Games took place 2 days after baseline testing. On game day, participants had a light standardized meal designed (13) and rested adequately before the game (18.00–20.00). Athletes played during the entire game. Athletes' HR was monitored (Polar Electro, Kempele, Finland) throughout the game (as a marker of game intensity). Participants consumed only water ad libitum during competition. Before and immediately after game, blood was collected and analyzed for metabolites that illustrate game's intensity. To examine whether athletes' daily dietary intake affected their inflammatory profile, they were asked to maintain their usual eating pattern and complete daily (during the course of the 2 trials) diet recall forms that were analyzed later with ScienceFit Diet 200A (Science Technologies, Athens, Greece).
A power analysis indicated that to detect statistically meaningful differences between consecutive measurements, a sample size of ≥18 athletes was necessary at a beta level of 0.90 (based on studies that used a similar design for similar sports) (13,19). Thus, 24 healthy elite adult TH players (age, 22.8 ± 1.4 years [range, 19.2–23.7 years]; training age, 9.1 ± 1.8 years; weekly training, 14.1 ± 0.7 hours; body mass, 82.2 ± 5.5 kg; height, 1.856 ± 4.2 m; body mass index, 23.8 ± 3.1 kg·m−2; body fat, 10.4 ± 2.6%; maximal oxygen consumption [V[Combining Dot Above]O2max], 55.7 ± 3.9 ml·kg−1·min−1; maximal HR, 194.6 ± 7.2 b·min−1) participated in the study. Participants abstained (≥6 months) from consumption of performance-enhancing supplements and medications, trained daily and participated in at least 1 match per week during their last in-season period, and were nonsmokers. All training and testing procedures and any possible risks and discomforts were fully explained in detail participants before the start of the study. A written informed consent for participation in the study was provided by all participants. The local Institutional Review Board approved the study. Experimental procedures conformed to the principles of the Declaration of Helsinki.
Anthropometrics (body mass, stature, and composition) were assessed as previously described (13). Open-circuit spirometry with an automated online gas exchange analyzer (breath-by-breath analysis) was used (SensorMedics 29C; SensorMedics Corporation, Yorba Linda, CA, USA) for V[Combining Dot Above]O2max measurement during a graded exercise test to exhaustion on a motor-driven treadmill following calibration of oxygen and carbon dioxide analyzers according to standard procedures (23). Certain criteria were used to ascertain that V[Combining Dot Above]O2max was attained (23).
An Ergojump contact platform (Newtest, Oulu, Finland) was used for the measurement (coefficient of variation [CV] for test-retest trials: 4.2%) of countermovement jump height (VJ) (7). Infrared light sensors (Newtest) were used to measure time to complete a 10-m sprint (speed assessment), a T-test (agility assessment), and a single-effort line drill test (LDT) on a TH court (6,14). Coefficient of variations for test-retest trials of speed, agility, and LDT testing were 2.2, 2.8, and 4%, respectively. Maximal strength of the upper and lower body was determined bilaterally on a leg press machine (Vita Fitness, Rome, Italy) and with free weights (bench chest press), respectively, using the 1 repetition maximal (1RM) protocol (24). Hand grip strength (GS) was measured with a calibrated Harpenden (British Indicators, Ltd, West Sussex, UK) handgrip dynamometer with visual feedback (21). Coefficient of variations for test-retest trials of upper- and lower-body 1RM and GS were 2.7, 3.1, and 2.9% respectively. The modified sit-and-reach test was used to measure low back and hamstring flexibility following a 5-minute warm-up (2).
Muscle soreness level was rated by the participants on a visual analog scale (1–10) following palpation of relaxed muscles' (knee extensors and flexors) belly and distal region after executing 3 repetitions of a full squat (31). The test-retest reliability CV of DOMS assessment was 0.93. Assessment of knee joint range of motion (ROM, index of muscle edema) by goniometry (Lafayette Instrument Company, Lafayette, IN, USA) was used to determine edema of knee extensors and flexors muscles (30). Coefficient of variations for test-retest trials of sit-and-reach testing and knee ROM were 2.6 and 2.4%, respectively.
