Post-acute exercise cardiovagal modulation in older male adults with and without type 2 diabetes.

PURPOSE: We examined heart rate variability (HRV) and baroreflex sensitivity (BRS) disease- and age-related response at 10-and 60-min after an acute high-intensity interval (HIIE) and moderate continuous exercise (MICE) in older adults with and without type 2 diabetes mellitus (T2DM) and healthy young adults. METHODS: Twelve older male adults with (57-84 years) and without T2DM (57-76 years) and 12 healthy young male adults (20-40 years) completed an isocaloric acute bout of HIIE, MICE, and a non-exercise condition in a randomized order. Time and Wavelets-derived frequency domain indices of HRV and BRS were obtained in a supine position and offline over 2-min time-bins using Matlab. RESULTS: HIIE but not MICE reduced natural logarithm root mean square of successive differences (Ln-RMSSD) (d = - 0.85; 95% CI - 1.15 to - 0.55 ms, p < 0.001), Ln-high-frequency power (d = - 1.60; 95% CI - 2.24 to - 0.97 ms2; p < 0.001), and BRS (d = - 6.32; 95% CI - 9.35 to - 3.29 ms/mmHg, p < 0.001) in adults without T2DM (averaged over young and older adults without T2DM), returning to baseline 60 min into recovery. These indices remained unchanged in older adults with T2DM after HIIE and MICE. Older adults with T2DM had lower resting Ln-RMSSD and BRS than aged-matched controls (Ln-RMSSD, d = - 0.71, 95% CI - 1.16 to - 0.262 ms, p = 0.001; BRS d = - 3.83 ms/mmHg), 95% CI - 6.90 to - 0.76, p = 0.01). CONCLUSIONS: Cardiovagal modulation following acute aerobic exercise is intensity-dependent only in adults without T2DM, and appears age-independent. These findings provide evidence of cardiac autonomic impairments in older adults with T2DM at rest and following aerobic exercise.

Intra and inter-rater repeatability of brachial artery ultrasound estimates of flow-mediated slowing and flow-mediated dilation.

Flow-mediated slowing (FMS) is a non-invasive measure of endothelial function measured through reactive hyperemia-induced changes in pulse wave velocity (PWV). FMS is suggested to mitigate known pitfalls of flow-mediated dilation (FMD) including suboptimal repeatability and high-operator dependency. However, the few single-rater studies that examined FMS repeatability have shown controversial results and used only regional measurements of PWV, which might not reflect local brachial artery stiffness responses to reactive hyperemia. We assessed the inter- and intra-rater repeatability of ultrasound-based changes in local PWV (FMS) and diameter (FMD). Twenty-four healthy male participants aged 23-75 yr, were examined on two separate days. Reactive hyperemia-induced changes in PWV were calculated using a tailored R-script. The inter- and intra-rater repeatability were tested with the intraclass correlation coefficient (ICC), coefficient of variation (CV), and the Bland-Altman plot estimates. The inter-rater repeatability of FMS (bias: -0.08%; ICC: 0.85; 95% CI: 0.65 to 0.93; CV: 11%) and FMD (bias: -0.02%; ICC: 0.98; 95% CI: 0.97 to 0.99; CV: 7%) showed overall good repeatability over different days. The intra-rater repeatability of FMD (1st rater: bias: 0.27%; ICC: 0.90; 95% CI: 0.78 to 0.96; CV: 14%; 2nd rater: bias: 0.60%; ICC: 0.85; 95% CI: 0.64 to 0.94; CV: 18%) was better than FMS (1st rater: bias: -1.03%; ICC: 0.76; 95% CI: 0.44 to 0.91; CV: 21%; 2nd rater: bias:-0.49%; ICC: 0.70; 95% CI: 0.34 to 0.80; CV: 23%) but not different between raters. Ultrasound-based local measurements of PWV deceleration reactive hyperemia were repeatable among the raters.

TNF-alpha, IL-1beta, IL-6, and cinc-1 levels in rat brain after meningitis induced by Streptococcus pneumoniae.

Bacterial meningitis caused by Streptococcus pneumoniae is associated with a significant mortality rate and persisting neurologic sequelae, including sensory-motor deficits, seizures, and impairment of learning and memory. The presence of proliferating bacteria within the subarachnoid and ventricular space compartments triggers an intense inflammatory host response at killing the invading microorganism. Proinflammatory mediators released in the process, including tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-1beta, and IL-6, were shown to contribute to the development of brain injury in bacterial meningitis. Thus, the aim of this study was to verify the levels of the TNF-alpha, IL-1beta, IL-6, and CINC-1 in the rat brain after pneumococcal meningitis. The animals underwent a magna cistern tap receiving either 10 microL of sterile saline as a placebo or an equivalent volume of a S. pneumoniae suspension at the concentration of 5x10(9) cfu/mL. The placebo group was killed immediately after the induction and the meningitis group at 0, 6, 12, 24, 48, and 96h after induction. The brains were removed followed by the isolation of the hippocampus and prefrontal cortex for determining TNF-alpha, IL-1beta, IL-6, and CINC-1 levels. In the hippocampus we found increased levels of the TNF-alpha only at 6h (p<0.01; F=3.777); CINC-1 levels increased at 6 and 24h (p<0.001; p<0.05; F=15.05); and IL-6 and IL-1beta levels were not altered. In the prefrontal cortex, the TNF-alpha levels were found to be increased only at 6h (p<0.05; F=4.921); IL-6 (p<0.05; F=11.69) and IL-1beta (p<0.001; F=132.0) levels were found to be increased only at 24h after meningitis induction; and CINC-1 levels were found to be increased at 6, 12, and 24h (p<0.01; p<0.01; p<0.01; F=16.86) after meningitis induction. Our data suggest that cytokine/chemokine levels can be putative biomarkers of brain damage in the first hours of the pneumococcal meningitis.