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Markers of Postmatch Fatigue in Professional Rugby League Players

McLellan, Christopher P; Lovell, Dale I; Gass, Gregory C

Journal of Strength and Conditioning Research: April 2011 - Volume 25 - Issue 4 - p 1030-1039
doi: 10.1519/JSC.0b013e3181cc22cc
Original Research
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McLellan, CP, Lovell, DI, and Gass, GC. Markers of postmatch fatigue in professional rugby league players. J Strength Cond Res 25(4): 1030-1039, 2011-The aim of the present study was to identify neuromuscular, biochemical, and endocrine markers of fatigue after Rugby League match play. Seventeen elite Rugby League players were monitored for a single match. Peak rate of force development (PRFD), peak power (PP), and peak force (PF) were measured during a countermovement jump (CMJ) on a force plate pre and postmatch play. Saliva and blood samples were collected 24 hours prematch, 30 minutes prematch, 30 minutes postmatch, and then at 24-hour intervals for a period of 120 hours to determine plasma creatine kinase concentration ([CK]) and salivary cortisol concentration ([sCort]). There were significant (p < 0.05) decreases in PRFD and PP up to 24 hours postmatch with PF significantly (p < 0.05) decreased immediately postmatch. The [sCort] significantly (p < 0.05) increased from 24 hours prematch to 30 minutes prematch and up to 24 hours postmatch compared with 24 hours prematch. Plasma [CK] significantly (p < 0.05) increased 30 minutes postmatch with a peak occurring 24 hours postmatch and remained elevated above 24 hours prematch for at least 120 hours postmatch. There were significant (p < 0.05) correlations between the increase in [CK] and reduction in PRFD 30 minutes postmatch and 24 hours postmatch. The [sCort] was significantly (p < 0.05) correlated with the reduction in PF 30 minutes postmatch. Results demonstrate that neuromuscular function is compromised for up to 48 hours after match play. Elevated [CK] despite 120-hour recovery indicate that damage to muscle tissue after Rugby League match play may persist for at least 5 days postmatch. Despite the prolonged presence of elevated [CK] postmatch, strength training 48 hours postmatch may have resulted in a compensatory increase in PRFD supporting the inclusion of strength training during the short-term postmatch recovery period.

1Faculty of Health Sciences and Medicine, Bond University, Gold Coast, Queensland, Australia; and 2School of Health and Sport Sciences, Faculty of Science, Health & Education, University of the Sunshine Coast, Maroochydore, Queensland, Australia

Address correspondence to Christopher P. McLellan, cmclella@bond.edu.au.

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Introduction

Participation in contact sport such as Rugby League that involves high-intensity, intermittent exercise, and blunt force trauma is a complex phenomenon, often associated with significant neuromuscular fatigue (for review, see [11]). Neuromuscular fatigue has been described in humans as any exercise-induced reduction in the maximal voluntary force or power produced by a muscle or muscle group (4,11) and is determined by the type of muscle contraction, the intensity of exercise, and the duration of the exercise (9). Traditionally, neuromuscular fatigue has been examined using isolated forms of isometric, concentric, or eccentric movements (11). However, recent evidence suggests the incorporation of movements involving the stretch-shortening cycle (SSC) (24) provides a more specific examination of neuromuscular fatigue (20,26).

Movements involving the SSC incorporate metabolic, mechanical, and neural elements of fatigue together with impairment of the stretch-reflex activation (26). Typically, the SSC involves a preactivated muscle that is first stretched (eccentric action) and then shortened (concentric action) and is common to activities that involve different phases of running, jumping, or hopping (20). Recovery after impaired SSC function occurs in 2 phases: (a) identified by a significant initial decrement in SSC function immediately postexercise and (b) a phase of transient recovery then followed by a subsequent decrement in performance, resulting in a peak reduction in SSC function some 48-72 hours postexercise (17,20,27).

Although the countermovement jump (CMJ) is commonly used to assess the SSC and athletic performance (7,15,16,36), there are limited data that have used the CMJ to determine the effect of competitive team match play on neuromuscular fatigue. Those data that are available are conflicting (7,15,16,36). Hoffman et al. (15) reported various changes in peak power (PP), peak force (PF), and peak rate of force development (PRFD) in American Football players, whereas Thorlund et al. (36) found no significant change in PF, PP, or rate of force development (RFD) immediately after a soccer match play. Similarly, Cormack et al. (7) found no significant change in mean force and mean power immediately after a game of elite Australian Rules Football and suggested that the CMJ may lack the sensitivity to detect neuromuscular fatigue from a single game. There appears to have been no investigation examining the influence of elite Rugby League match play on CMJ variables to assess their usefulness as measures of neuromuscular fatigue.

