Following prolonged sitting, G-PWV increased by 0.29 m/s (i.e., PRE vs. POST). However, the condition (P = 0.987) and time × condition (P = 0.954) effects were nonsignificant. The current findings support previous research showing an increase in arterial stiffness with prolonged sitting. However, in young and healthy adults, the arterial stiffness response was not worsened through HGI meal consumption.NEW & NOTEWORTHY We used novel statistical techniques and study design characteristics to examine how the cardiovascular disruptions due to prolonged sitting are changed after the consumption of low- and high-glycemic-index meals. Metabolism inhibitor The current study indicates that changes in arterial stiffness due to prolonged sitting are not worsened in young, healthy adults after the consumption of a high-glycemic-index meal.Right ventricular (RV) functional adaptation to afterload determines outcome in pulmonary hypertension (PH). RV afterload is determined by the dynamic interaction between pulmonary vascular resistance (PVR), characteristic impedance (Zc), and wave reflection. Pulmonary vascular impedance (PVZ) represents the most comprehensive measure of RV afterload; however, there is an unmet need for an easier bedside measurement of this complex variable. Although a recent study showed that Zc and wave reflection can be estimated from RV pressure waveform analysis and cardiac output, this has not been validated. Estimations of Zc and wave reflection coefficient (λ) were validated relative to conventional spectral analysis in an animal model. Zc, λ, and the single-beat ratio of end-systolic to arterial elastance (Ees/Ea) to estimate RV-pulmonary arterial (PA) coupling were determined from right heart catheterization (RHC) data. The study included 30 pulmonary artery hypertension (PAH) and 40 heart failure with preserved eje vascular impedance (PVZ) represents the most comprehensive measure of right ventricle (RV) afterload; however, measurement of this variable is complex. We demonstrate that characteristic impedance (Zc) and a wave reflection coefficient, λ, can be derived from RV pressure waveform analysis. In addition, RV dysfunction in left heart disease is independent of its afterload. The current study provides a platform for future studies to examine the pharmacotherapeutic effects and prognosis of different measures of RV afterload.Seasonal acclimatization from winter to summer is known to enhance thermoeffector responses in hot-dry environments during exercise whilst its impact on sweat evaporation and core temperature (Tcore) responses in hot-humid environments remains unknown. We therefore sought to determine whether seasonal acclimatization is able to modulate whole-body sweat rate (WBSR), evaporated sweat rate, sweating efficiency and thermoregulatory function during cycling exercise in a hot-humid environment (32∘C, 75% RH). We also determined whether the increase in air-velocity, could enhance evaporated sweat rate and sweating efficiency before and after seasonal acclimatization. Twelve males cycled for 1-hour at 40% VO2max in winter (pre-acclimatization) and repeated the trial again in summer (after-acclimatization). For the last 20-min of cycling at a steady-state of Tcore, air-velocity increased from 0.2 (0.04) m/s to 1.1 (0.02) m/s by using an electric fan located in front of the participant. Seasonal acclimatization enhanced WBSR, unevaporated sweat rate, local sweat rate and mean skin temperature compared to pre-acclimatization state (all P0.70). In conclusion, seasonal acclimatization enhances thermoeffector responses but does not attenuate Tcore during exercise in a hot-humid environment. Furthermore, increasing air-velocity enhances evaporated sweat rate and sweating efficiency irrespective of acclimated state.Dietary nitrate supplementation improves exercise performance by reducing the oxygen cost of exercise and enhancing skeletal muscle function. However, the mechanisms underlying these effects are not well understood. The purpose of this study was to assess changes in skeletal muscle energy metabolism associated with exercise performance in a zebrafish model. Fish were exposed to sodium nitrate (60.7 mg/L, 303.5 mg/L, 606.9 mg/L), or control water, for 21 days and analyzed at intervals (5, 10, 20, 30, 40 cm/s) during a 2-h strenuous exercise test. We measured oxygen consumption during an exercise test and assessed muscle nitrate concentrations, gene expression, and the muscle metabolome before, during, and after exercise. Nitrate exposure reduced the oxygen cost of exercise and increased muscle nitrate concentrations at rest, which were reduced with increasing exercise duration. In skeletal muscle, nitrate treatment upregulated expression of genes central to nutrient sensing (mtor), redox signaling (nrf2a), and, ATP, phosphocreatine, glycolytic intermediates). Overall, nitrate supplementation may lower oxygen cost of exercise through improved fuel availability resulting from metabolic programming of muscle prior to exercise.Altering dietary carbohydrate (CHO) intake modulates fuel utilization during exercise. However, there has been no systematic evaluation of metabolic responses to graded changes in short-term ( less then 1 wk) dietary CHO intake. Thirteen active men performed interval running exercise combined with isocaloric diets over 3 days before evaluation of metabolic responses to 60-min running at 65% V̇O2max on three occasions. Diets contained lower [LOW, 2.40 ± 0.66 g CHO·kg-1·day-1, 21.3 ± 0.5% of energy intake (EI)], moderate (MOD, 4.98 ± 1.31 g CHO·kg-1·day-1, 46.3 ± 0.7% EI), or higher (HIGH, 6.48 ± 1.56 g CHO·kg-1·day-1, 60.5 ± 1.6% EI) CHO. Preexercise muscle glycogen content was lower in LOW [54.3 ± 26.4 mmol·kg-1 wet weight (ww)] compared with MOD (82.6 ± 18.8 mmol·kg -1 ww) and HIGH (80.4 ± 26.0 mmol·kg-1 ww, P less then 0.001; MOD vs. HIGH, P = 0.85). Whole body substrate oxidation, systemic responses, and muscle substrate utilization during exercise indicated increased fat and decreased CHO metabolism in and decreased CHO metabolism during exercise.Skeletal muscle phenotype may influence the response sensitivity of myocellular regulatory mechanisms to contractile activity. To examine this, we employed an ex vivo endurance-type dynamic contraction model to evaluate skeletal muscle phenotype-specific protein signaling responses in rat skeletal muscle. Preparations of slow-twitch soleus and fast-twitch extensor digitorum longus skeletal muscle from 4-wk-old female Wistar rats were exposed to an identical ex vivo dynamic endurance-type contraction paradigm consisting of 40 min of stretch-shortening contractions under simultaneous low-frequency electrostimulation delivered in an intermittent pattern. Phosphorylation of proteins involved in metabolic signaling and signaling for translation initiation was evaluated at 0, 1, and 4 h after stimulation by immunoblotting. For both muscle phenotypes, signaling related to metabolic events was upregulated immediately after stimulation, with concomitant absence of signaling for translation-initiation. Signaling for translation-initiation was then activated in both muscle phenotypes at 1-4 h after stimulation, coinciding with attenuated metabolic signaling.