Plasma CK concentrations ([CK]) measured from 24 hours prematch to 120 hours postmatch are displayed in Figure 1. Plasma [CK] was not significantly correlated (p > 0.05) with total distance traveled (r = 0.28) during the match. In comparison to 30 minutes prematch, a significant increase in [CK] was established immediately postmatch (p < 0.05) with a further significant increase and peak measure at 24 hours postmatch (p < 0.05). Substantial increases in [CK] were identified immediately postmatch (+56%) and 24hours postmatch (+91%) with progressive decreases in [CK] from 48 hours postmatch (−32%), 72 hours postmatch (−3%), 96 hours postmatch (−18%), and 120 hours postmatch (−12%). In comparison with 24 hours prematch, significant increases in [CK] were identified at all subsequent sample-collection points. Despite 120 hours of recovery postmatch plasma, CK did not return to 24-hour prematch baseline levels.
No significant correlation (p > 0.05) was found for sCort and sTest and total distance traveled (r = 0.09 and r = −0.07, respectively) or during the whole match. The [sCort] response from 24 hours match to 120 hours postmatch is shown in Figure 2. Before the start of the match, a significant increase (p < 0.05; + 28%) in [sCort] was found between 24 hours prematch and 30 minutes prematch. The [sCort] continued to increase significantly (p < 0.05; +68%) from 30 minutes prematch to 30 minutes postmatch resulting in the peak [sCort]. A significant decrease in [sCort] was found at 24 hours postmatch (p < 0.01; −32%). A return of [sCort] to baseline measures was evident 48 hours postmatch (−37%), which remained below baseline measures for the remainder of the study.
The [sTest] response to competitive match play can be found in Figure 3. There was a significant decrease in [sTest] from 24 hours prematch to 30 minutes prematch (p < 0.01; −47%). Despite a small increase (+14%) in [sTest] 30 minutes postmatch, [sTest] remained significantly reduced (p < 0.05) in comparison to 24 hours prematch. The [sTest] increased (+33%) 24 hours postmatch resulting in a return to the 24 hours prematch baseline measures. There was a significant decrease in [sTest] after 96 hours (p < 0.05; −29.35%) and 120 hours (p < 0.05; −7.56%) of recovery, returning [sTest] concentration to below 24 hours prematch levels.
The T:C from 24 hours prematch to 120 hours postmatch is shown in Figure 4. A significant decrease in T:C was found from 24 hours prematch to 30 minutes prematch (p < 0.05; −58%) followed by a further decrease 30 minutes postmatch (p < 0.05; −33%). During the acute recovery phase, despite a considerable increase (+97%), T:C remained significantly reduced (p < 0.05) 24 hours postmatch in comparison to 24 hour prematch baseline measures. A substantial though not significant increase in T:C (+64%) was recorded at 48 hours postmatch, returning T:C to 24-hour prematch levels. After 120 hours of the short-term recovery phase, T:C decreased (p < 0.05) significantly in comparison to 24-hour prematch baseline measures.
The primary findings of the present study are that participation in competitive rugby league match play results in a significant increase in muscle damage postmatch, indicated by elevated [CK] that peaks within 24 hours postmatch and remained elevated in comparison to prematch values for at least 120 hours after competition. An anticipatory rise in the concentration of sCort was found before match play followed by an acute and considerable increase in [sCort] immediately postmatch. The [sCort] was found to peak immediately postmatch followed by a rapid return to resting concentrations within 24-48 hours postmatch. Conversely, a reduction in [sTest] was found prematch followed by an acute postmatch increase that progressively returned to baseline concentration within 24 hours postmatch.
