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1 Norwegian Olympic Sports Center and 3 Norwegian University of Sports and Physical Education, 0806 Oslo; and 2 Institute of Immunology, Rikshospitalet University Hospital, 0027 Oslo, Norway; and 4 Copenhagen Muscle Research Center and Rigshospitalet University Hospital, 2200 Copenhagen, Denmark
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The impact of repeated bouts of exercise on plasma levels of interleukin (IL)-6 and IL-1 receptor antagonist (IL-1ra) was examined. Nine well-trained men participated in four different 24-h trials: Long [two bouts of exercise, at 0800-0915 and afternoon exercise (Ex-A), separated by 6 h]; Short (two bouts, at 1100-1215 and Ex-A, separated by 3 h); One (single bout performed at the same Ex-A as second bout in prior trials); and Rest (no exercise). All exercise bouts were performed on a cycle ergometer at 75% of maximal O2 uptake and lasted 75 min. Peak IL-6 observed at the end of Ex-A was significantly higher in Short (8.8 ± 1.3 pg/ml) than One (5.2 ± 0.7 pg/ml) but not compared with Long (5.9 ± 1.2 pg/ml). Peak IL-1ra observed 1 h postexercise was significantly higher in Short (1,774 ± 373 pg/ml) than One (302 ± 53 pg/ml) but not compared with Long (1,276 ± 451 pg/ml). We conclude that, when a second bout of endurance exercise is performed after only 3 h of recovery, IL-6 and IL-1ra responses are elevated. This may be linked to muscle glycogen depletion.
glucose; recovery; muscle; glycogen
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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IT IS WELL DOCUMENTED THAT exercise induces marked increases in several plasma cytokines (20-22, 25, 26, 38). These cytokine responses are often closely linked; thus an increase in plasma tumor necrosis factor is accompanied by a subsequent increase in interleukin (IL)-6, which is followed by an increase in IL-1 receptor antagonist (IL-1ra) (22, 39). In relation to concentric as well as eccentric exercise, IL-6 is produced in larger amounts than any other cytokine (27). Recent studies have demonstrated that IL-6 is produced locally in the working muscle, as opposed to IL-1ra, which does not appear to be originating from muscle cells but from mononuclear and polymorphonuclear leukocytes (23, 27, 39). Moreover, IL-6 produced in contracting skeletal muscles is released in large amounts into the circulation. This can account for the exercise-induced increase in plasma IL-6 (34). Additionally, it has been demonstrated that the production rate and total production of IL-6 are further enhanced when muscle glycogen content is low (14, 32). It is well known that IL-6 stimulates the production of IL-1ra, which binds to and blocks the IL-1 receptor, thus exerting strong anti-inflammatory effects (6, 11, 39). With exercise, peak IL-1ra is found 1-2 h after peak IL-6 (17, 22). From this, it is assumed that the level of IL-1ra reflects the production of IL-6.
Most elite athletes perform more than one training session per day. Recently, it has been shown that the second bout of exercise on the same day induces more pronounced changes in leukocyte subsets and stress hormones, especially in epinephrine and growth hormone, compared with a single bout of identical exercise (29, 28). Although it has been suggested that epinephrine plays a mechanistic role in the exercise-induced cytokine production (5, 24), a recent study did not lend much support to this idea (33). However, during a second bout of endurance exercise, muscle glycogen content may be compromised by the previous exercise bout (35). This may induce an energy crisis in the working muscle, affecting both carbohydrate and fat metabolism, if the recovery period between the exercise sessions is short and the work intensity is high. Muscle-derived IL-6 has recently been suggested to work in a hormonelike fashion, mediating glucose homeostasis during exercise (27, 35-37, 40).
Several investigations have studied pro- and anti-inflammatory cytokine responses to various protocols of a single bout of exercise (17, 19, 21, 22, 38), but there is very limited information on how repeated bouts of exercise on the same day affects IL-6 and IL-1ra (18). Thus we designed a study that used two identical bouts of exercise but with a different duration of rest between the exercise sessions. We hypothesized that a second bout of exercise performed after only 3 h of rest and with incomplete glycogen resynthesis after the first bout would induce more pronounced increases in plasma IL-6 and IL-1ra levels compared with a single bout of exercise. Furthermore, we wanted to examine whether extending the rest period between the exercise sessions from 3 to 6 h would attenuate the IL-6 and IL-1ra responses.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects.
