Repeated high-intensity work is performed in sports such as soccer (36), basketball (35), and rugby (43) and taxes both the aerobic and anaerobic energy systems. The mean HR is around 85% of maximal HR in soccer (5) and basketball (35), with average blood lactate being 4-7 mM and peak values more than 10 mM (31,35). Nearly 40 sprints have been reported to occur for a player during a soccer game with the average distance being around 10-15 m (36). When comparing teams at different competitive standards, it is evident that the teams at the highest level carry out more high-intensity running during competition in soccer (36) and rugby (43). Furthermore, the players in the high-level teams perform better than players in lower ranked teams in the Yo-Yo intermittent recovery (Yo-Yo IR) tests consisting of 2 × 20-m runs with increasing speed interspersed by 10 s of recovery between work bouts until exhaustion (6). Thus, the players' ability to conduct repeated high-intensity work is an important factor for team success.
The aerobic energy system makes a significant contribution to energy turnover during repeated high-intensity work (8,12), and several studies have found a correlation between maximal oxygen uptake (V˙O2max) and performance in repeated sprint tests (RST) (44) and the Yo-Yo IR tests (6,41). In addition, recent studies have shown a correlation between fast pulmonary V˙O2 kinetics at 60% maximal aerobic speed (MAS) and performance in repeated 40-m sprints (19,42) and the Yo-Yo IR levels 1 (IR1) and 2 (IR2) tests (41) in trained soccer players. However, sprints in soccer have an average duration of ∼2 s (15 m) (36), and the validity of the results for match play may be questioned.
In untrained subjects, V˙O2 kinetics has been shown to be improved by different types of training ranging from low-intensity work at 60% V˙O2max in 6 wk (10) to high-intensity interval training using 4-7 × 30-s all-out sprints with 4 min of recovery for 2 wk (2), 20 × 1 min at 90% V˙O2max with 1-min recovery periods for 6 wk (10), and 15 × 1 min at 150% leg V˙O2max separated by 3 min of recovery for 7 wk (29). Limitations to oxygen uptake in the initial part of exercise is attributed either to local limitation in the muscles ("metabolic inertia") or in the oxygen delivery (40). In the aforementioned training studies performed on untrained subjects, it was unclear what caused the faster V˙O2 kinetics because the improvement was accompanied by increases in V˙O2max, capillary density, enzyme activity, and muscle blood flow during work. In trained runners, a combination of moderate continuous running and high-intensity interval training at intensities close to V˙O2max during 8 wk also resulted in faster V˙O2 kinetics, which seems to be caused by peripheral adaptations because V˙O2max was unaltered (18). This assumption is supported by results from another study performed on physical education students in which V˙O2 kinetics became faster and V˙O2max remained unchanged after 4 wk of intense interval training (11). A few weeks (4-9 wk) of intense intermittent and reduced amount of training have been shown to improve performance during short-term intense exercise in already trained runners (4,26). However, it is unclear whether a shorter period of intensified and reduced training can improve performance during repeated high-intensity work and V˙O2 kinetics of trained soccer players accustomed to high-intensity intermittent work.
The effect of inactivity on V˙O2 kinetics has not been investigated to the same extent as training. Inactivity causes among other things a decrease in oxidative enzymes (37), which may affect V˙O2 kinetics. Convertino et al. (17) found that V˙O2 kinetics became slower after 7 d of bed rest in untrained subjects. However, the time resolution was low (30-s intervals), and only one work period was used to describe the V˙O2 kinetics (33). In two other studies with untrained subjects, V˙O2 kinetics was not changed by 2 wk of bed rest (16) or 3 wk of inactivity in one leg after harness suspension (24), which may be because of the low training status of the subjects before the studies. Therefore, the effect of inactivity of trained subjects on V˙O2 kinetics and the relation to oxidative enzymes need to be studied.
Thus, the aim of the present study was to examine the effect of a 2-wk period of intensified training and cessation of training of trained soccer players on V˙O2 kinetics and how it is linked to muscle oxidative enzymes and the ability to perform repeated high-intensity work. In addition, another aim of the study was to evaluate whether V˙O2 kinetics was related to performance during repeated high-intensity work, using a higher intensity to describe V˙O2 kinetics and a shorter sprint distance than that used previously to mimic the work demands during intermittent sports such as soccer.