Blood Sampling and Assays
Blood samples (∼14 ml) were collected at 07:00–09:00 AM following an overnight fast from an antecubital arm vein by venipuncture using a disposable needle with a Vacutainer tube holder (Becton–Dickinson, Franklin Lakes, NJ, USA) in a recumbent position. One portion of blood was collected into ethylenediaminetetraacetic acid (EDTA) tubes either for plasma separation by centrifugation (1,370g, 4° C, 10 minutes) for the measurement of glucose, non-esterified fatty acids (NEFAs), urea, ammonia, glycerol, adhesion molecules, hemoglobin, malondialdehyde (MDA), and creatine kinase activity (CK). Another portion of blood was collected into SST-Gel/clot activator for serum separation by centrifugation (1,500g, 4° C, 15 minutes) after allowing it to clot at room temperature for the measurement of protein carbonyls (PC), catalase activity (CAT), cortisol, testosterone, cytokines, C-reactive protein (CRP), and total antioxidant capacity (TAC). After plasma separation, packed erythrocytes were collected and lysed (3) and the lysate was used for the determination of reduced (GSH) and oxidized glutathione (GSSG). Plasma, serum, and lysate samples were stored (in multiple aliquots) at −70° C until analyzed. A portion of whole blood was stored at −20° C and it was used subsequently for the measurement of glutathione peroxidase activity (GPX). For lactate analysis, a very small blood portion of (200 μl) was immediately added to thrichlororoacetic acid (TCA) (400 μl, 5%) tubes and centrifuged (2,500g, 15 minutes). After removal of the supernatant, samples were removed and stored at −75° C until analyzed for lactate concentration with an enzymatic assay with reagents purchased from Sigma Chemicals (St. Louis, MO, USA). Another blood portion (2 ml) was collected into EDTA tubes for immediate (within 24 hours) determination of leukocyte (white blood cell [WBC]) counts, hematocrit, and hemoglobin using an automated hematology analyzer (Shenzhen-Mindray, Shenzhen, China). All assays were performed in duplicate. Samples were protected from light and auto-oxidation and thawed only once before analyzed. Postgame results (only) were corrected for plasma volume changes based on hematocrit and hemoglobin values (11).
A Cobas Integra Plus-400 chemistry analyzer (Roche Diagnostics, Berlin, Germany) was used to measure glucose, triglycerides, uric acid, and urea by an enzymatic spectrophotometric method (32). Nonesterified fatty acids and free glycerol were measured spectrophotometrically by a commercially available kit (Wako Chemicals, Neuss, Germany). Ammonia was assayed spectrophotometrically (42). Creatine kinase activity was measured spectrophotometrically via a commercially available kit (Spinreact, Sant Esteve, Spain). Particle-enhanced immunonephelometry (Dade-Behring, Deerfield, IL, USA) was used for the determination of high-sensitivity CRP. Adhesion molecules (plasma soluble vascular adhesion molecule 1 [sVCAM-1] and sP-selectin) were analyzed on a Luminex-100 IS (Luminex, Austin, TX, USA) with a multiplex assay kit (Linco, St. Charles, MO, USA) (17). Testosterone and cortisol concentrations were measured with 2 commercially available ELISA kits (DRGDiagnostics, Marburg, Germany). Cytokines' (IL-6 and IL-1β) concentrations were measured with 2 commercially available ELISA kits (Immunokontact, Abingdon, Oxon, UK) (23).
Malondialdehyde concentration was determined by reverse-phase high-performance liquid chromatography with fluorimetric detection (excitation 532 nm, emission 550 nm) (13). For PC measurement (3), TCA (20%, 50 μl) was added to serum (50 μl), and after incubation (in an ice bath for 15 minutes) and centrifugation (15,000g, 5 minutes, at 4° C), the supernatant was discarded and 2,4-dinitrophenylhydrazine (500 μl, 10 mM) or HCl (500 μl, 2.5 N) was added in the pellet of the sample or the blank, respectively. After incubation in the dark (at room temperature for 1 hour with intermittent vortexing every 15 minutes), samples were centrifuged (15,000g, 5 minutes, 4° C). The resultant supernatant was discarded and TCA (10%, 1 ml) was added, and samples were then vortexed and centrifuged (15,000g, 5 minutes, 4° C). The resultant supernatant was discarded, ethanol–ethyl acetate (1:1 vol/vol—1 ml) was added and samples were vortexed and centrifuged (15,000g, 5 minutes, 4° C). After this washing step was repeated 2 more times, the final supernatant was discarded, urea (1 ml, 5M, pH 2.3) was added, and samples were vortexed and incubated (15 minutes, 37° C). Thereafter, samples were centrifuged (15,000g, 3 minutes, 4° C) and their absorbance was read spectrophotometrically at 375 nm.
For the spectrophotometric determination of GSH concentration (3), erythrocyte lysates (20 μl) were treated with TCA (5%) and were mixed with sodium potassium phosphate (660 μl, 67 mM, pH 8.0) and 5,5-dithio-bis-2 nitrobenzoate (DTNB; 330 μl, 1 mM). Samples were then incubated in the dark (room temperature, 45 minutes) and their absorbance was read at 412 nm. For the spectrophotometric determination of GSSG (3), erythrocyte lysates (50 μl) were treated with TCA (5%) and neutralized with NaOH (up to pH 7.0–7.5). Thereafter, 2-vinyl pyridine (1 μl) was added and samples were incubated (2 hours, room temperature). These samples (5 μl) were then mixed with sodium phosphate (600 μl, 6.3 mM EDTA, pH 7.5), NADPH (100 μl, 3 mM), DTNB (100 μl, 10 mM), and of distilled water (194 μl). The samples were then incubated (10 minutes, room temperature), mixed with glutathione reductase (1 μl), and the change in absorbance was read for 3 minutes at 412 nm. Calibration curves constructed of commercial standards were used to calculate the concentrations of GSH and GSSG.
