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Time Course of Changes in Performance and Inflammatory Responses After Acute Plyometric Exercise

Chatzinikolaou, Athanasios1; Fatouros, Ioannis G1; Gourgoulis, Vassilios1; Avloniti, Alexandra1; Jamurtas, Athanasios Z2; Nikolaidis, Michalis G2,3; Douroudos, Ioannis1; Michailidis, Yiannis1; Beneka, Anastasia1; Malliou, Paraskevi1; Tofas, Trifon2; Georgiadis, Ilias1; Mandalidis, Dimitrios4; Taxildaris, Kyriakos1

Journal of Strength and Conditioning Research: May 2010 - Volume 24 - Issue 5 - p 1389-1398
doi: 10.1519/JSC.0b013e3181d1d318
Original Article

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, and Taxildaris, K. Time course of changes in performance and inflammatory responses after acute plyometric exercise. J Strength Cond Res 24(5): 1389-1398, 2010-The objectives of the present investigation were to study the inflammatory and performance responses after an acute bout of intense plyometric exercise during a prolonged recovery period. Participants were randomly assigned to either an experimental group (P, n = 12) that performed intense plyometric exercises or a control group (C, n = 12) that rested. The delayed onset of muscle soreness (DOMS), knee range of motion (KROM), creatine kinase (CK) and lactate dehydrogenase (LDH) activities, white blood cell count, C reactive protein (CRP), uric acid (UA), cortisol, testosterone, IL-6, IL-1b strength (isometric and isokinetic), and countermovement (CMJ) and static (SJ) jumping performance were measured at rest, immediately postexercise and at 24, 48, 72, 96, and 120 hours of recovery. Lactate was measured at rest and postexercise. Strength remained unchanged throughout recovery, but CMJ and SJ declined (p < 0.05) by 8-20%. P induced a marked rise in DOMS, CK, and LDH (peaked 24-48 hours postexercise) and a KROM decline. An acute-phase inflammatory response consisting of leukocytosis (postexercise and at 24 hours), an IL-6, IL-1b, CRP, and cortisol elevation (during the first 24 hours of recovery) and a delayed increase of UA (peaked at 48 hours) and testosterone (peaked at 72 hours) was observed in P. The results of this investigation indicate that performing an acute bout of intense plyometric exercise may induce a short-term muscle damage and marked but transient inflammatory responses. Jumping performance seems to deteriorate for as long as 72 hours postexercise, whereas strength appears to remain unchanged. The acute-phase inflammatory response after a plyometric exercise protocol appears to follow the same pattern as in other exercise models. These results clearly indicate the need of sufficient recovery between successive plyometric exercise training sessions.

1Department of Physical Education and Sports Science, Democritus University of Thrace, Komotini, Greece; 2Department of Physical Education and Sports Science, University of Thessaly, Trikala, Greece; 3Institute of Human Performance and Rehabilitation, Center for Research and Technology-Thessaly, Trikala, Greece; and 4Department of Physical Education and Sports Science, University of Athens, Athens, Greece

Address correspondence to Dr. Ioannis G. Fatouros,

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Plyometrics is a widely used training approach to enhance the ability of muscle to generate power and refers to activities that assist athletes to reach maximal force in the shortest possible time (5). Plyometric exercise represents a rapid deceleration of the body immediately followed by a brief transition phase and a rapid acceleration to the opposite direction (39). This rapid combination of eccentric and concentric work by muscle is called stretch-shortening cycle during which the muscular force produced during the concentric phase is potentiated by the preceded negative phase (39). The use of plyometric training results in the improvement of vertical jumping ability (13), running economy (47), and overall athletic performance (42).

Lengthening or eccentric contractions have been documented to induce skeletal-muscle trauma in both human (31) and animal models (20). Eccentric contraction-associated trauma results in reductions of force output and range of motion (ROM) by the injured muscle, and edema that persist for several days during postexercise recovery (33,37). Strength has been shown to decline by 20-60% after an injurious exercise protocol that includes eccentric activity compared with baseline values (32,35). Muscle damage is mainly induced by mechanical stress and disturbances of calcium homeostasis while a sensation of discomfort within the muscle may be developed (4). The intensity of discomfort increases within the first 24 hours after exercise, peaks between 24 and 72 hours, subsides, and eventually disappears 5-7 days later, a phenomenon that is referred to as delayed onset of muscle soreness (DOMS) (10).

