Rugby union is characterized by repeated, high-intensity work periods of relatively short duration with varying recovery periods (15–17). Players are exposed to a high-frequency and magnitude of body-to-body contacts and collisions (40), with large contributions from high-intensity, stretch-shortening cycle-based movements (19). As a consequence of these large physical and metabolic demands, rugby union players demonstrate elevations in markers of muscle damage (10,40) and disruption in the testosterone and cortisol hormonal milieu postmatch (19). There is also potential that neuromuscular function (NMF) may be reduced over the post-game period (20,28,42).
After competing, rugby union players display elevations in markers of muscle damage (e.g., creatine kinase and myoglobin) for ∼48 hours postmatch (10,40). The degree of game-induced muscle damage, in rugby union, may relate directly to the number of collisions made (40); this has also been demonstrated in rugby league players (30,40). The muscle damage after high-intensity collisions may impact negatively on NMF in the days after competition (31,42). For example, McLellan et al. (31) found a ∼25% reduction in peak rate of force development and ∼20% reduction in peak power at 24 hours postmatch; the reduced NMF was associated with a ∼51% increase in salivary cortisol concentrations, in elite rugby league players. Acute and long-term changes in the postmatch hormonal milieu have also been demonstrated in other research examining rugby union players, with decreases and increases in testosterone and cortisol concentrations, respectively (10,11), and fluctuations in the T/C ratio for up to ∼72 hours postmatch (19).
Keeping in mind game-induced muscle damage, hormonal disruption, and potentially reduced NMF after a rugby union match, the postcompetition recovery period is an integral component in the management of the players. Insufficient recovery, with ensuing fatigue, could potentially lead to poor or inconsistent performances (1,33), injury (2), and eventually illness (9). This could also be magnified during the competitive season, with the potential for accumulative effects from both competition and training (27). There is evidence that a single strength and power training session, typically used in program design in rugby union, may also reduce NMF for ∼48 hours postexercise (20). Gee et al. (20) reported a significant decrease in countermovement jump (CMJ) height and peak power output (PPO) (range, 3–10% across participants) along with concomitant increases in creatine kinase for 48 hours after a strength training session in trained rowers. Thus, optimizing the postmatch recovery period, such that there are no accumulative adverse effects of games and training, is important. Therefore, being able to profile the long-term postmatch recovery of NMF and the hormonal milieu would be useful for player training program design in rugby union.
In addition to neuromuscular and hormonal changes, fatigue may also manifest itself in changes in athlete behavior (18,21) or psychologically with reduced motivation, disturbed mood, and increased perceived soreness (24,42). Mood, in particular, has shown a consistent dose-response relationship in reaction to overtraining (24) and has been assessed successfully in relation to performance and training recovery (34,37). Furthermore, there is evidence that psychological measures of fatigue/overtraining (including mood) are related to specific objective physiological markers of fatigue (3,27,35). However, there is limited data that have examined the acute changes in mood disturbance during the recovery period after a rugby union match.
Currently, there is a lack of literature that has collectively examined NMF, hormonal and mood disturbance responses in the long-term postmatch period in rugby union. Therefore, we examined the time-course changes of these measures for 60 hours after a competitive match in professional rugby union players.
Experimental Approach to the Problem
This study observed the NMF, hormonal and mood disturbance responses after a professional rugby union match. Baseline saliva samples, mood disruption (Brief Assessment of Mood [BAM] Questionnaire), and CMJ performance were collected 36 hours before a competitive professional rugby union match, with measures repeated at 12, 36, and 60 hours postmatch. Thus, testing was completed at the same time of day to avoid the effects of the circadian rhythm on hormonal concentrations and performance (5,41). Saliva was analyzed for testosterone and cortisol; CMJs were processed for PPO and jump height. Baseline measurements were taken after a midseason break (1 week) from competition.