The effects of high-intensity, intermittent contact sport match play on muscle enzyme (e.g., creatine kinase concentration [CK]) and endocrine (e.g., salivary cortisol concentration [sCort]) responses have been reported (14,15,21,35). Plasma [CK], an indirect marker of skeletal-muscle damage in humans (30), has been reported to be elevated after competitive match play in American Football (20) and Rugby Union (35). During a competitive Rugby Union match, there was a significant correlation (r = 0.92, p < 0.01) between the number of tackles performed and peak [CK] measured 24 hours postmatch (35). Although increases in plasma [CK] have also been reported in other contact sports (21), there are no data reporting the plasma [CK] response to a Rugby League match or during the subsequent 120 hours after a single match.

Cortisol has been used as both an acute and chronic marker of decreased protein synthesis and increased protein degradation during intense exercise (38). Ispirlidis et al. (18) reported plasma cortisol concentration [Cort] to be significantly increased immediately after a game of elite Soccer returning to pregame concentration 24 hours later. Similarly, Cormack et al. (7) found that salivary cortisol concentration [sCort] was substantially higher immediately and 24 hours after a game of elite Australian Rules Football (19). In contrast to these findings, other studies (15,25) have found no significant changes in [Cort] or [sCort] after intercollegiate American football and professional soccer match play, respectively. The usefulness of [CK] and [sCort] as markers of postmatch neuromuscular fatigue after high-intensity and short-duration sports is unclear, and particularly so for Rugby League match play.

Rugby League match play presents a unique model to study neuromuscular fatigue generated by high-intensity competition, combining movement patterns and sprinting profiles similar to Rugby Union, running volumes similar to soccer and blunt force trauma that is characteristic of American Football match play. Uncertainty remains regarding the pattern of neuromuscular fatigue, CK, and cortisol responses to elite contact sport, and the influence of elite Rugby League match play is unknown. A better understanding of the neuromuscular, biochemical, and endocrine response to competitive match play and the short-term postmatch recovery period is important to planning effective training over the subsequent week and may provide scope for improvement in individualized training and recovery strategies. The aim of the present study therefore was to examine the neuromuscular, biochemical, and endocrine responses to Rugby League match play to determine if the CMJ, CK activity, or sCort response could be used to monitor neuromuscular fatigue after a single match. We hypothesize that Rugby League match play will result in substantial skeletal muscle damage, considerable elevation in stress hormone levels and decreased neuromuscular performance during the CMJ postmatch. Further, the combination of neuromuscular performance data with CK and sCort provides a more detailed and specific analysis of the demands of Rugby League match play than achieved previously.

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Methods

Experimental Approach to the Problem

The present study examined SSC performance to determine neuromuscular fatigue after elite Rugby League match play. Measurement of the dependent variables of PRFD, PP, and PF during a CMJ was performed on a portable force plate pre- and post-match play. Plasma [CK] was examined to reflect skeletal-muscle damage in response to the demands of match play. The [sCort] was examined to represent the primary catabolic endocrine measure associated with metabolism pre and postmatch. To examine the acute and short-term postmatch response of the dependent variables, [CK] and [sCort] were measured via blood and saliva samples, respectively. An understanding of player neuromuscular fatigue, skeletal-muscle damage, and the endocrine response after match play is important to monitor recovery and effectively manage the prematch training and preparation process for subsequent matches.

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Subjects

Seventeen elite male Rugby League players, age 19.0 ± 1.3 years, height 188 ± 2.3 cm, and mass 89.6 ± 15.8 kg, representing a National Rugby League team volunteered to participate in the study. Data were collected during a single match of Rugby League with all participants completing a minimum of 30 minutes of match play in each of the 2 40-minute halves of the match. Before the commencement of the study, participants attended a presentation outlining the purpose, benefits and procedures associated with the study. Written informed consent was obtained from all participants. The study was approved by the Bond University Human Research Ethics Committee and the Gold Coast Titans Rugby League Football Club.

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Procedures

Saliva and blood samples were collected 24 hours prematch, 30 minutes prematch, within 30 minutes postmatch and at 24, 48, 7, 96, and 120 hours postmatch. The saliva and blood collection schedule is outlined in Table 1. Subjects were asked to refrain from strenuous exercise 24 hours before baseline prematch saliva and blood sample collection (24 hours prematch). Saliva and blood samples were collected daily between 1530 and 1630 h with the exception of the 30 minutes postmatch saliva and blood samples that were collected between 1830 and 1900 h because of the time of match play. Players provided saliva and blood samples within 30 minutes of match completion and before participation in postmatch team recovery activities (Table 1). The CMJ was performed on a force plate immediately after each saliva and blood sample collection. Throughout the postmatch data-collection period (30 minutes postmatch to 120 hours postmatch), all subjects participated in all standardized team-recovery sessions and weekly team training sessions (Table 1). Active and passive recovery activities are typically implemented after elite Rugby League match play. Player participation in all postmatch recovery sessions was maintained in the present study because of the impracticality of removing this procedure from the regular team routine after match play. An example of the standardized postmatch team recovery and team training week during the in-season period is outlined in Table 2.