Nine male, elite endurance athletes [four triathletes and five speed
skaters, age 21-27 yr, weight 74.7 ± 5.4 kg, maximal O2 uptake (
O2 max)
69.1 ± 3.7 ml · min
1 · kg1] from the
respective Norwegian national teams participated. All subjects were
accustomed to two daily training sessions as part of their normal
exercise schedule, including cycling as one of the training modalities.
A medical examination was performed on each subject before he entered
the study, and they were thoroughly informed about the purposes and
procedures of the study before a written consent was obtained. The
protocol was approved by the Regional Committee for Ethics in Medical
Research, Norway.
Design.
All subjects participated in four trials, each lasting from 0700 to
0800 the following day: 1) complete bed rest (Rest),
2) one bout of exercise from 1515-1630 (One),
3) two bouts of exercise (1100-1215 and 1515-1630)
with 3 h of rest in between (Short), and 4) two bouts
of exercise (0800-0915 and 1515-1630) with 6 h of rest
in between (Long) (Fig. 1). The trials
were separated by 12-17 days to ensure complete recovery among
trials and were randomized in a counterbalanced order with each subject
serving as his own control. The triathletes were tested between January and March, and the speed skaters between April and June, i.e., outside
the competitive season for both groups. Except for the last 2 days
before each trial, when exercise was regulated by the study protocol,
the subjects completed their regular training program without any
interruption during the study period.
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Pretrial procedures.
Approximately 2 wk before the start of the study, the subjects
performed an incremental exercise test on a cycle ergometer (Lode,
Groningen, The Netherlands), starting at a workload of 175 W with a
subsequent increase of 25 W every 5 min until they had reached a
workload of 275 W. The subjects then rested for 10 min before a
continuous ramp test was used to estimate
O2 max, starting at 275 W, with a
subsequent increase of 25 W every 30 s until volitional exhaustion
(i.e., the subject could not sustain the workload for a period of >30
s). A respiratory exchange ratio (RER) of >1.1 was used as an
additional criterion that O2 max had
been reached. The results were used to estimate a workload corresponding to 70% of O2 max for
each subject based on the regression line of O2 uptake vs.
workload from the incremental exercise test. However, in the next
experimental trials, performing at the individually estimated workload
resulted in a mean O2 uptake of ~75% of
O2 max.
Trial procedures. The subjects arrived in the laboratory at 7:00 AM, emptied their bladder, had their body weight measured, and were subsequently put to bed. A flexible temperature probe was inserted in the rectum, and the subjects were connected to a temperature, electrocardiogram, and heart rate monitor (Siemens SC 6000 P, Siemens Medical Systems, Danvers, MA). A flexible intravenous catheter (Venflon 1.2; 32 mm, BOC Health Care, Helsingborg, Sweden) was inserted into an antecubital vein and kept there for the whole trial.
The morning (Ex-M) and afternoon exercise (Ex-A) bouts were equal in intensity and duration and consisted of a 10-min warm-up period at 50% ofO2 max, immediately followed by 65 min at the subjects' predetermined workload with a cadence of
90-100 rpm. All subjects completed all of the exercise sessions,
but the workload had to be reduced temporarily on five occasions to avoid premature exhaustion. Subjects who had to have their workload reduced were excluded from the data analysis of O2 uptake
during exercise. The O2 uptake was measured for 60 s
after 15, 30, 45, 60, and 70 min of exercise, as well as continuously
during the first hour postexercise and for 10 min every hour during the
subsequent recovery period. Blood for cytokine analysis was sampled at
the start of all trials, 15 min before Ex-A, at the end of exercise, and 1, 2, 4, and 14 h postexercise.
The subjects rested in bed at all hours when they did not exercise and
spent the following night sleeping in the laboratory until 0700 the
next morning. The subjects were allowed to read and thus had a 45°
headrest, except for the last 15 min before each blood sampling. They
were allowed to listen to music during exercise and rest, but watching
television was restricted to a maximum of 3 h in the evening
between 1800 and 2200. No sleep was allowed during the daytime. During
each trial, the subjects were served four standardized meals at 0815 (1015 in trial Long), 1315, 1745, and 2145 h (Fig. 1). The meals
consisted of double sandwiches with butter, ham, cheese, jam, and
honey; there were three for breakfast, four for lunch, three for
dinner, and four for supper, for a total of 16 MJ. The same type and
number of sandwiches were served during each trial. Water was consumed
ad libitum during exercise and recovery, except for the first 60 min
postexercise, when O2 uptake was measured continuously. The ambient room temperature was kept at 20 ± 2°C, and humidity at 40 ± 10%.
