Competing within the elite-level professional soccer players are expected to possess a high level of physical conditioning in addition to proficient technical and tactical abilities to complement the demands associated with contemporary match play (7,13,41).
Characteristics imposed on players during modern match play necessitate that the physical performance of elite soccer players is based on the combination of aerobic endurance (3), muscular strength (7), power (45), and repeated sprint ability, respectively (41). The collective importance of these physical determinants is specific to soccer and as a result, the physiological demands placed on elite-level players are substantial (41). Because of this fact, soccer training needs to be well-prepared and structured in conjunction with the implementation of effective recovery strategies. Although the metabolic and physical demands characterizing the modern game are well-documented within the literature (24,25), to date, of the limited research available, evident disparity exists on the affect elite-level soccer has upon immune function (26,27,43,44).
Within the construct of the modern day soccer, given the limited time frame in the middle of a congested schedule, it is of great pertinence that optimal player recovery can be facilitated. Failure to recover fully after training and competitive performance, respectively, have been associated with the manifestation of immunodepression in athletes (12,22,43). As a result, within elite-level competition, monitoring athlete's immune status is receiving greater attention.
Much of the available immunological research in elite athletes has focused primarily on postexercise salivary immune response (42), with athletes seemingly experiencing a transitory decrease in immune function from 3- to 72-hour poststrenuous training or competition, respectively (39). It is during this “open window” period of immune depression, as proposed by Nieman's “J-shaped” relationship (35), that athletes after strenuous exercise, are considered to be at the greatest risk of developing an upper respiratory tract infection (URTI) (17,40).
Mucosal immunity constitutes the first line of defense against pathogen invasion (1), and approximately 95% of all reported URTIs are initiated at the mucosal surfaces (2). In view of this, saliva sampling has rapidly developed as a diagnostic tool for the assessment of physiological biomarkers associated with physical performance (5,31). Because the predominant immunoglobulin is expressed in mucosal fluids, salivary immunoglobulin A (s-IgA) is considered as the best indicator of mucosal immunity. As part of the innate immune response, s-IgA provides an immunological barrier to inhibit the attachment and replication of invading pathogenic viruses to the mucosal surfaces (23). Salivary IgA has been shown to correlate closely with or preceding the contraction of a URTI (32) and thus in accordance with the available research could assist in the evaluation of excessive training loads, individual recovery status, and assessment of potential immune suppression within athletes (20).
Nakamura et al. (33) demonstrated that saliva flow rate and s-IgA secretion rate tended to decrease 3 days before the appearance of URTI symptoms compared with the noninfection period for the same individual. While Neville et al. (36) highlighted that a significant decline (28%) in s-IgA occurred during 3 weeks before URTI episodes and returned to baseline 2 weeks after a URTI was contracted. Neville et al. (36) further proposed that when an athlete did not have, or was not recovering from URTI, an s-IgA value <40% of mean baseline s-IgA concentration indicated a 50% chance of contracting a URTI within 3 weeks.
Although there is clear evidence of an association between immunosuppression, volume, and duration of exercise, respectively within the literature (9,11,16,19,36), the influence of intensity of exercise and its interaction with volume and duration of training need further clarification. Intense training may compromise mucosal immunity. Engaging in heavy training involving bouts of high intensity (HI) or high volume for a prolonged time may cause decreases in s-IgA concentrations, thus leaving athletes susceptible to picking up infections. More pertinent to soccer, daily intense exercise during the long competitive season may have a cumulative suppressant effect on s-IgA output (18). Mackinnon and Hooper (20) reported a progressive decrease in s-IgA secretion rates after 90 minutes of running at 75% V̇o2peak performed on 3 successive days.
In light of these findings, given the demands of modern match-play in elite soccer, and the limited opportunity to avoid repeated stress when training and competitive fixtures are scheduled close together, players may be at greater risk of contracting URTIs as a result of decreased s-IgA concentrations. One day in-between matches and or consecutive intense training may be inadequate for full recovery to be elicited and thus leave players susceptible to URTI.
The primary aim of this investigation was to examine the effect of training intensity on s-IgA among elite professional soccer players by comparing the s-IgA values after HI sessions and low-intensity (LI) sessions. The secondary aim is to investigate the relationships between depressed s-IgA values and training parameters (e.g., GPS data, RPE, and training duration). We hypothesized that the s-IgA is depressed to a larger extent after HI training as compared with LI training. We also hypothesized that some training parameters are correlated with the depressed s-IgA.
