The effect of astaxanthin supplementation on performance and fat oxidation during a 40 km cycling time trial

ObjectivesThis study aimed to investigate whether supplementation with 12 mg?day^?1 astaxanthin for 7 days can improve exercise performance and metabolism during a 40 km cycling time trial.DesignA randomised, double-blind, crossover design was employed.MethodsTwelve recreationally trained male cyclists (VO_2peak: 56.5 ± 5.5  mL?kg^?1?min^?1, W_max: 346.8 ± 38.4  W) were recruited. Prior to each experimental trial, participants were supplemented with either 12 mg?day^?1 astaxanthin or an appearance-matched placebo for 7 days (separated by 14 days of washout). On day 7 of supplementation, participants completed a 40 km cycling time trial on a cycle ergometer, with indices of exercise metabolism measured throughout.ResultsTime to complete the 40 km cycling time trial was improved by 1.2 ± 1.7% following astaxanthin supplementation, from 70.76 ± 3.93 min in the placebo condition to 69.90 ± 3.78 min in the astaxanthin condition (mean improvement = 51 ± 71 s, p = 0.029, g = 0.21). Whole-body fat oxidation rates were also greater (+0.09 ± 0.13 g?min^?1, p = 0.044, g = 0.52), and the respiratory exchange ratio lower (?0.03 ± 0.04, p = 0.024, g = 0.60) between 39–40 km in the astaxanthin condition.ConclusionsSupplementation with 12 mg?day^?1 astaxanthin for 7 days provided an ergogenic benefit to 40 km cycling time trial performance in recreationally trained male cyclists and enhanced whole-body fat oxidation rates in the final stages of this endurance-type performance event.     

Myeloid Mixed Lineage Kinase 3 Contributes to Chronic Ethanol-Induced Inflammation and Hepatocyte Injury in Mice

Proinflammatory activity of hepatic macrophages plays a key role during progression of alcoholic liver disease (ALD). Since mixed lineage kinase 3 (MLK3)-dependent phosphorylation of JNK is involved in the activation of macrophages, we tested the hypothesis that myeloid MLK3 contributes to chronic ethanol-induced inflammatory responses in liver, leading to hepatocyte injury and cell death. Primary cultures of Kupffer cells, as well in vivo chronic ethanol feeding, were used to interrogate the role of MLK3 in the progression of liver injury. Phosphorylation of MLK3 was increased in primary cultures of Kupffer cells isolated from ethanol-fed rats compared to cells from pair-fed rats. Kupffer cells from ethanol-fed rats were more sensitive to LPS-stimulated cytokine production; this sensitization was normalized by pharmacological inhibition of MLK3. Chronic ethanol feeding to mice increased MLK3 phosphorylation robustly in F4/80⁺ Kupffer cells, as well as in isolated nonparenchymal cells. MLK3^−/− mice were protected from chronic ethanol-induced phosphorylation of MLK3 and JNK, as well as multiple indicators of liver injury, including increased ALT/AST, inflammatory cytokines, and induction of RIP3. However, ethanol-induced steatosis and hepatocyte apoptosis were not affected by MLK3. Finally, chimeric mice lacking MLK3 only in myeloid cells were also protected from chronic ethanol-induced phosphorylation of JNK, expression of inflammatory cytokines, and increased ALT/AST. MLK3 expression in myeloid cells contributes to phosphorylation of JNK, increased cytokine production, and hepatocyte injury in response to chronic ethanol. Our data suggest that myeloid MLK3 could be targeted for developing potential therapeutic strategies to suppress liver injury in ALD patients.Key words: Alcoholic liver disease (ALD), Kupffer cells, Necroptosis, Toll-like receptor 4 (TLR4), Cytokines     

Electrochromic Os-based metallo-supramolecular polymers: electronic state tracking by in situ XAFS,IR, and impedance spectroscopies

In this study, the electronic states of Os-based metallo-supramolecular polymers (poly(OsL)²⁺) during electrochromism were tracked by in situ X-ray absorption fine structure (XAFS), infrared (IR), and impedance spectroscopies. The XAFS spectra suggested electronic charge migration in the polymer, and the in situ spectra revealed reversible changes caused by electrochemical redox reactions. The IR spectra of the polymers showed an IVCT band, and we also confirmed the reversible changes by applying a voltage to the redox cell. During the impedance measurements, we found a drastic decrease in the charge transfer resistance (R_CT) of the polymer films near the electrochemical redox potential.

In this study, the electronic states of Os-based metallo-supramolecular polymers (poly(OsL)²⁺) during electrochromism were tracked by in situ X-ray absorption fine structure (XAFS), infrared (IR), and impedance spectroscopies.     

Growth and Proximate Composition of Scenedesmus obliquus and Selenastrum bibraianum Cultured in Different Media and Condition

Proceedings of the National Academy of Sciences, India Section B: Biological Sciences - Microalgae are natural producers of various biochemical compounds such as protein, lipid, carotenoids and...     

Discovery of Thienoimidazole-Based HCV NS5A Genotype 1a and 1b Inhibitors

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DNA methylation is a reversible biological signal

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