Metabolic measurements. During the pretrial test, the O2 uptake was measured during the last 90 s at each increment with an automated Oxycon Champion System (Erich Jaeger) with a nose clip and a Rudolph mouthpiece, and gas exchange was recorded for every expiration. In the three study trials, the O2 uptake was measured by collection of expired air in Douglas bags (Hans Rudolph, Kansas City, MO). The bags were emptied through a flow controller (Flow Transducer K 520, K. L. Engineering) and volume counter (Spirometric module, K. L. Engineering). The CO2 and O2 contents were measured on an O2 analyzer (Ametek Oxygen Analyzer, model S-3A, and Ametek Oxygen Sensor, model N-22M, Pittsburgh, PA) and a CO2 analyzer (Ametek Carbon Dioxide Analyzer, model CD-3A, and Ametek Carbon Dioxide Sensor, model P-61B). Additional measurements of air pressure and temperature were performed on an EOS-sprint system (Erich Jaeger).
Cytokine and glucose measurement.
For cytokine measurement, a 5-ml blood sample was drawn into a glass
tube containing 35 µmol dipotassium-EDTA and 1,500 kallikrein- inactivator units of Trasylol (Bayer, Leverkusen, Germany). The tube
was kept on ice for 15 min before centrifugation at 2,500 rpm for 15 min at 4°C (Biofuge 17RS, Heraeus SEPATECH, Osterade, Germany).
Plasma was separated from the cells and stored at 
80°C until
subsequent analysis for IL-6 and IL-1ra. The cytokines were analyzed by
commercially available high-sensitivity ELISA, according to the
manufacturer's instructions (Quantikine HS, R&D Systems Europe, Oxon,
UK). All measurements were performed in duplicate. For IL-6, the lower
and upper detection limits were 0.7 and 300 pg/ml, and for IL-1ra the
corresponding limits were 10 and 3,000 pg/ml, respectively. According
to information provided by R&D Systems, the ELISA used for measuring
IL-6 is insensitive to the addition of the recombinant forms of the
soluble receptor, thus measuring both soluble and receptor-bound IL-6.
Plasma glucose was determined by using the Roche Glucose HK liquid
enzymatic assay (Roche Diagnostics, Manheim, Germany) on a
Roche/Hitachi 917 analyzer. Blood for catecholamine analysis was
collected in a 3-ml precooled 143-USP heparinized tube, kept on ice for
15 min before centrifugation at 6°C for 10 min at 3,000 rpm, frozen immediately, and stored at 70°C. Plasma epinephrine was analyzed by
HPLC with electrochemical detection, according to a previously described method (28).
Statistical analyses. In three of the nine subjects, IL-6 concentrations >4 pg/ml were measured in the resting state. These were considered outliers and were, therefore, excluded from the statistical analysis. The same subjects were also excluded from the IL-1ra analysis. The plasma glucose data were analyzed by using all subjects (n = 9). A two-way ANOVA procedure for repeated measures, testing for main effects of trial and time, was used to compare the individual trials, including measurements from 1500 to 2030 h. Student's t-test and Pearson correlation test were used for between-trial comparisons at the same time point (peak values) or time period (delta values). P levels < 0.05 were considered significant, but specific P values are generally given. Results are presented as means ± SE, unless otherwise noted.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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IL-6.
Plasma levels of IL-6 increased in all exercise trials during the Ex-A
compared with trial Rest (time effect; P < 0.001) and remained elevated for at least 2 h (Fig.
2). Peak IL-6 was significantly higher in
trial Short (8.8 ± 1.3 pg/ml) compared with trial One (5.2 ± 0.7 pg/ml; P = 0.014) but not compared with trial
Long (5.9 ± 1.2 pg/ml; P = 0.160). When
concentration is compared during the entire period from 1500 to
2030 h, the increase in concentrations of IL-6 was more pronounced
in trial Short compared with trial One (P = 0.025).