Eighteen male soccer players participated in the study. All subjects were members of teams from the Danish second division (third best league), with the exception of one player coming from the first division. All subjects were healthy, and none was on medication. Age, height, weight, and pulmonary V˙O2max were 23.4 ± 3.5 (mean ± SD) yr, 181.8 ± 6.7 cm, 78.5 ± 8.5 kg, and 55.0 ± 3.1 mL O2·kg−1·min−1, respectively. The subjects had been training and competing on the elite level on a regular basis for at least 2 yr. Their normal week schedule consisted of three to four training sessions and one match. After receiving oral and written information about any possible risks and discomforts associated with the experimental procedures, all participants gave their written informed consent to participate. The study conformed to the Code of Ethics of the World Medical Association (Declaration of Helsinki) and was approved by the Ethics Committee of the Copenhagen and Frederiksberg communities.
Experimental Protocol and Design
The present study was conducted as a randomized two-group longitudinal experiment. After the last match of the season, the subjects were either assigned to a high-intensity training group (HI, n = 7) or to a training cessation group (TC, n = 11) for a period of 2 wk. Before the intervention period, the subjects completed an incremental running test for determination of maximal oxygen uptake (V˙O2max), MAS, and HRmax. Furthermore, both before and after the intervention period, the subjects carried out approximately six runs at 75% MAS for estimation of V˙O2 kinetics (see below), the Yo-Yo IR2 test, and an RST. The tests were performed during two separate days with three submaximal exercise bouts and the Yo-Yo IR2 being performed on the first day and three submaximal exercise running bouts and the RST on the second day using the same test order before and after the intervention period. All the testing took place at least 36 h after the last practice or test session and more than 72 h after a match. In addition, TC performed the Yo-Yo IR2 test 72 h into the inactivation period. A muscle biopsy was obtained from the musculus Vastus lateralis with the Bergström technique at rest during the first visit to the laboratory both for HI and TC as well as 36-40 h after the last training in the intervention period for HI and after 14 d with training cessation for TC. The biopsies were split into two parts. One part was immediately frozen in liquid nitrogen, and the other part was embedded in Tissue-Tek (Sakura Finetek, Zoeterwoude, The Netherlands) and frozen in isopentane. The biopsies were stored at −80°C until analyzed.
During the intervention period, HI had 10 training sessions including five aerobic high-intensity (AHI) sessions and five speed endurance training (SET) sessions. Each training session included an approximately 25-min warm-up program. The AHI sessions were performed as small-sided soccer drills (four vs four and three vs three) on artificial grass consisting of eight repetitions of 2 min of exercise interspersed by 1 min of recovery. HR was recorded at 5-s intervals (Polar Team System; Polar Electro Oy, Kempele, Finland) during every session and afterward downloaded to a personal computer for further analysis. Mean HR during the 2-min exercise period in AHI was 87.7% ± 1.2% of HRmax (determined during incremental running), and the total duration of the exercise in AHI was 75.4 ± 7.8 min. Four of the SET sessions consisted of 10-12 × 25- to 30-s all-out sprinting bouts including changes of directions and parts with ball contacts. Peak HR was 88.4% ± 1.9% of HRmax, and the total duration of the exercise periods was 19.9 ± 0.6 min. In one of the SET sessions, the players performed 16 exercise bouts lasting 40-60 s separated by a recovery time between the work bouts of a similar duration. Mean HR during the exercise periods was 84.4% ± 1.7% of HRmax, and the total duration of exercise periods was 14 min. SET was performed the day after an AHI session, and no training was performed the day after an SET session. Overall, the players in HI reduced the total training duration during the 2-wk training intervention by ∼30% compared with their normal training.
The subjects in TC did not perform any training during the 2-wk intervention period, and they maintained their normal daily activities but refrained from intense physical activity.
On the days of testing, subjects reported to the laboratory at least 2 h after consuming a light meal. Subjects refrained from strenuous physical activity in the last 36 h before testing and abstained from alcohol and caffeine consumption 24 h before the testing. During all testing sessions, the HR was recorded during 5-s intervals (Polar Team System; Polar Electro Oy).
