Purpose:To establish the reliability of various measures obtained during single and repeated countermovement jump (CMJ) performance in an elite athlete population.Methods:Two studies, each involving 15 elite Australian Rules Football (ARF) players were conducted where subjects performed two days, separated by one week, of AM and PM trials of either a single (CMJ1) or 5 repeated CMJ (CMJ5). Each trial was conducted on a portable force-plate. The intraday, interday, and overall typical error (TE) and coefficient of variation (CV%) were calculated for numerous variables in each jump type.Results:A number of CMJ1 and CMJ5 variables displayed high intraday, interday, and overall reliability. In the CMJ1 condition, mean force (CV 1.08%) was the most reliable variable. In the CMJ5, fight time and relative mean force displayed the highest repeatability with CV of 1.88% and 1.57% respectively. CMJ1Mean force was the only variable with an overall TE < smallest worthwhile change (SWC).Conclusion:Selected variables obtained during CMJ1 and CMJ5 performance can be used to assess the impact of both acute and chronic training and competition. Variables derived from the CMJ5 may respond differently than their CMJ1 counterparts and should provide insights into differential mechanisms of response and adaptation.

The purpose of this study was to evaluate the reliability and validity of a new test of agility, the reactive agility test (RAT), which included anticipation and decision-making components in response to the movements of a tester. Thirty-eight Australian football players took part in the study, categorized into either a higher performance group (HPG) (n=24) or lower performance group (LPG) (n=14) based on playing level from the previous season. All participants undertook testing of a 10m straight sprint (10mSS), a 8-9m change of direction speed test (CODST), and the RAT. Test-retest and inter-tester reliability testing measures were conducted with the LPG. The intra-class correlation (ICC) of the RAT was 0.870, with no significant (p<0.05) difference between the test results obtained on the first and second test sessions using a t-test. A dependent samples t-test revealed no significant (p<0.05) difference between the test results of two different testers with the same population. The HPG were significantly (p=0.001) superior to those of the LPG on the RAT, with no differences observed on any other variable. The RAT is an acceptably reliable test when considering both test-retest reliability, as well as inter-rater reliability. In addition, the test was valid in distinguishing between players of differing performance level in Australian football, while the 10mSS and CODST were not. This result suggests that traditional closed skill sprint and sprint with direction change tests may not adequately distinguish between players of different levels of competition in Australian football.

Peroxynitrite (PN, ONOO−) and its reactive oxygen precursor superoxide (SO, O2·−), are critically important in the development of pain of several etiologies including in the development of pain associated with chronic use of opiates such as morphine (also known as opiate-induced hyperalgesia and antinociceptive tolerance). This is now an emerging field in which considerable progress has been made in terms of understanding the relative contribution of SO, PN, and nitroxidative stress in pain signaling at the molecular and biochemical levels. Aggressive research in this area is poised to provide the pharmacological basis for development of novel non-narcotic analgesics that are based upon the unique ability to selectively eliminate SO and/or PN. As we have a better understanding of the role of SO and PN in pathophysiological settings, targeting PN may be a better therapeutic strategy than targeting SO. This is due to the fact that unlike PN, which has no currently known beneficial role, SO may play a significant role in learning and memory [1]. Thus, the best approach may be to spare SO while directly targeting its downstream product, PN. Over the last 15 years, our team has spearheaded research concerning the roles of SO/PN in pain and these results are currently leading to the development of solid therapeutic strategies in this important area.

Chemotherapy-induced peripheral neuropathy (CIPN) accompanied by chronic neuropathic pain is a major dose-limiting side effect of a large number of antitumoral agents including paclitaxel (Taxol). We also demonstrate the prevention of CIPN with our two new orally active PNDCs, SRI6 and SRI110. The improved chemical design of SRI6 and SRI110 also affords selectivity for PN over other reactive oxygen species (such as superoxide). Our findings identify PN as a critical determinant of CIPN, while providing the rationale toward development of superoxide-sparing and "PN-targeted" therapeutics.

Chronic pain is a global burden that promotes disability and unnecessary suffering. To date, efficacious treatment of chronic pain has not been achieved. Thus, new therapeutic targets are needed. Here, we demonstrate that increasing endogenous adenosine levels through selective adenosine kinase inhibition produces powerful analgesic effects in rodent models of experimental neuropathic pain through the A3 adenosine receptor (A3AR, now known as ADORA3) signalling pathway. Similar results were obtained by the administration of a novel and highly selective A3AR agonist. These effects were prevented by blockade of spinal and supraspinal A3AR, lost in A3AR knock-out mice, and independent of opioid and endocannabinoid mechanisms. A3AR activation also relieved non-evoked spontaneous pain behaviours without promoting analgesic tolerance or inherent reward. Further examination revealed that A3AR activation reduced spinal cord pain processing by decreasing the excitability of spinal wide dynamic range neurons and producing supraspinal inhibition of spinal nociception through activation of serotonergic and noradrenergic bulbospinal circuits. Critically, engaging the A3AR mechanism did not alter nociceptive thresholds in non-neuropathy animals and therefore produced selective alleviation of persistent neuropathic pain states. These studies reveal A3AR activation by adenosine as an endogenous anti-nociceptive pathway and support the development of A3AR agonists as novel therapeutics to treat chronic pain.