However, there was no statistical difference between changes in Il-6 in
trials Short and Long (P = 0.084). After 4 h of
recovery, IL-6 had reached baseline levels in all exercise trials.
There was no correlation between pre- to post-Ex-A changes in IL-6 and
plasma glucose concentrations in trials Short (r = 0.48) or Long (r = 0.03). When the pre- to post-Ex-A
changes in IL-6 are compared with the corresponding changes in
epinephrine (Table 1) (28),
we found a significant correlation in trial Short (r = 0.91, P < 0.02) but not in trial Long
(r = 0.79, 0.05 < P < 0.10).
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IL-1ra.
As shown in Fig. 3, the plasma level of
IL-1ra was elevated before the Ex-A in trial Short compared with Rest
(P = 0.022), but no significant change in IL-1ra was
observed from before to after Ex-A in the three exercise trials.
However, IL-1ra increased in all exercise trials during the first hour
of recovery (time effect; P < 0.02). Peak IL-1ra was
higher in trial Short (1,774 ± 373 pg/ml) compared with trial One
(454 ± 109 pg/ml; P = 0.015) but was not
statistically higher compared with trial Long (1,276 ± 451 pg/ml). When concentration is compared during the entire period from
1500 to 2030, the increase in concentrations of IL-1ra was more
pronounced in trial Short compared with trial One (P = 0.002). There was no statistical difference between IL-1ra changes in
trials Short and Long (P = 0.219) during this period.
After 4 h of recovery, IL-1ra was still elevated in trial Short
compared with One (P = 0.031) but not compared with
trial Long (P = 0.137).
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Plasma glucose and epinephrine.
Compared with trial Rest, there was a significant decrease in plasma
glucose during Ex-A in trials One (P = 0.030), Short (P = 0.011), and Long (P = 0.001; Fig.
4). Furthermore, during Ex-A, there was a
trend toward a larger decrease in trial Short compared with trial One
(P = 0.059), but there was no difference in the
magnitude of decrease between trials Short and Long (P = 0.865). During the recovery period after Ex-A, plasma glucose showed
a larger magnitude of changes in all three exercise trial compared with
trial Rest (trial × time effect; P < 0.001);
however, there were no differences in the magnitude of change between
trials One and Short (P = 0.523) or trials Short and
Long (P = 0.112). Concentrations of epinephrine in the
four trials during the time period for Ex-A and the first hour of
recovery (1500-1730) are given in Table 1. Peak epinephrine at the
end of Ex-A was higher in trial Short (9.1 nmol/l) compared with trial
One (1.6 nmol/l; P < 0,0005) and trial Long (6.1 nmol/l; P < 0.005).
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O2 uptake and RER. Mean O2 uptake during exercise was 3.7 ± 0.1 l/min in trial One, 3.9 ± 0.1 l/min during the second bout in trial Short, and 3.8 ± 0.1 l/min in trial Long. Mean O2 uptake during Ex-A in trial Short was 0.21 ± 0.04 l/min higher than in trial One (P = 0.040) and 0.09 ± 0.03 l/min higher than in trial Long (P = 0.025). The average RER during Ex-A was lower in trial Short (0.84 ± 0.02) compared with trial One (0.87 ± 0.02; P = 0.005) and trial Long (0.86 ± 0.02; P = 0.010). During the first 5 h of recovery, RER was lower in trial Short than trial One (P = 0.006), but there was no difference between trials Short and Long (P = 0.242).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The main finding in the present study was that the second bout of exercise in trial Short provoked more pronounced increases in plasma levels of IL-6 and IL-1ra compared with the first (single) bout in trial One. Furthermore, the increased levels of these cytokines during and after the second bout of exercise were attenuated when the period of rest between the exercise sessions was extended from 3 h in trial Short to 6 h in trial Long (Figs. 2 and 3). Plasma glucose decreased during Ex-A in trials One, Short, and Long, but there was no significant difference in magnitude of change among the three exercise trials.
To our knowledge, there is only one published study examining the effect of repeated bouts of exercise on plasma levels of IL-6 (18). Using a protocol with three bouts of exhaustive rowing, each lasting 6 min and separated by 4 h of rest, Nielsen et al. (18) showed a trend toward augmented peak values after each consecutive bout of exercise. Despite the differences in exercise protocol, the findings of Nielsen et al. correspond with the results of the present study. The more pronounced IL-6 and IL-1ra responses observed on the second bout after only 3 h of rest in the present study were according to our hypothesis. There may be several explanations for this finding, but we propose incomplete resynthesis of muscle glycogen during recovery between the two bouts of exercise as the most plausible explanation (27).