Incremental running test.
The subjects completed an incremental running protocol on a motorized treadmill, starting with 5 min at 10 km·h−1 followed by 4 min at 14 km·h−1, and then, the running speed was increased by 1 km·h−1 every minute until exhaustion. Throughout the test, pulmonary oxygen uptake was measured by a breath-by-breath gas analyzing system (JAEGER MasterScreen CPX; Viasys Healthcare GmbH, Hoechberg, Germany). The analyzer was calibrated before each test with two gases of known O2 and CO2 concentrations as well as by the use of a 3-L syringe for the tube flow meter calibration. V˙O2max was determined as the highest value achieved during a 20-s period. A plateau in oxygen uptake, despite an increased power output, and an RER >1.10 were used as criteria for V˙O2max achievement. MAS was determined as the lowest running speed when V˙O2max was achieved, and HRmax was determined as the highest value observed during the test.
The subjects performed approximately six runs at 75% MAS (average speed = 14.1 km·h−1) corresponding to ∼85% V˙O2max on two separate days both before and after the intervention period to describe V˙O2 kinetics. This intensity was chosen because it is well known that high-intensity aerobic exercise is of great importance for elite soccer players (30,36). The pulmonary V˙O2 was measured breath by breath with the same equipment as in the V˙O2max test. Each bout consisted of 1 min of rest standing on the treadmill followed by 4 min of running at 75% MAS. Because preceding work can influence V˙O2 kinetics (14), the work bouts were separated by a 30-min rest period, and the first run was not included in the calculations. Thus, V˙O2 kinetics was modeled from four transitions both before and after HI and TC. To estimate V˙O2 kinetics, the average pulmonary V˙O2 in 5-s intervals was calculated for each running bout. The cardiopulmonary phase corresponding to 15-20 s was removed before modeling of the V˙O2 responses for each individual (9,15,45). The individual V˙O2 values for the four transitions were modeled using monoexponential fitting (Mathcad; Parametric Technology Corp., Needham, MA):
where t = time, V˙O2 baseline = average V˙O2 at standing rest, A′ = asymptote for the exponential rise in V˙O2, Td = time delay (s), and τ = time constant (s)-63% of time to reach the final V˙O2 value. In addition, the mean response time (MRT) was calculated as time delay + τ (9). An iterative process was used to minimize the sum of the squared errors between the fitted function and the observed values. The 4-min work period was chosen to avoid fatiguing the subjects before the RST and the Yo-Yo IR2 test. This procedure allowed for a calculation of the overall response by the monoexponential fitting procedure described previously but did not allow a prober two-component exponential fitting and determination of the slow component. Instead, the rise in pulmonary V˙O2 in the last phase of exercise was evaluated as the difference in V˙O2 from 120-150 to 210-240 s. Running economy (RE) (mL O2·kg−1·km−1), RER (V˙CO2/V˙O2), and HR (%HRmax) were calculated during the final 30 s of each 4-min running bout.
The RST was performed indoor on a wooden floor. A standardized 15-min warm-up procedure was performed with the last part consisting of two 20-m sprints separated by 1 min of recovery. The RST was then performed 2 min after the last sprint. The subjects carried out ten 20-m sprints interspersed by 15 s of active recovery. All sprints started from a standing position. In the recovery period, the subjects ran slowly back to the starting point before the next sprint. Time to cover the 20-m sprint was measured with ports of light sensors (Newtest Powertimers; Newtest Oy, Oulu, Finland). Fastest sprint time (FST) and total time for all 10 sprints (TST) were determined. If the fastest sprint was obtained during the warm-up, this was used as FST. In addition, a sprint fatigue index (SFI) was calculated as SFI = (1 − FST × 10 × TT−1)100%. Furthermore, the reliability of RST was determined in six subjects, who performed the RST twice separated by 4 d. The coefficients of variance for TST, FST, and SFI were 0.7% ± 0.2%, 0.6% ± 0.2%, and 7.7% ± 3.0%, respectively.
Yo-Yo IR2 test.
