The purpose of this study was to determine potential adverse cardiac effects of chronic endurance training by comparing sympathovagal modulation via heart rate variability (HRV) and heart rate recovery (HRR) in middle-aged endurance athletes (EA) and physically-active individuals (PA) following maximal exercise. 36 (53±5 years) EA and 19 (56±5 years) PA were recruited to complete a two-week exercise diary and graded exercise to exhaustion. Time domain and power spectral HRV analyses were completed on recorded R-R intervals. EA had a greater HRR slope following exercise (95%CI, 0.0134-0.0138 vs. 0.0101-0.0104 beats/second;p less then 0.001). While EA had greater HRR 1-5 minutes post-exercise (all p less then 0.01), PA and EA did not differ when expressed as a percentage of baseline HR (130±19 vs. 139±19; p=0.2). Root mean square of successive differences in R-R intervals (rest and immediately post-exercise) were elevated in EA (p less then 0.05). Low frequency (LF) and high frequency (HF) spectral components were non-significantly elevated post-exercise (p=0.045-0.147) in EA while LF/HF was not different (p=0.529-0.986). This data suggests greater HRR in EA may arise in part due to a lower resting HR. While non-significant elevations in HF and LF in EA produces a LF/HF similar to PA, absolute spectral component modulation differed. These observations require further exploration. Novelty Bullets • Acute effects of exercise on HRV in EA compared to a relevant control group, PA, are unknown. • EA had greater HRR, and non-significant elevations in LF and HF compared to PA, yet LF/HF was not different. • Future work should explore the implications of this observation.Introduction Optical Coherence Tomography (OCT) is an intravascular imaging providing high-resolution images of morphological features of arterial wall. Nowadays, OCT is an accepted intravascular modality to study coronary arteries, stent implantation, and vessel injury. In the last decade, an increasing interest have been focused on the application of OCT in carotid arteries.Areas covered Literature evidence in the application of OCT in carotid arteries still remains debated. So far, OCT has been used as a research tool, aiming to evaluate atherosclerotic plaques’ features and stents’ behavior after implantation. This paper is intended to summarize clinical evidences and practices in the use of OCT in carotid arteries district and during CAS procedures. Literature review was completed via Pubmed search using Keywords.Expert opinion CAS is a safe and effective procedure when performed by trained physicians with a tailored approach. In this scenario, ambiguous pictures at ultrasound, angiography, and IVUS might be clarified using OCT.By providing unprecedented microstructural information on atherosclerotic plaques, OCT may identify the features of vulnerable carotid plaque and, by identifying possible defects after stent implantation as malapposition and plaque prolapse, it may help the tailoring approach to CAS.BACKGROUND Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is used as rescue for severe cardiopulmonary failure. We tested whether the ratio of CO2 elimination at the lung and the ECMO (VCO2ECMO/VCO2Lung) would reflect the ratio of respective blood flows and could be used to estimate changes in pulmonary blood flow (QLUNG), i. e. native cardiac output. METHODS Four healthy pigs were centrally cannulated for VA-ECMO. We measured blood flows with an ultrasonic flow probes. VCO2ECMO and VCO2Lung were calculated from sidestream capnographs under constant pulmonary ventilation during ECMO weaning with changing sweep gas and/or ECMO blood flow. If ventilation/perfusion (V/Q) ratio of ECMO was not one, the VCO2ECMO was normalized to V/Q=1 (VCO2ECMONORM). Changes in pulmonary blood flow were calculated using the relationship between changes in CO2 elimination and ECMO blood flow. RESULTS QECMO correlated strongly with VCO2ECMONORM (r2 0.95 – 0.99). QLUNG correlated well with VCO2LUNG (r2 0.65 – 0.89, p less then =0.002). Absolute QLung could not be calculated in a non-steady state. Selleck Iadademstat Calculated pulmonary blood flow changes had a bias of 76 (-266 to 418) ml/min and correlated with measured QLUNG (r2 0.974 – 1.000, p = 0.1 to 0.006) for cumulative ECMO flow reductions. CONCLUSIONS VCO2 of the lung correlated strongly with pulmonary blood flow. Our model could predict pulmonary blood flow changes within clinically acceptable margins of error. The prediction is made possible with a normalization to a V/Q of 1 for ECMO. This approach depends on measurements readily available and may allow immediate assessment of the cardiac output response.Type 2 diabetes mellitus is a major health problem and a societal burden. Individuals with pre-diabetes are at increased risk of type 2 diabetes mellitus. Catalpol, an iridoid glycoside, has been reported to exert a hypoglycaemic effect in db/db mice, but its effect on the progression of pre-diabetes is unclear. In this study, we established a mouse model of pre-diabetes and examined the hypoglycaemic effect, and the mechanism of any such effect, of catalpol. Catalpol (200 mg/kg/day) had no effect on glucose tolerance or the serum lipid level in a mouse model of impaired glucose tolerance (IGT)-stage pre-diabetes. However, catalpol (200 mg/kg/day) increased insulin sensitivity and decreased the fasting glucose level in a mouse model of impaired fasting glucose/impaired glucose tolerance-stage pre-diabetes. Moreover, catalpol increased the mitochondrial membrane potential (1.52-fold) and ATP content (1.87-fold) in skeletal muscle and improved skeletal muscle function. These effects were mediated by activation of the IRS-1/GLUT4 signalling pathway in skeletal muscle. Our findings will facilitate the development of a novel approach to suppressing the progression of diabetes at an early stage. Novelty bullets • Catalpol prevents the progression of pre-diabetes in a mouse model of pre-diabetes. • Catalpol improves insulin sensitivity in skeletal muscle. • The effects of catalpol are mediated by activation of the IRS-1/GLUT4 signalling pathway.