Earlier studies have observed a 60-80% reduction in glycogen
content of working muscles after a single bout of exercise with similar
intensity and duration as in the present study (2-4, 8, 13,
15, 41). Furthermore, these and other studies have demonstrated
that restoring muscle glycogen completely after strenuous endurance
exercise may take as long as 24 h and that the rate of resynthesis
is, to a great extent, dependent on the glucose availability during the
postexercise period. We did not obtain muscle biopsies in the present
study, but, on the basis of the aforementioned investigations, a
substantial reduction in glycogen stores could be expected at the end
of the first bout of exercise. By analyzing multiple muscle biopsies
after exhaustive work of 78-113 min at 75%
O2 max, Blom et al. (3) estimated a maximal rate of glycogen synthesis of ~6
mmol · kg1 · h1 and found
only 40-44% of the preexercise muscle glycogen content after
4 h of recovery (varying with the amount of glucose in the refeeding regime) (3). Therefore, we must assume that
muscle glycogen was incompletely restored during the rest period
between the two bouts of exercise, particularly in trial Short in which only 3 h of rest and one meal containing 4 MJ were given.
The assumption that glycogen stores were compromised during the second
bout of exercise is supported by the lower mean RER found in trial
Short (0.84 ± 0.02) compared with One (0.87 ± 0.02; P = 0.005), both during and after the second bout of
exercise. This indicates a shift toward decreased carbohydrate and
increased fat oxidation on the second bout of exercise. Furthermore, in a recent study that used a glucose clamp technique, Galassetti et al.
(9) demonstrated an increased turnover of carbohydrate fuels during a second bout of endurance exercise, even at
moderate intensity. When two equal bouts of 90-min exercise are
performed at 48% of O2 max separated
by 3 h of rest, a fivefold higher rate of exogenous glucose
infusion was needed during the last 30 min of the second bout of
exercise to maintain euglycemia. This further substantiates the
argument that muscle glycogen stores in the subjects of the present
study must have been minimal toward the end of the second bout of
exercise, particularly because exogenous carbohydrates were not
provided during exercise.
Interestingly, two recent studies have demonstrated that IL-6 production in contracting muscle is influenced by preexercise muscle glycogen content, showing a larger IL-6 production when exercise is performed in glycogen-depleted states (14, 32). Other studies have altered carbohydrate supply before (10) or during (17, 31) strenuous endurance exercise and observed an attenuating effect of increased carbohydrate availability on the IL-6 and IL-1ra responses to prolonged exercise. Furthermore, recombinant IL-6 has proved to have dose-dependent effects on glucose regulation (40) and to mediate metabolic effects during catabolic states (37). Thus we suggest that the more pronounced IL-6 at the end of the second bout of exercise observed in the present study, and the subsequently increased IL-1ra response, may be a result of muscle glycogen depletion. It could be speculated that increased IL-6 reflects an energy crisis within the working muscle, thus mediating a signal for increased substrate mobilization in other organs and tissues in the body, i.e., performing a hormonelike action (27). It has been demonstrated that IL-6 can arrest fasting-induced decline in blood glucose in a dose-dependent fashion, possibly through direct action on hepatocytes or through glucose counterregulatory hormones like glucagon, cortisol, GH, and epinephrine (40). Furthermore, infusion of IL-6 seems to mimic many of the metabolic alterations associated with a catabolic state, including increased lipolysis and fat oxidation, increased oxygen consumption and energy expenditures, and increased hepatic glucose output, although the mechanisms of action are not clear (37).
In accordance with previous studies on blood glucose regulation during strenuous endurance exercise, we observed a fall in plasma glucose during Ex-A (1, 7, 13). However, the new observation from this study is that glucose concentration appears to remain well regulated during a second bout of exercise, even in the absence of exogenous carbohydrate supply during the exercise. Moreover, a reduction from 6 to 3 h of the rest and a 50% reduction in caloric intake between the two exercise sessions did not seem to further affect plasma glucose concentrations during the second bout. Also, there was no correlation between changes in plasma glucose and IL-6 concentrations from pre- to postexercise on the second bout. Thus, assuming IL-6 is involved in signaling carbohydrate substrate shortage during prolonged strenuous exercise, our observations lend support to the contention that muscle glycogen content rather than blood glucose concentration is the dominant stimulus for increased IL-6 production during high-intensity endurance exercise (27).