The Yo-Yo IR2 test was performed indoor on a wooden floor after a 15-min standardized warm-up procedure. The Yo-Yo IR2 test consists of 2 × 20-m shuttle runs at increasing speeds, interspersed with 10 s of active recovery controlled by audio signals from a CD (30). The test was terminated when the subject was no longer able to maintain the required speed. The total distance covered represented the test result.
To determine the maximal activity of citrate synthase (CS) and 3-hydroxyacyl-CoA (HAD), muscle samples were freeze-dried, and all connective tissue, visible fat, and blood were removed under a stereomicroscope in a room with a temperature of 18°C and a relative humidity below 30%. About 2 mg dry weight of muscle tissue was homogenized (1:400) in a 0.3-M phosphate buffer adjusted to pH 7.7 containing 0.5 mg·mL−1 of bovine serum albumin. Maximal activities of CS and HAD were determined by using fluorometric methods with nicotinamide adenine dinucleotide-coupled reactions (Fluoroskan Ascent; Thermo Scientific, Waltham, MA) (34).
The amount of pyruvate dehydrogenase (PDH) was determined by western blotting. Approximately 3 mg dry weight of muscle tissue taken at rest was homogenized in a fresh batch of buffer (10% glycerol, 20 mM of Na pyrophosphate, 150 mM of NaCl, 50 mM of HEPES, 1% NP-40, 20 mM of β-glycerophosphate, 10 mM of NaF, 2 mM of phenylmethylsulfonyl fluoride, and 1 mM of EDTA and EGTA, aprotinine, leupeptine, and benzamidine) two times of 30 s (QIAGEN TissueLyser II; Retsch GmbH, Haan, Germany). After rotation end over end for 1 h, the samples were centrifuged for 30 min at 17,500g at 4°C, and the lysate was collected as the supernatant. Protein concentrations were determined in the lysates using bovine serum albumin standards (Pierce Reagents, Chicago, IL). The lysates were diluted to appropriate protein concentrations in a 6X sample buffer (0.5 M of Tris base, dithiothreitol (DTT), sodium dodecyl sulfate, glycerol, and bromphenol blue), and an equal amount of total protein was loaded for each sample in different wells on precasted gels (Bio-Rad Laboratories, Copenhagen, Denmark). For comparisons, samples from the same subject were always loaded on the same gel. After gel electrophoresis, the proteins were blotted to a polyvinylidene fluoride (PVDF) membrane, which was incubated with ∼10 mL of a primary antibody overnight and then washed for 5 min in Tris-buffered saline-Tween 20 (TBST) before incubation with a secondary antibody for 1 h. PDH-E1α protein expression was measured in muscle samples by sodium dodecyl sulfate polyacrylamide gel electrophoresis (Tris-HCl 10% gel; Bio-Rad Laboratories) and western blotting using the PVDF membrane and semidry transfer. After the transfer, the PVDF membrane was blocked overnight at 4°C (TBST + 2% skim milk). The following day, the membrane was incubated with the primary antibody (39) in TBST + 2% skim milk for 2 h at room temperature and thereafter washed in TBST and incubated with a horseradish peroxidase-conjugated secondary antibody (Dako, Glostrup, Denmark) for 1 h at room temperature (TBST + 2% skim milk). Immobilon Western (Millipore Corp., Billerica, MA) was used as a detection system. Bands were visualized using an Eastman Kodak Co. Image Station 2000MM. Bands were quantified using the Kodak Molecular Imaging Software v. 4.0.5 (Eastman Kodak Co., Rochester, NY), and protein content was expressed in units relative to control samples loaded on each gel. The changes in PDH are expressed as an arbitrary unit and relative to the levels before the interventions. On the basis of our experience with variation in results from western blotting, observations were removed if the delta ratio (before vs after) differed more than the average delta ratio ± 2 SD for the two groups separately. This resulted in removal of data from one subject from TC.
Muscle fiber types and size.
Ten-micrometer-thick sections of the muscle samples embedded in Tissue-Tek were cut at −20°C and incubated for myofibrillar ATPase reactions at pH 9.4, after preincubation at pH 4.3, 4.6, and 10.3 (13). On the basis of the myofibrillar ATP staining, slow-twitch (ST) and fast-twitch a, x, and c (FTa, FTx, and FTc) fiber types were defined under light microscopy. The number and size of fibers were determined using a computer program (TEMA 1995; CheckVision, Hadsund, Denmark). On average, 170 muscle fibers were included in each of the four analyses before and after HI and TC.
