Nutritional Ergogenic Aids — Macronutrients
Luke Bucci in Nutrients as Ergogenic Aids for Sports and Exercise, 2020
Nutritional ergogenic aids fall into three major categories: macronutrient manipulations, essential micronutrient and intermediate metabolite supplementation, and addition of other dietary substances. This chapter examines the results from studies on each type of nutrient and provides guidelines on use of nutrients to foster applicability of latest data. Water repletion during exercise appears to be the most important nutritional ergogenic aid yet studied, and is recommended by every expert on exercise performance. Athletes, especially weightlifters, have imbedded in their psyche a desire to consume large amounts of protein. This desire stems from the tradition, fostered by centuries of anecdotal, but not totally correct, conclusions that meat ingestion increases muscle mass. It is now apparent that protein catabolism can account for 5 to 10 percent of energy production during endurance exercise. Unlike other fats, Medium-Chain Triglycerides possess unique physiological properties that strongly indicate a need for further study as an ergogenic aid.
Coupling and pleiotropy
Hugo van den Berg in Hormones as Tokens of Selection, 2019
Pleiotropic suites emerge automatically within the coupling graph, which charts how each pressure ‘spreads out’ over the entire system. In the case of transport fluxes or transformations, the coupling coefficients are typically positive in both directions, as the following example illustrates. Fluxes that are supplied by the pool can then be efficiently regulated by up- or down-regulating the machinery that mediates these fluxes, since their substrate species is maintained at a near-constant level; in this manner the usage traffic is shielded off from the fluctuations at the level of supply to this substrate pool. An additional consideration is that the hub substrate is typically an osmotically active species of small-molecular weight. Catabolic and anabolic pathways both converge on, and depart from, a small number of interconnected pools of metabolites with low molecular weight, and temporary surpluses are absorbed by polymeric reserve compounds, which can occupy substantial portions of the total intracellular volume in bacteria.
Surgery
David McCollum in The Easy Guide to Focused History Taking for OSCEs, 2017
This chapter presents information or guidance regarding surgery for use by medical, scientific or health-care professionals. The pathophysiology of abdominal pain may be divided into parietal, visceral and referred. Parietal or somatic pain is well localised and is caused by local inflammation and is a consequence of infection, irritation etc. Visceral pain is usually due to distension of a viscus and is poorly localised. Upper abdominal pain usually reflects stomach, duodenal, gallbladder, liver or pancreas pathology; central abdominal pain reflects those areas supplied by the superior mesenteric artery i.e. small bowel, appendix and proximal colon; lower abdominal pain reflects pathology in the lower colon and genito-urinary tract. Referred pain is usually secondary to cardiopulmonary conditions but may also be secondary to abdominal wall problems such as herpes zoster or muscle haematoma. Weight loss is due to either inadequate intake, malabsorption, reduced anabolism, increased catabolism or a combination.
Rapamycin Inhibits Nf-ΚB Activation by Autophagy to Reduce Catabolism in Human Chondrocytes
Published in Journal of Investigative Surgery, 2020
Yibin Liu, Xiaojun Li, Aunhua Jin
Background and Aim: Osteoarthritis is a disease that is accompanied by inflammation and catabolic disorders in the cartilage. Rapamycin is a good autophagy activator and has an inhibitory effect on inflammation, and autophagy can remove waste generated by catabolic disorders and delay the destruction of cartilage by inflammation. This study was designed to evaluate the effect of rapamycin upon the catabolism in human chondrocytes and unravel underlying mechanism. Methods and Results: C57 mice and SW1353 cells were cultured and osteoblastic arthritis was formed by destabilization of the medial meniscus surgery; 10 ng/ml of IL-1β was added to the cells to produce inflammatory chondrocytes, and a non-cytotoxic concentration of 20 nM Rapamycin was used as the self-activator. Autophagy levels were verified by quantitative analysis of autophagy markers of LC3 and ATG5, and it was verified that rapamycin can activate autophagy. Autophagy inhibition was induced by ATG5 siRNA by comparing the presence of rapamycin treatment in inflammatory chondrocytes. The expression of the degrading gene and chemokine was evaluated by qPCR. Rapamycin down-regulated the expression of MMP-3 and -9, ADAMTS5, CCL-1, -2, and -5 induced by inflammation. Quantitative analysis of IκBα and P-P65 was used to analyze the interaction between the NF-κB pathway and autophagy in inflammation. Activation of the NF-κB pathway by inflammatory stimulation, P-P65 nuclear translocation, and degradation of IκBα protein were attenuated, respectively. Autophagy inhibited the activation of NF-κB signaling pathway in inflammatory chondrocytes. Conclusions: Rapamycin can inhibit the overexpression of inflammatory catabolic genes by activating autophagy, and can suppress the NF-κB signaling pathway in chondrocytes to break the positive feedback loop with inflammatory factors and reduce the rate and level of inflammation progression.
Bacterial catabolism of nonulosonic (sialic) acid and fitness in the gut
Published in Gut Microbes, 2010
Salvador Almagro-Moreno, E. Fidelma Boyd
The term nonulosonic acid or sialic acid encompasses a varied group of nine-carbon amino sugars widely distributed among mammals and higher metazoans. Among bacteria, the ability to synthesize sialic acid was first examined in a small number of human pathogenic species that deposit sialic acid residues on their outer surface. New phylogenomic data suggest that the ability to synthesize sialic acid and sialic acid-like compounds is not a novel bacterial innovation but a much more widespread ancient trait. In contrast, the genes required for the catabolism of sialic acid are found only among pathogenic and commensal bacterial species. This ability to utilize sialic acid as a carbon source is correlated with bacterial virulence, especially, in the sialic acid rich environment of the gut. In this article, we present the most recent findings in sialobiology with a focus on sialic acid catabolism.
Malignant manipulaTORs of metabolism: suppressing BCAA catabolism to enhance mTORC1 activity
Published in Molecular & Cellular Oncology, 2019
Russell E. Ericksen, Weiping Han
The mammalian target of rapamycin complex 1 (mTORC1) plays an important role in the development and progression of multiple cancers. Its activity is regulated by both growth factor and nutrient signals, and the branched-chain amino acid (BCAA) leucine plays an important and unique role in this process. Recently we found that cancers of the liver and multiple other tissues suppress the catabolism of BCAAs, thereby facilitating the chronic activation of mTORC1. Our results unveil how mTORC1’s nutrient-sensing arm can be manipulated by tumors, and suggest that restoring BCAA catabolism may help control mTORC1 activity in cancer cells.