Table 1

Table 1

Table 2

Table 2

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The Countermovement Jump

Before performing the unloaded CMJ test, subjects completed a warm-up session consisting of 10 minutes of self-paced stationary cycling followed by 5 minutes of prescribed dynamic stretching. Once positioned on the force plate, subjects performed 1 submaximal practice jump. Each subject then performed 3 CMJ, with 3 minutes of rest between each CMJ. The CMJ was commenced in the standing position; the subject then dropped into the squat position and immediately jumped vertically incorporating arm swing to jump as high as possible. The depth of knee flexion and the amount of arm movement used during the CMJ was individually determined by each subject. Take-off from 2 ft was strictly monitored with no preliminary steps or shuffling permitted during the eccentric or transition phases of the CMJ technique. The best result from the 3 CMJs was used for analysis.

The CMJ was performed on a commercially available force plate (ONSPOT 2000-1) which sampled at a rate of 1,000 Hz and the analog signal was converted to a digital signal using a PowerLab 30 series data acquisition system (ADInstruments, Sydney, Australia). The vertical force-time data were filtered using a fourth-order Butterworth low-pass filter with a cutoff frequency of 17 Hz.

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Calculation of Force Variables

The force-time data from the CMJ included PRFD, PP and PF. A CMJ was deemed to have started when the vertical force exceeded 10 N greater than the mass of the subject. The PRFD was calculated from the maximum force that occurred over the first derivative of the force-time curve. The PF was calculated as the maximum force achieved over the force-time curve during the CMJ. The vertical velocity was calculated from the integration of the force-time trace and was used to calculate PP. The vertical force was multiplied by the velocity throughout the propulsive phase of the CMJ to determine PP.

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Plasma Creatine Kinase Sampling and Analysis

Plasma [CK] was determined from 30-μL capillarized whole-blood samples collected via fingertip puncture made using a spring-loaded single-use disposable lancet. Blood samples were collected from subjects simultaneously at the time of saliva sample collection. Whole-blood samples were centrifuged (Heraeus, Function Line) at 3,000 rpm for 10 minutes; separated plasma was stored at a temperature of −30°C until analysis. Plasma samples were analyzed using a Reflotron spectrophotometer (Abbott Architect) via an optimized UV test.

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Salivary Cortisol Sampling and Analysis

Unstimulated saliva was collected via passive drool into a plastic tube for analysis of Cortisol. The [sCort] are independent of salivary flow rate (31), and a significant correlation has been reported between saliva and serum unbound cortisol concentration at rest (r = 0.93) and during exercise (r = 0.90) (28). All subjects were requested to avoid the ingestion of food and fluids other than water during the 60 minutes before providing each saliva sample and refrain from brushing their teeth 2 hours before each saliva sample-collection session. Subjects were instructed to wait for a period of 10 minutes after their last consumption of water before commencing the saliva sample-collection process. Saliva samples were stored at −80°C until analysis.

[sCort] was analyzed in duplicate via a commercially available enzyme-linked immunosorbent assay (Salimetrics LLC, State College, PA, USA) using a microplate reader (SpectraMax 190, Molecular Devices, Fullerton, CA, USA). Standard curves were constructed as per the manufacturer's instructions, and commercially available standards and quality control samples were used for the assays (Salimetrics LLC). Cortisol sensitivity was 0.007 ng·mL−1 with an average intraassay CV of 2.6%. All samples were analyzed in the same series to avoid interassay variability.

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Statistical Analyses

Endocrine and biochemical variables analyzed prematch and postmatch included [sCort] and [CK]. Before statistical analysis, log transformation was applied to the endocrine and biochemical data to normalize the distribution and reduce nonuniformity bias. All data are expressed as mean ± SD. Changes in force-power characteristics, biochemical concentrations and endocrine concentrations were analyzed using a 1-way repeated measures analysis of variance. Significant differences were located by a Bonferroni post hoc test. The criterion level for statistical significance was set at p ≤ 0.05. The correlation between peak changes in force-power characteristics, biochemical and endocrine characteristics was analyzed using the Pearson Product-Moment Correlation Coefficient. The mean coefficient of variation (CV) for CK assays was 6.1%. All statistical analyses were performed using the Statistical Package for the Social Sciences (SPSS for Windows, version 14.0; SPSS, Inc., Chicago, IL).

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Results

Force-Power Characteristics

Changes in the force-power characteristics after elite Rugby League match play are shown in Table 3. The PRFD was significantly lower 30 minutes postmatch (p = 0.026) and 24 hours postmatch (p = 0.042) compared with 30 minutes prematch. Peak rate of force development values returned to 24 hours prematch values 48 hours postmatch. However, at 72 and 96 hours postmatch, the PRFD values were significantly higher than both prematch values (p = 0.012, p = 0.044, respectively). Peak power was significantly lower 30 minutes postmatch (p = 0.005) and 24 hours postmatch (p = 0.034) when compared with 30 minutes prematch. Peak power had returned to 24 hours prematch and 30 minutes prematch levels after 48 hours postmatch. Peak force was significantly lower 30 minutes postmatch (p = 0.031) but had returned to 30 minutes prematch levels after 24 hours.