The TAC was measured spectrophotometrically as previously described (24). Briefly, samples (20 μl) were added to sodium potassium phosphate (480 μl, 10 mM, pH 7.4) and 2,2-diphenyl-1-picrylhydrazyl (DPPH·) free radical (500 μl, 0.1 mM) and incubated in the dark (30 minutes, room temperature). Thereafter, samples were centrifuged (20,000g, 3 minutes) and their absorbance was read at 520 nm. The TAC is expressed as millimoles of DPPH· reduced to 1,1-diphenyl-2-picrylhydrazine by serum's antioxidants. Catalase activity was measured spectrophotometrically as previously described (3). Briefly, sodium potassium phosphate (67 mM, pH 7.4) was added to erythrocyte lysates (4 μl) and samples were incubated (37° C, 10 minutes). Thereafter, H2O2 (30%) was added to the samples and the change in absorbance was immediately read at 240 nm for 1.5 minutes. The GPX activity was determined spectrophotometrically at 37° C using cumene hydroperoxide as the oxidant of glutathione (Ransel RS 505; Randox, Crumlin, UK).
Spectrophotometric assays were performed on a Hitachi 2001 UV–VIS spectrophotometer (Hitachi Instruments, Tokyo, Japan). The interassay and intra-assay CVs of all analyses were 2.5–6.8 and 3.7–7.2, respectively.
Data normality was evaluated with a 1-sample Kolmogorov-Smirnoff test. A 2-way (trial × time) repeated measure analysis of variance with planned contrasts on different time points was used for data analysis. A Bonferroni test was used for post-hoc analysis when a significant effect was detected. Significance was accepted at p ≤ 0.05. Data are presented as mean ± SE.
Mean HR was markedly elevated (p ≤ 0.05) during both halves of the game (66.4 ± 4.5 b·min−1 at rest vs. 163.4 ± 7.6 b·min−1 during first half and vs. 168.7 ± 8.1 b·min−1 during second half). No differences were noted in HR elevation between the 2 halves of the game. The handball game was metabolically stressful as evidenced by the marked increase (p ≤ 0.05) of lactate (∼8-fold), glucose (∼14%), NEFA (105%), glycerol (61%), and ammonia (∼60%) concentration following the game (Table 2). However, urea did not show any changes postgame (Table 2). No differences were detected in nutrient intake among groups (data not shown).
Table 3 illustrates performance changes following a TH. Upper- and lower-body strength and hand GS declined (p ≤ 0.05) 24 hours postgame by ∼7, ∼6.5, and ∼9%, respectively, and recovered thereafter. Speed deteriorated (∼5%; p ≤ 0.05) for 24 hours following the game and returned to baseline values thereafter. Vertical jumping performance decreased (∼9%; p ≤ 0.05) until 24 hours of recovery and normalized thereafter. Anaerobic power (LDT performance) and agility (T-test performance) declined (∼11% and ∼5.5, respectively; p ≤ 0.05) at 24 hours and recovered thereafter.
Table 4 shows DOMS and knee ROM changes following a handball game in both groups. Delayed onset of muscle soreness of knee extensor increased postgame (2.1-fold; p ≤ 0.05), peaked at 24 hours (3.7-fold; p ≤ 0.05). and recovered thereafter. Delayed onset of muscle soreness of knee flexors increased postgame (2.4-fold; p ≤ 0.05), peaked at 24 hours (4.4-fold; p ≤ 0.05), remained elevated at 48 hours (2.2-fold; p ≤ 0.05), and returned to baseline thereafter. It must be noted that DOMS elevation at 24 hours of knee flexors was of a greater (p ≤ 0.05) magnitude than that of knee extensors. Knee ROM of the dominant limb declined at 24 hours (∼5%, p ≤ 0.05) and recovered thereafter, whereas knee ROM of the nondominant limb remained unaffected.