The present study found no significant difference in the total distance traveled between backs and forwards in either half of play or over the full match. The total full-match mean distances reported for backs and forwards were 5,747 ± 1,095 and 4,774 ± 1,186 m, respectively. The maximum distances traveled by players in the present study are similar to the findings of others (15,31) using match video recordings to analyze movement characteristics in Rugby League match play. The similarity of distances covered between backs and forwards and the consistency of running characteristics in each half of the match indicate that match intensity was maintained and the characteristics of running performance did not deteriorate during the whole match. Further, similarity in the distances recorded by GPS and video analysis methods suggests that GPS may be a useful alternative to the measurement of distances traveled by players during competitive match play in Rugby League.
In the present study, significant differences in the running speeds used to cover the total distances traveled during match play were recorded between forwards and backs. In the first half, backs traveled a significantly greater distance during maximal sprinting in comparison to forwards (110 ± 32 and 68 ± 13 m, respectively). During the second half, backs traveled significantly greater distance during striding (267 ± 68 m), high-intensity running (87 ± 30 m), and maximal sprinting (177 ± 38 m) in comparison to forwards (168 ± 56; 39 ± 13; and 82 ± 14 m, respectively). Subsequently, on the basis of whole-match performance, backs traveled significantly greater distance during high-intensity running and sprinting (135 ± 49 and 290 ± 69 m) compared with forwards (82 ± 21 and 149 ± 32 m). To our knowledge, no previous studies have quantified distances traveled by players according to speed profile characteristics and playing position during Rugby League match play.
The significant positional differences in striding, high-intensity running, and sprinting during match play is reflective of the fundamental characteristics of positional play in Rugby League. Forwards are positioned in closer proximity to the center of play, requiring those players to run shorter distances at high speed to perform game-specific tasks. Alternatively, backs are often positioned a greater distance from their opponent and therefore are required to travel greater distances at higher speeds (10) thereby providing greater ability to achieve higher velocity running. Backs have the additional tasks of sprinting into position over greater distances to perform kick return and kick chase activities thereby increasing their opportunity to achieve maximum sprint velocities. Overall, the data indicate that backs participate in a greater amount of high-intensity locomotor activity over similar total distances in comparison to forwards during match play.
Although eccentric muscular work has traditionally been considered the predominant contributor to increased [CK] after exercise (1), recent evidence suggests that significant increases in plasma [CK] may occur as a result of physical collisions and blunt force trauma (13,32). The present study found that participation in Rugby League match play, which is characterized by repeated eccentric muscle contractions of the lower limbs, intermittent high-intensity exercise and blunt force trauma resulting from high-speed collisions between and among players, significantly increased plasma [CK] and is consistent with the findings of others (17,35).
Creatine Kinase values were found to be elevated in players 24 hours prematch after a period of complete rest (∼256 ± 123.049 U·L−1). Other research has also reported elevated CK levels precompetition (11,34,35). Suzuki et al. (34) and Takarada (35) reported [CK] of approximately 351.6 and 400 U·L−1 48 hours prematch and same day prematch, respectively, in Japanese college rugby players. Gill et al. (11) reported CK activity of 1,023.0 U·L−1 3.5 hours prematch in elite rugby players. The elevated prematch [CK] found in the present study is likely to indicate residual muscle damage because of game-simulated contact-training activities or the result of cumulative muscle damage associated with the rigors of competitive game participation before the commencement of the present investigation.
Creatine kinase mean values increased from 30 minutes prematch to 30 minutes postmatch (302.83 ± 144.07 to 454.83 ± 209.36 U·L−1) followed by a significant increase of 91% in [CK] 24 hours postmatch (454.83 ± 209.36 to 889.25 ± 538.27 U·L−1). The increase in [CK] 30 minutes postmatch agrees with results of others (11,34,35) and indicates an acute response in CK activity to match-play trauma associated with the degree of impact during collisions. Other research has reported similar (Suzuki et al.  715.4 ± 438.3 U·L−1) and greater CK levels after competitive match play in rugby union (Takarada  1,081 ± 159 U·L−1 and Gill et al.  2,194.0 ± 833.7 U·L−1).