Differences between the two groups HI and TC before the intervention period were examined by an unpaired t-test. Changes in V˙O2 kinetics, RE, RER, enzyme activity, and muscle fiber distribution and size were examined by a paired Student's t-test separately for HI and TC. Changes in TST and SFI in RST and Yo-Yo IR2 performance were tested by a two-way ANOVA for repeated measurements (one-factor repetition) with group (HI vs TC) and time (before vs after) as factors. Changes in Yo-Yo IR2 performance for TC were examined by a one-way ANOVA for repeated measurements (before, 72 h, after). When a significant main effect was detected in the one- or two-way ANOVA repetition maximum, a Student-Newman-Keuls post hoc analysis was performed for pairwise multiple comparison. The Pearson correlation coefficient was calculated to test the relationship between two variables. All the statistical analyses were made in SigmaPlot version 11.0 (Systat Software, Inc., Chicago, IL), and the level of statistical significance was set at P < 0.05. Data are expressed as means ± SD.
V˙O2 kinetics was unaffected in HI (Fig. 1), but in the last 30 s of the 4-min exercise bout, the oxygen uptake was lower (P < 0.05), and the RE was improved after the intensified training period (197.8 ± 10.2 (before) vs 192.8 ± 7.2 (after) mL O2·kg−1·km−1, P < 0.05) (Table 1). After TC, V˙O2 kinetics became slower (P < 0.05) reflected as an increase in the time constant from 21.5 ± 2.9 to 23.8 ± 3.2 s and an increase in the MRT from 45.0 ± 1.8 to 46.8 ± 2.2 s (Fig. 1 and Table 1). The increase in the oxygen uptake during the last 2 min was not changed after the intervention period either in HI (72 ± 48 vs 63 ± 33 mL O2·min−1) or in TC (101 ± 51 vs 91 ± 44 mL O2·min−1).
HR response and RER during submaximal running.
HR and RER during submaximal running were not changed in HI. In TC, HR was elevated (P < 0.05) throughout exercise, and RER was higher (P < 0.05) from 80 s of exercise after the inactivity period (Table 1).
RST and Yo-Yo IR2 test performance.
Performance in the RST is displayed in Figure 2. In HI, the fastest sprint (3.15 ± 0.08 and 3.16 ± 0.13 s) and fatigue index (5.8% ± 2.8% and 3.9% ± 1.6%) were not changed, but performance was improved (P < 0.05) in the fourth (3.35 ± 0.13 vs 3.26 ± 0.14 s), sixth (3.43 ± 0.21 vs 3.32 ± 0.10 s), and tenth (3.39 ± 0.20 vs 3.29 ± 0.12 s) sprints. In addition, total sprint time was reduced (P < 0.05) after the intervention period (33.44 ± 1.17 vs 32.81 ± 1.01 s). In TC, the fastest sprint (3.14 ± 0.08 and 3.15 ± 0.14 s) and fatigue index (5.9% ± 2.3% and 7.6% ± 2.8%) were the same. Performance was reduced (P < 0.05) in the fifth (3.38 ± 0.11 vs 3.46 ± 0.14 s), sixth (3.41 ± 0.15 vs 3.48 ± 0.11 s), seventh (3.41 ± 0.13 vs 3.50 ± 0.11 s), eighth (3.42 ± 0.13 vs 3.50 ± 0.12 s), ninth (3.42 ± 0.10 vs 3.56 ± 0.09 s), and tenth (3.35 ± 0.12 vs 3.46 ± 0.09 s) sprints. Total sprint time was also longer (P < 0.01) after the inactivity period (33.41 ± 0.96 vs 34.11 ± 0.92 s). In HI, no change in performance of the Yo-Yo IR2 test was observed (937 ± 56 and 994 ± 72 m), whereas it was reduced (P < 0.01) in TC from 845 ± 160 m before the intervention to 801 ± 162 and 654 ± 99 m after 3 and 14 d of inactivity, respectively.
V˙O2 kinetics and performance during repeated intense work.