Creatine kinase activity increased (∼95%, p ≤ 0.05) at 24 hours and returned to baseline values thereafter (Figure 2A). Leukocyte count (Figure 2B) increased (∼25%, p ≤ 0.05) only postgame and recovered thereafter. C-reactive protein (∼65%, Figure 2C) demonstrated a modest elevation (p ≤ 0.05) at 24 hours and normalized thereafter. Uric acid (Figure 2D) increased at 24 hours (∼20%, p ≤ 0.05) and normalized thereafter. The sVCAM-1 (Figure 2E) peaked postgame (∼50%, p ≤ 0.05), remained elevated at 24 hours (∼20%, p ≤ 0.05) and normalized thereafter, whereas sP-selectin (Figure 2F) remained unchanged throughout the postgame microcycle. Both cytokines (IL-1β and IL-6; Figures 3A and 3B) increased (∼65 and ∼50%, respectively, p ≤ 0.05) immediately postgame and returned to baseline thereafter. Cortisol (Figure 3C) increased only postgame (∼25%, p < 0.1), whereas testosterone (Figure 3D) remained unaltered throughout recovery.
The GSH (Figure 4A) declined immediately postgame (∼30%, p ≤ 0.05), remained below baseline at 24 hours postgame (∼16%, p < 0.1) and recovered thereafter, whereas GSSG (Figure 4B) decreased by ∼10% immediately after the game and at 24 hours (p < 0.1) and normalized thereafter. Accordingly, GSH/GSSG ratio (Figure 4C) decreased postgame (∼35%, p ≤ 0.05) and at 24 hours (∼23%, p < 0.1) and recovered thereafter. The GPX (Figure 4D) increased postgame (∼24 and ∼17%, respectively, p ≤ 0.05), remained elevated at 24 hours (∼14 and ∼10%, respectively, p < 0.1), and returned to baseline values thereafter. The TAC (Figure 4E) and CAT (Figure 4F) increased postgame (∼25%, p ≤ 0.05) and returned to baseline thereafter. Malondialdehyde (Figure 4G) and PC (Figure 4H) increased postgame (47 and 65%, respectively, p ≤ 0.05) and returned to baseline values thereafter.
The main purpose of this study was to record the magnitude and the time frame of changes of acute inflammatory response and performance during a simulated in-season training microcycle following a single TH game. Results indicate that a single TH game elicits only a short-lived inflammatory response and performance deterioration. Although the game performed was unofficial, it induced a significant physiological and metabolic overload as evidenced by the rise in game's mean HR and lactate values that were comparable with those observed in official TH games (8,10). To our knowledge, this is the first study to monitor the changes of specific metabolites in response to a handball game. Glycerol and NEFA upregulation indicates that a single game activates the lipolytic pathway as previously reported for another team indoor sport, that is, basketball (1). A potential rise in catecholamine secretion in response during multiple burst of powerful actions (i.e., sprints, jumps) that are incorporated in team sports, such as handball, basketball, and soccer, explains the rise of blood glucose concentration as a result of increased hepatic glycogenolysis (1,22). The intense nature of the TH game in this study is also supported by the augmented ammonia concentration that indicates a rise in ATP turnover, an adaptation commonly observed during or after intense team sport events (22).
It is well established that intense eccentric contractions may lead to exercise-induced muscle damage that results in marked ultrastructural alterations, DOMS, and performance deterioration (7,13,19). Although TH incorporates a large number of movement patterns of intense eccentric component (i.e., sprinting, jumping, throwing, shuffling) that determine team's effectiveness or success, only 2 previous studies have examined the effects of a handball game on inflammatory muscle damage and performance responses (25,40). However, these 2 studies examined these responses for only 24 hours postgame. In this study, we followed inflammatory and performance responses throughout a 6-day microcycle while they were training daily according an in-season weekly training plan to simulate an in-season training environment. In this context, DOMS (a marker of muscle edema) remained elevated for 24 hours for knee extensors and 48 hours for knee flexors. Moreover, knee flexors' DOMS was of a greater magnitude than that of knee extensors, indicating that the former require a longer recovery period than the later. This phenomenon may be attributed to extended eccentric contraction of hamstrings in their effort to control knee's extension and hip's flexion when athletes plant the foot to the ground while performing explosive eccentric movements involving the lower limbs that decelerate the body (i.e., during sprinting or jumping). Another interesting finding was that while knee ROM of dominant limb was reduced for 24 hours, that of the nondominant limb remained unaltered, indicating that the former may be more involved in handball's explosive movements. Although no such data exist for TH, similar findings have been reported for sport activities of similar nature, such as plyometric exercises and soccer (7,13,19). Creatine kinase activity increased for only 24 hours postgame, reaching a peak value of ∼350 U L−1. This CK rise is shorter and much less pronounced than that seen following other team sports or training modalities of similar nature, such as soccer or rugby (7,19,38). In agreement with our findings, Marin et al. (25) also reported a very modest rise (∼160 U L−1) of CK 24 hours following a single TH. The lower CK value at 24 hours reported by Marin et al. (25) may be explained by the fact that CK demonstrates a highly variable response postexercise (28). The rise in CK activity indicates the increased muscle fibers' membrane permeability that coincides with the onset of DOMS and exercise-induced muscle damage after the game (5). Nevertheless, based on the values and the time frame of changes in response of muscle damage markers, it seems that a handball game induces a limited and transient muscle damage response as compared with that reported for other intermittent-type sports, such as soccer or hockey (13,19,39).
