The Efficacy of a Calamansi-Containing Energy Drink on Running Performance and Recovery in NCAA Division I Middle-Distance Runners: A Preliminary Study.

This study examined the effects of a non-caffeinated energy drink (ED) that contained calamansi juice, glucose, and taurine on 3-km running performance and recovery. Eleven NCAA Division I middle-distance runners (20.8 ± 1.5 years old) were randomly assigned to consume either the ED or a placebo drink 60 min before 3-km running on a 400-m official track. Performance time and speed were recorded every 500-m interval. Recovery blood lactate concentration (BLC), systolic (SBP), diastolic blood pressure (DBP), and heart rate (HR) were measured at baseline, 60-min after ingesting the drinks, and post-running measurements were performed at 1-min, 5-min, and 10-min. Repeated analysis of variance and paired t-test were applied to examine the effects of time, trials, and their interaction on performance and recovery. Statistical significance was set a priori at p < 0.05. No significant difference was observed in performance time and speed between trials (p < 0.05). No interaction effect was found on performance time, speed, recovery BLC, DBP, and HR (p < 0.05). However, an interaction effect for trial by time was observed on SBP (p = 0.01). Recovery SBP continues to decrease from 5-min to 10-min in the ED trial (∆ = -13.9 mmHg) and slightly increased in the placebo trial (∆ = 1.1 mmHg). This study suggests that acute consumption of a calamansi-containing ED can positively impact the SBP recovery but not running performance. Further studies are needed to examine the acute and chronic effects of this ED on exercise performance and recovery among different populations.

Inhibition of the TGF-beta receptor I kinase promotes hematopoiesis in MDS.

MDS is characterized by ineffective hematopoiesis that leads to peripheral cytopenias. Development of effective treatments has been impeded by limited insight into pathogenic pathways governing dysplastic growth of hematopoietic progenitors. We demonstrate that smad2, a downstream mediator of transforming growth factor-beta (TGF-beta) receptor I kinase (TBRI) activation, is constitutively activated in MDS bone marrow (BM) precursors and is overexpressed in gene expression profiles of MDS CD34(+) cells, providing direct evidence of overactivation of TGF-beta pathway in this disease. Suppression of the TGF-beta signaling by lentiviral shRNA-mediated down-regulation of TBRI leads to in vitro enhancement of hematopoiesis in MDS progenitors. Pharmacologic inhibition of TBRI (alk5) kinase by a small molecule inhibitor, SD-208, inhibits smad2 activation in hematopoietic progenitors, suppresses TGF-beta-mediated gene activation in BM stromal cells, and reverses TGF-beta-mediated cell-cycle arrest in BM CD34(+) cells. Furthermore, SD-208 treatment alleviates anemia and stimulates hematopoiesis in vivo in a novel murine model of bone marrow failure generated by constitutive hepatic expression of TGF-beta1. Moreover, in vitro pharmacologic inhibition of TBRI kinase leads to enhancement of hematopoiesis in varied morphologic MDS subtypes. These data directly implicate TGF-beta signaling in the pathobiology of ineffective hematopoiesis and identify TBRI as a potential therapeutic target in low-risk MDS.