Although plyometric exercise includes a strong eccentric component, information regarding its effects on muscle damage and DOMS is scarce. An acute bout of plyometric exercise has been shown to cause a marked increase of muscle damage (22) and collagen breakdown markers (45). It appears that plyometric work elicits higher DOMS than concentric exercise but less than eccentric exercise (22). Two previous studies showed that drop jump performance resulted in prolonged marked reduction of jumping ability and elevation of circulating creatine kinase (CK) (17,30). In contrast, Tofas et al. (45), reported a similar CK elevation but no change in muscle performance. This discrepancy may be attributed to differences in exercise protocols, testing modalities, subjects' fitness status, and experience in plyometric training. Exercise-induced muscle damage is associated with an acute-phase inflammatory response characterized by phagocyte infiltration into muscle, free radical production, and elevation of cytokines and other inflammatory molecules (3). Although a few investigations (12,19) attempted to study the plyometric exercise-induced muscle damage, limited data exist regarding the acute-phase inflammatory response after an acute session of plyometric exercise. Therefore, the purpose of the present study was to employ a holistic approach by investigating the time course of changes in inflammatory, hormonal, and performance markers involved in the inflammatory response during a 5-day recovery period after an acute bout of plyometric exercise.

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Experimental Approach to the Problem

Frequency of plyometric training is an important issue in muscle power training methodology. The time frame of inflammation development and performance deterioration is crucial when practitioners need to decide when their next training session must be placed within the training microcycle (i.e., when inflammation subsides and performance is regained). Several studies have examined the effect of eccentric contractions on the acute-phase inflammatory response, but there are no such data regarding plyometric exercise. To determine the time course of inflammatory and performance responses after an acute bout of plyometric exercise, a 2-group (including a control group to account for the day-to-day variation of the physiological and biochemical assays), repeated-measures design was employed. To this end, we monitored performance changes through jumping ability by measuring countermovement (CMJ) and squat (SJ) jumping and isokinetic assessment of knee extensors strength (at 2 different velocities). Vertical jumping is a valid performance indicator because it is an integral component of plyometric exercise drills, whereas lower limb strength is a major determinant of jumping performance. Inflammatory markers chosen represent the various phases of the inflammatory cycle that follows exercise-induced muscle damage such as clinical symptoms (muscle damage [DOMS] and knee range of motion [KROM] as muscle edema marker), white blood cell activation (leukocyte count), the cytokine cascade (cytokines IL-6 and IL-1b), sarcolemma disruption (CK and lactate dehydrogenase [LDH] activities), acute phase reaction (C-reactive protein [CRP]), respiratory burst activity (uric acid [UA]) and hormonal regulation (cortisol and testosterone) markers before exercise, immediately postexercise, and 24, 48, 72, 96, and 120 hours within recovery.

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Twenty-four healthy men who volunteered to participate in the present study were randomly assigned to either a control group (C, N = 12, age 25.5 ± 1.9 years, height 1.84 ± 0.05 m, weight 82.7 ± 6.1 kg, body fat 13.3 ± 1.6%, o2max 50.4 ± 5.9 ml·kg−1·min−1) that participated only in the measurements or an experimental group (P, N = 12, age 23.1 ± 2.6 years, height 1.86 ± 0.04 m, weight 84.2 ± 8.2 kg, body fat 12.1 ± 4.8%, and o2max 52.1 ± 6.4 ml·kg−1·min−1) underwent an acute plyometric exercise bout. Subjects were familiar with plyometric exercise training, but they did not performed this type of exercises at least 6 months before the study although they were regularly training (participated in at least 3 training sessions per week, performing both cardiovascular and resistance exercises). All participants were able to lift at least 2 times their body weight in squat exercise before the study. Participants abstained from any strenuous physical activity for at least 7 days before and after the experimental period. To examine if there were differences in dietary intake between groups, 5-day diet recalls were completed. Participants were instructed to maintain their normal eating pattern for 2 weeks before data collection and during the experiment. Participants were not taking any medication or dietary supplements with anti-inflammatory action for 6 months before the study. During exercise, participants were allowed to drink only water ad libitum. All subjects were informed about the nature of the study and the associated risks and benefits, and appropriate consent has been obtained pursuant to law. The study was approved by the Institutional Board, and procedures were in accordance with the Helsinki declaration.