A dissociation was observed between CK, DOMS, and performance recovery rates after the game with CK demonstrating a slower rate than the other 2. This dissociation between blood CK concentration and muscle function postexercise occurs because while a large number of myofibers demonstrate structural abnormalities they maintain their functional integrity without releasing CK into the circulation (16). Therefore, CK levels offer a gross estimation of exercise-induced muscle damage but not of its magnitude. In fact, plasma CK levels depend on rate of its release by the muscle and its clearance from the blood. After its release from the muscle, CK enters the interstitium where it is cleared by the reticuloendothelial system and then enters the circulation slowly through the thoracic duct (18). The slower recovery of circulating CK levels may attribute to its sow clearance from the blood, which also explains its dissociation from DOMS and performance recovery curves (18).
Typically, exercise-induced muscle damage is followed by a marked immune and inflammatory response characterized by elevated WBC count and increased levels of proinflammatory cytokines, adhesion molecules, and acute phase proteins (15). In this study, a single TH game induced a marked elevation of WBC for only a few hours postgame that was accompanied by a similar elevation of IL-1β, IL-6, and cortisol, which has been shown to mediate immune and cytokine elevation postexercise (36). These results coincide with findings reported by Marin et al. (25) who showed that a single TH game upregulates IL-6 and tumor necrosis factor–alpha 24 hours in the circulation after a handball game. However, because limited muscle damage was observed in this study, IL-6 elevation immediately postgame may be associated with the increased metabolic demands imposed by the game (34). C-reactive protein, a protein that regulates the inflammatory response in response to cytokine action in the liver, increased after cytokines' elevation, that is, 24 hours postexercise (15). Similarly, sVCAM-1, an adhesion molecule that facilitates WBC mobilization into traumatized muscle in response to cytokine stimulation, increased simultaneously with and following cytokine's rise (i.e., immediately postgame and at 24 hours), which is in agreement with previous research (33).
During exercise-induced inflammatory response, increased leukocytes in the injured muscle produce superoxide and ROS that subsequently are converted to hydrogen peroxide (H2O2) that forms the toxic hydroxyl radical, which then readily oxidizes lipid and protein molecules (20). This well-described mechanism explains the elevation of PC (protein oxidation marker) and MDA (a lipid periodization marker) immediately after the game. However, this response was very short-lived because it disappeared at 24 hours, further supporting the notion that TH elicits a less pronounced inflammatory response than other team sports, such as soccer, rugby, and team hockey (13,19,38,39). Similar findings have been presented by Marin et al. (25) as well. The short-lived upregulation of oxidative stress is also supported by brief reduction of GSH/GSSG ratio, a valid oxidative stress marker reflecting the system's redox status (29). This transient rise in oxidative stress was accompanied by a rise of TAC and antioxidant enzyme activity for as long as 24 hours. Surprisingly, a previous report (43) showed that TAC may actually deteriorate following a basketball game, which is a way that may be similar to a handball game in respect to the movement pattern of these 2 indoor team sports. This is, however, in contrast to responses monitored following intermittent-type sports that include intense eccentric actions (3,7,13,24). The TAC rise was verified also by the elevation of uric acid concentration within the same time frame because it has been estimated that the later accounts for one-third of TAC concentration (44) and changes in the same direction and magnitude with TAC. In general, it seems that TH induced a brief upregulation of oxidative stress and antioxidant activity in relation to other similar sports, probably suggesting a smaller exposure to eccentric activity because of a shorter total duration as compared with team sports, such as soccer (27).
The main purpose of a training microcycle design during in-season is the recovery following a competitive event, training, tapering, and participation in the upcoming event. Based on that, it is useful for coaches to know when players fully recover after a game and are ready to fully participate in the next intense training session or competition. However, the only study that examined the effect of a handball game on performance measured neuromuscular performance only immediately postgame and reported a marked reduction (40). In fact, ammonia, which was markedly increased postgame, has been implicated in central and peripheral fatigue (4). Specifically, it was shown that a single handball game induces a preferential fatigue of vastus lateralis and biceps femoris muscles that may predispose athletes to knee instability and increased risk for knee injury (40). However, we are unaware how long within a microcycle this impairment of performance may persist. This study attempted to monitor various aspects of physical performance during the entire training microcycle. It seems that strength of lower and upper body, hand-GS, speed, anaerobic capacity, and agility performance deteriorated for as long as 24 hours postgame and returned to baseline values thereafter. This time frame of changes seems to differ from that reported for other team sports, such as soccer, where performance deterioration may persist for as long as 48–72 hours (13,19). This brief performance reduction observed in this study is probably associated with muscle damage induced by the game that creates a catabolic environment in muscle because of impaired protein synthesis and increased protein degradation (33). This catabolic state is also evidenced by the augmented cortisol response. This catabolic response is associated with increased breakdown of contractile proteins and neurotransmitters that ultimately result in loss of muscular force (33). This phenomenon may be exacerbated if this catabolic state is accompanied by a decline or an absence of change in testosterone levels because it occurred here and in other similar studies (13,19). This short-lived performance impairment coincides with the brief rise in muscle damage and inflammatory markers. Therefore, our results verify previous reports (40) and extend their results in respect to the time frame of performance changes following a handball game.