Peak [CK] in the present study was found 24 hours postmatch (889.25 ± 538.27 U·L−1) and is consistent with the findings of others (35). Our findings contrast the results reported by Gill et al. (11), however, who observed peak [CK] immediately after rugby match play. The findings of the present study therefore are consistent with the concept that peak [CK] is delayed 24-96 hours postcompetition (13,17,25,35) and support the practice of prolonging the sample collection period postcompetition to accurately assess muscle damage and provide direction with respect to the postmatch recovery process.
Methodological differences may explain the discrepancy between [CK] observed in the present study and the studies of Takarada (35), Suzuki et al. (34), and Gill et al. (11). The present study reported [CK] at each time point prematch and postmatch as mean values, whereas Takarada (35), Suzuki et al. (34), and Gill et al. (11) only reported peak CK activity. The rationale for reporting mean [CK] in the present study at each time point prematch and postmatch was to identify the overall adaptation of players from all positions during competitive match play. Peak [CK] in response to competition highlights the response of a single player to match participation and the [CK] response of any single player may therefore be determined by playing position or skill level leading to error in match-play analysis.
Although no significant positional difference was evident between [CK] and total distances traveled during the match, the backs covered greater distance at high-intensity running (135 ± 49 m; p = 0.03) and sprinting speeds (290 ± 69 m; p < 0.01) compared with the forwards (82 ± 21 and 149 ± 32 m, respectively). The repeated high-intensity acceleration and deceleration associated with sprinting efforts seen in backs, requires considerable eccentric muscle activity in the hamstring muscles. An increased likelihood of structural damage associated with eccentric muscle activity may contribute to the CK response of backs. Alternatively, the exposure of forwards to repetitive high-intensity collisions may contribute to acute soft-tissue trauma and structural damage to muscle tissue.
Sampling differences may also offer an alternative explanation for variation between the present study and others regarding greater [CK] in response to match play in contact sports reported previously (11,35). The present study examined capillary blood samples, whereas Takarada (35) examined venous blood samples and Gill et al. (11) sampled interstitial fluid. On the basis that muscle-damage results in CK leakage from the muscle cells into the interstitial fluid before entering the blood through the lymphatic system, it is conceivable that [CK] in the interstitial fluid is greater than in blood because of partitioning effects (11).
The present study examined 2 hormones that represent the major catabolic and anabolic profile in response to contact-sport participation. Testosterone is the dominant anabolic marker for protein signaling and glycogen synthesis (33). Cortisol was also examined in the present study on the basis that it is dependent on the type, intensity, and duration of exercise (24) and is influenced by psychological stress (29), whereas the T:C was used to monitor the balance between anabolism and catabolism in players throughout the game preparation and recovery process.
The pattern of increased cortisol measured precompetition in contact sport is well documented (9,29). An increase in [sCort] from 24 hours prematch to 30 minutes prematch in the present study is consistent with others (29). Increased prematch cortisol is thought to reflect a psychophysiological mechanism influenced in part by cognitive anticipation and anxiety used by athletes as a precompetitive arousal and coping mechanism used to manage pregame stress (12).
Elevated postmatch [sCort] found in the present study is consistent with other studies (3,9,17) after competitive performance. During match play, [sCort] increased 69% from 30 minutes prematch to 30 minutes postmatch and is consistent with the results of others (3,9,23) who have reported increases in sCort during exercise and competition involving high-intensity collision between opposing competitors. The mean [sCort] 30 minutes postmatch was more than double baseline measures recorded 24 hours prematch. Several factors associated with Rugby League match play provide an explanation for the sharp increase in sCort found 30 minutes postmatch.