Table 3

Table 3

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Creatine Kinase

There was a significant (p = 0.003) increase in plasma [CK] 30 minutes postmatch with a further significant (p = 0.002) increase in [CK], peaking at 24 hours postmatch (Table 4). Significant increases in plasma [CK] were also found 48 hours postmatch (p < 0.006), 72 hours postmatch (p = 0.004), 96 hours postmatch (p = 0.013), and 120 hours postmatch (p = 0.043) compared with 30 minutes prematch. There was a significant correlation between plasma [CK] and PRFD 30 minutes postmatch (p = 0.044, r = −0.64) and 24 hours postmatch (p = 0.033, r = −0.58) compared to 30 minutes prematch values.

Table 4

Table 4

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Cortisol

The [sCort] was significantly (p = 0.043) higher 30 minutes prematch compared with 24 hours prematch. Significant increases in [sCort] were also found 30 minutes postmatch (p < 0.001) and 24 hours postmatch (p < 0.000) when compared to 24 hours prematch (Table 4). The [sCort] was significantly (p = 0.042) lower 96 hours postmatch compared with 24 hours prematch. There was a significant correlation between the percent change in [sCort] and PF 30 minutes postmatch (p = 0.048, r = −0.58) compared with 30 minutes prematch values.

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Discussion

The present study examined the neuromuscular, biochemical and endocrine responses to Rugby League match play to determine if the CMJ, plasma [CK] or [sCort] response could be used to monitor neuromuscular fatigue after competition. The main findings of the present study were (a) PRFD and PP measured during a CMJ were decreased for up to 48 hours postmatch with PF decreased 30 minutes postmatch. Peak rate of force development also increased above prematch values 72 and 96 hours postmatch; (b) plasma [CK] and [sCort] increased postmatch with plasma [CK] remaining elevated for up to 120 hours postmatch; (c) significant correlations between the change in plasma [CK] and PRFD and the change in [sCort] and PF were found postmatch.

Previous work examining force-power variables including PRFD, PF, and PP subsequent to team sport participation during Australian Rules Football (7), American Football (15), and Soccer (36) found no significant difference between pre and postmatch force and power measures and suggested that team sport athletes may be able to maintain PRFD, PF, and PP after match play. The results of these studies (7,15,36) when compared with the results of the present study are surprising. The competitive requirements of Australian Rules Football, American Football and Soccer that involve periods of sprinting, jumping, rapid changes of direction, and blunt trauma could be expected to have an effect on the SSC and a reduction in CMJ performance as found in the present study.

Peak rate of force development, a measure of explosive muscle strength, is an important measure of performance in Rugby League. In the present study, PRFD significantly decreased 30 minutes postmatch and 24 hours postmatch in comparison to 24 hours prematch. Peak rate of force development remained below prematch values for 48 hours postmatch, and may reflect the influence of impaired excitation-contraction coupling reported with low-frequency fatigue (LFF) (22) on decreased PRFD, PP, and PF 24 hours after Rugby League match play.

The reduction in PRFD 30 minutes postmatch (35%) in the present study agrees with some (37) but not others (15,36). The differences in PRFD, PP, and PF between the present study and other studies (15,36) may be because of the running volumes, sprinting profiles, tackling and wrestling, and heavy blunt force trauma demands placed on Rugby League players but not upon Soccer or American Football players during match play. Although American Football players are likely to experience heavy contact during match play, episodes of contact involving blunt force trauma are dispersed through protective padding so as to reduce the effect of such trauma upon skeletal muscle tissue. Fewer total blunt force trauma episodes combined with reduced running volumes and extended rest periods between competitive efforts may contribute to the maintenance of PRFD, PP, and PF after American Football match play.

We observed a significant increase in PRFD at 72 hours (18%) and 96 hours (17%) postmatch that preceded a return to prematch values 120 hours postmatch. Our results regarding PRFD at 72 and 96 hours postmatch appear to be in contrast to the reported bimodal trend of neuromuscular fatigue involving SSC exercise (20,26). An immediate decrease in neuromuscular performance after exhaustive SSC exercise has been attributed primarily to metabolic disturbances, (e.g., metabolite accumulation, depletion of energy substrates and phosphate, and decrease in mitochondrial respiratory control) (22), whereas the secondary decrease in neuromuscular performance may coincide with the inflammatory processes associated with muscle damage during exhaustive SSC exercise (10). Studies that reported a bimodal trend of neuromuscular fatigue and recovery (20,27) used exhaustive eccentric exercise and not team sport activity as used in the present study. Therefore, the pattern of PRFD recovery observed at 72 and 96 hours postmatch may reflect the specific sprinting, SSC activity, blunt force trauma, and high-intensity intermittent nature of Rugby League match play and the influence of postmatch recovery methods.

