009) area under the curve (AUC). The BICARB session had lower acylated ghrelin at 60 (P=0.014) and 90 min post-exercise (P=0.016) with a decreased AUC (P=0.039). The BICARB session had increased PYY (P=0.034) with an increased AUC (P=0.031). The BICARB session also tended (P=0.060) to have increased GLP-1 at 30 (P=0.003) and 60 min post-exercise (P less then 0.001) with an increased AUC (P=0.030). The BICARB session tended (P=0.059) to reduce overall appetite, though there was no difference in AUC (P=0.149). These findings support a potential role for lactate in the high-intensity exercise-induced appetite-suppression.Reduced exercise capacity and impaired physical performance are observed in nearly all patients with liver cirrhosis. Physical activity and exercise are physiological anabolic stimuli that can reverse dysregulated protein homeostasis or proteostasis and potentially increase muscle mass and contractile function in healthy subjects. Cirrhosis is a state of anabolic resistance and unlike the beneficial responses to exercise reported in physiological states, there are few systematic studies evaluating the response to exercise in cirrhosis. Hyperammonemia is a mediator of the liver-muscle axis with net skeletal muscle ammonia uptake in cirrhosis causing signaling perturbations, mitochondrial dysfunction with decreased ATP content, modifications of contractile proteins and impaired ribosomal function, all of which contribute to anabolic resistance in cirrhosis and have the potential to impair the beneficial responses to exercise. English language publications in peer reviewed journals that specifically evaluated the impact of exercise in cirrhosis were reviewed. Most studies evaluated responses to endurance exercise and readouts included peak or maximum oxygen utilization, grip strength, and functional capacity. Endurance exercise for up to 12 weeks is clinically tolerated in well-compensated cirrhosis. Data on the safety of resistance exercise is conflicting. Nutritional supplements enhance the benefits of exercise in healthy subjects but have not been evaluated in cirrhosis. Whether the beneficial physiological responses with endurance exercise and increase in muscle mass with resistance exercise that occur in healthy subjects also occur in cirrhotics is not known. Specific organ-system responses, changes in body composition, or improved long-term clinical outcomes with exercise in cirrhosis need evaluation.It is unknown if simultaneous stimulation of the respiratory and locomotor muscle afferents via inspiratory loading (IL) and locomotor subsystolic cuff inflation (CUFF) influences the cardiovascular responses during exercise. We hypothesized that combined IL and CUFF (IL+CUFF) will result in greater increases in blood pressure (MAP) and systemic vascular resistance (SVR) than IL and CUFF alone during exercise. Eight adults (6M/2W) were enrolled and performed four 10 min bouts of constant-load cycling eliciting 40% maximal oxygen uptake on a single day. For each exercise bout, the first 5 min consisted of spontaneous breathing. The second 5 min consisted of voluntary hyperventilation (i.e. breathing frequency of 40 breaths/min) with IL (30% maximum inspiratory pressure (PIMAX)), CUFF (80 mmHg), IL+CUFF or no intervention (CTL) in randomized order. During exercise, cardiac output and MAP were determined via open-circuit acetylene wash-in and manual sphygmomanometry, respectively and SVR was calculated. Across CTL, IL, CUFF, and IL+CUFF, MAP was greater with each condition (CTL 97±14; IL 106±13; CUFF 114±14; IL+CUFF 119±15mmHg) (all, p0.05). These data demonstrate that simultaneous stimulation of respiratory and locomotor muscle afferent feedback results in additive MAP and SVR responses than IL and CUFF alone during submaximal exercise. These findings have important clinical implications for populations with exaggerated locomotor and respiratory muscle reflex feedbacks.Both lipid oversupply and poor mitochondrial function (low respiration and elevated H2O2 emission) have been implicated in the development of hepatic steatosis and liver injury. Mitophagy, the targeted degradation of low functioning mitochondria, is critical for maintaining mitochondrial quality control. Here, we used intralipid injections combined with acute (4day) and chronic (4-7wk) high-fat diets (HFD) to examine if hepatic mitochondrial respiration would decrease and H202 emission would increase with lipid overload. We tested these effects in male and female wild type (WT) mice and mice null for a critical mediator of mitophagy, BNIP3 (BNIP3 KO) housed at thermoneutral temperatures. Intralipid injection was successful in elevating serum triglycerides and NEFAs but had no impact on hepatic mitochondrial respiratory function or H2O2 emission. However, female mice had greater mitochondrial respiration on the acute HFD, lower H2O2 emission across both HFD durations, and were protected against hepatic steatosis. Unexpectedly, BNIP3 KO animals had greater hepatic mitochondrial respiration, better coupled respiration, and increased electron chain protein content after the 4day HFD compared to WT animals. Altogether, these data suggest that acute lipid overload delivered by a single intralipid bolus does not alter hepatic mitochondrial outcomes, but rather sex and genotype profoundly impact hepatic mitochondrial respiration and H2O2 emission.In 2005 the scientific misconduct case of a noted researcher concluded with, among other things, the retraction of 10 papers. However, these articles continue to be cited at relatively high rates. The objectives of this paper are (1) to track the retraction process of these papers, (2) to assess the impact of retraction on subsequent citation rates of these papers, and (3) to compare the citation history of these retracted articles and five other high-profile retraction cases. For Objective #1, all 5 articles to be Retracted were retracted and of the 4 to be Corrected, 2 were Retracted and 2 were Corrected. Opaganib Eight PubMed and journal sites were identified where retraction messages could be conveyed; the number of retraction messages averaged 3.4+2.5 for these 9 articles. For Objective #2, an absolute “cleansing” did not occur. While it initially appears there was a relative “cleansing”, as citation rates for these articles did decrease after retraction, the reductions in citation rates for these articles (-28%) were the same as those for matched non-retracted publications both by the same author (-28%) and by another investigator (-29%) over the same time frame.