Exercise-induced muscle damage has been examined in humans (16,20) with plasma creatine kinase (CK) activity commonly reported as an indirect marker of skeletal muscle damage in sports (15,26,34). The extent of skeletal muscle damage has been related to the intensity and duration of exercise (35). High-intensity eccentric exercise has been traditionally considered the primary factor associated with skeletal muscle damage (28). Typically, skeletal muscle damage is associated with morphological changes within the muscle cell that is accompanied by the leakage of proteins such as CK out of the cell and into the blood circulation via the lymphatic system (17).
Elite Rugby League match play is synonymous with high-intensity exercise, repeated blunt force trauma, skeletal muscle damage, and postexercise muscle soreness. Elevated plasma CK concentration ([CK]) has been reported after competitive match play in various contact sports (12,15,19,32-34) suggesting that significant skeletal muscle damage occurs during such contact sports. Takarada (34) reported a significant correlation between the number of tackles performed during Rugby Union match play with peak [CK] measured 24 hours postmatch. Suzuki et al (33) also found significant increases in [CK] immediately after Rugby Union match play that remained elevated 24 hours postmatch. Although increases in plasma [CK] have been reported in contact sports (12,19,32,34), the CK response to impact associated with collisions during elite Rugby League match play is unknown.
Although the effects of competitive contact sport on the acute endocrine response (5,10,16,19) and postcompetition recovery period (10,19) have been reported, this is not the case for elite Rugby League. Cortisol has a role as a stress hormone, and its presence has been identified as a marker of the endocrine response to competitive high-intensity combative sports (10,11). Salivary cortisol concentration ([sCort]) provides a valid and reliable estimation of serum unbound cortisol (2,37). Repeated high-velocity collisions and high running volumes that are characteristic of Rugby League match play provide a unique model in which to examine the time course of endocrine responses to competition. Previous work with other collision-based sports has reported increased [sCort] immediately after, and 24 hours after competition (5,10). No studies have examined the time course of [sCort] in response to repeated blunt force trauma and high velocity collisions during elite Rugby League competition beyond 24 hours postmatch.
Recent studies have added to our understanding of player movement characteristics during Rugby League match play (18,31). Advances in match analysis technologies, such as the global positioning system (GPS), have enabled investigators to accurately quantify activity profiles and the impact associated with collisions in contact sports. Further, accurate determination of G forces experienced by players during repeated collisions with opponents during match play provides new insight into the physical consequences of competition.
The movement patterns of elite Rugby League players during competitive match play using GPS technology have been reported (23); however, there are no data that describe the G forces experienced by players during high-velocity collisions that are synonymous with elite Rugby League match play. Skeletal muscle damage because of high-intensity eccentric exercise such as that found in Rugby League match play has been associated with decreased muscle function and performance (4). Uncertainty remains regarding the pattern of CK and endocrine responses to elite-level contact sport, and the influence of blunt force trauma and impact during Rugby League match play is unknown. A greater understanding of the biochemical and endocrine responses to elite Rugby League match play may provide scope for improved individualized postmatch strategies, reduce the risk of residual and cumulative fatigue, and potentially decrease the incidence of musculoskeletal injury.
The aim of this study was to examine the acute and short-term biochemical and endocrine responses to the intensity, number, and distribution of impact associated with collisions during competitive Rugby League match play. We hypothesize that blunt force trauma associated with impacts that are characteristic of Rugby League match play will result in substantial skeletal muscle damage and considerable elevation in stress hormone levels postmatch. Further, the combination of impact-related GPS performance data with CK, sCort, and sTest provides a more detailed and specific analysis of the demands of Rugby League match play than achieved previously.
Experimental Approach to the Problem
A single group repeated-measures prepost match design was used in this study. To examine the impact characteristics of the independent variable of player collisions during elite Rugby League match play, GPS data and accelerometer data were collected from players during a match of 80-minute duration between 2 National Rugby League (NRL) teams. Plasma [CK] was examined to reflect skeletal muscle damage in response to collisions experienced by players during match play. Salivary cortisol was examined to represent the primary catabolic endocrine measure associated with metabolism pre and postmatch. To examine the pre during, and postmatch response of the dependent variables, [CK] and [sCort] were measured via blood and saliva samples, respectively. All participants played a minimum of 30 minutes in each of the 2 40-minute halves of the match. Players were separated into forwards and backs for comparison. An understanding of the influence of blunt force trauma and impact on endocrine responses and skeletal muscle damage markers after elite Rugby League match play is important to determine postmatch recovery strategies, monitor residual and or cumulative fatigue throughout the competitive season and effectively manage player preparation for subsequent matches.