Experimental Approach to the Problem
Within the construct of the modern day soccer, given the limited time frame in the middle of a congested schedule, it is of great pertinence that optimal player recovery can be facilitated. Failure to recover fully after training and subsequent performance has been associated with the manifestation of immunodepression in athletes.
To test the aforementioned hypotheses, 10 elite soccer players performed a week's training. Subjects provided resting saliva samples 30 minutes before training session (PRE) and after session (POST). Saliva samples were collected immediately after the conclusion of the training session. The aim was to model the actual training load the players are subjected to on a typical weekly basis within elite-level soccer and demonstrate if this affects the immune function (measured by s-IgA). To quantify the intensity of the training sessions, GPS, HR response, and RPE using Borg's 6-20 scale were recorded respectively. Before this study, the players were familiarized with this procedure during the regular training sessions.
Ten elite male professional soccer players participated in this investigation, and all subjects had been playing soccer for a minimum of 10 years. The team had been among the most successful teams in domestic and European competitions throughout the last 5 years, culminating in a European competition finals. Seven of the players used in this investigation were members of their respected national teams. Players' age, height, body mass, maximal aerobic capacity, and sum of 8 skinfold sites (taken at the biceps, triceps, subscapular, iliac crest, supraspinal, abdominal, mid-thigh, and calf) were 26.8 ± 4.1 years, 185.4 ± 6.0 cm, 79.3 ± 7.8 kg, 56 ± 6 ml·kg−1·min−1, and 54 ± 15 mm, respectively. Participants were provided verbal and written information of experimental procedures and signed informed consent statements and medical history forms before study initiation. Players were detailed on the benefits and potential risks associated with participation and were informed they were free to withdraw from the study at any time without penalty. The study was conducted according to the Declaration of Helsinki, and the protocol was fully approved by the Sports Science Department at Rangers Football Club.
All players were fully familiarized with the experimental procedures within this study because of the testing and training protocols being implemented within the club as part of its sport science and conditioning structure. During the study, players were instructed to maintain normal daily food and water intake, and no dietary interventions were undertaken.
The basic rules of hygiene were recalled to avoid methodological bias. To reduce the influence on the immune system, participants were asked not to ingest caffeine, alcohol, or anti-inflammatory medications 24 hours before testing. Moreover, the subjects should abstain from using large doses of vitamin/mineral supplements at least 30 days before the experiment starting. They were also instructed not to engage in exercise during the 24 hours before each testing session. Participants were excluded from the study if they had any oral, dental, or other symptoms of infection at the time of testing (immunocompromised condition such as an autoimmune disease [i.e., lupus, multiple sclerosis, rheumatoid arthritis, or insulin-dependent diabetes mellitus], tested positive for human immunodeficiency virus, or had been diagnosed with acquired immune deficiency syndrome) and taking any medication for at least 1 month before testing. Subjects were also excluded if they had experienced high psychological stress. Finally, before each testing session, subjects exhibiting any symptoms associated with URTI illness known to affect immune-cell parameters, were excluded from the study.
The experiment took place during the first period of the in-season (e.g., October–November). The training sessions performed during the investigation were representative of a training structure expected to be implemented within top-level elite soccer, constituting a controlled periodized training week encompassing low, moderate, and HI sessions in preparation for match performance. The players involved within this study undertook tactical, technical (LI sessions), and conditioning sessions (inclusive of repeated sprint activity, aerobic intervals, and small-sided games) within the training week. Training intensity was closely monitored during each session throughout the study. For each session, a profile of the internal load (individual training response) was established through heart rate responses (Polar Team System 2; Kempele, Finland) and session-RPE respectively, in response to the imposed external load (training session), determined through GPS.
As part of the presampling protocol, players were required to complete a daily wellness questionnaire and provide an RPE (Borg's 6-20 scale RPE) in response to the preceding training session. Saliva samples were collected at 2 different time points on the testing days throughout the investigation. Before the investigation started, 3 separate samples were taken 30 minutes before training on consecutive days to develop the baseline values used in this study. During the testing days, samples were taken 30 minutes before the commencement of training (Pretraining) and the other one immediately after the cessation of training (Post-training). Samples were collected as close to the same time of day where possible to minimize the effects of circadian variation on salivary immunoglobulin. Testing sessions were situated after a recovery day or 24 hours of nonactivity to ensure players had no existing fatigue from repeated bouts of HI work.
