Similar to IL-1β, TNF-α was undetected in 15 of the 21 participants and therefore due to the small data set available, no statistical analysis was performed on TNF-α data (data not shown).
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Figure 6.1: Comparison between groups for changes in myoglobin pre-match and throughout the 48 h recovery period. * Significantly greater than pre-match (P < 0.001). # Significant difference between PAS and CWI (P < 0.05). White bar = passive recovery, hatch bar = cold water immersion, lack bar = Contrast water immersion.
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Figure 6.2: Comparison between groups for changes in interleukin-6 pre-match and throughout the 48 h recovery period. * Significantly lower than post-match (P < 0.01). White bar = Passive recovery, Hatch bar = Cold water immersion, Black bar = Contrast water immersion.
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Figure 6.3: Comparison between groups for changes in interleukin-10 pre-match and throughout the 48 h recovery period. * Significantly greater than pre-match (P < 0.001). White bar = Passive recovery, Hatch bar = Cold water immersion, Black bar = Contrast water immersion.
6.4 Discussion
This is the first study to examine the effects of both CWI and CWT on muscle damage markers as well as on both pro- and anti-inflammatory cytokine concentrations after an AF match. Each of Mb, IL-10 and IL-6 increased substantially after an AF match and that the inflammatory process was unaffected by the type of recovery players undertook post-match. Players covered an average of 107 m.min-1 during the 75 min match which is similar to the lower range of distances covered in Australian Football League competition matches (Aughey, 2011b). This distance indicates that the practice match was at a sufficient intensity to replicate the demands of a typical in-season match.
Intense and damaging exercise results in an acute phase inflammatory response and it is clear than an AF match induces this response. Both [IL-6] and [IL-10] increased substantially in response to the match, and it was clear that compared to PAS, the magnitude and time course
of the inflammatory response was not moderated by the use of either CWI or CWT. This lack of difference signifies that in well trained AF players, the application of cold temperatures via CWI and CWT did not disturb the normal inflammatory response. Interleukin-6 is an important moderator of satellite cell proliferation (Serrano et al., 2008) and as undertaking CWI and CWT led to no reduction in IL-6 compared to PAS, there was likely no blunting of the pathways leading to muscle repair and regeneration and no disturbance to the adaptive response resulting from the normal inflammatory response. This is a significant finding and indicates that both CWI and CWT should not be discounted as post-exercise recovery modalities. When used acutely, they do not have a negative impact on the normal inflammatory response and offer substantial benefits in reducing post-match soreness and fatigue improving physical performance (see chapter 5). Similar responses occur following repeated basketball matches where no differences in IL-6 and IL-10 were observed between a control or CWI group (Montgomery et al., 2008a) and also following a muscle damaging exercise protocol where CWI or CWT failed to elicit changes in IL-6 compared to a PAS recovery (Vaile et al., 2008c). Although likely similar to the acute use investigated here, the effects of prolonged use of either CWI or CWT are as yet unknown and requires further investigation.
Post-match changes in [IL-1β] and/or [TNF-α] were not detected in most players during this investigation. These results are not uncommon following prolonged and strenuous exercise, with low or no in [IL-1β] and/or [TNF-α] values being reported following 1, 2.5 and 6 h of running and following 2 h of strenuous cycling (Drenth et al., 1995, Ostrowski et al., 1998, Scott et al., 2011, Ullum et al., 1994). Additionally, the lack of detectable changes observed may have resulted from a lack of sensitivity in the kits used which has been confirmed by the manufacturer. Increases in pro-inflammatory cytokines are balanced by the release of the anti- inflammatory cytokine IL-10 (Jenkins et al., 1994). This in turn can up-regulate the release of the cytokine inhibitor IL-1ra and cause down regulation of IL-1β and TNF-α (Drenth et al., 1995, Jenkins et al., 1994) and may explain why both cytokines in this study were undetectable across all time points.
Increased serum/plasma [Mb] indicates damage to a muscle (Clarkson and Hubal, 2002, Clarkson and Sayers, 1999). During this investigation, substantial increases in [Mb] of between 328-333 µg.L-1 were observed all 3 groups immediately following the match, similar in magnitude to that detected after several soccer matches (Ascensao et al., 2008, Magalhaes et al., 2010). The similarity of these results may be due to the activity profile where the AF players in this investigation covered 107 m.min-1 compared to that of soccer matches where players can cover between 110 and 118 m.min-1 (Bradley et al., 2009, Burgess et al., 2006). The post-match use of both CWI and CWT both successfully reduced [Mb], similar to responses seen following after a soccer match and 90 min of shuttle running (Ascensao et al., 2011, Bailey et al., 2007). Furthermore, CWI substantially reduced [Mb] 1 h post-match compared to PAS similar to results following 90 min of team sport shuttle running (Bailey et al., 2007). The observed reductions in [Mb] for both CWI and CWT corresponded with improvements in post-match sprint performance (see chapter 5) where CWI was more successful at restoring repeat 20 m sprint and squat jump than CWT with both methods being more successful than PAS. It therefore appears that a reduction in muscle damage as measured by [Mb] corresponds with an improvement in sprint performance.
The mechanism(s) responsible for the attenuation of myoglobin by cold temperatures are unclear. Previously, cold application has been proposed to reduce the amount of post-exercise muscle damage and/or reduce the efflux of muscle proteins into the lymphatic system (Eston and Peters, 1999). Cold application is associated with a reduced permeability of cellular, lymphatic and capillary vessels and when combined with the physiological effects of hydrostatic pressure (Wilcock et al., 2006a), it is possible that CWI caused a reduction in protein efflux and may explain why CWI and CWT were more successful than PAS at attenuating [Mb] increases. Unsurprisingly, the application of heat can have an opposing effect by increasing blood flow and vasodilatation (Wilcock et al., 2006a). This can increase the efflux of proteins, and in turn increase the level of circulating Mb and may help explain the differences between the CWT and CWI groups in this investigation. Although the mechanisms leading to reduced [Mb] are not evident, it is clear that in well trained AF
players, reductions in [Mb] are positively related to physical performance (see chapter 5) which can only be of benefit for players in their preparation for their next training session or match.
6.5 Conclusion
It is clear that participating in a game of AF induces muscle damage and an acute phase inflammatory response. This investigation established that in well trained team sport athletes, neither CWT nor CWI interfered with the regular post-exercise inflammatory response leading to muscle regeneration. This should allay any concerns that acute cold application will blunt the regenerative pathways associated with post-exercise inflammation. Throughout this investigation, CWI emerged as a more effective modality in attenuating post-match increases in myoglobin and when combined with the positive effects that CWI had on restoring physical performance (see chapter 5) it is recommended that 14 min of CWI be utilised as an acute recovery tool post-match in team sport athletes.