Seventeen elite male Rugby League players, age 24.2 ± 7.3 years, height 188 ± 20.1 cm, and mass 94.6 ± 26.8 kg; mean ± SD, representing an NRL team volunteered to participate in the study. Because of the minimum time on field match-play requirements, data were analyzed from 15 players (Forwards n = 8; Backs n = 7). Before the commencement of the study, players attended a presentation outlining the purpose, benefits, and procedures associated with the study. All players were made aware of their ability to withdraw from testing at any time. Written informed consent was obtained from all players who participated in the study. The study was approved by the Bond University Human Research Ethics Committee and the NRL club from which players volunteered.
Saliva and blood samples were collected 24 hours prematch, 30 minutes prematch, within 30 minutes postmatch, and at 24, 48, 72, 96, and 120 hours postmatch. The daily training and saliva and blood collection schedule is outlined in Table 1. Subjects were asked to refrain from strenuous exercise during the 24 hours before baseline saliva and blood sample collection 24 hours prematch. Saliva and blood samples were collected daily between 1530 and 1630 hours with the exception of the 30-minute postmatch saliva and blood samples that were collected between 1830 and 1900 hours because of the scheduled time of match play. Players provided saliva and blood samples within 30 minutes of match completion and before participation in postmatch recovery activities. Data were examined for each subject at each saliva and blood sample collection time point. Throughout the postmatch data collection period, subjects participated in all of the teams scheduled postmatch recovery and daily training sessions (Table 1).
Plasma Creatine Kinase Sampling and Analysis
Plasma [CK] was determined from 30 μL capilliarized 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 (Table 1). Whole blood samples were centrifuged (Hereaus Function Line, Labofuge 400, Kendro Laboratory Products, Hanau, Germany) at 3,000 rpm for 10 minutes, and separated plasma was stored at a temperature of −30°C until analysis. Plasma samples were analyzed using a Reflotron spectrophotometer (Abbott Architect, Abbott Park, IL, USA) via an optimized UV test.
Salivary Cortisol Sampling and Analysis
Unstimulated saliva was collected via passive drool into a plastic tube for analysis of [sCort]. Saliva measures of [sCort] are independent of flow rate (29), and there is a significant relationship between saliva and serum unbound cortisol at rest (r = 0.93) and during exercise (r = 0.90) (24). All subjects were requested to avoid the ingestion of food and fluids other than water in the 60 minutes before providing each saliva sample and to 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 a temperature of −80°C until analysis. Saliva Cortisol [sCort] (μg·dL−1) 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). A standard curve was constructed per the manufacturer's instructions, and commercially available standard and quality control samples were used for both assays (Salimetrics LLC). The assay sensitivity was 0.007 ng·mL−1 for sCort with intraassay coefficient of variation as a percentage of 2.6%. All samples were analyzed in the same series to avoid possible interassay variability.
This study used commercially available 5-Hz GPS receivers (SPI-Pro, GPSports, Canberra, Australia), which operated in nondifferential mode and provided data in real time. The GPS is a satellite-based navigation system that enables real time data collection during training and competition (6,9,22). Information with respect to the intensity, number, and distribution of gravitational forces (G) experienced by players during collision are recorded simultaneously via satellite communication with a portable GPS receiver and integrated accelerometer worn by a player. The GPS typically uses a network of 24 satellites in orbit around the Earth. Each satellite is equipped with an atomic clock that emits, at the speed of light, the exact time and position of the satellite. The GPS receiver compares the time emitted by each satellite signal with the lag time, measured by each receiver, translated into distance by trigonometry. By calculating the distance to at least 4 satellites, the exact position and altitude of the receiver on the Earth's surface can be determined (36). Speed of displacement is determined via the Doppler shift method, by measuring the rate of change of the satellites' signal frequency attributable to movement of the receiver (36).