To accurately quantify the external load, players' activity profiles were monitored by means of portable GPS devices (MinimaxX, version 4.0; Catapult Innovations, Melbourne, Australia) operating at a sampling frequency of 5 Hz. The validity of this device for use within team sports performance has been determined previously (6,25). Each player wore a special harness to allow the unit to be fitted in a secured pouch, positioned on the upper back of the player. After the training session, GPS files were downloaded and analyzed with the software package provided by the manufacturer (Logan Plus version 4.2.3; Melbourne, Australia).
The activity profiles were verified using the speed categories: walking (0–7.2 km·h−1), jogging (7.3–14.3 km·h−1), running (14.4–21.5 km·h−1), HI running (21.6–25.2 km·h−1), and sprinting (>25.3 km·h−1). For the purposes of this study, indicators of external load were as follows: (a) total distance (TD) covered (m), (b) total HI distance covered (THID), defined as TD covered (m) at HI speeds >21.6 km·h−1, (c) frequency of efforts at HI (FEHS), expressed as the number of times a player was able to achieve a speed >21.6 km·h−1, (d) HI distance covered as a percentage of the TD covered within the training session, and (e) meterage per minute, taken as an average of the TD covered within the session divided by session duration.
In addition to measuring HR response to quantify the individual training response, session-RPE was also implemented within this investigation. The session-RPE assessment was conducted in accordance with the procedures previously described by Foster et al. (6). Briefly, this method of monitoring training and competition load required each athlete to provide a session-RPE value using Borg's 6-20 scale to represent the perceived exertion of the whole training session. To ensure that the perceived exertion was reflective of the entire session rather than the last effort, data were collected in the proceeding morning after each training session.
In conjunction with detailing session-RPE, players were required to answer and provide scores (1 = very poor, 5 = excellent) on the listed simple questions within a questionnaire, intended to establish a picture of individual daily wellness. The questions and aggregation of scores provided an insight into players' perception of their current energy levels, quality of sleep, readiness to train, and lower-body soreness in response to the previous days' training session (14). The data were recorded by the same investigator on every occasion throughout the investigation period.
Saliva Sampling and Analysis
Player provided saliva samples 30 minutes before training session commencement and immediately after training. Additionally, before saliva sampling, to regulate saliva secretion, players were required to ensure adequate hydration (consumed 500 ml of water) because dehydration has been associated with reduced resting saliva flow rates (42).
A total of 90 saliva samples were collected and analyzed from this cohort of players, using the IPRO OFC collection kits in combination with a real-time lateral flow device (LFD), respectively. This method has been validated previously for oral fluid collection in the immunoassay of immunoglobulins in sports persons (5) and correlates well with other methods (enzyme-linked immunosorbent assay) adopted in the determination of s-IgA (31).
In accordance to the manufacturer's guidelines, after thoroughly rinsing their mouths with water, unstimulated saliva samples were collected as follow. Players were required to place a synthetic polymer-based swab material attached to a volume adequacy indicator stem in their mouth. Once the OFC kits collect 0.5 ml of oral fluid (collection times typically in the range of 20–50 seconds), the volume adequacy indicator changed color and indicated to the player to place the swab in the dropper bottle containing a known volume of extraction buffer. The bottle was then shaken vigorously for a period of 60 seconds, and the collected sample was ready to be analyzed through a real-time LFD (IPRO interactive). For the LFD, 2 drops of saliva/buffer mix were added to the sample window of the LFD cassette. The liquid in turn then ran length of the test strip through capillary action creating a control and test line visible in the test window. Five minutes after the sample was added, the test line intensity was measured in an IPRO reader. The test line intensity was inversely proportional to the s-IgA concentration in the sample analyzed.
Data were expressed as mean ± SD. After testing for normal distribution (Kolmogorov-Smirnov test), differences within and between the training periods (low and intense period) were analyzed using a 2-way analysis of variance for repeated measurements: factor 1 was the time of test (Pre vs. Post) and factor 2 was the intensity of training session (low vs. high). Pearson correlation coefficient evaluated the correlation between the indicators of external or internal load and s-IgA values. The magnitude of the correlations was determined using the modified scale by Hopkins (15): r < 0.1, trivial; 0.1–0.3, small; >0.3–0.5, moderate; >0.5–0.7, large; >0.7–0.9, very large; >0.9, nearly perfect; and 1, perfect (21). The reliability was assessed by intraclass correlations. The difference was considered statistically significant when p ≤ 0.05, and we conclude that the difference was not significant when the power >0.8 (<0.2) (type II errors). The data were analyzed by using SPSS for Windows (version 16.0; SPSS Inc, Chicago).