Utilization of a randomized order of the control and ETs could be a valid alternative for our experimental design. However, such a design would not allow us to obtain a close simulation of an in-season microcycle that precedes and follows a TH game. Nevertheless, the lack of trial randomization might have affected our outcome variables because of the “repeated bout” effect, that is, reduced inflammation after the game because of training microcycle that preceded the game. Although this possibility exists, several reasons suggest otherwise: (a) daily practices performed before the game were characterized by low training intensity and volume because they included mostly tactical drills and (b) the baseline values of CK and other inflammatory indices were similar between the 2 trials, indicating that participants entered both trials with very low inflammatory levels. This may also be attributed to participants' excellent conditioning level and the fact that these athletes are accustomed to frequent high training loads. This is further supported by the minimal muscle damage and inflammatory response produced by practices during the control trials on a daily basis, suggesting that in-season practices induce limited inflammation.
In conclusion, a single TH game induces only limited and transient performance reduction and inflammatory response that persist for as long as 24 hours. These data indicate that handball players may need approximately 24 hours to recover and be able to fully participate in the next high-intensity training session or game.
The findings of the present investigation suggest that a single TH game represents a strong metabolic stimulus and induces a brief and moderate inflammatory response that may affect physical performance for as long as 24 hours postgame. These data clearly suggest that a TH game is characterized by a unique time frame of inflammatory/performance responses as compared with other intermittent-type sports and athletes may need ∼24 hours of recovery after a match before participating in the next intensive practice or match. These results indicate that trainers may be able to schedule an intense practice session as early as 24 hours postgame (late during the day after the match) because inflammation subsides and performance recovers within this time frame. In other words, the intensity of in-season daily practices may be maintained at maximal levels based on the fast recovery of inflammatory and performance markers. It also seems that daily training during a simulated in-season training microcycle does not further affect athletes' performance and inflammatory responses. This notion will allow TH coaches and strength and conditioning trainers to design their daily practices, in respect to intensity and volume, with a greater flexibility.
The authors thank all participants for their contribution and commitment to this study. This study was supported by departmental funding, a grant received by Bodosakis Foundation (Greece) for instrument purchase, and grant funding CE-80739.
1. Ben Abdelkrim N, Castagna C, El Fazaa S, Tabka Z, El Ati J. Blood metabolites during basketball competitions. J Strength Cond Res 23: 765–773, 2009.
2. American College of Sports Medicine. Guidelines for Exercise Testing and Prescription. Philadelphia, PA: Lippincott Williams & Wilkins, 2000. pp. 85.
3. Barbas I, Fatouros IG, Douroudos II, Chatzinikolaou A, Michailidis Y, Draganidis D, Jamurtas AZ, Nikolaidis MG, Parotsidis C, Theodorou AA, Katrabasas I, Margonis K, Papassotiriou I, Taxildaris K. Physiological and performance adaptations of elite Greco-Roman wrestlers during a one-day tournament. Eur J Appl Physiol 111: 1421–1436, 2011.
4. Bassini-Cameron A, Monteiro A, Gomes A, Werneck-de-Castro JP, Cameron LL. Glutamine protects against increases in blood ammonia in football players in an exercise intensity dependent way. Br J Sports Med 42: 260–266, 2008.
5. Cannon J, Orencole R, Fielding R, Meydani M, Meydani SN, Fiatarone MA, Blumberg JB, Evans WJ. Acute phase response in exercise: Interaction of age and vitamin E on neutrophils and muscle enzyme release. Am J Physiol 259: R1214–R1219, 1990.
6. Chaouachi A, Brughelli M, Chamari K, Levin GT, Ben Abdelkrim N, Laurencelle L, Castagna C. Lower limb maximal dynamic strength and agility determinants in elite basketball players. J Strength Cond Res 23: 1570–1577, 2009.