Rugby League is a form of high-intensity, intermittent exercise of 80-minute duration involving frequent collisions with opponents and is influenced by psychological factors associated with anxiety and perceived stress. Passelergue et al. (24) identified that raised levels of anxiety and stress associated with competition contribute to elevated cortisol concentration in simulated Olympic weight-lifting competition. Lac and Berthon (18) reported that the higher the intensity and the longer the duration, the greater the cortisol response to such exercise, whereas Vanhelder et al. (36) highlighted a stronger adrenal response to intermittent anaerobic exercise in comparison to aerobic exercise. The sharp postmatch increase in [sCort] found in the present study may be explained by the interplay of psychological, exercise type, and the duration of exercise experienced during Rugby League match play.
After the peak in [sCort] measured 30 minutes postmatch, there was a significant reduction in [sCort] 24 hours postgame (−32%) and 48 hours postmatch (−37%), decreasing [sCort] to below 24 hours prematch concentrations. The return of [sCort] toward 24-hour prematch levels within 24-48 hours postmatch is consistent with others (9,17,23) who have reported a progressive decrease in cortisol postcompetition.
During the postmatch recovery phase, sCort sampling took place at 4 pm on a daily basis at 24-hour intervals for 5 days postmatch. There were further reductions in sCort at 48, 72, and 96 hours postmatch compared with 24 hours prematch. Elloumi et al. (9) reported a similar pattern of progressively reduced cortisol levels in rugby players from the first to fourth days postmatch. The progressive decline in [sCort] identified during the recovery phase in the present study is in agreement with previous reports describing the sCort response after competition (3,23) and is reflective of a return to hormonal homeostasis and removal of the psychological and physical stress associated with match play.
A nonsignificant increase in [sCort] was found 120 hours postmatch; however, [sCort] remained below 24 hours prematch levels. The trend for cortisol to become elevated toward the end of the training week in preparation for the next game is consistent with other research (9) and in the present study is indicative of a return to high-intensity precompetition sport-specific training and the accompanying stress associated with team selection and performance expectations.
In contact sports, changes in testosterone concentration typically do not occur immediately postcompetition; however, increases have been identified during a subsequent period of recovery (9,23). The expected pattern of response of sTest during competitive Rugby League match play is unclear. In the present study, [sTest] decreased significantly (p < 0.05; −47%) 30-minutes prematch in comparison to 24-hour prematch baseline levels. Although the match itself produced a small increase in sTest (+14%), [sTest] remained significantly reduced compared with 24 hours prematch, supporting the results of others that have reported a reduction (3,9) in [sTest] postcontact sport participation. The present results disagree with the findings of others (13,17) who reported no change in testosterone in American Football players after match play. The inconsistency between our results and others (13,17) is likely because of considerably greater metabolic requirements of Rugby League match play in comparison to a game of American Football.
After the match a return to normalized [sTest] was evident with no significant difference between [sTest] at 24 hours postmatch in comparison to 24 hours prematch. The return to 24-hourprematch [sTest] within 24 hours of competitive match play are in contrast to the work of Elloumi et al. (9) who reported higher testosterone levels in Rugby Union players in the presence of reduced cortisol during a 6-day postcompetition period in comparison to rested values. Considerable variation in the positional play requirements, match-play intensity and postmatch recovery protocols may have contributed to inconsistency between our results and those reported after Rugby Union match play (9).
The results of the present study clearly identify a precompetition anticipatory decrease in T:C influenced by prematch anxiety and perceived stress in elite Rugby League players. The combination of substantially increased [sCort] and reduced [sTest] identified 30 minutes prematch in comparison to 24-hour prematch baseline measures resulted in a low T:C and predominant catabolic hormonal environment. The subsequent catabolic environment associated with a low T:C before match play in the present study is likely to be a reflection of the diversity of [sTest] and [sCort] prematch. Our results are in contrast to the findings of Elloumi et al. (9) who reported game day [sCort] and [sTest] was unchanged in comparison to rest. Subsequently, Elloumi et al. (9) found similar game day T:C in comparison to resting levels in rugby union players. Our results are consistent with Cormack et al. (3) who identified a similar pregame pattern in Australian Rules Football players and reported a substantial decrease in T:C immediately prematch in comparison to 48 hours prematch.