Indicators of external load (GPS data) and indicators of internal load are presented in Table 1. As shown in this table, players covered significantly lower TDs (p < 0.01) during LI sessions than during HI ones. Hence, during HI sessions, the THID were significantly higher than during LI sessions. Likewise, the %HID ([HID/TD] × 100) was significantly higher (p ≤ 0.05 for session 2 and 4 and p < 0.01 for session 1 and 3) during HI sessions compared with LI sessions. Frequency of efforts at HI was also significantly higher (p ≤ 0.05 for session 1, 2, and 4 and p < 0.01 for session 3) during HI sessions compared with LI sessions. Meterage per minute, taken as an average of the TD covered within the session divided by session duration was significantly higher (p < 0.01) during HI sessions compared with LI sessions.
Concerning the indicators of internal load (Table 1), only the RPE differ significantly between HI and LI sessions. In fact, RPE values were significantly higher after HI sessions than after LI ones (p < 0.01).
As shown in Figure 1, s-IgA baseline concentrations did not differ significantly between the 4 different sessions of training both for HI and LI (Figure 1). On the same way, there were no significant differences between HI and LI across the different training sessions concerning s-IgA concentrations determined just before the training sessions (s-IgA pretraining) (Figure 2).
Figure 3 showed the s-IgA values determined after the training sessions (s-IgA post-training). When there were no significant differences between HI and LI sessions at the first 3 sessions (S1, S2, and S3), s-IgA post-training concentration determined after the fourth HI session was significantly lower (p ≤ 0.05) than the value determined after the fourth LI session (Table 2).
On the same way, the percentage change between s-IgA post-training and s-IgA baseline concentrations differ significantly (p ≤ 0.05) only at the fourth session between HI and LI training sessions (Figure 4).
In addition, negative significant relationships were observed in our study during HI training sessions.
- RPE/s-IgA after training: r = −0.57, p ≤ 0.05 at S1; r = −0.60, p ≤ 0.05 at S2; and r = −0.59, p ≤ 0.05 at S4.
- TD/s-IgA baseline change: r = −0.69, p ≤ 0.05 at S1.
- RPE/s-IgA baseline change: r = −0.72, p ≤ 0.05 at S2.
- TD/s-IgA after training: r = −0.64, p ≤ 0.05 at S4.
Hence, a positive relationship was observed between RPE and s-IgA after training (r = 0.72, p ≤ 0.05) after the LI training at session 1.
The key finding of this investigation was that a significant reduction in the expression of s-IgA was observed in the postexercise window after the completion of HI training when compared against LI training. This is in agreement with the study's primary hypothesis, which postulated that the intensity of training within elite professional soccer would be reflected in s-IgA concentration levels.
Various authors have used s-IgA concentration to investigate the relationship between changes in mucosal immune function with training and the incidence of URTI (11,18,19,33,36,43). Consistent with available literature, this study displays a characteristic, albeit nonsignificant, reduction in s-IgA concentration postexercise after acute, prolonged HI exercise (19,21,27).
Moreira et al. (28) recently reported significant relationships between stress tolerance, training loads, s-IgA, and the incidence of URTI in elite basketball players over the course of a 4-week training period. A reduction in s-IgA among the players coincided with a proliferation in weekly training load and increased reports of URTI symptoms. In a corresponding publication by the same author (27), the immune response to 2 highly competitive 40-minute futsal matches, separated by 7 days, was observed in elite Brazilian professional futsal players. The findings presented indicated that the matches induced reductions in both s-IgA concentration and secretion rates.
While these studies lend support to the existence of a relationship between exercise and immune suppression, evident disparity exists within the literature with respect to the s-IgA response to exercise. In contrast to the aforementioned findings, other investigations have provided conflicting results about the acute exercise response demonstrated in IgA. Both the IgA concentration and secretion rate have been reported to remain unchanged after completion of 70-minute professional soccer match (26) or actually increase after simulated 90-minute soccer-specific treadmill protocol (43). The large SDs observed in s-IgA response to a given exercise session (Table 1, Figure 4) show consensus with the large within- and between-variations in s-IgA concentration reported within the literature (8,34). As such, the marked variability makes it difficult to establish a direct link between exercise, s-IgA, and the incidence of URTI in elite athletes.
