Grees with previous studies that have shown that PYC AOX supplementation improves high intensity cycling and running performance [28,29]. This study was unique in that performance was monitored for each repetition and did not rely solely on the total volume for the session. Instead, concentric performance was measured by mean power output. The key finding from the performance data was that AOX supplementation was effective in attenuating the decrease in mean power which occurred in the placebo trial, meaning concentric power output was greater during the AOX trial (see Figure 1). During the placebo trial PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28212752 the mean power decrements per set ranged from 5 to 10 (specific data not shown). These observations are similar to the decrements observed by Baker and Newton [38], however their study employed a series of jump squats to elucidate a ROS response, and therefore comparisons between the two studies should be approached with caution.The present study also found the oxidative stress response as measured by the marker XO was significantly increased after the HTS following both the placebo and AOX trials. This is similar to other studies which also observed an elevated XO response following BAY 11-7083MedChemExpress BAY 11-7083 strenuous exercise [13,39]. The significant rise in XO would suggest that the HTS in the present study invoked a substantial ROS response, which can lead to skeletal muscle injury and fatigue [1,39,40]. Indeed, reduced XO activity during RT has been linked to less oxidative damage and enhanced recovery from RT sessions [13]. It was therefore hypothesised that the AOX treatment would blunt the oxidative stress response, preserving skeletal muscle integrity and force production when performing strenuous RT such as BS exercise. Yet, there was no significant difference in XO levels between the placebo and AOX trials, although a slight trend towards a reduction in XO following the AOX trials was observed (p = 0.069). There was also no difference in blood lactate concentration between the two conditions suggesting that differences in anaerobic fatigue were not the cause for the disparity in performance. This data suggests other mechanisms of muscular fatigue may have been involved in the performance changes observed. One possible mechanism is a decrease in Na+/K + ATPase pump activity [41]. A previous study found AOX supplementation in the form of N-acetylcysteine is effective in preserving Na+/K + ATPase activity during strenuous exercise, acting as a reduced thiol donor and promoting the regeneration of the endogenous AOX glutathione (GSH) [1,42]. Similarly, PYC supplementation has been shown to enhance GSH activity and decrease the levels of GSSG [43]. It is therefore possible that in the present study, the PYC based AOX supplement supported GSH levels which then lead to decreased thiol oxidation thus maintaining Na+/K + ATPase activity and attenuating muscular fatigue. Another possibility for the attenuation of muscular fatigue during the AOX trial may be a result of nitric oxide (NO) stimulated increased blood flow during exercise [44]. It has been repeatedly shown that PYC can enhance blood flow [23,25] and decrease platelet aggregation [45] which can decrease peripheral blood flow to contracting muscles during high intensity exercise [45]. At present it can only be speculated that these mechanisms were involved as GSH or muscular blood flow were not measured in this study. Further research with additional measures of oxidative stress is required to help.