Before the interventions, there was no correlation between V˙O2 kinetics (expressed as τ and MRT, respectively) and total sprint time (r2 = 0.03 and 0.001, NS), fatigue index (r2 = 0.02 and 0.02, NS), and Yo-Yo IR2 performance (r2 = 0.002 and 0.003, NS). A correlation (P < 0.05) was observed between the changes in V˙O2 kinetics and in fatigue index (r2 = 0.43 for τ and 0.27 for MRT) and total sprint time and τ (r2 = 0.25) but not MRT (r2 = 0.21, NS). No correlation was found between the changes in τ and MRT and the change in Yo-Yo IR2 performance (r2 = 0.18 and 0.03, NS).
Muscle enzymes and fiber type distribution.
In HI, the maximal activity of CS (30.8 ± 2.8 and 32.7 ± 3.6 μmol per dry weight per minute) and HAD (23.7 ± 2.1 and 22.5 ± 2 μmol per dry weight per minute) did not change (Fig. 3), whereas the amount of PDH was elevated by 17% ± 14% from before level (P < 0.05) after the intervention period (Fig. 4). In TC, CS (32.7 ± 2.9 and 28.8 ± 4.8 μmol per dry weight per minute) and HAD (25.3 ± 3.6 and 20.8 ± 3.1 μmol per dry weight per minute, P < 0.05) were lowered (P < 0.01) by 12% and 18% after the inactivation period, and the amount of PDH decreased by 17% ± 11% (P < 0.01) from before level (Figs. 3 and 4).
In HI, no changes in muscle fiber distribution and size were observed (Table 2). In TC, the relative number (56% ± 18% and 47% ± 15%) and area (51% ± 18% and 39% ± 16%) of ST fibers were lowered (P < 0.05) after the inactivation period, whereas fiber size was unaltered (Table 2).
The main findings of the present study performed on trained soccer players were impaired V˙O2 kinetics after 2 wk of training cessation, which was associated with a lowered activity and amount of oxidative enzymes as well as a reduced performance in repeated sprint work and the Yo-Yo IR2 test. In addition, 2 wk of intensified training improved RE as well as performance in an RST and content of PDH.
To our knowledge, this is the first controlled study, using several exercise bouts to describe V˙O2 kinetics for elite athletes, showing slower V˙O2 kinetics after a period of inactivity. Convertino et al. (17) found that V˙O2 kinetics was slower after 7 d of bed rest in untrained subjects with a V˙O2max of 38 mL O2·kg−1·min−1 before the bed rest period, although it should be mentioned that only one work bout was used to estimate V˙O2 kinetics, which may reduce the validity of the calculations (33). In contrast to the present finding, several studies did not find any effect of inactivity on V˙O2 kinetics (16,24). A possible explanation is the low training status of the subjects, indicating that they had limited activities already before the intervention period. Although the fitting procedure used in the present study does not allow for a clear distinction between fast and slow components of the V˙O2 response, the finding that the rise in V˙O2 during the last 2 min of exercise was unchanged after the inactivity period suggests that the slower V˙O2 kinetics after inactivity was primarily related to the early phase of exercise. There is good evidence to support that a limited extraction of oxygen by the contracting muscle cells causes the delay in oxygen utilization in the initial phase of exercise (7,20,29,40), often termed "metabolic inertia." The slower V˙O2 kinetics in the present study was associated with a 17% decrease in the amount of PDH and a lowering of the maximal activity of CS and HAD by 12% and 18%, respectively. In agreement with this, several studies using short periods of detraining on well-trained subjects have shown reductions in oxidative enzymes (37). The reduction in PDH and CS may have slowed the V˙O2 kinetics, but it is questionable whether these enzymes are limiting for muscle oxygen uptake per se. In several studies where the PDH activity was increased by ingestion of dichloroacetate, no effect was seen on muscle and pulmonary V˙O2 (3,27). In addition, when correlating the changes in τ with the alterations in PDH and CS in the inactivity group, no correlations were observed, and in the HI, PDH was elevated by 17% after the 2-wk training period without V˙O2 kinetics being changed. Furthermore, after 5 d of training V˙O2 kinetics was improved in untrained subjects despite no changes in CS (38). The lowering of the HAD activity probably also had little influence on the slower V˙O2 kinetics because glucose metabolism dominates while running at 75% MAS (∼85% V˙O2max) (1), which is supported by the high RER values of 0.93-0.97 at the end of the running bouts (Table 1). Nevertheless, further studies also including measurements of oxygen delivery are needed to clarify the effect of inactivity on V˙O2 kinetics. After TC, the distribution of ST fibers was lowered. This is in contrast to observations in some other studies with detraining of trained subjects where fiber type distribution is reported to be unaltered (37) but in agreement with observations after 11 d of space flight in astronauts (46), after 3 wk of knee immobilization in recreationally active subjects (23), and 6 wk after knee surgery in trained athletes (21). Nevertheless, it may be speculated that a larger recruitment of FT fibers during exercise may have slowed V˙O2 kinetics because support for slower V˙O2 kinetics in FT fibers can be found in the literature. Thus, an increase in τ during moderate work after inactivation of ST fibers by cisatracurium has been observed (32), and τ is often reported higher when the relative workload is increased (28,29), which may be explained by a higher activation of the FT fibers.