With university ethical approval and informed consent, 14 male professional rugby union players volunteered to take part in this study (mean ± SD; 24.9 ± 4.4 years, 1.85 ± 0.10 m, 105.18 ± 12.31 kg). All subjects were full-time members of a professional squad and engaged in a full-time training and competition schedule. Subjects played for a team in the South of Wales, United Kingdom, competing in the professional Celtic League and European Cup competitions. Subjects were considered healthy and injury-free at the time of this study. Before any data being collected, subjects attended a session outlining the purpose of the study and the procedures involved.
Testing was completed over a 96-hour period, with baseline data collected at 36 hours before a match with an evening kick off (19:30 hours); further data were collected at 12, 36, and 60 hours postmatch (6,30). Upon arrival to the laboratory, subjects provided a 2-ml saliva sample and then completed the BAM Questionnaire. Subjects then performed a 5-minute standardized warm-up, which consisted of jogging and dynamic stretching, before completing 3 maximal effort CMJs on a portable force platform. This protocol was replicated at the postmatch data collection time points. Subjects rested throughout the 60-hour postmatch period with no training taking place during this time.
Saliva Collection and Analysis
Two milliliters of saliva was collected via passive drool (8) into sterile containers during a standardized collection period of 2 minutes, with samples subsequently stored at −20° C until assay. After thawing and centrifugation (2000 rpm × 10 min), the saliva samples were analyzed in duplicate for testosterone and cortisol concentrations using commercial kits (Salimetrics, LLC, State College, PA, USA). The minimum detection limit for the testosterone assay was 6.1 pg·ml−1, with interassay coefficient of variation (CV) of <10%. The cortisol assay had a detection limit of 0.12 ng·ml−1 with interassay CV of <7%.
Countermovement Jump Testing
For the measurement of lower-body PPO, the CMJ was completed on a portable force platform (Type 92866AA; Kistler Instruments Ltd, Farnborough, United Kingdom; (43)). All players were familiar with CMJ testing and received verbal instructions before testing. To isolate the lower limbs, participants were instructed to stand with arms akimbo (22). After an initial stationary phase of at least 2 seconds in the upright position, for the determination of body mass, participants performed a CMJ, dipping to a self-selected depth and then exploding upward in an attempt to gain maximum height. Participants landed back on the force platform and their arms were kept akimbo throughout the movement.
Calculating Peak Power Output
Peak power output was calculated from the CMJ as per West et al. (43). The vertical component of the ground reaction force (GRF) during performance of the CMJ was used in conjunction with the participant's body mass to determine instantaneous velocity and displacement of his center of gravity (22). Instantaneous power was determined using the following standard relationship:
Mood Questionnaire and Scoring
Mood state was assessed using the BAM Questionnaire. This 6-item measure of mood is designed as a brief version of the Profile of Mood State (32) and consists of a 5-point scale, where players describe how they feel at that particular instant in 6 mood adjectives (anger, tension, vigor, confusion, fatigue, and depression). This is often used in applied settings where quick accurate measures of mood are required. This information was provided at the same time of day on each testing occasion. Total mood disturbance scores were calculated from subtracting the vigor score from the sum of the remaining 5 negative items, with higher scores indicating elevated mood disturbance. The BAM Mood Disturbance Scores have been highly correlated with Profile of Mood State Total Mood Disturbance Scores (r = 0.88, 13).
Data were analyzed using repeated measures analysis of variance. Where significant main effects of time were identified, data were further explored with Bonferroni corrected pairwise comparisons. Relationships between changes in each variable, from baseline, across all postmatch sample points were examined using Pearson's product moment correlation. Percentage changes from baseline at each time point are also presented. Statistical analysis was performed using SPSS software (version 16; SPSS, Inc., Chicago, IL, USA), with significance set at p ≤ 0.05. Where significant differences have been identified, 95% confidence intervals (CIs) are presented for an estimation of the population mean difference. Partial-eta2 is presented as a measure of effect size; the reader should square root these values for correlation coefficients that can be compared with the effect sizes described by Hopkins et al. (23). Data are presented as mean ± SD.