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Plyometric Exercise Protocol

Two weeks after a familiarization period and exercise technique instruction, subjects in P performed an intense bout of plyometric exercises. Briefly, after a 10-minute warm-up (light running and stretching), subjects performed a plyometric protocol consisting of 50 jumps over 50-cm hurdles (5 sets of 10 repetitions) and 50 drop jumps from 50-cm plyometric box (5 sets of 10 repetitions). Two- and 5-minute rest was allowed between sets and exercises, respectively. A majority of training injuries (e.g., meniscal damage, patellar tendonitis, achilles tendon strains, and heel bruises) have been attributed to the repetitive ballistic movements of plyometrics because of high external forces acting upon a joint that momentarily surpass the structural integrity of the muscles, bones, and connective tissue (2). Therefore, plyometrics were performed on a rubber mat that produces less strain on muscle, bones, and connective tissue without absorbing a great amount of shock without diminishing the effectiveness of the training method (18).

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Anthropometric Profile and Maximal Oxygen Consumption Assessment

Body mass was measured to the nearest 0.5 kg (Beam Balance 710, Seca, United Kingdom) with subjects wearing their underclothes and barefooted. Standing height was measured to the nearest 0.5 cm (Stadiometer 208, Seca). Percent body fat was calculated from 7 skinfold measures (average of 2 measurements of each site) using a Harpenden calliper (John Bull, United Kingdom). o2max was determined as previously described (21).

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Vertical Jump Height Assessment

All jumps were performed on a Kistler force platform with the arms akimbo (sampling rate: 1,000 Hz). The starting position for all countermovement jumps was the upright posture (the degree of knee bend used by each subject was self-determined); the goal was to jump as high as possible. Jump height was calculated from the impulse of the vertical ground reaction force during the stance phase, and the trial resulting in the highest jump (total 3 attempts) (15).

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Assessment of Leg Strength

Knee extensor peak torque was measured using an isokinetic dynamometer (Cybex 6000) in a seated position. The dynamometer was calibrated before testing according to procedures suggested by the manufacturer. The test was preceded by a 5-minute cycling warm-up. Each subject was familiarized with the testing protocol and underwent 4 submaximal (75% perceived effort) and 1 maximal (100% perceived effort) trial before the actual testing. The testing protocol included 1 bout of 5 maximal knee extension-flexion repetitions for each tested speed (0, 60 and 180°·s−1) in a random order, separated by 120-second rest intervals. The highest value tested for each velocity was recorded. Maximal testing began with the knee flexed (100°) and ended at full extension (zero position of the knee, i.e., 0° flexion). Correction was applied for the elimination of errors against the effect of gravity on the lower leg and lever arm. To verify torque measurement reliability, knee extensor peak torque at all tested speeds was measured twice (within a week, at the same time of day) on the dominant leg. The intraclass correlation coefficients for repeated measurements were 0.98, 0.94, and 0.90, respectively.

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Muscle Damage Markers

The delayed onset of muscle soreness was determined by palpation of the muscle belly and the distal region of relaxed the vastus medialis, vastus lateralis, and rectus femoris in a seated position. Perceived soreness was then rated on a scale ranging from 1 (normal) to 10 (very, very sore) as previously described (7). Reliability coefficient for repetitive measurements in DOMS was 0.98. Knee range of motion was measured as an index of muscle edema. A 3-minute warm-up on a Monark stationary bicycle preceded KROM testing. Range of motion for knee extension-flexion was determined by the use of a goniometer (Lafayette Instrument Company, Lafayette, IN, USA) as previously described (34). After warm-up, 3 consecutive measurements were taken, and the best score was recorded. The coefficient of variation for test-retest trials for knee flexion/extension was 3.1% (n = 48).