The SPI-Pro GPS units used in this study contain a triaxis (x, y, z axes) integrated accelerometer, which measures accelerations in gravitational force (G force) on 3 planes, namely, forwards/backwards, up/down, and tilt left/right. The integrated accelerometer within the GPS unit measures accelerations and decelerations (m·second−2) for each plane, with known gravity of 9.8 m·second−2 equal to 1G. The integrated accelerometer measures the rate of acceleration and deceleration on each plane and divides the value by 9.8 m·second−2 to determine the combined G force as the sum of the G force measured on each directional axis. The GPS model used in this study (76g; 48 mm × 20 mm × 87 mm) was worn in a purpose designed vest (GPSports) to ensure that range of movement of the upper limbs was not restricted. The GPS unit was worn in a padded mini backpack contained in the vest and positioned in the center area of the upper back slightly superior to the shoulder blades at the level of approximately first thoracic vertebrae.
Participants had previously worn the GPS units in outdoor training sessions that included Rugby League-specific running, skill-related and match-simulated contact activities during a 12-week preseason training period. Participants had also worn the units in 2 preseason practice matches conducted 7 and 14 days before the match examined in this study. No participants complained of discomfort or impediment to their normal range of movement or performance from wearing the GPS equipment during training or competitive match play. Data provided from the GPS unit for examination in this study included impact (G Force) data (intensity,number, and distribution), total distance, speed, and heart rate characteristics. Raw accelerometer data were available in real time via Wireless Fidelity communication and were displayed using commercially available software (Team AMS, GPSports). The reliability of the SPI-Pro has been reported previously (27) and has been assessed by our laboratory over distances from 5 to 8,000 m on a synthetic 400-m athletics track with <3% variation in total distance and the reliability of speed assessed with electronic light gates (Smartspeed, Fusion Sports, Brisbane, Australia) from walking speed (6.0 km·h−1) to maximum sprint speed (>22.0 km·h−1) with a variation <5.5%. Our results are similar to the results of others (27).
Impact Classification System
Player exposure to impact was determined via accelerometer data provided in G force. A zone classification system forms the basis of the analysis performed by the Team AMS software, allowing 6 ranges impact (zone 1-6) to be preset and used for subsequent analysis. Zone 1 indicates the lowest impact or lowest velocity of collision with each zone progressively categorizing impact force and movement intensity to zone 6 indicting the highest impact and intensity of movement. The impact classification system used in this study was based on methods used in Rugby Union (9) and manufacturer guidelines (GPSports). Each impact was coded to 1 of 6 zones based on acceleration G force characteristics recorded by the GPS unit. Impact zone characteristics used in this study are listed in Table 2.
Tackle Count and Hit-Up Number Data
The average number of tackles and the number of ball carries (hit-ups) completed by forwards and backs were determined via postmatch analysis of video recordings of the match (Table 3). For the purposes of this study, a tackle was defined as an event that halted the progress of an opponent in possession of the ball. A ball carry (hit-up) was defined as a player being tackled in possession of the ball during match play.
Biochemical and endocrine variables analyzed prematch and postmatch included CK and [sCort]. Before statistical analysis, log transformation was applied to the biochemical and endocrine data to normalize the distribution and reduce nonuniformity bias. The data for each of the dependent variables are represented as mean (±SEM) using standard statistical methodology. Changes in biochemical and endocrine concentrations were analyzed using 1-way repeated-measures analysis of variance. Significant differences were identified via a Bonferroni post hoc test. Differences in tackles, hit-ups, impact zones, and peak biochemical data between backs and forwards were determined using Student's unpaired t-test. The criterion level for statistical significance was set at p ≤ 0.05. The correlation between peak changes in biochemical and endocrine markers, total tackles, number of hit-ups, and impact zones were analyzed using the Pearson Product-Moment Correlation Coefficient. The data are expressed as mean ± SD. All statistical analyses were performed using the Statistical Package for the Social Sciences (SPSS for Windows, version 14.0; SPSS, Inc., Chicago, IL, USA).
