Speed and power predictors of change of direction ability in elite snow athletes

Change of direction ability (COD speed) is an important physical component of snow sports. The aim of this study was to investigate the relationships between regular speed and vertical jumping ability, and COD speed in elite snow athletes. Moreover, the correlations between relative mean propulsive power (assessed in the jump squat exercise) and COD speed were quantified. Sixteen elite snow sport athletes executed squat jumps, countermovement jumps, jump squats, and 25 m sprint tests, in addition to a Zig-zag change of direction speed test. The outcomes revealed that vertical jumping height and mean propulsive power are strongly correlated (r ≈ 0.90) with COD speed. Furthermore, snow athletes capable of sprinting faster in a linear course of 25 m performed better in COD speed tests ( r = 0.91). Our results support the use of loaded and unloaded vertical jumping and regular speed tests to evaluate/monitor predictors of COD speed in elite snow athletes. Finally, these relationships suggest that plyometrics and regular speed training should be considered by coaches as effective strategies to enhance COD ability in this specific group of subjects

Impact of COVID-19 on cardiovascular testing in the United States versus the rest of the world

Objectives: This study sought to quantify and compare the decline in volumes of cardiovascular procedures between the United States and non-US institutions during the early phase of the coronavirus disease-2019 (COVID-19) pandemic. Background: The COVID-19 pandemic has disrupted the care of many non-COVID-19 illnesses. Reductions in diagnostic cardiovascular testing around the world have led to concerns over the implications of reduced testing for cardiovascular disease (CVD) morbidity and mortality. Methods: Data were submitted to the INCAPS-COVID (International Atomic Energy Agency Non-Invasive Cardiology Protocols Study of COVID-19), a multinational registry comprising 909 institutions in 108 countries (including 155 facilities in 40 U.S. states), assessing the impact of the COVID-19 pandemic on volumes of diagnostic cardiovascular procedures. Data were obtained for April 2020 and compared with volumes of baseline procedures from March 2019. We compared laboratory characteristics, practices, and procedure volumes between U.S. and non-U.S. facilities and between U.S. geographic regions and identified factors associated with volume reduction in the United States. Results: Reductions in the volumes of procedures in the United States were similar to those in non-U.S. facilities (68% vs. 63%, respectively; p = 0.237), although U.S. facilities reported greater reductions in invasive coronary angiography (69% vs. 53%, respectively; p < 0.001). Significantly more U.S. facilities reported increased use of telehealth and patient screening measures than non-U.S. facilities, such as temperature checks, symptom screenings, and COVID-19 testing. Reductions in volumes of procedures differed between U.S. regions, with larger declines observed in the Northeast (76%) and Midwest (74%) than in the South (62%) and West (44%). Prevalence of COVID-19, staff redeployments, outpatient centers, and urban centers were associated with greater reductions in volume in U.S. facilities in a multivariable analysis. Conclusions: We observed marked reductions in U.S. cardiovascular testing in the early phase of the pandemic and significant variability between U.S. regions. The association between reductions of volumes and COVID-19 prevalence in the United States highlighted the need for proactive efforts to maintain access to cardiovascular testing in areas most affected by outbreaks of COVID-19 infection

26th Annual Computational Neuroscience Meeting (CNS*2017): Part 3 - Meeting Abstracts - Antwerp, Belgium. 15–20 July 2017

This work was produced as part of the activities of FAPESP Research,\ud Disseminations and Innovation Center for Neuromathematics (grant\ud 2013/07699-0, S. Paulo Research Foundation). NLK is supported by a\ud FAPESP postdoctoral fellowship (grant 2016/03855-5). ACR is partially\ud supported by a CNPq fellowship (grant 306251/2014-0)

Oxidative stress is associated with arterial dysfunction and enhanced intima-media thickness in children with hypercholesterolemia: The potential role of nicotinamide-adenine dinucleotide phosphate oxidase