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Blood Sampling and Biochemical Assays

Blood samples were drawn from an antecubital arm vein using a 20-gauge disposable needle equipped with a Vacutainer tube holder (Becton Dickinson, Franklin Lakes, NJ, USA) with the subject in a seated position. Samples (8 mL) were collected into a Vacutainer tube containing SST-Gel and Clot Activator. Serum was allowed to clot at room temperature and subsequently centrifuged (1,500g, 4°C, and 15 minutes). The resulting serum was placed into separate microcentrifuge Eppendorf™ tubes in multiple aliquots and frozen at −75°C for later analyses of the concentration of cortisol, testosterone, IL-6, IL-1B, and CRP and the activities of LDH and CK. Blood samples were thawed only once before analysis. A small quantity of blood (200 μL) was immediately added to 400 μL of 5% trichloroacetic acid and centrifuged (2,500g, 15 minutes). The supernatant was removed and frozen at −75°C until analysis for lactate by an enzymatic method with reagents purchased from Sigma Chemicals (St. Louis, MO, USA). A blood aliquot (1 mL) was immediately mixed with ethylenediaminetetraacetic acid to prevent clotting for hematology. Complete blood count and UA was determined within 24 hours via matching duplicate counts using an automated hematology analyzer (Sysmex K-1000 autoanalyzer, TOA Electronics, Kobe, Japan).

Creatine kinase was determined spectrophotometrically using a commercially available kit (Spinreact, Sant Esteve, Spain). Lactate dehydrogenase activity was determined spectrophotometrically by means of a commercial diagnostic test kit (Sigma Diagnostics, Saint Louis, MO). C-reactive protein was measured with the COBAS INTEGRA 800 Clinical Chemistry System (Roche Diagnostics, Indianapolis, IN, USA). Cortisol and testosterone were analyzed by using 2 commercially available enzyme-linked immunosorbent assay (ELISA) kits (DRG Diagnostics, Germany). Serum IL-6 and IL-1b concentrations were measured using 2 commercially available ELISA kits (Immunokontact, United Kingdom) based on an immunoenzymatic method. Postexercise changes in plasma volume were computed based on hematocrit and hemoglobin (11). Quality control procedures relating to the measurements of lactate, CK, LDH, CRP, uric acid, cortisol, testosterone, IL-1b, and IL-6 were also performed. Spectrophotometric assays were performed on a Hitachi 2001 UV-VIS spectrophotometer (Hitachi Instruments Inc., Tokyo, Japan) in duplicate (with all values expressed as a mean of the 2 determinations). The inter and intra-assay coefficients of variation in all assays performed were 2.8-7.1 and 4.2-7.4, respectively.

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Statistical Analyses

Data are presented as mean ± SE. Data normality was verified with the 1-sample Kolmogorov-Smirnoff test; therefore, a nonparametric test was not necessary. Data were analyzed through 2-way (group × time) repeated-measures ANOVA with planned contrasts on different time points. When a significant effect was found, post hoc analysis was performed through the Bonferonni test. Significance was set at an alpha of 0.05.

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There were no differences between groups with respect to their anthropometric profile, age, o2max, and diet composition (data not shown).

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Performance Responses

Performance changes are shown in Figure 1. Countermovement jumping declined (8-12%, p < 0.05) 24 hours postexercise and remained below baseline until 72 hours within recovery. Static jumping decreased (8-20%, p < 0.05) 24-72 hours during recovery, demonstrating its lowest value at 72 hours. No significant changes (p > 0.05) were observed in isometric and in isokinetic peak of knee extensors during recovery.