Plasma [CK] values measured from 24 hours prematch to 120 hours postmatch are given in Table 4. In comparison to 30 minutes prematch, a significant (p = 0.003) increase in [CK] was established 30 minutes postmatch with a further significant (p = 0.002) increase and peak measures at 24 hours postmatch (Table 4). Peak [CK] for forwards and backs was 979 ± 415 and 922 ± 380 U·L−1, respectively. Significant increases in [CK] were also found 48 hours post (p < 0.006), 72 hours post (p = 0.004), 96 hours post (p = 0.013), and 120 hours post (p = 0.043) compared to 30 minutes prematch. Impact zones 5 and 6 were significantly correlated to [CK] 30 minutes postmatch and at 24, 48, and 72 hours postmatch (Table 5). The number of zone 4 entries was significantly correlated to [CK] 30 minutes postmatch and 24 hours postmatch (Table 5). The number of hit-ups performed during match play was significantly correlated (p < 0.05) to [CK] at 24, 48, and 72 hours postmatch (Table 5).
The [sCort] from 24 hours prematch to 120 hours postmatch is listed in Table 4. [sCort] was significantly (p = 0.043) >30 minutes prematch compared to 24 hours prematch. Significant increases in [sCort] were also found 30 minutes postmatch (p < 0.001) and 24 hours postmatch (p < 0.001) compared to 24 hours prematch (Table 4). There was no significant difference between [sCort] at 48 hours postmatch in comparison to 24 hours prematch. Despite significant increases in [sCort] immediately postmatch and 24 hours postmatch, there was no significant correlation between [sCort] and the number of tackles performed, the number of hit-ups or the number of impact related entries in zone 4, 5, or 6 by forwards or backs during match play or throughout the 120 hours short-term postmatch recovery period.
The number (mean ± SD) of tackles and ball carries for forwards and backs during the match are listed in Table 3. Although there were no significant differences in the number of hit-ups between forwards and backs, forwards completed significantly (p = 0.043) more tackles during the match compared to backs (Table 3). There was no significant difference between forwards and backs in peak [CK] and [sCort] after match play (Table 3). Impact zone entries during the match are listed in Table 6. There was no significant difference in the number of recorded impacts in each zone between forwards and backs. The grouping of match impacts within zones 4-6 (heavy + very heavy + severe) revealed that players experience high-level impacts approximately every 50 seconds during match play.
The findings of this study indicate that competitive elite Rugby League match play induces significant damage to skeletal muscle that remains elevated in comparison to prematch measures for at least 120 hours postmatch. The extent of skeletal muscle damage is related to the player impact associated with repeated high-intensity collisions during match play.
Increases in the concentration of muscle enzymes such as CK in the blood are indicative of increased skeletal muscle membrane permeability and suggestive of skeletal muscle damage (3). 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 because of physical collisions and blunt force trauma (16,32,34). Rugby League match play is characterized by repeated eccentric muscle contractions, intermittent high-intensity exercise and frequent blunt force trauma. This study found that participation in Rugby League match play induces structural damage to skeletal muscle tissue and is consistent with others that have used CK to assess the degree of skeletal muscle damage in contact sports (12,15,19,33,34).
The [CK] was found to be elevated in players 24 hours prematch after a period of complete rest (∼256 ± 113 U·L−1). Other research has also reported elevated CK levels precontact sport participation (8,12,33,34). Cunniffe et al. (8) reported elevated [CK] in elite Rugby players in a rested state (497 U·L−1) and preinternational level match play (333 U·L−1), whereas Suzuki et al. (33) and Takarada (34) 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. (12) reported CK activity of 1,023.0 U·L−1 3.5 hours prematch in elite rugby players. The elevated prematch [CK] found in this study is likely to indicate residual skeletal muscle damage arising from Rugby League oriented contact training activities and cumulative skeletal muscle damage resulting from the rigors of competitive match play before the commencement of the present investigation.