As offered by Moreira et al. (27), the reason for these inconsistent and discrepant findings may be related to the modality of exercise adopted, differences in the training and nutritional status of the subjects, the discrepancies in both exercise duration and intensity, and the various methods employed to express IgA data. In our study, we have minimized these variations by controlling the factors known to affect the concentration of salivary IgA. Indeed, all the subjects realized the same training session and have approximately the same training level (elite players) and sporting past (minimum of 10 years). Moreover, all our subjects were in a fasted state and were required to abstain from food and caffeine products for a minimum of 2 hours before the collection of saliva. Additionally, before saliva sampling, to regulate saliva secretion, players were required to ensure adequate hydration (consumed 500 ml of water). To minimize residual effect of exercise and circadian variations, salivary samples were collected as close to the same time of day for all subjects. Finally, the same method was used for all subjects to collect and measure salivary IgA.
Currently, there is much deliberation within the literature regarding the most suitable method to express s-IgA changes after exercise. It has been postulated that the expression of s-IgA as a secretion rate could be more important to immune defense (1). Expressing s-IgA data in this way has been advocated by some authors (1,27), particularly for acute exercise responses because the s-IgA rate takes into account and represents the actual availability of s-IgA on the mucosal surfaces. In this light, the inability to express s-IgA responses as a secretion rate may represent a possible limitation to this investigation.
However, in line with a recent study (36), examining salivary IgA as a risk factor for URTI in professional America's Cup yachtsmen, this study, in addition to reporting salivary IgA as an absolute value, documented s-IgA as a relative percentage to a baseline measure. This method of expressing salivary IgA has been demonstrated to be a strong predictor of the risk of URTI within the available published literature. The findings from the longitudinal study conducted by Neville et al. (36) longitudinal study, were able to conclude from their cohort of athletes, that a decrease of 40% in s-IgA from baseline correlated in a 50% chance of developing URTI symptoms.
The marked change (%) identified after training in mucosal immune function after HI training relative to baseline measures for sessions 1 and 4 specifically (both >40%) provides support for the assumption that salivary IgA may reflect the intensity of training undertaken within elite professional soccer. More pertinently, it suggests that elite soccer professionals are potentially at an increased risk of contracting a URTI, and therefore, it may be necessary to ensure that appropriate strategies are implemented to effectively manage this period of compromised mucosal immunity.
It has been suggested that the mechanisms underlying the alterations in markers of mucosal immunity (s-IgA) with exercise are probably largely related to the activation of the sympathetic nervous system, that innervate the salivary glands directly or the blood vessels that supply the glands, and its associated effects on salivary protein exocytosis and IgA transcytosis. The stimulation of saliva glands by sympathetic nervous activity reduces saliva flow rate through vasoconstriction of the blood vessels supplying the glands (4). All these factors are known to vary with the intensity of training. Supplementation with carbohydrate (CHO) has offered promise in attenuating the post-exercise changes observed in mucosal immunity (37–39). Given the requirement to undertake heavy training cycles during training, e.g., preseason in soccer, athletes, and conditioning practitioners may be more receptive to ingesting a nutrient supplement that could potentially counter the induced immunosuppression associated with prolonged HI exercise rather than reduced training workloads to accommodate states of depressed immune function. This is an area, which has received little interest within the literature and more work is merited.
The increased frequency of URTI attributable to decreased s-IgA in elite athletes may be due, at least in part, to the repetitive intensive exercise sessions undertaken without sufficient recovery between them (10,11,43). Given the limited time frame in the middle of a congested schedule within the construct of modern day soccer, it has been suggested that an imbalance between training/competition stress and recovery has the capacity to facilitate high levels of fatigue, underperformance and immunodepression (12). It could be inferred, from the significant differences seen in indicators of external loading between the first and fourth HI sessions in Table 1 and the coinciding large postexercise baseline percentage changed after HI session 4 in Table 2, respectively, that undertaking prior HI sessions may have manifested to elicit the significant decrease seen in s-IgA and activity profile markers after the fourth HI session.
Given the periodized training structure implemented within this study however, this seems unlikely. The combination of HI and LI sessions in unison with recognized recovery days facilitate the maintenance of performance levels while eliciting optimal player recovery in preparation for subsequent competition/performance. The likelihood of these findings being attributable to the high levels of variability in s-IgA sampling rather than an accumulative fatiguing effect are supported by the recovery kinetics demonstrated in s-IgA within this study. As reported within the literature, a period of typically 24 hours is required for the recovery kinetics of s-IgA to promote a return to baseline after the transitory decrease identified after HI exercise (36). In reference to Table 2, pre-exercise IgA concentration collected display strong agreement with baseline measures about the recovery kinetics displayed in IgA.