Figure 1

Figure 1

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Muscle Damage and Inflammatory Marker Responses

The delayed onset of muscle soreness (Table 1) increased (p < 0.05) in P immediately postexercise, peaked at 24 hours postexercise (fourfold) and remained elevated for 72 hours during recovery. Knee range of motion (Table 1) declined (p < 0.05) in P at 24 and 48 hours postexercise and returned to baseline thereafter. Creatine kinase activity (Table 1) increased (p < 0.05) at 24 hours until 72 hours of recovery (0.5- to 2.6-fold), demonstrating its peak at 48 hours. Lactate dehydrogenase activity (Table 1) increased (p < 0.05) immediately after exercise (∼30%), peaked at 24 hours postexercise (∼65%), and remained elevated for 72 hours within recovery.

Table 1

Table 1

Leukocytosis developed (Figure 2) immediately postexercise, which persisted for 24 hours within recovery. C reactive protein (Figure 2) increased (p < 0.05) immediately postexercise (∼twofold), peaked at 24 hours of recovery (2.8-fold), and normalized thereafter. Uric acid (Figure 2) increased (p < 0.05) at 24 hours postexercise (28%) and remained elevated for 96 hours, peaking at 48 hours (40%) of recovery.

Figure 2

Figure 2

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Hormonal and Lactate Responses

Hormonal responses are shown in Figure 3. Cortisol concentration increased (p < 0.05) postexercise (60%), remained elevated for 96 hours of recovery, exhibiting its peak value at 48 hours (4.7-fold, p < 0.05). Free testosterone concentration increased (p < 0.05) between 48 and 72 hours of recovery. IL-6 concentration increased (twofold, p < 0.05) immediately after plyometric exercise, remained elevated for 24 hours, and returned to resting levels thereafter. Testosterone to cortisol ratio declined (p < 0.05) 24 hours postexercise and remained below baseline values until 96 hours within recovery. IL-1b values remained below the assay kit's lowest detection limit in almost all measurement times except immediately postexercise. Plyometric exercise increased (p < 0.001) blood lactate levels (1.1 ± 0.2 mM at rest vs. 7.1 ± 0.9 mM postexercise, p < 0.05).

Figure 3

Figure 3

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Our intention was to monitor changes in specific inflammatory markers and performance for a prolonged period (5 days) after a plyometric session. The present investigation suggests that an acute bout of intense plyometric exercise induces time-dependent changes in various inflammatory markers indicative of muscle trauma and acute performance deterioration.

The substantial decline in KROM and the marked elevation of DOMS, CK, and LDH levels provide indirect evidence of muscle microtrauma after an acute bout of plyometrics. Only a few previous investigations have suggested that plyometric exercise may induce muscle damage because of the forces produced during ground impact and the associated eccentric contraction (22,30). In accordance with Tofas et al. (45), the plyometrics group demonstrated higher DOMS levels compared with the control group for as long as 72 hours postexercise and subsided thereafter. The present DOMS rise (∼3-4) may be considered moderate compared with the respective values after eccentric and other exercise protocols (9,21) in a 10-point scale that may be interpreted as limited muscle damage. This limited DOMS response coincides with the lack of changes in isometric and isokinetic torques (although jumping performance deteriorated). However, in contrast to the work of Tofas et al. (45) that used an identical exercise protocol (that induced a similar lactate response), KROM declined for 48 hours within recovery indicating increased muscle edema. This discrepancy may be attributed to different modes of KROM assessment. Peak CK activity, 48 hours postexercise, was somewhat over 200 U·L−1, which is almost as high as the increase observed in the study of Tofas et al. (45) and well below the values seen with eccentric exercise protocols (35,36). This finding may be attributed to the lower eccentric component of the present protocol and the execution of the plyometric jumps on a soft surface (wrestling-type mat) that induces less muscle damage than a firm surface (30). The 48 hours peak of the CK response after acute plyometric exercise seems a relatively constant finding (12,19,22,45). The CK and LDH protein efflux from muscle may be attributed to the increased permeability of plasma membrane or intramuscular vasculature (8). During the negative phase of a plyometric jump, eccentric activation produces higher tension per cross-sectional area of active muscle mass compared with concentric actions (4) resulting in significant structural muscle damage (10). Therefore, muscle trauma seen after plyometrics is, at least partially, attributed to intermittent repetitions of intense eccentric activation that may cause strains or tears accompanied by marked collagen breakdown (45).