The increase in [CK] 30 minutes postmatch is consistent with the results of others (8,12,32-34) and indicates an acute [CK] response to trauma associated with high-speed collisions between and among players during match play. The peak in [CK] found 24 hours postmatch in this study agrees with results of previous studies in Rugby Union and American Football (8,19,33,34). This study is the first to examine [CK] after elite Rugby League match play and adds further support to delayed increase in [CK] for approximately 18-96 hours postcompetition (3,19). Our results are in contrast to those of Gill et al. (12), who recorded the highest [CK] immediately after Rugby Union match play. The difference between the results of this study and those of Gill et al. (12), may reflect the differences in experimental design between the 2 studies. This study examined plasma [CK] 30 minutes after elite Rugby League match play and subsequently at 24-hour intervals for a period of 120 hours. The immediate postmatch [CK] reported by Gill et al. (12) may not represent peak [CK] because of subsequent sample collection not taking place until 36 hours postmatch and 84 hours postmatch.
The findings of this study are consistent with those of other studies that have reported that peak [CK] may not take place until 24-48 hours postmatch (33,34). Sampling differences may also offer an alternative explanation for the greater [CK] reported after Rugby Union match play (12,34). This study examined capillary blood samples, whereas Gill et al. (12), sampled interstitial fluid. Muscle damage resulting in CK leakage from the muscle cells into the interstitial fluid before entering the blood stream through the lymphatic system (17) may result in the [CK] in interstitial fluid to be greater than in blood because of partitioning effects (12). Plasma [CK] may be further reduced because of metabolism of CK in interstitial fluid before entering the circulation, resulting in decreased [CK] by comparison.
An increase in [sCort] from 24 hours prematch to 30 minutes prematch is consistent with that of other studies (10,30) that have examined cortisol levels precontact sport competition. The pattern of increased prematch cortisol is thought to reflect a psychophysiological mechanism influenced in part by cognitive anticipation and self-perceived anxiety used by athletes as a precompetition coping and arousal mechanism to manage prematch stress (14). Elevated [sCort] found in thist study 30 minutes postmatch is consistent with the results of others (5,10,19), who have identified a significant increase in cortisol (p < 0.001) after competitive performance. The [sCort] increased significantly from 30 minutes prematch to 30 minutes postmatch and supports the findings of others (5,10,19) who have reported increased cortisol levels in response to exercise and competition involving repeated collisions between opposing competitors. Several performance-related factors associated with elite Rugby League match play provide an explanation for significantly increased [sCort] 30 minutes postmatch in this study.
Rugby League is a collision sport characterized physically by high-intensity intermittent exercise and repeated blunt force trauma of 80 minutes in duration and influenced psychologically by perceived stress and anxiety. Lac and Berthon (21) have reported that the greater the intensity and duration of exercise, the greater the cortisol response, whereas Passelergue et al. (25) have identified increased cortisol in response to raised anxiety and stress during simulated weight lifting competition. The sharp postmatch increase in [sCort] found in this study is likely to have been influenced by an interplay of psychological factors and the type and duration of exercise experienced by players during elite Rugby League match play.
After the peak in [sCort] 30 minutes postmatch a significant reduction in [sCort] was found 24 hours postmatch, followed by a further decrease in [sCort] at 48 hours postmatch to below 24 hours prematch [sCort]. The return to 24 hours prematch levels within 24-48 hours postmatch is consistent with the findings of others (10,19) who have reported a similar pattern of progressively reduced cortisol levels postcompetition and reflects the removal of match-related psychological and physical stressors during the short-term recovery period.
Despite significant elevations in [sCort] 30 minutes postmatch and during the 24-48 hours postmatch period, no relationship was found between [sCort] and the number of collisions experienced by players in this study. Further, [sCort] was not related to the number of entries in impact zones 1-6 during match play. No studies have investigated [sCort] in response to elite Rugby League match play using GPS to quantify the impact associated with collisions. The results indicate that competitive Rugby League match play is an intense form of exercise, generating sufficient physiological and psychological (11) stress to cause an elevation in [sCort] followed by a return to homeostasis within 48 hours postmatch.
A nonsignificant increase in [sCort] was found 120 hours postmatch; however, [sCort] remained <24 hours prematch levels. The trend for cortisol to increase in preparation of subsequent match play is consistent with other research (10) and in this study is indicative of a return to high-intensity Rugby League-specific training and the accompanying stress associated with individual and team performance expectations.
