We propose a Theory of Challenge and Threat States in Athletes (TCTSA) which is an amalgamation and extension of the biopsychosocial model of challenge and threat, the model of adaptive approaches to competition and the debilitative and facilitative competitive state anxiety model. In the TCTSA we posit that selfefficacy, perceptions of control, and achievement goals determine challenge or threat states in response to competition. Distinct patterns of neuroendocrine and cardiovascular responses are indicative of a challenge or threat state. Increases in epinephrine and cardiac activity, and a decrease in total peripheral vascular resistance (TPR) characterise a challenge state and increases in cortisol, smaller increases in cardiac activity and either no change or an increase in TPR characterise a threat state. Positive and negative emotions can occur in a challenge state while a threat state is associated with negative emotions only. Emotions are perceived as helpful to performance in a challenge state but not in a threat state. Challenge and threat states influence effort, attention, decision-making and physical functioning and accordingly sport performance. The TCTSA provides a framework for practitioners to enhance performance, through developing a challenge state, and encourages researchers to explore the mechanisms underlying performance in competition.Keywords: Challenge; threat; appraisal; emotion; cardiovascular. In proposing the TCTSA we draw on the biopsychosocial (BPS) model of challenge and threat (Blascovich & Mendes, 2000;Blascovich & Tomaka, 1996), the model of adaptive approaches to competition (Skinner & Brewer, 2004) and other related contemporary approaches to understanding athletes' perceptions and experiences of an upcoming competition (e.g., achievement goal theory, interpretation of anxiety symptoms). Although the TCTSA concerns athletes' preparedness for competition, because it explains how athletes respond to an upcoming competition, we also consider how the cognitions, emotions and physiological responses associated with challenge and threat states may influence sport performance. That is, we posit athletes' psychophysiological states before competition will predict, at least partly, performance levels in competition. 4We propose that the TCTSA outlines more fully than existing approaches why athletes may perceive an upcoming competition as either a challenge or threat, how they respond emotionally and physiologically when they do, and how challenge and threat states can influence performance. While the TCTSA draws on existing models, a number of aspects unique to the TCTSA contribute to the literature.Specifically, the TCTSA outlines: how a unique combination of psychological constructs interact to determine challenge and threat states; that high intensity negative emotions can be experienced in a challenge state; how challenge and threat states influence performance through effort, attention, decision-making and physical functioning.Challenge and threat are motivational state...
BackgroundAcute kidney injury (AKI) remains a deadly condition. Tissue inhibitor of metalloproteinases (TIMP)-2 and insulin-like growth factor binding protein (IGFBP)7 are two recently discovered urinary biomarkers for AKI. We now report on the development, and diagnostic accuracy of two clinical cutoffs for a test using these markers.MethodsWe derived cutoffs based on sensitivity and specificity for prediction of Kidney Disease: Improving Global Outcomes Stages 2–3 AKI within 12 h using data from a previously published multicenter cohort (Sapphire). Next, we verified these cutoffs in a new study (Opal) enrolling 154 critically ill adults from six sites in the USA.ResultsOne hundred subjects (14%) in Sapphire and 27 (18%) in Opal met the primary end point. The results of the Opal study replicated those of Sapphire. Relative risk (95% CI) in both studies for subjects testing at ≤0.3 versus >0.3–2 were 4.7 (1.5–16) and 4.4 (2.5–8.7), or 12 (4.2–40) and 18 (10–37) for ≤0.3 versus >2. For the 0.3 cutoff, sensitivity was 89% in both studies, and specificity 50 and 53%. For 2.0, sensitivity was 42 and 44%, and specificity 95 and 90%.ConclusionsUrinary [TIMP-2]•[IGFBP7] values of 0.3 or greater identify patients at high risk and those >2 at highest risk for AKI and provide new information to support clinical decision-making.Clinical Trials RegistrationClintrials.gov # NCT01209169 (Sapphire) and NCT01846884 (Opal).
BackgroundHydrogen sulfide (H2S) therapy is recognized as a modulator of vascular function during tissue ischemia with the notion of potential interactions of nitric oxide (NO) metabolism. However, little is known about specific biochemical mechanisms or the importance of H2S activation of NO metabolism during ischemic tissue vascular remodeling. The goal of this study was to determine the effect of H2S on NO metabolism during chronic tissue ischemia and subsequent effects on ischemic vascular remodeling responses.Methods and ResultsThe unilateral, permanent femoral artery ligation model of hind‐limb ischemia was performed in C57BL/6J wild‐type and endothelial NO synthase–knockout mice to evaluate exogenous H2S effects on NO bioavailability and ischemic revascularization. We found that H2S selectively restored chronic ischemic tissue function and viability by enhancing NO production involving both endothelial NO synthase and nitrite reduction mechanisms. Importantly, H2S increased ischemic tissue xanthine oxidase activity, hind‐limb blood flow, and angiogenesis, which were blunted by the xanthine oxidase inhibitor febuxostat. H2S treatment increased ischemic tissue and endothelial cell hypoxia‐inducible factor‐1α expression and activity and vascular endothelial growth factor protein expression and function in a NO‐dependent manner that was required for ischemic vascular remodeling.ConclusionsThese data demonstrate that H2S differentially regulates NO metabolism during chronic tissue ischemia, highlighting novel biochemical pathways to increase NO bioavailability for ischemic vascular remodeling.
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