Epinephrine has been proposed to possess a mechanistic role in the increased levels of plasma IL-6 during exercise (16, 24, 30, 37). In an earlier publication from the present study, we reported a fivefold higher increase in epinephrine during the second bout in trial Short compared with the first bout in trial One (28). When comparing the pre- to post-Ex-A changes in IL-6 with the corresponding changes in epinephrine, we found a significant correlation in trial Short but only a trend in trial Long. However, because peak epinephrine was 500% higher, whereas peak IL-6 was only 40% higher, during the second bout compared with the first bout, this does not indicate a strong relationship. Furthermore, Steensberg et al. (33) have shown that the exercise-induced increase in plasma IL-6 could not be mimicked by epinephrine infusion, thus suggesting only a minor role for epinephrine in stimulating IL-6 production during exercise.
All exercise sessions in the present study lasted 75 min, and the
subjects performed all exercise bouts at the same relative workload,
corresponding to ~75% of O2 max.
However, mean oxygen uptake was slightly higher during the second bout
of exercise in trial Short (3.9 ± 0.1 l/min) compared with the
first bout in trial One (3.7 ± 0.1 l/min). This may be a result
of increased exertion [rating of perceived exertion was higher in
trial Short (15.5 ± 0.9) than One (13.0 ± 0.7;
P = 0.006), data not published], increased fat
oxidation relative to carbohydrate (RER was lower in trial Short than
One), altered muscle fiber recruitment, or a combination of these
factors. Nevertheless, it is our opinion that this minor (4%)
elevation of oxygen uptake may only account for a smaller part of the
augmented IL-6 and IL-1ra responses associated with the second bout of exercise.
Three of the nine subjects showed initial resting levels of IL-6 >4 mmol/l and consistently high levels throughout the trial in one or more of the four exercise trials. IL-6 concentrations of this magnitude have not been observed at rest in previous investigations (14, 27, 34). Because all samples were analyzed in duplicates and all samples from each trial were analyzed in kits from the same batch, analytic error does not appear to be the most plausible explanation. Rather, some form of immunological activation, i.e., infection or inflammation, may have triggered a cytokine response before entering the trial (12). Interestingly, among the four subjects who needed to reduce their workload temporarily because of near exhaustion during Ex-A (see METHODS), we found all three subjects who were excluded on the basis of high resting levels of IL-6. However, none of these subjects had reported any illness symptoms within the last 5 days before or the day after the trials. In any case, it appeared reasonable to exclude these subjects from both the IL-6 and IL-1ra analysis, because changes in IL-1ra are known to be related to elevations in IL-6 (39).
Conclusion. On the basis of this study, we conclude that a second bout of high-intensity endurance exercise on the same day is associated with a more pronounced increase in IL-6 and IL-1ra compared with a single bout of similar exercise. Furthermore, a trend toward attenuation in the augmented cytokine response was observed when the rest period between the two bouts of exercise was extended from 3 to 6 h and an additional meal was served. The augmented IL-6 and IL-1ra response may be linked to glycogen depletion in the working muscle, thus representing a signal of energy shortage in the muscle and a need for increased substrate mobilization from other tissues. Further studies that use a design with repeated bouts of exercise are warranted to elucidate the mechanism(s) and biological significance behind the augmented increases in IL-6 and IL-1ra.
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ACKNOWLEDGEMENTS |
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We are grateful for the skillful assistance of Øystein Haugen and Tone Rassmussen Øritsland at the Norwegian University of Sport and Physical Education.
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FOOTNOTES |
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This study was supported by a grant from The Norwegian Research Council and The Norwegian Olympic Committee and Confederation of Sport.
Address for reprint requests and other correspondence: O. Ronsen, Norwegian Olympic Sports Center, Box 4004, Ullevaal Stadion, 0806 Oslo, Norway (E-mail: ola.ronsen{at}olympiatoppen.no).
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.
First published January 18, 2002;10.1152/japplphysiol.01263.2001
Received 27 December 2001; accepted in final form 17 January 2002.
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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