Conversely, it could be inferred that an inherent drawback of this investigation was that a 2-week sampling period undertaken was not a long-enough window to appropriately assess the s-IgA response within elite soccer players and so may be inferred seen as a limitation of this study. It has been proposed that the typical deadline in an individual's relative s-IgA concentration over a 3-week period before the appearance of a URTI seems to pre-empt and contribute to URTI risk, with the level of risk being related to the extent of the decline in s-IgA. Neville et al. (36) highlighted that a significant decline (28%) in s-IgA occurred during 3 weeks before URTI episodes.
After the fourth HI session, where a significant decrease in postexercise relative to baseline was detected, this investigation may have benefited from possessing a longer sampling window to monitor subsequent IgA levels and players' wellbeing. Nakamura et al. (33) demonstrated that saliva flow rate and s-IgA secretion rate tended to decrease 3 days before the appearance of URTI symptoms compared with the noninfection period. Thus, more research on the role of these acute postexercise changes in s-IgA expression in elite-level professional soccer players is needed and within a longitudinal study approach.
The secondary aim of this investigation was to attempt to reveal any key variables that may significantly contribute to depressed s-IgA values. Both indicators of internal and external player loading were recorded for each session throughout the investigation period. Although RPE has been used extensively within soccer and also IgA research (29,30), to our knowledge, this is the first study to use motion analysis within elite-level soccer to assess its potential impact on s-IgA concentration. To date, Thorpe and Sunderland (44) are the only other known to publish research to use motion analysis to assist in quantifying match play, albeit within semi-professional soccer players, while also monitoring the immune response pre- and post-match. However, within this study no correlations were made between player activity profiles and the s-IgA response to match play.
Analysis of player activity profiles in Table 1 demonstrates a clear distinction between HI and LI sessions throughout the study. Significant differences (p ≤ 0.05) were evident for every indicator of external load measured between HI and LI sessions. This finding is also reflected in players' RPE after each session of HI and LI exercise performed. In attempting to correlate the GPS data to the immune response, a significant, negative relationship (r = −0.7; p ≤ 0.05) was found between IgA percentage change pre- to post- HI exercise and TD covered in session 1. Similarly after HI session 4, TD was significantly negatively correlated to s-IgA post concentration (r = −0.6, p ≤ 0.05). Importantly, in both of these sessions, the greatest baseline percentage change in s-IgA was reported (>40%) and was in line with previous published literature support the opinion that players may be at increased risk of developing URTI symptoms (36).
Importantly, TD as an indicator of external loading is more commonly associated with the volume of training rather than training intensity per se and so, these results oppose the main finding of this investigation and advocate that training volume may present a useful indicator of monitoring s-IgA response to HI exercise within elite-level soccer. In support for this interpretation, the TD covered in HI session 2 (<12,000 km), the highest of the sessions undertaken with the study, exhibited the largest mean percentage IgA change pre to post within this study (−21%). This is the first study to attempt to correlate markers of external loading with immune responses to exercise, and thus more research is needed to verify this novel association between TD covered in elite professional soccer and s-IgA concentration.
As the main indicator of internal load, players were asked to provide an RPE score after each session. In line with the GPS data collected and available literature (30), RPE demonstrated strong negative correlations with s-IgA postexercise (r = −0.6; −0.6; −0.6 for sessions 1, 2, and 4 of HI exercise, respectively).
The findings from this particular investigation have indicated that HI soccer training sessions may cause a significant decrease in players' s-IgA values during the postexercise window when compared against LI training. They also suggest that s-IgA values may be considered as an intensity/volume (TD)-dependant marker. This investigation further shows that the intensity and volume of the training sessions may be more appropriate to monitor to determine the impact of the IgA value. This study encourages coaches and practitioners to monitor s-IgA in routine, and in particular, during HI training periods so as to take precautions to avoid URTI in highly trained athletes.
The authors gratefully acknowledge the soccer players participated in this study. The results of this study do not constitute endorsement of the product by the authors or the National Strength and Conditioning Association. The authors declare no conflict of interest. The research did not receive funding from the National Institutes of Health, Welcome Trust, Howard Hughes Medical Institute, or any other source requiring deposit.
1. Bishop NC, Gleeson M. Acute and chronic effects of exercise on markers of mucosal immunity
. Front Biosci (Landmark Ed) 14: 4444–4456, 2009.