Although few studies have investigated plyometrics impact on indirect indices of muscle damage, limited knowledge exists regarding plyometrics effects on indices of the inflammatory reaction. Acute intense exercise elicits an acute-phase inflammatory response characterized by leukocyte infiltration in the damaged area resulting in leukocytosis with neutrophils representing 50-60% of the total circulating pool (40). Leukocytes exhibit a transient rise immediately postexercise followed by a delayed increase several hours later, a response that was also observed in the present investigation (38). Similarly, Doussett et al. (12) observed a transient leukocyte rise that persisted for only 2 hours after stretch-shortening type exercise. However, in that study, there were no data on 24-hour leukocyte response (they sampled immediately postexercise, 2 hours post, and 2 days post). These 2 studies indicate that plyometric exercise-induced leukocytosis may persist for 24 hours. This postexercise immune reaction has been partially attributed to cortisol increase in the circulation, which has a complex effect on leukocyte subpopulations (14). The increase in cortisol is induced by IL-6, which is in agreement with our findings of a simultaneous postgame increase of IL-6 and cortisol (43). Cortisol may be also involved in IgM production and leukocyte adhesion capacity after intense exercise (26). Although acute resistance exercise and field sports appear to elevate cortisol (21,24), there is no information regarding cortisol responses after acute plyometric exercise. It has been shown that exercise protocols that induce the greatest cortisol response, induce the greatest lactate response (41). In support of our findings, acute increase in circulating cortisol has been highly associated with blood CK concentrations measured 24 hours postexercise (23). It appears that the greatest cortisol and lactate response is induced by metabolically demanding exercise regimens characterized by high total volume, mild to high intensity with short rest intervals (16). Nevertheless, more studies employing plyometric exercise protocols are needed to verify our results. Interestingly, testosterone increased not immediately postexercise but 48-72 hours later. Testosterone has been associated with leukocyte number in injured muscle tissue (27) and immunological responses after acute exercise (26). This delayed testosterone rise may be explained as an attempt to oppose the postexercise catabolic state. Unfortunately, no information exists regarding testosterone responses to acute plyometric exercise. Resistance exercise, which also has a strong eccentric component, has been shown to acutely increase total testosterone concentrations in most exercise studies in men (24). However, only few studies measured testosterone responses after 24 hours of recovery after various forms of exercise. Kraemer et al. (25) reported that although circulating testosterone increased immediately after resistance exercise, it declined to below resting values on day 3 despite a simultaneous CK rise. However, that was an entirely exercise model involving 3 exercise bouts that may elicit a repeated bout effect in relation to muscle inflammation responses. In another study, a hypertrophy-oriented resistance exercise protocol induced a prolonged (48 hours) testosterone response as in the present study but that exercise model was entirely different than the one used in this study (29). Therefore, it is difficult to compare our results with those of other investigators.

Secretion of anabolic and catabolic hormones, such as testosterone and cortisol, depends on the severity of previously performed exercise. These 2 hormones demonstrate quantitative alterations indicating a catabolic state that may be reversed by suitable regenerative approaches (48). Adlerreutz et al. (1) proposed that a decline in the ratio of testosterone-to-cortisol >30% or <0.35/10−3 may serve as a marker for the diagnosis of overtraining. In this study, the testosterone-to-cortisol ration declined more than 75% 24-48 hours postexercise although it did not reach the 0.35/10−3 threshold. However, overtraining implies a cumulative stress of multiple training session without appropriate resting, a condition that does not apply in this study where participants performed only 1 training session while their adequate rest before and during the experimental protocol was a prerequisite.

IL-1B and IL-6 are 2 of the primary cytokines involved in the cytokine cascade that is involved in the control of immune reaction during the acute-phase inflammatory response and the subsequent repair process (6). Our results are in line with previous reports of IL-1B elevation immediately postexercise (12,14). IL-1B may also be involved in muscle adaptation by inducing protein degradation and muscle atrophy (3,6). IL-6 is implicated in hepatocyte-derived acute-phase proteins production, cortisol production, and neutrophil degranulation (6,43). Muscle damage per se causes a repair response with macrophage entry into the muscle, eliciting an additional delayed IL-6 production of a smaller magnitude. In the present investigation, IL-6 increased only during the first 24 hours of recovery and at a lesser extent (twofold to threefold) compared with other studies (44), which is probably related to the smaller extent of muscle trauma induced by plyometrics as compared with other exercise models.

