Gut-related symptoms and an increase in markers of gut dysfunction have been observed in patients with chronic obstructive pulmonary disease (COPD). It remains unclear whether exercise, in relation to inducing hypoxia, plays a role in disturbances in protein digestion and amino acid absorption and whole body protein kinetics. Sixteen clinically stable patients with moderate-to-very severe COPD and 12 matched healthy subjects completed the study. Protein digestion and amino acid absorption, whole body protein kinetics were measured in the postabsorptive state via a continuous infusion of stable tracers in combination with orally administered stable tracer sips during 20 min of walking exercise and up to 4 h post exercise. In addition, concentrations of short-chain fatty acid (SCFA) and amino acids were measured. Patients with COPD completed one study day, walking at maximal speed, whereas healthy subjects completed two, one matched to the speed of a patient with COPD and one at maximal speed. The patients withge of the response of the gut to aerobic exercise is of importance.One in three Americans suffer from kidney diseases such as chronic kidney disease, and one of the etiologies is suggested to be long-term renal hypoxia. Interestingly, sympathetic nervous system activation evokes a renal vasoconstrictor effect that may limit oxygen delivery to the kidney. In this report, we sought to determine if sympathetic activation evoked by lower body negative pressure (LBNP) would decrease cortical and medullary oxygenation in humans. LBNP was activated in a graded fashion (LBNP; -10, -20, and -30 mmHg), as renal oxygenation was measured (T2*, blood oxygen level dependent, BOLD MRI; n = 8). At a separate time, renal blood flow velocity (RBV) to the kidney was measured (n = 13) as LBNP was instituted. LBNP significantly reduced RBV (P = 0.041) at -30 mmHg of LBNP (Δ-8.17 ± 3.75 cm/s). Moreover, both renal medullary and cortical T2* were reduced with the graded LBNP application (main effect for the level of LBNP P = 0.0008). During recovery, RBV rapidly returned to baseline, whereas medullary T2* remained depressed into the first minute of recovery. In conclusion, sympathetic activation reduces renal blood flow and leads to a significant decrease in oxygenation in the renal cortex and medulla.NEW & NOTEWORTHY In healthy young adults, increased sympathetic activation induced by lower body negative pressure, led to a decrease in renal cortical and medullary oxygenation measured by T2*, a noninvasive magnetic resonance derived index of deoxyhemoglobin levels. In this study, we observed a significant decrease in renal cortical and medullary oxygenation with LBNP as well as an increase in renal vasoconstriction. We speculate that sympathetic renal vasoconstriction led to a significant reduction in tissue oxygenation by limiting oxygen delivery to the renal medulla.In the neonatal (NRDS) and acute (ARDS) respiratory distress syndromes, mechanical ventilation supports gas exchange but can cause ventilation-induced lung injury (VILI) that contributes to high mortality. Further, surface tension, T, should be elevated and VILI is proportional to T. Surfactant therapy is effective in NRDS but not ARDS. Sulforhodamine B (SRB) is a potential alternative T-lowering therapeutic. In anesthetized male rats, we injure the lungs with 15 min of 42 ml/kg tidal volume, VT, and zero end-expiratory pressure ventilation. Then, over 4 hrs, we support the rats with protective ventilation - VT of 6 ml/kg with positive end-expiratory pressure. At the start of the support period, we administer intravenous non-T--altering fluorescein (targeting 27 mM in plasma) without or with therapeutic SRB (10 nM). Throughout the support period, we increase inspired oxygen fraction, as necessary, to maintain >90% arterial oxygen saturation. At the end of the support period we sacrifice the rat; sample systemic venous blood for injury marker ELISAs; excise the lungs; combine confocal microscopy and servo-nulling pressure measurement to determine T in situ in the lungs; image fluorescein in alveolar liquid to assess local permeability; and determine lavage protein content and wet-to-dry ratio (W/D), both to assess global permeability. Lungs exhibit focal injury. Surface tension is elevated 72% throughout control lungs and in uninjured regions of SRB-treated lungs, but normal in injured regions of treated lungs. Sulforhodamine B administration improves oxygenation, reduces W/D and reduces plasma injury markers. Intravenous SRB holds promise as a therapy for respiratory distress.Diet-induced obesity (DIO) is associated with glucose intolerance, insulin resistance (IR), and an increase in intramyocellular lipids (IMCL), which may lead to disturbances in glucose and protein metabolism. To this matter, it has been speculated that chronic obesity and elevated IMCL may contribute to skeletal muscle loss and deficits in muscle function and growth capacity. Thus, we hypothesized that diets with elevated fat content would induce obesity and insulin resistance, leading to a decrease in muscle mass and an attenuated growth response to increased external loading in adult male mice. Male C57BL/6 mice (8 wk of age) were subjected to five different diets, namely, chow, low-dat-diet (LFD), high-fat-diet (HFD), sucrose, or Western diet, for 28 wk. At 25 wk, HFD and Western diets induced a 60.4% and 35.9% increase in body weight, respectively. https://www.selleckchem.com/products/BMS-754807.html Interestingly, HFD, but not Western or sucrose, induced glucose intolerance and insulin resistance. Measurement of isometric torque (ankle plantar flexor and auced growth; however, only a 45% HFD resulted in attenuated growth following 30 days of functional overload.Obesity has become one of the most pressing public health issues of the 21st century and currently affects a substantial proportion of the older adult population. Although the cardiometabolic complications are well documented, research from the past 20 years has drawn attention to the detrimental effects of obesity on physical performance in older adults. Obesity-related declines in physical performance are due, in part, to compromised muscle strength and power. Recent evidence suggests there are a number of mechanisms potentially underlying reduced whole muscle function, including alterations in myofilament protein function and cellular contractile properties, and these may be related to morphological adaptations, such as shifts in fiber type composition and increased intramyocellular lipid content within skeletal muscle. To date, even less research has focused on how exercise and weight loss interventions for obese older adults affect these mechanisms. In light of this work, we provide an update on the current knowledge related to obesity and skeletal muscle contractile function and highlight a number of questions to address potential etiologic mechanisms as well as intervention strategies, which may help advance our understanding of how physical performance can be improved among obese older adults.