Body impacts experienced by players during high-intensity collisions between opposing players are associated with impact forces in zones 4-6. This study found no significant difference between the total number of impacts or the number of entries in each impact zone between forwards and backs during offensive and defensive match play. The total number of impacts for forwards and backs during match play (858 ± 125; 795 ± 145, respectively) was consistent with the total number of impacts recorded for backs (798) but substantially less than forwards (1,274) during a case study analysis of the physiological demands of elite Rugby Union match play using accelerometer data (9). It is likely that considerable time spent in match play-specific activities such as rucks, mauls, scrums, and repetitive contact between opposing players at the breakdown generally in Rugby Union resulted in a high number of total impacts in Rugby Union forwards in comparison to Rugby League forwards. Rugby League match play however resulted in considerably more very high intensity zone 6 (forwards 21 ± 8; backs 20 ± 5) entries in comparison to forwards and backs during a game of elite Rugby Union (>10G: 13 and 4, respectively) (9).
This study found a significant correlation between the number of zone 4-6 entries and plasma [CK] 30 minutes postmatch and 24 hours postmatch (Table 6). Further, a significant correlation was found between the number of zone 5 and 6 entries and [CK] 48 and 72 hours postmatch. Our results indicate that regardless of the nature of contact, exposure to high impact collisions >7.1G caused significant skeletal muscle damage during match play that peaked 24 hours postmatch. Collisions that involved heavy impacts >8.1G, resulted in a prolonged increase in [CK] that remained significantly elevated for at least 72 hours postmatch (Table 6). These results have not been reported previously and are likely to reflect greater skeletal muscle damage associated with heavy blunt force trauma during repeated high-intensity collisions.
This study found a significant correlation between the total number of hit-ups and tackles and [CK] 30 minutes postmatch and at 24, 48, and 72 hours postmatch. To differentiate the physical consequences of offensive vs. defensive match play, this study investigated the relationship between the number of tackles, the number of hit-ups and plasma [CK] independently within 30 minutes postmatch and for a period of 120 hours postmatch. Although this study found no significant correlation between the number of tackles a player performed and [CK] immediately postmatch, or during the 120 hours postmatch recovery period, a significant correlation was found between the number of hit-ups performed by players and [CK] 24 hours (p = 0.043), 48 hours (p = 0.038), and 72 hours (p = 0.041) postmatch (Table 5).
Our results are consistent with the findings of others who have examined [CK] and match-related impacts during Rugby Union match play (8,32,34). Takarada (34) reported a significant correlation between the number of tackles and peak [CK] 24 hours after Rugby Union match play in Japanese college players. We note that Takarada (34) referred to a tackle as the “total number of times a player tackled or was tackled from in front” (34) and ignored multidirectional impacts and all other match-related contact between players that did not constitute a tackle. This study referred to a tackle as the total number of times that the player was involved in a tackle that halted the progress of an opponent in possession of the ball regardless of the direction of the collision. The classification of a tackle vs. a hit-up in this study is representative of a “tackle” as defined by Takarada (34). Our findings also support the results of Smart et al. (32) who reported significant correlations between game time, time defending, and hit-ups and [CK] in forwards and backs during Rugby Union match play. In their analysis of immunoendocrine markers after an international level Rugby match, Cunniffe et al. (8) reported significant correlations between serum CK activity and player involvement in tackles and match-related contact events and support the findings of this study.
The relationship between [CK] and the impact of collisions during Rugby League match play using integrated accelerometry in portable GPS units has not been investigated previously. Variation in mean total tackles and hit-ups (Table 2) in comparison to the total number of zones 4-6 entries (Table 3) during match play was found in this study. The disparity in the total number of tackles and hit-ups compared to the number of impact zone entries is likely to be because of impact experienced by players during missed tackles, incomplete tackles, line breaks during hit-ups and second effort during tackles and or hit-ups that were not included in this study. Our findings with respect to the number of zones 4-6 entries and [CK] postmatch indicated that skeletal muscle damage during Rugby League match play is dependent upon the number and intensity of collisions experienced by players.