During inflammation, CRP, an acute-phase protein, is synthesized and released by the liver after stimulation by IL-6 and cortisol (43). In the present study, cortisol and IL-6 peaks preceded or coincided with CRP peak in the circulation. It appears that, plyometrics caused a marked but transient CRP increase within 24 hours of recovery as previously reported for other exercise models (21,27). In contrast, Dussett et al. (12) reposted that CRP increased only 2 days after a plyometric exercise protocol and subsided thereafter, whereas CRP values were lower than in the present study. This discrepancy may be associated with the conditioning status of the subjects or the intensity of the exercise protocol. C reactive protein rise has been associated with monocyte activation and adhesion molecules synthesis that recruit leukocytes (46).

Exercise-induced inflammation is accompanied by an upregulation of oxidative stress response and antioxidant capacity in serum (28,33). Uric acid elevation postexercise usually parallels total antioxidant capacity changes (28). Uric acid elevation has been estimated to account for nearly one-third of total antioxidant capacity increase (49). High-intensity exercise-associated muscle ischemia upregulates purine nucleotide metabolism leading to adenosine elimination of monoposphate adenosine (AMP) and accumulation of hypoxanthine in the muscle compartment and plasma. Although hypoxanthine may be converted back to AMP at rest and during mild exercise, it is converted to uric acid and oxygen radicals. Uric acid elevation in the present study is consistent with these observations. The involvement of purine nucleotide metabolism in plyometric exercise training, not previously reported, indicates an ATP reduction and IMP rise in muscle after plyometric activity.

Strength loss after muscle-damaging exercise is one of the most commonly used indicators of exercise-induced muscle trauma (35,36). In this study, we measured performance through isometric and isokinetic peak torque and 2 forms of vertical jumping (CMJ and SJ). In a previous study, Tofas et al. (45) reported no changes in peak isometric and isokinetic peak torque at knee extensions after an identical plyometric exercise protocol. In line with that study, isometric and isokinetic peak torque remained unchanged during 120 hours of recovery in the present investigation. In contrast, CMJ and SJ jumping deteriorated by 8-20% 24-72 hours postexercise, returning to baseline levels only after 96 hours of recovery suggesting that there may be a refractory period for successive plyometric exercise training sessions. To our knowledge, this is the first study that measured jumping ability after plyometric exercise-induced muscle damage. This variation in results between isometric-isokinetic strength and jumping performance may be attributed to different kinematic characteristics of knee extensions during isometric-isokinetic leg model and jumping motion, revealing a movement-specific adaptation.

In conclusion, an acute plyometric exercise bout induces marked but transient inflammatory responses and decrements in vertical jumping (but not strength) for as long as 72 hours postexercise. These data clearly indicate the need of sufficient recovery for athletes after a plyometric exercise session.

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Practical Applications

The findings of the present study confirm previous observations that an acute bout of plyometric exercise does induce muscle damage and DOMS but of a smaller magnitude compared with other exercise forms. Plyometric exercise-induced muscle damage is accompanied by a marked acute inflammatory response that persists for as long as 72 hours. Furthermore, acute plyometric exercise may induce a substantial decline in jumping performance but not in other forms of muscle strength. Sport professionals in numerous sports use plyometric training to enhance power performance. Physical conditioning trainers and other practitioners should consider that successive plyometric exercise training sessions may need adequate recovery (∼72 hours) to allow performance recovery and inflammation withdrawal. More research is needed to determine the relationship between different combinations of volumes and intensities of plyometric exercise and acute inflammatory response.

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The authors wish to thank all the subjects for their participation and commitment to the study.

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plyometric exercise; muscle soreness; stress hormones; strength

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