Prematch and postmatch force plate data are presented in Figures 1A–C. Player body weight did not change during the 60-hour postmatch period (baseline 105.2 ± 12.7 kg; 12 h 104.43 ± 12.0 kg; 36 h 105.6 ± 12.6 kg; 60 h 105.1 ± 12.3 kg; p = 0.543). There was a significant time effect in the postmatch changes in PPO (p < 0.001; Partial-eta2 = 0.508; Figure 1A), relative PPO (P < 0.001; Partial-eta2 = 0.443; Figure 1B), and jump height (p = 0.001; Partial-eta2 = 0.301; Figure 1C).
Peak power output had decreased below baseline at 12 hours (p = 0.004; 95% CI = −235 to −606 W; −7 ± 6%) and 36 hours (p < 0.001; 95% CI = −223 to −457 W; −6 ± 4%) but was similar at 60 hours (p = 0.151; −2 ± 4%; Figure 1A). Both relative concentric power and jump height followed similar time-course changes (Figures 1B,C).
The time-course changes in testosterone, cortisol, and the T/C ratio are presented in Figures 2A–C, respectively. There was a significant time effect in the postmatch changes in testosterone (p = 0.011; Partial-eta2 = 0.246), cortisol (p = 0.003; Partial-eta2 = 0.296), and the T/C ratio (p < 0.001; Partial-eta2 = 0.466).
Testosterone concentrations had declined from baseline at 12 hours (p = 0.023; 95% CI = −28.07 to −97.62 pg·ml−1; −26 ± 30%) and 36 hours (p = 0.016; 95% CI = −12.12 to −69.84 pg·ml−1; −15 ± 34%) postmatch but returned to concentrations similar to baseline at 60 hours (p = 0.986; −8 ± 28%; Figure 2A). Cortisol concentrations had increased from baseline at 12 hours (p = 0.004; 95% CI = 0.11–0.29 µg·dl−1; 56 ± 49%) and 36 hours (p = 0.027; 95% CI = 0.09–0.31 µg·dl−1; 59 ± 64%) but returned to concentrations similar to baseline at 60 hours (p = 0.189; 34 ± 51%; Figure 2B). The T/C ratio decreased from baseline at 12 hours (p = 0.001; 95% CI = −182 to −389; −50 ± 20%) and 36 hours (p = 0.027; 95% CI −133 to −349; −40 ± 31%) before returning to baseline at 60 hours (p = 0.144; −23 ± 36%; Figure 2C). The changes in testosterone, cortisol, and T/C ratio did not relate to any changes in PPO (absolute or relative) or jump height (p > 0.05).
The mood disturbance scores are presented in Figure 3. There was a significant time effect (p = 0.013; Partial-eta2 = 0.274) in player mood disturbance scores. Mood disturbance increased above baseline at 12 hours (p = 0.031; 95% CI = 1.2–4.3; 56 ± 49%) before returning to baseline at 36 hours (p = 0.220; 33 ± 60%) and 60 hours (p = 0.954; 8 ± 15%; Figure 3). Changes in mood were not related to changes PPO (p = 0.321), jump height (p = 0.133), testosterone (p = 0.232), cortisol (p = 0.166), or the T/C ratio (p = 0.103) at any time point postmatch.
The aim of this study was to examine the postmatch time-course recovery of NMF, the salivary hormonal milieu, and mood disturbance in professional rugby union players. We have demonstrated that NMF, testosterone, and the T/C ratio are reduced, while cortisol is elevated, for 36 hours, before returning to baseline at 60 hours postmatch. Moreover, players displayed an increased mood disturbance at 12 hours postmatch only.
Power output was reduced by approximately−7% for 36 hours, before returning to baseline levels at 60 hours postmatch. Similar findings have been demonstrated in professional rugby league players; McLellan and Lovell (28) demonstrated reductions in PPO of ∼10% for up to 48 hours postmatch, before recovering at 72 hours. This transient reduction in NMF is potentially because of an impairment of excitation-contraction coupling, which is a result of low-frequency fatigue (4,26,28). It is likely that muscle damage, induced by collisions during match play (39), is a contributing factor in the reduced NMF (4). Research in rugby union players has demonstrated elevated creatine kinase concentrations for 48 hours, before returning to baseline concentrations at 70 hours postmatch (40). Furthermore, there is potential that repeated stretch-shortening cycle using movements in rugby union game play (19) may also result in some focused damage of type II muscle fibers (4), further contributing to the reduced power output over this time.
