This study determined if 6-weeks vitamin D₂ supplementation (vitD₂, 3800 IU/day) had an influence on muscle function, eccentric exercise-induced muscle damage (EIMD), and delayed onset of muscle soreness (DOMS) in National Association for Stock Car Auto Racing (NASCAR) NASCAR pit crew athletes. Subjects were randomized to vitD₂ (n = 13) and placebo (n = 15), and ingested supplements (double-blind) for six weeks. Blood samples were collected and muscle function tests conducted pre- and post-study (leg-back and hand grip dynamometer strength tests, body weight bench press to exhaustion, vertical jump, 30-s Wingate test). Post-study, subjects engaged in 90 min eccentric-based exercise, with blood samples and DOMS ratings obtained immediately after and 1- and 2-days post-exercise. Six weeks vitD₂ increased serum 25(OH)D₂ 456% and decreased 25(OH)D₃ 21% versus placebo (p < 0.001, p = 0.036, respectively), with no influence on muscle function test scores. The post-study eccentric exercise bout induced EIMD and DOMS, with higher muscle damage biomarkers measured in vitD₂ compared to placebo (myoglobin 252%, 122% increase, respectively, p = 0.001; creatine phosphokinase 24 h post-exercise, 169%, 32%, p < 0.001), with no differences for DOMS. In summary, 6-weeks vitD₂ (3800 IU/day) significantly increased 25(OH)D₂ and decreased 25(OH)D₃, had no effect on muscle function tests, and amplified muscle damage markers in NASCAR pit crew athletes following eccentric exercise.

The purpose of this study was to assess the effect of 8-weeks ingestion of a commercialized joint pain dietary supplement (InstaflexTM Joint Support, Direct Digital, Charlotte, NC) compared to placebo on joint pain, stiffness, and function in adults with self-reported joint pain. InstaflexTM is a joint pain supplement containing glucosamine sulfate, methylsufonlylmethane (MSM), white willow bark extract (15% salicin), ginger root concentrate, boswella serrata extract (65% boswellic acid), turmeric root extract, cayenne, and hyaluronic acid. Subjects included 100 men and women, ages 50-75 years, with a history (>3 months) of joint pain, and were randomized to Instaflex™ or placebo (3 colored gel capsules per day for 8 weeks, double-blind administration). Subjects agreed to avoid the use of non-steroidal anti-inflammatory drugs (NSAID) and all other medications and supplements targeted for joint pain. Primary outcome measures were obtained pre- and post-study and included joint pain severity, stiffness, and function (Western Ontario and McMaster Universities [WOMAC]), and secondary outcome measures included health-related quality of life (Short Form 36 or SF-36), systemic inflammation (serum C-reactive protein and 9 plasma cytokines), and physical function (6-minute walk test). Joint pain symptom severity was assessed bi-weekly using a 12-point Likert visual scale (12-VS). Joint pain severity was significantly reduced in Instaflex™ compared to placebo (8-week WOMAC, ↓37% versus ↓16%, respectively, interaction effect P = 0.025), with group differences using the 12-VS emerging by week 4 of the study (interaction effect, P = 0.0125). Improvements in ability to perform daily activities and stiffness scores in Instaflex™ compared to placebo were most evident for the 74% of subjects reporting knee pain (8-week WOMAC function score, ↓39% versus ↓14%, respectively, interaction effect P = 0.027; stiffness score, ↓30% versus ↓12%, respectively, interaction effect P = 0.081). Patterns of change in SF-36, systemic inflammation biomarkers, and the 6-minute walk test did not differ significantly between groups during the 8-week study Results from this randomized, double blind, placebo-controlled community trial support the use of the Instaflex™ dietary supplement in alleviating joint pain severity in middle-aged and older adults, with mitigation of difficulty performing daily activities most apparent in subjects with knee pain. ClinicalTrials.gov Identifier: NCT01956500

