Objectives-Controversy exists over the effect of acute hyperglycemia on vascular function. In this systematic review, we compared the effect of acute hyperglycemia on endothelial and vascular smooth muscle functions across healthy and cardiometabolic diseased subjects. Approach and Results-A systematic search of MEDLINE, EMBASE, and Web of Science from inception until July 2014 identified articles evaluating endothelial or vascular smooth muscle function during acute hyperglycemia and normoglycemia. Meta-analyses compared the standardized mean difference (SMD) in endothelial and vascular smooth muscle functions between acute hyperglycemia and normoglycemia. Subgroup analyses and metaregression identified sources of heterogeneity. Thirty-nine articles (525 healthy and 540 cardiometabolic subjects) were analyzed. Endothelial function was decreased (39 studies; n=1065; SMD, −1.25; 95% confidence interval, −1.52 to −0.98; P<0.01), whereas vascular smooth muscle function was preserved (6 studies; n=144; SMD, −0.07; 95% confidence interval, −0.30 to 0.16; P=0.55) during acute hyperglycemia compared with normoglycemia. Significant heterogeneity was detected among endothelial function studies (P<0.01). A subgroup analysis revealed that endothelial function was decreased in the macrocirculation (30 studies; n=884; SMD, −1.40; 95% confidence interval, −1.68 to −1.12; P<0.01) but not in the microcirculation (9 studies; n=181; SMD, −0.63; 95% confidence interval, −1.36 to 0.11; P=0.09). Similar results were observed according to health status. Macrovascular endothelial function was inversely associated with age, blood pressure, and low-density lipoprotein cholesterol and was positively associated with the postocclusion interval of vascular assessment. Conclusions-To our knowledge, this is the first systematic review and meta-analysis of its kind. In healthy and diseased subjects, we found evidence for macrovascular but not microvascular endothelial dysfunction during acute hyperglycemia. Loader et al Acute Hyperglycemia Impairs Vascular Function 2061in vitro studies suggest that acute hyperglycemia may also impair VSM function by disrupting VSM cell apoptosis, causing subsequent VSM cell proliferation and desensitization to NO. [19][20][21] However, whether endothelial and VSM functions are transiently impaired during acute hyperglycemia in humans is unclear because of discrepant results. Given this, we conducted a systematic review and meta-analysis of available studies comparing endothelial function alone or in combination with VSM function during acute hyperglycemia in healthy and cardiometabolic diseased individuals. To our knowledge, this represents the first systematic review and meta-analysis to assess the effect of acute hyperglycemia on vascular function. Materials and MethodsMaterials and methods are available in the online-only Data Supplement. Results Study Selection and CharacteristicsA flowchart of study selection is shown in Figure 1. The systematic search resulted in the inclusion of 39 from 394 potential a...

URL: https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=366442&isReview=true. Australian New Zealand Clinical Trials Registry Number: ACTRN12614000614695.

This study shows that endothelial dysfunction occurs early in the pathophysiology of diabetes and is a link between cardiovascular risk factors and DPN.

Time-motion data was used to classify a selection of training drills. Ten midfielders (age=23.8±1.8yr; height=183.9±3.8cm; mass=83.2±5.0 kg) from an Australian Football League team participated in 17 training drills and four quarters of an official competitive match. Heart rate and time-motion data were collected using Global Positioning and Heart Rate Systems. Cluster analysis of mean distance travelled in the seven velocity zones identified three clusters: 1) game-specific conditioning; 2) skill refining/moderate intensity dominant; and 3) skill refining/low intensity dominant. Differences between the three clusters in distance travelled at the speed zones were confirmed using one-way ANOVA. Differences between clusters were also assessed for number of efforts in velocity zones and percentage time in heart rate zones. When compared to drills with a focus on skill refining or performed on a reduced playing area, drills utilising the entire playing field better replicated the movement characteristics of competitive game play.

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Background Considering the widespread risk of collider bias and confounding by indication in previous research, the associations between renin‐angiotensin aldosterone system (RAAS) inhibitor use and COVID‐19 remain unknown. Accordingly, this study tested the hypothesis that RAAS inhibitors influence the summation effect of COVID‐19 and its progression to severe outcomes. Methods and Results This nationwide cohort study compared all residents of Sweden, without prior cardiovascular disease, in monotherapy (as of January 1, 2020) with a RAAS inhibitor to those using a calcium channel blocker or a thiazide diuretic. Comparative cohorts were balanced using machine‐learning‐derived propensity score methods. Of 165 355 people in the analysis (51% women), 367 were hospitalized or died with COVID‐19 (246 using a RAAS inhibitor versus 121 using a calcium channel blocker or thiazide diuretic; Cox proportional hazard ratio [HR], 0.97; 95% CI, 0.74–1.27). When each outcome was assessed separately, 335 people were hospitalized with COVID‐19 (HR, 0.92; 95% CI, 0.70–1.22), and 64 died with COVID‐19 (HR, 1.22; 95% CI, 0.68–2.19). The severity of COVID‐19 outcomes did not differ between those using a RAAS inhibitor and those using a calcium channel blocker or thiazide diuretic (ordered logistic regression odds ratio, 1.01; 95% CI, 0.89–1.14). Conclusions Despite potential limitations, this study is among the best available evidence that RAAS inhibitor use in primary prevention does not increase the risk of severe COVID‐19 outcomes; presenting strong data from which scientists and policy makers alike can base, with greater confidence, their current position on the safety of using RAAS inhibitors during the COVID‐19 pandemic.

This study demonstrates that linagliptin tends to improve endothelial and neurovascular microvascular function and is associated with decreased markers of inflammation in patients with type 2 diabetes. There was no significant effect of linagliptin on mitochondrial function, macrovascular function, or endothelial progenitor cells.