2. Bosch JA, Ring C, de Geus EJ, Veerman EC, Amerongen AV. Stress
and secretory immunity. Int Rev Neurobiol 52: 213–253, 2002.
3. Chamari K, Hachana Y, Kaouech F, Jeddi R, Moussa-Chamari I, Wisloff U. Endurance training and testing with the ball in young elite soccer players. Br J Sports
Med 39: 24–28, 2005.
4. Chicharro JL, Lucía A, Pérez M, Vaquero AF, Ureña R. Saliva
composition and exercise. Sports
Med 26: 17–27, 1998.
5. Fahlman MM, Engels H-J. Mucosal IgA and URTI in American college football
players: A year longitudinal study. Med Sci Sports
Exerc 37: 374–380, 2005.
6. Foster C, Florhaug JA, Franklin J, Gottschall L, Hrovatin LA, Parker S, Doleshal P, Dodge C. A new approach to monitoring exercise training. J Strength Cond Res 15: 109–115, 2001.
7. Fousekis K, Tsepis E, Vagenas G. Multivariate isokinetic strength asymmetries of the knee and ankle in professional soccer players. J Sports
Med Phys Fitness 50: 465–474, 2010.
8. Francis JL, Gleeson M, Pyne DB, Callister R, Clancy RL. Variation of salivary immunoglobulins in exercising and sedentary populations. Med Sci Sports
Exerc 37: 571–578, 2000.
9. Fricker PA, McDonald WA, Gleeson M, Clancy RL. Exercise-associated hypogammaglobulinemia. Clin J Sport Med 9: 46–48, 1999.
10. Gleeson M. Mucosal immunity
and respiratory illness in elite athletes. Int J Sports
Med 21(Suppl 1): S33–S43, 2005.
11. Gleeson M, McDonald WA, Pyne DB, Cripps AW, Francis JL, Fricker PA, Clancy RL. Salivary IgA levels and infection risk in elite swimmers. Med Sci Sports
Exerc 31: 67–73, 1999.
12. Gleeson M, Walsh NP, Blannin AK, Robson PJ, Cook L, Donnelly AE, Day SH. The effect of severe eccentric exercise induced muscle damage on plasma elastase, glutamine and zinc concentrations. Eur J Appl Physiol Occup Physiol 77: 543–546, 1998.
13. Hoff J. Training and testing physical capacities for elite soccer players. J Sports
Sci 23: 573–582, 2005.
14. Hooper SL, Mackinnon LT. Monitoring overtraining in athletes. Recommendations. Sports
Med 20: 321–327, 1995.
15. Hopkins WG. A scale of magnitudes for effect statistics. 2009. Available at: http://www.sportsci.org/resource/stats/index.html
16. Levando VA, Suzdal'nitskii RS, Pershin BB, Zykov MP. Study of secretory and antiviral immunity in sportsmen. Sports
Train Med Rehab 1: 49–52, 1988.
17. Libicz S, Mercier B, Bigou N, Le Gallais D, Castex F. Salivary IgA response of triathletes participating in the French iron tour. Int J Sports
Med 27: 389–394, 2006.
18. Mackinnon LT, Ginn E, Seymour GJ. Effects of exercise during sports
training and competition on salivary IgA levels. In: Behaviour and Immunity. Husband A.J., eds. Boca Raton, Florida: CRC Press, Inc, 1992. pp. 169–177.
19. Mackinnon LT, Ginn E, Seymour GJ. Decreased salivary immunoglobulin A secretion after intense interval exercise in elite kayakers. Eur J Appl Physiol Occup Physiol 67: 180–184, 1993.
20. Mackinnon LT, Hooper S. Mucosal (secretory) immune system responses to exercise of varying intensity and during overtraining. Int J Sports
Med 15(Suppl 3): S179–S183, 1994.
21. Mackinnon LT, Jenkins DG. Decreased salivary immunoglobulins after intense interval exercise before and after training. Med Sci Sports
Exerc 25: 678–683, 1993.
22. Malm C, Ekblom O, Ekblom B. Immune system alteration in response to two consecutive soccer games. Acta Physiol Scand 180: 143–155, 2004.
23. Mazanec MB, Nedrud JG, Kaetzel CS, Lamm ME. A three-tiered view of the role of IgA in mucosal defence. Immunol Today 14: 430–435, 1993.
24. Mohr M, Krustrup P, Bangsbo J. Match performance of high-standard soccer players with special reference to development of fatigue. J Sports
Sci 21: 519–528, 2003.
25. Mohr M, Krustrup P, Bangsbo J. Fatigue in soccer: A brief review. J Sports
Sci 26: 593–599, 2005.