BACKGROUND. Endothelial dysfunction and intima-media thickness are precocious manifestations of hypercholesterolemia, but the mechanism is unclear. OBJECTIVE. The aim of the study was to analyze the interplay among endothelial dysfunction, intima-media thickness, and oxidative stress in children with hypercholesterolemia. METHODS. We performed a cross-sectional study comparing flow-mediated dilation, intima-media thickness, lipid profile, urinary isoprostanes as markers of oxidative stress, and platelet expression of gp91(phox), the catalytic unit of nicotinamide-adenine dinucleotide phosphate oxidase, in a population of 50 children with hypercholesterolemia (mean age +/- SD: 10.0 +/- 3.7 years) and 50 children without hypercholesterolemia (mean age: 9.2 +/- 3.5 years). Four children with hereditary deficiency of gp91(phox) were studied also. RESULTS. Children with hypercholesterolemia had reduced flow-mediated dilation (mean +/- SD: 6.2 +/- 2.4 vs 9.2 +/- 2.5%) and enhanced intima-media thickness (0.45 +/- 0.07 vs 0.40 +/- 0.06 mm), urinary isoprostanes (86.9 +/- 51.6 vs 45.9 +/- 25.6 pg/mg creatinine), and gp91(phox) platelet expression (4.4 +/- 3.8 vs 2.0 +/- 1.7 mean fluorescence) compared with control subjects. At bivariate analysis, flow-mediated dilation was correlated with low-density lipoprotein cholesterol, intima-media thickness, urinary isoprostanes, and platelet gp(91phox). Stepwise multiple linear regression analysis showed that, in children with hypercholesterolemia, flow-mediated dilation and intima-media thickness were significantly associated with low-density lipoprotein cholesterol and urinary isoprostanes; also, gp91(phox) platelet expression was an independent predictor of urinary isoprostanes. Children with gp91(phox) hereditary deficiency showed downregulation of platelet gp91(phox) and reduced urinary excretion of isoprostanes. CONCLUSIONS. The study suggests that gp91(phox)-mediated oxidative stress may have a pathogenic role in the anatomic and functional changes of the arterial wall occurring in children with premature atherosclerosis

LDL oxidation by platelets propagates platelet activation via an oxidative stress-mediated mechanism

OBJECTIVES: Platelets generate oxidized LDL (ox-LDL) via NOX2-derived oxidative stress. We investigated if once generated by activated platelets ox-LDL can propagate platelet activation. METHODS: Experiments were performed in platelets from healthy subjects (HS), hyper-cholesterolemic patients and patients with NOX2 hereditary deficiency. RESULTS: Agonist-stimulated platelets from HS added with LDL were associated with a dose-dependent increase of reactive oxidant species and ox-LDL. Agonist-stimulated platelets from HS added with a fixed dose of LDL (57.14 μmol/L) or added with homogenized human atherosclerotic plaque showed enhanced ox-LDL formation (approximately +50% and +30% respectively), which was lowered by a NOX2 inhibitor (approximately -35% and -25% respectively). Compared to HS, ox-LDL production was more pronounced in agonist-stimulated platelet rich plasma (PRP) from hyper-cholesterolemic patients but was almost absent in PRP from NOX2-deficient patients. Platelet aggregation and 8-iso-PGF2α-ΙΙΙ formation increased in LDL-treated washed platelets (+42% and +53% respectively) and PRP (+31% and +53% respectively). Also, LDL enhanced platelet-dependent thrombosis at arterial shear rate (+33%) but did not affect platelet activation in NOX2-deficient patients. Platelet activation by LDL was significantly inhibited by CD36 or LOX1 blocking peptides, two ox-LDL receptor antagonists, or by a NOX2 inhibitor. LDL-added platelets showed increased p38MAPK (+59%) and PKC (+51%) phosphorylation, p47phox translocation to platelet membrane (+34%) and NOX2 activation (+30%), which were inhibited by ox-LDL receptor antagonists. CONCLUSION: Platelets oxidize LDL, which in turn amplify platelet activation via specific ox-LDL receptors; both effects are mediated by NOX2 activation

Different degrees of NADPH oxidase 2 regulation and in vivo platelet activation: lesson from chronic granulomatous disease.

Background: In vitro study showed that NADPH oxidase (NOx), the most important enzyme producing reactive oxygen species (ROS), plays a role in the process of platelet activation. However, it is unclear if changes in its activity affect platelet activation in vivo. Methods and Results: In vivo and ex vivo experiments assessing platelet activation were investigated in healthy subjects, obese patients, and subjects with different low rates of NOx2 activity, namely X-linked chronic granulomatous disease (X-CGD) patients and X-CGD carriers. We included 27 X-CGD patients, 31 women carriers of hereditary deficiency of NOx2, 31 obese women, and 62 healthy subjects matched for sex and age. Plasma levels of soluble sCD40 L (sCD40L) and soluble P (sP)-selectin, 2 markers of in vivo platelet activation, were reduced in X-CGD patients (sCD40L=-55%; sP-selectin=-51%, P < 0.001) and in X-CGD carriers (sCD40L=-41%; sP-selectin=-57%, P < 0.001) compared with respective controls. Conversely, obese women, who disclosed NOx2 upregulation, had significantly higher plasma levels of sCD40L (+47%, P < 0.001) and sP-selectin (+70%, P < 0.001) compared with controls. Ex vivo study showed platelet isoprostane downexpression and enhanced platelet NO generation in both X-CGD patients and X-CGD carriers compared with controls; opposite findings were observed in obese patients. Correlation analysis showed that platelet NOx2 regulation was directly associated with plasma levels of sCD40L (R=0.336, P < 0.001) and sP-selectin (R=0.441; P < 0.001). Conclusions: The study provides the first evidence that in vivo platelet activation is significantly and directly associated with NOx2 activity. Platelet NOx2 may be a novel target for platelet activation inhibition