7. Chatzinikolaou A, Fatouros IG, Gourgoulis V, Avloniti A, Jamurtas AZ, Nikolaidis MG, Douroudos I, Michailidis Y, Beneka A, Malliou P, Tofas T, Georgiadis I, Mandalidis D, Taxildaris K. Time course of changes in performance and inflammatory responses after acute plyometric exercise. J Strength Cond Res 24: 1389–1398, 2010.
8. Chelly MS, Hermassi S, Aouadi R, Khalifa R, Van den Tillaar R, Chamari K, Shephard RJ. Match analysis of elite adolescent team handball players. J Strength Cond Res 25: 2410–2417, 2011.
9. Clarkson PM, Tremblay I. Exercise-induced muscle damage, repair, and adaptations in humans. J Appl Physiol (1985) 65: 1–6, 1988.
10. Delamarche P, Gratas A, Beillot J, Dassonville J, Rochcongar P, Lessard Y. Extent of lactic anaerobic metabolism in handballers. Int J Sports Med 8: 55–59, 1987.
11. Dill DB, Costill DL. Calculation of percentage changes in volumes of blood, plasma, and red cells in dehydration. J Appl Physiol 37: 247–248, 1974.
12. Draganidis D, Chatzinikolaou A, Jamurtas AZ, Barbero JC, Tsoukas D, Theodorou AS, Margonis K, Michailidis Y, Avloniti A, Theodorou A, Kambas A, Fatouros IG. The time-frame of acute resistance exercise effects on football skill performance: The impact of exercise intensity. J Sports Sci 31: 714–722, 2013.
13. Fatouros IG, Chatzinikolaou A, Douroudos II, Nikolaidis MG, Kyparos A, Margonis A, Michailidis Y, Vantarakis A, Taxildaris K, Katrabasas I, Mandalidis D, Kouretas D, Jamurtas AZ. Time-course of changes in oxidative stress
and antioxidant status responses following a soccer game. J Strength Cond Res 24: 3278–3286, 2010.
14. Fatouros IG, Laparidis K, Kambas A, Chatzinikolaou A, Techlikidou E, Katrabasas I, Douroudos I, Leontsini D, Berberidou F, Draganidis D, Christoforidis C, Tsoukas D, Kelis S, Taxildaris K. Validity and reliability of the single-trial line drill test of anaerobic power in basketball players. J Sports Med Phys Fitness 51: 33–41, 2011.
15. Fehrenbach E, Schneider ME. Trauma-induced systemic inflammatory response
versus exercise-induced immunomodulatory effects. Sports Med 36: 373–384, 2006.
16. Friden J, Lieber RL. Serum creatine kinase level is a poor predictor of muscle function after injury. Scand J Med Sci Sports 11: 126–127, 2001.
17. Goussetis E, Spiropoulos A, Tsironi M, Skenderi K, Margeli A, Graphakos S, Baltopoulos P, Papassotiriou I. Spartathlon, a 246 kilometer foot race: Effects of acute inflammation induced by prolonged exercise on circulating progenitor reparative cells. Blood Cells Mol Dis 42: 294–299, 2009.
18. Hyatt JP, Clarkson PM. Creatine kinase release and clearance using MM variants following repeated bouts of eccentric exercise. Med Sci Sports Exerc 30: 1059–1065, 1998.
19. Ispirlidis I, Fatouros IG, Jamurtas AZ, Michailidis I, Douroudos I, Michailidis K, Margonis K, Chatzinikolaou A, Nikolaidis MG, Kalistratos E, Katrabasas I, Alexiou V, Taxildaris K. Time course of changes in performance and inflammatory responses following a soccer match. Clin J Sport Med 18: 423–431, 2008.
20. Jaeschke H. Mechanisms of oxidant stress-induced acute tissue injury. Proc Soc Exp Biol Med 209: 104–111, 1995.
21. Kraemer WJ, Fry AC, Rubin MR, Triplett-McBride T, Gordon SE, Koziris LP, Lynch JM, Volek JS, MeuVels DE, Newton RU, Fleck SJ. Physiological and performance responses to tournament wrestling. Med Sci Sports Exerc 33: 1367–1378, 2001.
22. Krustrup P, Mohr M, Steensberg A, Bencke J, Kjær M, Bangsbo J. Muscle and blood metabolites during a soccer game: Implications for sprint performance. Med Sci Sports Exerc 38: 1165–1174, 2006.
23. Malm C, Ekblom O, Ekblom B. Immune system alteration in response to two consecutive soccer games. Acta Physiol Scand 180: 143–155, 2004.
24. Margonis K, Fatouros IG, Jamurtas AZ, Nikolaidis MG, Douroudos II, Chatzinikolaou A, Mitrakou A, Mastorakos G, Papassotiriou I, Taxildaris K, Kouretas D. Oxidative stress
biomarkers responses to physical overtraining: Implications for diagnosis. Free Radic Biol Med 43: 901–910, 2007.
