A comprehensive review focusing specifically on altitude training for team-sports suggests that repeat-sprint training performed in hypoxia (RSH) may be a promising avenue for improving match-related performance (Faiss et al., 2013a). Indeed, a number of studies across a range of sports (e.g. football, rugby, lacrosse) have reported performance benefits following a RSH protocol (Brocherie et al., 2015; Faiss et al., 2013b; Galvin et al., 2013; Hamlin et al., 2017; Kasai et al., 2015), and a recent meta-analysis found that RSH induces greater improvements in mean repeatedsprint performance during sea-level repeated sprinting than the same training performed in normoxia (Brocherie et al., 2017). Conversely, select studies have not observed performance benefits following RSH (Goods et al., 2015; Montero and Lundby, 2017). Nevertheless, given the encouraging findings reported in some of the literature and the growing awareness of RSH as a training method (Girard et al., 2017), it is likely that RSH will be increasingly utilised within the team-sport setting.
To date, performance factors (e.g., power output, repeat-sprint ability) have been the main variable of interest in the RSH literature. However, relatively little is known regarding the effect of RSH on inflammatory markers, despite the fact that studies of the hypoxia signalling pathway consistently indicate that hypoxia induces inflammation (see review by Eltzschig and Carmeliet, 2011). This may be an important consideration for team-sport athletes given that inflammatory status has the potential to influence recovery and subsequent training performance (Davis et al., 2007). Indeed, athletes are already more susceptible to illness and infection during periods of intense training or competition (Gleeson, 2007), and there is recent evidence to suggest that a RSH program may alter immune functioning (Born et al., 2016). While select studies have investigated the acute inflammatory response following exercise in hypoxia (e.g., Badenhorst et al., 2014; Govus et al., 2014; Sumi et al., 2017), to the current authors' knowledge only one previous study has measured an inflammatory biomarker (interleukin-6; IL-6) after the completion of a RSH protocol (Goods et al., 2016). Goods and colleagues (2016) had ten trained male team-sport athletes perform a repeat-sprint session in both simulated altitude (3000 m) and at sea level. This study reported increases in IL-6 concentrations in response to the sprint protocol in both conditions, but a large effect size (d = 0.80) indicated a trend for higher IL-6 concentrations one-hour post-exercise in the hypoxic environment. However, the authors noted that the IL-6 response elicited by the protocol was moderate, likely due to the use of cycling as the exercise modality (Nieman et al., 1998). Indeed, a reduced IL-6 response has been observed when comparing cycling exercise to running (Nieman et al., 1998), which is more specific to most team sports. Moreover, this previous study is limited by its sole use of IL-6 as a marker of inflammation; it is well understood that IL-6 has both pro-inflammatory and anti-inflammatory properties, with elevated post-exercise IL-6 concentrations playing a role in inhibiting pro-inflammatory (i.e., tumour necrosis factor-[alpha]; TNF-[alpha]) cytokines and facilitating anti-inflammatory cytokine (i.e., IL-1ra, IL-10) production (Petersen and Pedersen, 2005). Thus, the results obtained by Goods et al (2016) could be indicative of either an enhanced inflammatory status following RSH or a positive adaptive response to the training stimulus.
The present study aimed to assess the acute inflammatory response to one RSH session performed on a non-motorised treadmill when compared to the same exercise performed at sea level. Specifically, TNF[alpha], IL-1[beta], IL-1ra, IL-6, IL-8, and IL-10 were measured before and after the performance of a team-sport specific RSH session. It was hypothesised based on the (albeit limited) existing literature that the RSH session would illicit a greater inflammatory response when compared to the same session performed in normoxic conditions.
Eleven amateur team-sport athletes (seven Australian rules footballers, three soccer players and a touch football player) volunteered to participate in the present study and provided their written informed consent. The Griffith University Human Research Ethics Committee approved all procedures used in the study (AHS/72/14/HREC). All participants had competed for a minimum of two consecutive years in their respective sport immediately prior to participation in the study, trained for a mean ([+ or -] SD) of 152 [+ or -] 35 min x [week.sup.-1], and competed in their sport for a mean ([+ or -] SD) of 108 [+ or -] 17 min x [week.sup.-1]. Familiarisation commenced 3-4 weeks after each participant's last competitive match for the season (i.e., at the beginning of their off-season). The physical characteristics of the participants are presented in Table 1.
All participants performed a repeat-sprint running test (i.e., the [RSR.sub.444]; Morrison et al. (2015)) on two occasions. The [RSR.sub.444] consisted of sixteen (four sets of four) 4-s sprints separated by 26 s (and 2 min 26 s between sets) of passive recovery in a standing position, performed in a commercial normobaric hypoxic chamber (Synergy Physical Conditioning Systems, Yatala, Australia). During one trial participants breathed air with an inspired oxygen fraction (Fi[O.sub.2]) of 0.209, and in the other trial a Fi[O.sub.2] of 0.145 was used to simulate an altitude of 3000 m (i.e., hypoxia). This Fi[O.sub.2] at sea level creates a Pi[O.sub.2] of approximately 110 mmHg. The study followed a crossover design with five of the participants performing the [RSR.sub.444] in normoxia and then in hypoxia 7-10 d later at the same time of day, whereas the remaining participants (n = 6) performed the [RSR.sub.444] tests in the reverse order with the same number of days between trials. Participants were required to: 1) refrain from caffeine consumption on testing days; 2) refrain from alcohol consumption 24 h prior to testing; 3) refrain from performing any exercise of moderate intensity or greater for 72 h prior to testing, as well as refrain from performing any exercise between POST and 3h blood samples; 4) consume only food/beverages that they would ordinarily consume during the 24 h prior to testing; 5) keep a detailed food diary so that food/beverage consumed prior to trial 1 could be replicated for trial 2, and; 6) consume only water in the 4 h prior to testing. Water was consumed ad libitum between POST and 3h, and no food was consumed during this time. The hypoxic environment was created via the extraction of oxygen from air that was subsequently pumped into the chamber. Oxygen concentration was monitored using a gas detector (KB-501, Kingsby Electronics,) which utilises an electrochemical sensor. Relative humidity and temperature were maintained between 45-50% and 19-21[degrees]C, respectively. Tests were performed on a non-motorised treadmill (Curve 3.0, Woodway, Waukesha, Wisconsin, USA). While we acknowledge that a passive recovery does not replicate team-sport movement demands, the protocol was designed to allow the...