An interesting finding was that the RE was improved after just 2 wk with 10 high-intensity training sessions substituting the normal training of the soccer players. Similarly, two recent studies with trained runners performing speed endurance production training consisting of runs at 95% of maximal speed for 30 s either for 4 (25) or 6-9 wk in combination with AHI training (4) found an improved RE. It may be related to a specific adaptation of the high-order motor units (FT fibers), e.g., an improved P:O ratio, because these fibers were likely maximally taxed during the sprints used in the training. In support, Henriksson and Reitman (22) have demonstrated a training-specific fiber adaptation in the aerobic enzyme succinate dehydrogenase (SDH) after an 8-wk training period. However, this issue warrants more investigation. The high-intensity training was not sufficient to improve the V˙O2 kinetics in the soccer players in the present study, which may have been because of the high initial fitness level and the short intervention period. Many studies involving training of untrained subjects have shown improvement within 2 wk (2,38), and intervention periods lasting 4-8 wk have shown faster kinetics in moderately (11,29) and highly trained subjects (18).
Previous soccer studies have demonstrated a correlation between τ at 60% MAS and performance in both Yo-Yo IR2 (41) and repeated 40-m sprints (19,42). In the present study, no association was observed before the intervention between the V˙O2 kinetics and performance in repeated intense exercise, which may be related to the protocol used to determine V˙O2 kinetics and intermittent exercise performance. We used four repetitions at 75% MAS in comparison with two repetitions at 60% MAS (18,41) and a 20-m sprint distance making the aerobic contribution to the total energy turnover less pronounced compared with the 40-m sprints applied in the previous studies (19,42). Considering that the time constants become greater with increasing work intensity (28,29), the kinetics was fast in the present study with time constants of ∼22 s before the interventions in comparison with values of 23 and 27 s in the other studies using 60% MAS (19,41,42). Interestingly, the observed changes in τ and MRT after the two interventions were correlated with the changes in RST performance, and Yo-Yo IR2 was markedly reduced after inactivity in association with slower V˙O2 kinetics, confirming a link between V˙O2 kinetics and intermittent exercise capacity.
In summary, 2 wk of training cessation of elite soccer players led to slower V˙O2 kinetics, which was associated with a reduced content and activity of oxidative enzymes and a lower fraction of ST fibers. In addition, performances in the Yo-Yo IR2 test and the RST were also impaired. A 2-wk training period with 10 high-intensity training sessions substituting the normal training improved work efficiency during submaximal running and performance during repeated sprinting. No association between fast V˙O2 kinetics and performance during repeated high-intensity work was observed, but the changes found after the interventions indicate that they may be related.
This work was supported by the Danish Ministry of Culture (Kulturministeriets Udvalg for Idrætsforskning).
There are no conflicts of interest.
The authors thank Jens Jung Nielsen, Rikke Leihof, and Benjamin Leisvig for excellent technical assistance.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
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Keywords:©2011The American College of Sports Medicine
REPEATED SPRINTING; YO-YO INTERMITTENT RECOVERY TEST; RUNNING ECONOMY; OXIDATIVE ENZYMES