To our knowledge, no studies have examined CK activity in response to elite Rugby League match play or during the postmatch recovery period. Further, although [CK] remained elevated for at least 5 days postmatch, a gradual reduction in mean [CK] was identified during the short-term postmatch recovery phase that coincided with reduced training loads and physical trauma. Similar reductions in CK activity have been observed in studies that have examined endocrine and biochemical responses to tapering in team sport athletes (7,13). The most likely cause for the reduction in [CK] during the postmatch recovery period is the removal of blunt force trauma characteristic of Rugby League training and match play, and a global reduction in the volume and intensity eccentric muscle contractions during training. On that basis, we suggest that CK can be used to monitor acute recovery from elite Rugby League match play.
This study provides an insight into the relationship between the prematch and short-term postmatch biochemical and endocrine responses to the intensity, number, and distribution of impacts associated with collisions during elite Rugby League match play using contemporary GPS and accelerometer performance analysis methods that have not been reported previously. The findings of this study suggest that repeated high-intensity collisions during elite Rugby League match play are associated with significant skeletal muscle damage with [CK] peaking 24 hours postmatch. Players can also expect to sustain blunt force trauma and impact >7.1G because of high-intensity collision approximately every 50 seconds during match play. The number of heavy to severe impacts experienced by players during match play is correlated with significantly increased [CK] for at least 72 hours postmatch. The prolonged and significantly elevated [CK] that remained for at least 120 hours postmatch indicates that training loads should be carefully monitored for at least 5 days postmatch to optimize recovery of skeletal muscle damage sustained during Rugby League match play.
The endocrine profile depicted in the present study revealed an absence of any correlation between [sCort] and impacts experienced by players during match play. A substantial acute increase in [sCort] in response to match play was identified, however, followed by a return to homeostasis within 48 hours, substantiating the value of [sCort] as a viable analysis measure and supporting the implementation of 2 days of modified activity to facilitate the short-term postmatch recovery phase. When integrated with GPS technologies, biochemical and endocrine measures can assist coaches to determine the demands of performance and establish a comprehensive profile of individual responses and adaptations to elite Rugby League match play.
The author wises 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.
1. Brancaccio, P, Maffiuletti, NA, and Limongelli, FM. Creatine kinase monitoring in sport medicine. Br Med Bull
81-82: 209-230, 2007.
2. Cadore, E, Lhullier, F, Brentano, M, Silva, E, Ambrosini, M, Spinelli, R, Silva, R, and Kruel, L. Correlations between serum and salivary hormonal concentraions in response to resistance exercise. J Sports Sci
26: 1-6, 2008.
3. Clarkson, PM, Nosaka, K, and Braun, B. Muscle function after exercise-induced muscle damage and rapid adaptation. Med Sci Sport Exerc
24: 512-520, 1992.
4. Connolly, DA, Sayers, SP, and McHugh, MP. Treatment and prevention of delayed onset muscle soreness. J Strength Cond Res
17: 197-208, 2003.
5. Cormack, SJ, Newton, RU, and McGuigan, MR. Neuromuscular and endocrine responses of elite players to an Australian Rules football match. Int J Sports Phys Perf
3: 359-374, 2008.
6. Coutts, A and Duffield, R. Validity and reliability of GPS devices for measuring movement demands of team sports. J Sci Med Sport
11: 500-509, 2008.
7. Coutts A, Reaburn P, Piva TJ, and Murphy A. Changes in Selected Biochemical, Muscular Strength, Power, and Endurance Measures during Deliberate Overreaching and Tapering in Rugby League Players. Int J Sports Med
28: 116-124, 2007.
8. Cunniffe B, Hore AJ, Whitcombe DM, Jones KP, Baker JS, and Davies B. Time course of changes in immuneoendocrine markers following an international rugby game. Eur J Appl Physiol
9. Cunniffe, B, Proctor, W, Baker, JS, and Davies, B. An evaluation of the physiological demands of elite rugby union using global positioning system tracking software. J Strength Cond Res
23: 1195-1203, 2009.
10. 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.
11. Filaire, E, Sagnol, M, Ferrand, C, Maso, F, and Lac, G. Psychophysiological stress in judo athletes during competitions. J Sports Med Phys Fitness
41: 263-268, 2001.
12. Gill, ND, Beaven, CM, and Cook, C. Effectiveness of post-match recovery strategies in rugby players. Br J Sports Med
40: 260-263, 2006.