The cause of the significant increase in PRFD after 72 and 96 hours postmatch in the present study is unclear. The CMJ is an effort-dependent SSC activity that may have been performed submaximally by players 30 minutes post and 24 hours postmatch. Submaximal CMJ effort 30 minutes post and 24 hours postmatch may be one of the consequences of competitive Rugby League match play, influenced by skeletal muscle soreness and SSC fatigue resulting from high-intensity intermittent exercise and repeated blunt force trauma. During competitive Rugby League match play however, the extent of SSC fatigue may not be exhaustive. Incomplete exhaustion of SSC performance during Rugby League match play may result in a pattern of postmatch PRFD recovery that is not consistent with the bimodal concept of fatigue-induced SSC performance decreases and the subsequent short-term recovery process.

During the short-term postmatch recovery period, players completed a structured recovery program of cold water immersion therapy (12°C), low-intensity deep water running and low-intensity mobility-resistance exercise (<40% 1RM). Strength training that included complex training methods incorporating high-intensity loads (>85% 1RM) coupled with explosive SSC exercise for the upper and lower limbs was conducted 48 hours postmatch. Rugby League specific speed and agility exercise consisting of high-intensity, short-duration sprint and SSC exercise was conducted 72 hours postmatch.

Our results suggest that the explosive strength, speed, and SSC exercise conducted during the structured recovery period (48 and 72 hours postmatch) may have resulted in a compensatory effect observed in PRFD at 72 hours post and 96 hours postmatch. The impaired excitation-contraction coupling reported with LFF (34) in the presence of exercise-induced muscle damage (20,22) may have been attenuated by the structured postmatch recovery strategies. These structured recovery strategies, if responsible for the increase in PRFD 72 and 96 hours postmatch reinforce the need for recovery strategies that enhance the return to prematch function so that the optimal training stimulus can be provided to players in preparation for subsequent match play.

Peak power in the present study was significantly lower 30 minutes postmatch and 24 hours postmatch compared with 30 minutes prematch values. It would appear that both the velocity of the CMJ, evidenced by the reduction in PRFD, and the force as evidenced by the reduction in PF 30 minutes postmatch, may have contributed to the decrease in PP. The decrease in PP remained until 48 hours postmatch suggesting that the velocity component of PP was more sensitive to fatigue than the force component. Peak force decreased significantly 30 minutes postmatch, returning to prematch values within 24 hours postmatch. Not all studies (7,15,16) have reported a decrease in PP and PF after competitive match play or sporting activity. The cause of the decrease in PF observed 30 minutes postmatch as suggested by others (1,34) may be because of a combination of central fatigue in the form of reduced central drive, and peripheral fatigue in the form of an impairment in action potential propagation over the sarcolemma (high-frequency fatigue) or impaired excitation-contraction coupling (LFF). The difference between PP and PF found 30 minutes postmatch in the present study and other studies (7,15,16) is most likely because of physical demands placed on players from different sports and the incorporation of a structured recovery program during the short-term recovery period. Our results indicate that PF (also referred to as maximal strength) recovers more quickly than PP or PRFD after rugby league match play.

Other studies (6,32) have found that PF recovers more rapidly than PP and PRFD. Byrne and Eston (6) reported the recovery of PP after exhausting squat exercise was 2 days longer than the recovery of isometric strength and suggested that PP, unlike strength that recovers more rapidly, may be affected by delayed onset muscle soreness (39) and the inflammatory responses to exercise-induced muscle damage. Although both PF and PP are important qualities in elite Rugby League players (3), PP and PRFD measured during a CMJ may be more useful than PF in monitoring neuromuscular fatigue post-Rugby League match play. The nature of Rugby League match play includes sprinting, jumping, high-speed directional changes, and a rapid summation of forces characteristic of PP and PRFD. Significant reductions in PP and PRFD found beyond 24 hours postmatch in the present study may reflect the continued influence of LFF and delayed recovery of the neuromuscular system.

In the present study, plasma [CK] and [sCort] were used as indirect markers of muscle damage and physiological stress after Rugby League match play. Although eccentric muscular work has traditionally been seen as the major contributor to increases in plasma [CK] after exercise (5), recent evidence suggests that significant increases in plasma [CK] may occur as a result of physical impact and blunt force trauma (15,32,34). The present study found that participation in Rugby League match play, which is characterized by physical impact and blunt force trauma, significantly increased plasma [CK] 30 minutes postmatch, with a peak plasma [CK] occurring 24 hours postmatch. Plasma [CK] remained significantly elevated above 24 hours prematch concentrations for up to 120 hours postmatch. The present study adds new knowledge in the time course of [CK] after Rugby League match play.