Exercise induces blood flow redistribution among tissues, leading to splanchnic hypoperfusion. Intestinal epithelial cells are positioned between the anaerobic lumen and the highly metabolic lamina propria with an oxygen gradient. Hypoxia-inducible factor (HIF)-1α is pivotal in the transcriptional response to the oxygen flux. In this study, the pimonidazole hydrochloride staining was applied to observe the tissue hypoxia in different organs, which might be affected by the blood flow redistribution. The HIF-1α luciferase reporter ROSA26 oxygen-dependent degradation domain (ODD)-Luc/+ mouse model (ODD domain-Luc; female, n = 3-6/group) was used to detect the HIF-1α expression in the intestine. We used 3 swimming models: moderate exercise for 30 min, heavy-intensity exercise bearing 5% bodyweight for 1.5 h, and long-time exercise for 3 h. We found that 1 session of swimming at different intensities could induce tissue hypoxia redistribution in the small intestine, colon, liver and kidney, but not in the spleen, heart, and skeletal muscle. Our data showed that exercise exacerbated the extent of physiological hypoxia in the small intestine. Next, using ODD-Luc mice, we found that moderate exercise increased the in vivo HIF-1α level in the small intestine. The post-exercise HIF-1α level was gradually decreased in a time-dependent manner. Interestingly, the redistribution of tissue hypoxia and the increase of HIF-1α expression were not related to the exercise intensity and duration. This study provided evidence that the small intestine is the primary target organ for exercise-induced tissue hypoxia and HIF-1α redistribution, suggesting that HIF-1α may be a potential target for the regulation of gastrointestinal functions after exercise.

A novel synthesis approach for the construction of 2-trifluoroethyl-substituted benzofurans under copper-catalyzed conditions has been developed. The reaction of salicylaldehyde p-tosylhydrazones with 2-bromo-3,3,3-trifluoropropene proceeded through a sequential process to afford products in moderate to excellent yields (up to 93%). This method is also applicable to the formation of 2-trifluoroethylated indoles.

This paper is Part A of a two paper series seeking a systematical investigation of the feasibility of separating binary solvent mixtures with solvent resistant nanofiltration (SRNF) membranes.

Background: The process of muscle protein synthesis (MPS) plays a pivotal role in the enhancement of muscle function. Following a bout of exercise, the rate of MPS experiences an elevation for a brief period, known as the “anabolic window.” Despite whey protein supplementation has been demonstrated to augment the post-exercise anabolic window, the optimal timing and dosage remain controversial. Therefore, the present systematic review and meta-analysis were conducted to evaluate the effects of whey protein supplementation on post-exercise MPS and its protein kinase B (AKT)/mammalian target of the rapamycin (mTOR) pathway in healthy adults. Methods: Following PRISMA guidelines, this review included 21 RCTs, with 15 studies subjected to meta-analysis and 6 studies to qualitative analysis. Eligible studies examined myofibrillar fractional synthetic rate (FSR) or the AKT/mTOR pathway-related protein phosphorylation levels in muscle biopsy samples. Results: The combination of whey protein supplementation and exercise has been shown to significantly enhance FSR (Hedge’s g = 1.24, 95% CI: 0.71–1.77; p < 0.001), with increases ranging from 1.3 to 1.6 folds when consumed immediately after exercise and up to 2.5 folds when given 45 min prior to multiple-set resistance exercise. A dose-dependent increase in FSR was observed in response to whey protein supplementation, ranging from 10 to 60 g. In comparison to the placebo group, whey protein supplementation enhanced the phosphorylation levels of AKT, mTOR, eukaryotic translation initiation factor 4E-binding protein-1 (4E-BP1), 70 kDa ribosomal protein S6 kinase (p70S6K), and ribosomal protein S6 (rpS6) at 1–2 h post-exercise. Phosphorylation levels of p70S6K and rpS6 decreased 4–5 h after exercise. Conclusions: The combination of whey protein supplementation and exercise improves MPS in a time- and dose-dependent manner. Consumption of 20–40g of whey protein before multiple sets of resistance exercise may enhance myofibrillar FSR and activate the AKT/mTOR pathway, thereby augmenting MPS and extending the anabolic window.