13. Hartmann, U and Mester, J. Training and overtraining markers in selected sport events. Med Sci Sports Exerc
32: 209-215, 2000.
14. Hoffman, JR. Endocrinology of sport competition. In: The Endocrinology of Physical Exercise and Sport
. Kraemer, WJ and Rogol, AD, eds. Oxford, United Kingdom: Blackwell Publishing, 2005. pp 600-612.
15. 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.
16. 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.
17. Hortobagyi, T and Denahan, T. Variability in creatine kinase: Methodological, exercise and clinically related factors. Int J Sports Med
10: 69-80, 1989.
18. King, T, Jenkins, DG, and Gabbett, TJ. A time motion analysis
of professional rugby league match play. J Sports Sci
27: 213-219, 2009.
19. 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, Häkkinen, K, and Maresh, CM. Recovery from a national collegiate athletic association division 1 football game: Muscle damage and hormonal status. J Strength Cond Res
23: 2-10, 2009.
20. Kyrolainen, H, Takala, T, and Komi, P. Muscle damage induced by stretch-shortening cycle exercise. Med Sci Sport Exerc
30: 415-420, 1998.
21. Lac, G and Berthon, P. Changes in cortisol and testosterone levels and T/C ratio during an endurance competition and recovery. J Sports Med Phys Fitness
40: 139-144, 2000.
22. MacLeod, H, Morris, J, Nevill, A, and Sunderland, C. The validity of a non-differential global positioning system for assessing player movement patterns in field hockey. J Sports Sci
27: 121-128, 2009.
23. McLellan CP, Lovell D, and Gass GC. Creatine kinase and endocrine responses of elite players pre, during and post rugby league match-play. J Strength Cond Res
24 (11): 2908-2919, 2010.
24. O'Connor, P and Corrigan, D. Influence of short-term cycling on salivary cortisol levels. Med Sci Sport Exerc
19: 224-228, 1987.
25. Passelergue, P, Robert, A, and Lac, G. Salivary cortisol and testosterone variations during an official and a simulated weight-lifting competition. Int J Sports Med
16: 298-303, 1995.
26. 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.
27. Petersen, C, Pyne, D, Portus, M, and Dawson, B. Validity and reliability of GPS units to monitor cricket-specific movement patterns. Int J Sports Phys Perform
4: 381-393, 2009.
28. Proske, U and Morgan, DL. Muscle damage from eccentric exercise: Mechanism, mechanical signs, adaptation and clinical applications. J Physiol
537: 333-345, 2001.
29. Riad-Fahmy, D, Read, GF, and Walker, RF. Salivary steroid assays for assessing variation in endocrine activity. J Steroid Biochem
19: 265-272, 1983.
30. Salvador, A, Suay, F, Gonzalez-Bono, E, and Serrano, MA. Anticipatory cortisol, testosterone and psychological responses to judo competition in young men. Psychoneuroendocrinology
28: 364-375, 2003.
31. Sirotic, A, Coutts, A, Knowles, H, and Catterick, C. A comparison of match demands between elite and semi-elite rugby league competition. J Sports Sci
27: 203-211, 2009.
32. 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. Br J Sports Med
42: 198-201, 2008.
33. Suzuki, M, Umeda, T, Nakaji, S, and Al, E. Effect of incorporating low intensity exercise into the recovery period after a rugby match. Br J Sports Med
38: 436-440, 2004.
34. Takarada, Y. Evaluation of muscle damage after a rugby match with special reference to tackle plays. Br J Sports Med
37: 416-419, 2003.
35. Tiidus, PM and Ianuzzo, CD. Effects of intensity and duration of muscular exercise on delayed soreness and serum enzyme activities. Med Sci Sport Exerc
15: 461-465, 1983.
36. Townshend, AD, Worringham, CJ, and Stewart, IB. Assessment of speed and position during human locomotion using non-differential GPS. Med Sci Sport Exerc
40: 124-132, 2008.
37. Vining, RF, McGinley, RA, Maksvytis, JJ, and Ho, KY. Salivary cortisol: A better measure of adrenal cortical function than serum cortisol. Ann Clin Biochem
20: 329-335, 1983.