
endurance-trained athletes; +, strength-trained athletes.