25. Marin D, dos Santos Rde C, Bolin AP, Guerra BA, Hatanaka E, Otton R. Cytokines and oxidative stress
status following a handball game in elite male players. Oxid Med Cell Longev 2011: 804873, 2011.
26. Michailidis Y, Karagounis LG, Terzis G, Jamurtas AZ, Spengos K, Tsoukas D, Chatzinikolaou A, Mandalidis D, Stefanetti RJ, Papassotiriou I, Athanasopoulos S, Hawley JA, Russell AP, Fatouros IG. Thiol-based antioxidant supplementation alters human skeletal muscle signaling and attenuates its inflammatory response
and recovery after intense eccentric exercise. Am J Clin Nutr 98: 233–245, 2013.
27. Mohr M, Krustrup P, Bangsbo J. Match performance of high-standard soccer players with special reference to development of fatigue. J Sports Sci 21: 519–528, 2003.
28. Mougios V. Reference intervals for serum creatine kinase in athletes. Br J Sports Med 41: 674–678, 2007.
29. Nikolaidis MG, Jamurtas AZ, Paschalis V, Fatouros IG, Koutedakis Y, Kouretas D. The effect of muscle-damaging exercise on blood and skeletal muscle oxidative stress
: Magnitude and time-course considerations. Sports Med 38: 579–606, 2008.
30. Norkin CC, White DJ. Measurement of Joint Motion: A Guide to Goniometry. Philadelphia, PA: FA. Davis Company, 2009.
31. Nosaka K, Newton M, Sacco P. Muscle damage and soreness after endurance exercise of the elbow flexors. Med Sci Sports Exerc 34: 920–927, 2002.
32. Panayiotou G, Paschalis V, Nikolaidis MG, Theodorou AA, Deli CK, Fotopoulou N, Fatouros IG, Koutedakis Y, Sampanis M, Jamurtas AZ. No adverse effects of statins on muscle function and health-related parameters in the elderly: An exercise study. Scand J Med Sci Sports 23: 556–567, 2013.
33. Peake J, Nosaka K, Suzuki K. Characterization of inflammatory responses to eccentric exercise in humans. Exerc Immunol Rev 11: 64–85, 2005.
34. Pedersen BK, Fischer CP. Physiological roles of muscle-derived interleukin-6 in response to exercise. Curr Opin Clin Nutr Metab Care 10: 265–271, 2007.
35. Povoas SCA, Seabra AFT, Ascensao AAMR, Magalhaes J, Soares JMC, Rebelo ANC. Physical and physiological demands of elite team handball. J Strength Cond Res 26: 3365–3375, 2012.
36. Steensberg A, Fischer CP, Keller C, Møller K, Pedersen BK. IL-6 enhances plasma IL-1ra, IL-10, and cortisol in humans. Am J Physiol Endocrinol Metab 285: E433–E437, 2003.
37. Stone WJ, Steingard PM. Year-round conditioning for basketball. Clin Sports Med 12: 173–191, 1993.
38. Takarada Y. Evaluation of muscle damage after a rugby match with special reference to tackle plays. Br J Sports Med 37: 416–419, 2003.
39. Thompson D, Nicholas CW, Williams C. Muscular soreness following prolonged intermittent high-intensity shuttle running. J Sports Sci 17: 387–395, 1999.
40. Thorlund JB, Michalsik LB, Madsen K, Aagaard P. Acute fatigue-induced changes in muscle mechanical properties and neuromuscular activity in elite handball players following a handball match. Scand J Med Sci Sports 18: 462–472, 2008.
41. Tofas T, Jamurtas AZ, Fatouros IG, Nikolaidis MG, Koutedakis Y, Sinouris EA, Papageorgakopoulou N, Theocharis DA. The effects of plyometric exercise on muscle performance, muscle damage and collagen breakdown. J Strength Cond Res 22: 490–496, 2008.
42. Toubekis AG, Smilios I, Bogdanis GC, Mavridis G, Tokmakidis SP. Effect of different intensities of active recovery on sprint swimming performance. Appl Physiol Nutr Metab 31: 709–716, 2006.
43. Tsakiris S, Parthimos T, Tsakiris T, Parthimos N, Schulpis KH. Alpha-tocopherol supplementation reduces the elevated 8-hydroxy-2-deoxyguanosine blood levels induced by training in basketball players. Clin Chem Lab Med 44: 1004–1008, 2006.
44. Whitehead TG, Thorpe HG, Maxwell S. Enhanced chemiluminescent assay for antioxidant capacity in biological fluids. Anal Chim Acta 226: 265–277, 1992.
Keywords:Copyright © 2014 by the National Strength & Conditioning Association.
inflammatory response; team sports; oxidative stress; periodization