Although plasma [CK] as a marker of exercise-induced muscle damage has been challenged (40), plasma [CK] continues to be used as an indirect marker of skeletal-muscle damage (5,20). Our results using plasma [CK] suggests that the exercise-induced muscle damage after Rugby League match play does occur in significant amounts and remains elevated for at least 120 hours postmatch. Peak plasma [CK] (941 ± 392 U·L−1) found in the present study is similar to plasma [CK] reported in other sports that involve high-impact collisions between players (33,35). Although Takarada (35) recorded similar peak plasma [CK] 24 hours postcollege Rugby Union match play, the return to prematch [CK] was shorter (48 hours) postmatch than in the present study. The prolonged elevation of plasma [CK] found from 48 hours postmatch until 120 hours postmatch in the present study may have also been influenced by recovery strategies during the first 24 hours postmatch and the subsequent training sessions undertaken by the players after 48 hours postmatch.

The effect of elevated [CK] upon athletic performance is unclear. We observed a significant correlation between the increase in plasma [CK] and decreased PRFD 30 minutes postmatch (p = 0.044, r = −0.65) and 24 hours postmatch (p = 0.033, r = −0.58). Our results suggest that the decrease in PRFD in the present study at 30 minutes postmatch and 24 hours postmatch is causally related to the increase in plasma [CK], consistent with the findings of others (2,27). Andersson et al. (2) reported that CMJ height was reduced in the presence of a significant rise in plasma [CK] after elite female soccer match play. Nicol et al. (27) also reported an association between an increase in plasma [CK] and decreased drop jump performance during the first 2 days after exhaustive SSC exercise.

The associated increase in [CK] with decreased PRFD suggests that a CMJ may be used as an indirect estimate of the exercise-induced muscle damage from Rugby League match play. Support for a CMJ as an indirect estimate of PRFD is based on the reported relationship between [CK] and decreased SSC performance (20). The use of the CMJ as a functional indicator of PRFD, PP, PF, and exercise-induced muscle damage may therefore provide an appropriate method of functional impairment analysis associated with skeletal-muscle damage and recovery times after Rugby League match play. The association between increased [CK] and decrements in PRFD may be modified by structured recovery programs during the short-term postmatch recovery period.

In the present study, there was a significant increase in [sCort] 30 minutes prematch, 30 minutes postmatch, and 24 hours postmatch compared with 24 hours prematch. Cortisol is used as an indicator of “physiological stress” imposed during strenuous physical activity (23) and “psychological stress” because of the competitive environment of sport (25). The increase in prematch [sCort] found in the present study is consistent with the results of others (12) and is likely to be associated with prematch “psychological stress” because of anticipation and anxiety (29).

In the present study, the peak [sCort] was found 30 minutes postmatch, and by 48 hours postmatch [sCort] had returned to 24 hours prematch levels. Similar postmatch cortisol levels have been reported after games of Australian Rules Football (7), American Football (15), and Rugby Union (8). Elevations in [sCort] have been reported to be dependent on the duration and intensity of exercise (13). The increase in postmatch [sCort] found in the present study may be a reflection of exercise duration, intensity, and combative nature of Rugby League match play and psychological influences of anxiety and perceived stress of competition (29).

The present study found a significant correlation between change in [sCort] and the decrease in PF 30 minutes postmatch (p = 0.048, r = −0.58). No other study has examined the relation between [sCort] and PRFD, PP, and PF after Rugby League match play. Although it is not clear what the relationship between decreased PF and increased [sCort] may be, our results indicate that those players with the largest decrement in PF also produced the highest [sCort] 30 minutes postmatch. Decreased PF may reflect neuromuscular fatigue via a Rugby League match play-induced decline in central drive and failure of the excitation contraction mechanism (1) in players who experienced greater psychological stress or completed more high-intensity activity for longer duration, resulting in higher postmatch [sCort].

In summary, the findings of the present study indicate that the PRFD measured during a CMJ may be used as a mechanism to determine the neuromuscular fatigue associated with competitive Rugby League match play. Elevated plasma [CK] for up to 120 hours postmatch suggests significant damage to muscle tissue as a result of the blunt force trauma associated with high-speed collisions among Rugby League players. These neuromuscular and biochemical markers show promise as predictors of fatigue, recovery, and readiness for subsequent training after a Rugby League match play.

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Practical Applications

The ability to quantify decrements in key performance indicators such as lower body force and power characteristics and establish the neuromuscular status of players postmatch via an easy to administer functional test enables coaches to make informed decisions regarding recovery protocols and subsequent training programs and schedules. Our findings indicate skeletal-muscle damage occurs as a result of the rigors of elite Rugby League match play, and is reflected by peak [CK] measured 24 hours postmatch. Elevated [CK] persisted in comparison to prematch levels despite 120 hours of modified activity postmatch suggesting a prolonged recovery phase of at least 5 days is required to achieve a full recovery of muscle damage after match play. The [sCort] profile depicted in the present study identified a substantial acute [sCort] increase in response to Rugby League match play followed by a return to homeostasis within 48 hours. A minimum period of 48 hours of modified activity postmatch is therefore recommended to enable [sCort] to return to prematch rested levels.