26. Moreira A, Arsati F, Cury PR, Franciscon C, Oliveira R, de Araujo VC. Salivary immunoglobulin A response to a match in top level Brazilian soccer players. J Strength Cond Res 23: 1968–1973, 2009.
27. Moreira A, Arsati F, de Oliveira Lima-Arsati YB, Simoes AC, de Araujo VC. Monitoring stress
tolerance and occurrences of upper respiratory illness in basketball players by means of psychometric tools and salivary biomarkers. Stress
Health 27: 166–172, 2011.
28. Moreira A, Arsati F, de Oliveira Lima-Arsati YB, de Freitas CG, de Araujo VC. Salivary Immunoglobulin A responses in professional top-level fustal players. J Strength Cond Res 25: 1932–1936, 2011.
29. Moreira A, Freitas CG, Nakamura FY, Drago G, Drago M, Aoki MS. Effect of match importance on salivary cortisol and immunoglobulin A responses in elite young volleyball players. J Strength Cond Res 27: 202–207, 2013.
30. Moreira A, McGuigan MR, Arruda AF, Freitas CG, Aoki MS. Monitoring internal load parameters during simulated and official basketball matches. J Strength Cond Res 26: 861–866, 2012.
31. Mortatti AL, Moreira A, Aoki MS, Crewther BT, Castagna C, de Arruda AF, Filho JM. Effect of competition on salivary cortisol, immunoglobulin A, and upper respiratory tract infections in elite young soccer players. J Strength Cond Res 26: 1396–1401, 2012.
32. Nakamura D, Akimoto T, Suzuki S, Kono J. Decreased salivary s-IgA levels before appearance of upper respiratory tract infection in collegiate soccer players. In: Science and Football
V. Reilly T., Cabri J., Araujo D., eds. Lisbon, Portugal: Routledge, 2003. pp. 526–533.
33. Nakamura D, Akimoto T, Waku T, Suzuki S, Kono J. Daily changes of salivary secretory immunoglobulin A and appearance of upper respiratory symptoms during physical exercise. J Sports
Med Phys Fitness 46: 152–157, 2006.
34. Nehlson-Cannarella SL, Nieman DC, Fagoaga OR, Kelln WJ, Henson DA, Shannon M, Davis JM. Saliva
immunoglobulins in elite woman rowers. Eur J Appl Physiol 81: 222–228, 2000.
35. Neiman DC. Exercise, infection and immunity. Int J Sports
Med 15: 131–141, 1994.
36. Neville V, Gleeson M, Folland JP. Salivary IgA as a risk factor for upper respiratory infections in elite professional athletes. Med Sci Sports
Exerc 40: 1228–1236, 2008.
37. Nieman DC. Influence of carbohydrate on the immune response to intensive, prolonged exercise. Exerc Immunol Rev 4: 64–76, 1998.
38. Nieman DC, Nehlsen-Cannarella SL, Fagoaga OR, Henson DA, Utter A, Davis JM, Williams F, Butterworth DE. Influence of mode and carbohydrate on the cytokine response to heavy exertion. Med Sci Sports
Exerc 30: 671–678, 1998.
39. Nieman DC, Pedersen BK. Exercise and immune function
. Recent developments. Sports
Med 27: 73–80, 1999.
40. Novas AM, Rowbottom DG, Jenkins DG. Tennis, incidence of URTI and salivary IgA. Int J Sports
Med 24: 223–229, 2003.
41. Owen A, Wong D, Dellal A. Effects of a periodised small-sided game training intervention on physical performance in elite professional soccer. J Strength Con Res 26: 2748–2754, 2012.
42. Pedersen BK, Kappel M, Klokker M, Nielsen HB, Secher NH. The immune system during exposure to extreme physiologic conditions. Int J Sports
Med 15(Suppl 3): S116–S121, 1994.
43. Sari-Sarraf V, Reilly T, Doran D, Atkinson G. Effects of repeated bouts of soccer specific intermittent exercise on salivary IgA. Int J Sports
Med 29: 366–371, 2008.
44. Thorpe R, Sunderland C. Muscle damage, endocrine and immune marker response to a soccer match. J Strength Cond Res 26: 2783–2790, 2012.
45. Wisloff U, Castagna C, Helgerud J, Jones R, Hoff J. Strong correlation of maximal squat strength with sprint performance and vertical jump height in elite soccer players. Br J Sports
Med 38: 285–288, 2004.