A substantial drop in T:C 30 minutes postmatch in comparison with 24 hours prematch produced the lowest T:C found during the prematch or postmatch data collection period in the present study. Despite a 97% increase in T:C 24 hours postmatch in comparison to the 30-minute postmatch level, T:C remained significantly lower than baseline levels, representing a persistent catabolic hormonal profile. The prolonged catabolic hormonal profile of players after Rugby League match play has implications for postmatch recovery and subsequent match preparation on the basis that matches may be scheduled with as few as 4 days separating match play in the NRL.
A return to baseline measures of both [sTest] and [sCort] at 48 hours postmatch is reflected in a reciprocal recovery of T:C to baseline levels within the same time period. The normalization of T:C remained evident in the present study at 72 and 96 hours postmatch and preceded a drop in T:C 120 hours postmatch in comparison to baseline levels. The reduction in T:C that occurred 5 days postmatch may reflect a return to higher intensity precompetition sport-specific training and the associated increased demand on the endocrine system.
The acute and short-term recovery phase findings with respect to T:C in the present study reflect the findings of others (3,9) that have examined the recovery status of contact-sport athletes after competitive performance. With respect to the acute 30 minute postmatch T:C response, Elloumi et al. (9) reported a substantial reduction in T:C at the end of an international level Rugby Union match. Conversely, however, during the short-term recovery phase, our findings contrast those of Elloumi et al. (9) who reported a high T:C from day 1 to day 5 postmatch in excess of baseline measures. Our results reflect the findings of Cormack et al. (3) who reported a 36% decrease in T:C from prematch to postmatch. The acute decrease in T:C is likely a function of significantly increased [sCort] and little or no change in [sTest] immediately after match play. During the short-term postmatch recovery phase, however, our results are inconsistent with those of Cormack et al. (3) who found substantially reduced T:C in all comparisons from 48 hours pregame to 120 hours postgame following Australian Rules Football performance suggesting a prolonged catabolic hormonal profile despite 5 days of recovery.
The explanation for variation in short-term recovery rates in athletes from collision sports such as Rugby League is multifactorial. The influence of individual biological responses, specialized team recovery protocols including nutrition and hydration regimes, travel commitments, and weekly team training schedules all contribute to a player's ability to recover from match play in an optimal time frame. The use of T:C to represent the anabolic:catabolic hormonal profile of athletes after competition has implications for the design and implementation of training programs, particularly in a team sport environment competing in a prolonged regular season period such as 24 matches in a 26-week period as seen in the NRL. The return of the postmatch T:C to baseline measures identified in the present study within 48 hours is indicative of a successful recovery of [sTest] and [sCort] and thereby represents an restoration of resting anabolic:catabolic hormone profile in elite rugby league players.
The present study provides an insight into player movement patterns during elite Rugby League match play using contemporary GPS performance analysis methods that have not been reported previously. Our findings indicate that the rigors of elite Rugby League matchplay result in skeletal-muscle damage 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 that a prolonged recovery phase of at least 5 days is required to achieve full recovery of muscle damage after match play.
The endocrine profile depicted in the present study identified a substantial acute sCort and small sTest response to Rugby League match play followed by a return to homeostasis within 48 hours. A minimum period of 48 hours is therefore recommended to enable hormonal homeostasis to be achieved postmatch. The evolution of real-time data acquisition with respect to player-movement characteristics in team sports will continue to facilitate a more robust analysis approach and enable sports scientists and coaches to further quantify the requirements of performance. By comparing endocrine and CK responses to performance, coaches are able to establish a more tangible identification of individual responses and adaptation to performance will be achieved in team sports such as Rugby League.
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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Keywords:© 2010 National Strength and Conditioning Association
muscle enzyme; salivary testosterone; cortisol ratio; GPS; monitoring