Peak rate of force development, PP, and PF returned to prematch levels within 48 hours postmatch, indicating an absence of neuromuscular fatigue and a preparedness of players to undertake strength training despite a prolonged presence of muscle damage as indicated by elevated [CK]. The present study found that a return to modified strength training activities 48 hours postmatch may result in a compensatory increase in PRFD and supports the early implementation of strength training methods to facilitate the short-term postmatch recovery period. By comparing neuromuscular, biochemical and endocrine responses to match play, coaches are able to establish a comprehensive profile of individual responses and adaptation to elite Rugby League match play.

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Acknowledgments

The author wishes to thank the players and staff of the Gold Coast Titans Rugby League Football Club, Australia, for participation and facilitation of this study. No grant aid was received in conjunction with this study and no conflicts of interest are declared.

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References

1. Abbiss, CR and Laursen, PB. Models to explain fatigue during prolonged endurance cycling. Sports Med 35: 865-898, 2005.
2. Andersson, H, Raastad, T, Nilsson, J, Paulsen, G, Garthe, I, and Kadi, F. Neuromuscular fatigue and recovery in elite female soccer: Effects of active recovery. Med & Sci Sport Ex 40: 372-380, 2008.
3. Baker, DG and Newton, RU. Comparison of lower body strength, power, acceleration, speed, agility, and sprint momentum to describe and compare playing rank among professional rugby league players. J Strength Cond Res 22: 153-158, 2008.
4. Bigland-Ritchie, B and Woods, J. Changes in muscle contractile properties and neural control during human muscular fatigue. Muscle Nerve 7: 691-699, 1984.
5. Brancaccio, P, Maffulli, N, and Limongelli, FM. Creatine kinase monitoring in sport medicine. Br Med Bull 81-82: 209-230, 2007.
6. Byrne, C and Eston, R. Maximal-intensity isometric and dynamic exercise performance after eccentric muscle actions. J Sports Sci 20: 951-959, 2002.
7. Cormack, SJ, Newton, RU, and McGuigan, MR. Neuromuscular and endocrine responses of elite players to an Australian rules football match. Int J Sports Physiol Perform 3: 359-374, 2008.
8. Elloumi, M, Maso, F, Michaux, O, Robert, A, and Lac, G. Behaviour of saliva cortisol [C], testosterone [T] and the T/C ratio during a rugby match and during the post-competition recovery days. Eur J Appl Physiol 90: 23-28, 2003.
9. Enoka, RM. Neuromechanics of human movement. Champaign, IL: Human Kinetics, 2002.
10. Faulkner, JA, Brooks, SV, and Opiteck, JA. Injuiry to skeletal muscle fibers during contractions: conditions of occurrence and prevention. Physical Therapy 73: 911-921, 1993.
11. Gandevia, SC. Spinal and supraspinal factors in human muscle fatigue. Physiological reviews 81: 1725-1789, 2001.
12. Gonzalez-Bono, E, Salvador, A, Serrano, MA, and Ricarte, J. Testosterone, cortisol, and mood in a sports team competition. Horm Behav 35: 55-62, 1999.
13. Haneishi, K, Fry, AC, Moore, CA, Schilling, BK, Li, Y, and Fry, MD. Cortisol and stress responses during a game and practice in female collegiate soccer players. J Strength Cond Res 21: 583-588, 2007.
14. Hoffman, JR, Kang, J, Ratamess, NA, and Faigenbaum, AD. Biochemical and hormonal responses during an intercollegiate football season. Med Sci Sports Exerc 37: 1237-1241, 2005.
15. Hoffman, JR, Maresh, CM, Newton, RU, Rubin, MR, French, DN, Volek, JS, Sutherland, J, Robertson, M, Gomez, AL, Ratamess, NA, Kang, J, and Kraemer, WJ. Performance, biochemical, and endocrine changes during a competitive football game. Med Sci Sports Exerc 34:1845-1853, 2002.
16. Hoffman, JR, Nusse, V, and Kang, J. The effect of an intercollegiate soccer game on maximal power performance. Can J Appl Physiol 28: 807-817, 2003.
17. Horita, T, Komi, PV, Nicol, C, and Kyrolainen, H. Effect of exhausting stretch-shortening cycle exercise on the time course of mechanical behaviour in the drop jump: possible role of muscle damage. Eur J Appl Physiol Occup Physiol 79: 160-167, 1999.
18. Ispirlidis, I, Fatouros, IG, Jamurtas, AZ, Nikolaidis, MG, Michailidis, I, Douroudos, I, Margonis, K, Chatzinikolaou, A, Kalistratos, E, Katrabasas, I, Alexiou, V, and Taxildaris, K. Time-course of changes in inflammatory and performance responses following a soccer game. Clin J Sport Med 18: 423-431, 2008.