Cortisol concentrations increased from baseline by ∼56 and ∼ 59% at 12 and 36 hours, respectively, and remained ∼34% above baseline at 60 hours (although not statistically) postmatch. Concomitantly, testosterone declined by ∼26% at 12 hours and ∼15% at 36 hours and remained ∼8%, but not significantly, below baseline at 60 hours. Cortisol is a primary stress hormone, and postexercise rises are suggested to reflect the metabolic demand placed on the body (25). This cortisol response has been shown to be largely dependent on the exercise type, intensity, and duration (36). Moreover, increases in cortisol concentrations may be due to psychological stress (38); for example, the stress and pressures of competition may raise cortisol concentrations in athletes (36). In our players, the physiological demands (e.g., large metabolic stress, muscle damage, negative energy balance, and depleted glycogen reserves) of the match are likely to be major contributors to the prolonged elevation in cortisol concentrations observed at 12 and 36 hours. The adrenal release of cortisol in the days after sports competition is relatively unclear, with research tending to focus on immediate post-game period (21).
It is suggested that increases in cortisol concentrations may reduce testosterone synthesis (7,12,14), which would explain the opposing time-course changes in testosterone and the T/C ratio. Similar findings have been demonstrated in rugby league players where average testosterone concentrations were below basal concentrations for ∼48 hours after a professional rugby league match, with the T/C ratio being ∼45% below resting levels for 24 hours postmatch (29). However, our data are conflicting with that of Elloumi et al. (19) who showed that the T/C ratio may increase above basal (rested) levels for 5 days postmatch in 20 international rugby union players. The exact reasons behind the conflicting findings are unclear but may be attributed to the level of competition/match intensity, the opposition players and overall outcome, and postmatch recovery protocols.
Players reported increased mood disturbance at 12 hours postmatch, but this had dissipated by 36 and 60 hours. Mood disturbance can increase because of stress derived from competition (21), but in this instance, as the team won the game, significant psychological stress in the 12 hours postgame is less likely. However, athletes may display reduced vigor and increased fatigue after sporting competition, irrespective of outcome (21,42), which could be exacerbated by increased perceived soreness after high-intensity collision sport (42).
Our data demonstrate the individual nature of recovery; at 60 hours, 7 players' PPO had not fully recovered to baseline levels. Further to this, at 60 hours postmatch, 5 players elicited a recovery/slight increase (2–25% across players) in the T/C ratio, whereas 9 players displayed a T/C ratio decreased by approximately −6 to −65%. Interestingly, just 2 players elicited full recovery of NMF and the T/C ratio at 60 hours. Potential contributors to this individual variation in the data could be factors such as playing position and the number of collisions and contacts during the game, and the amount of high-intensity running performed throughout the game. Additionally, there were no relationships between changes in testosterone, cortisol, and the T/C ratio, with changes in NMF in our group of athletes. Although T/C did follow similar time-course patterns to NMF, particularly during the earlier postmatch time points, this did not hold up across the full measurement period. Potentially, neuromuscular recovery is somewhat independent from the testosterone and cortisol hormonal milieu. This is perhaps not surprising as recent arguments suggest that these hormones may have a greater influence of athlete psychology (e.g., motivation, willingness to perform) rather than muscle physiology, especially in elite athletes (7).
In conclusion, the profiling of a professional rugby union match revealed postmatch changes in CMJ power, salivary hormones, and mood disturbance. The directions of the changes in these measures varied up to 36 hours, but all were returned to baseline by 60 hours postmatch. Thus, a professional rugby union match elicits transient changes in important markers of recovery, with a large degree of individual variation.
Our data have highlighted an important recovery window (1.5–2.5 days) after a professional rugby union match, and knowledge of this could benefit player training and management. The content or timing of any postmatch recovery strategies can be modified to facilitate NMF, hormonal, and mood restoration. Coaches should also be aware of the individual nature of the recovery of these outcomes, which may necessitate an individual approach to recovery strategies.
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