19. Jaffe, AS, Garfinkel, BT, Ritter, CS, and Sobel, BE. Plasma MB creatine kinase after vigorous exercise in professional athletes. Am J Cardiol 53: 856-858, 1984.
20. Komi PV. Stretch-shortening cycle: a powerful model to study normal and fatigued muscle. J Biomech 33: 1197-1206, 2000.
21. Kraemer, WJ, Spiering, BA, Volek, JS, Martin, GJ, Howard, RL, Ratamess, NA, Hatfield, DL, Vingren, JL, Ho, JY, Fragala, MS, Thomas, GA, French, DN, Anderson, JM, Hakkinen, K, and Maresh, CM. Recovery from a national collegiate athletic association division I football game: muscle damage and hormonal status. J Strength Cond Res 23: 2-10, 2009.
22. MacLaren, D, Gibson, H, Parry-Billings, M, and Edwards, R. A review of metabolic and physiological factors in fatigue. Exerc & Sport Sci Rev 28: 29-66, 1989.
23. Mastorakos, G, Pavlatou, M, Diamanti-Kandarakis, E, and Chrousos, GP. Exercise and the stress system. Hormones (Athens) 4: 73-89, 2005.
24. Meeusen, R, Piacentini, MF, Busschaert, B, Buyse, L, De Schutter, G, and Stray-Gundersen, J. Hormonal responses in athletes: the use of a two bout exercise protocol to detect subtle differences in (over)training status. Eur J Appl Physiol 91: 140-146, 2004.
25. Moreira, A, Arsati, F, de Oliveira Lima Arsati, YB, da Silva, DA, and de Araujo, VC. Salivary cortisol in top-level professional soccer players. Eur J Appl Physiol 106: 25-30, 2009.
26. Nicol, C, Avela, J, and Komi, PV. The stretch-shortening cycle: a model to study naturally occurring neuromuscular fatigue. Sports Med 36: 977-999, 2006.
27. Nicol, C, Komi, PV, Horita, T, Kyrolainen, H, and Takala, TE. Reduced stretch-reflex sensitivity after exhausting stretch-shortening cycle exercise. Eur J Appl Physiol Occup Physiol 72: 401-409, 1996.
28. O'Connor, PJ and Corrigan, DL. Influence of short-term cycling on salivary cortisol levels. Med Sci Sports Exerc 19: 224-228, 1987.
29. Passelergue, P and Lac, G. Saliva cortisol, testosterone and T/C ratio variations during a wrestling competition and during the post-competitive recovery period. Int J Sports Med 20: 109-113, 1999.
30. Peake, JM, Suzuki, K, Wilson, G, Hordern, M, Nosaka, K, Mackinnon, L, and Coombes, JS. Exercise-induced muscle damage, plasma cytokines, and markers of neutrophil activation. Med Sci Sports Exerc 37: 737-745, 2005.
31. Riad-Fahmy, D, Read, GF, and Walker, RF. Salivary steroid assays for assessing variation in endocrine activity. Journal of steroid biochemistry 19: 265-272, 1983.
32. Sargeant, AJ and Dolan, P. Human muscle function following prolonged eccentric exercise. European journal of applied physiology and occupational physiology 56: 704-711, 1987.
33. Smart, DJ, Gill, ND, Beaven, CM, Cook, CJ, and Blazevich, AJ. The relationship between changes in interstitial creatine kinase and game-related impacts in rugby union. British journal of sports medicine 42: 198-201, 2008.
34. Strojnik, V and Komi, PV. Neuromuscular fatigue after maximal stretch-shortening cycle exercise. J Appl Physiol 84: 344-350, 1998.
35. Takarada, Y. Evaluation of muscle damage after a rugby match with special reference to tackle plays. British journal of sports medicine 37: 416-419, 2003.
36. Thorlund, JB, Aagaard, P, and Madsen, K. Rapid muscle force capacity changes after soccer match play. Int J Sports Med 30: 273-278, 2009.
37. Thorlund, JB, Michalsik, LB, Madsen, K, and Aagaard, P. Acute fatigue-induced changes in muscle mechanical properties and neuromuscular activity in elite handball players following a handball match. Scandinavian journal of medicine & science in sports 18: 462-472, 2008.
38. Urhausen, A, Gabriel, H, and Kindermann, W. Blood hormones as markers of training stress and overtraining. Sports Med 20: 251-276, 1995.
39. Vanhelder, WP, Radomski, MW, and Good, RC. Hormonal and metabolic response to three type of exercise of equal duration and external work output. Eur J Appl Physiol 54: 337-342, 1985.
40. Warren, GL, Lowe, DA, and Armstrong, RB. Measurement tools used in the study of eccentric contraction-induced injury. Sports Med 27: 43-59, 1999.
Keywords:

countermovement jump; creatine kinase; cortisol; contact sport

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