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Many sports employ caloric restriction (CR) to reduce athletes’ body mass. During these phases, resistance training (RT) volume is often reduced to accommodate recovery demands. Since RT volume is a well-known anabolic stimulus, this review investigates whether a higher training volume helps to spare lean mass during CR. A total of 15 studies met inclusion criteria. The extracted data allowed calculation of total tonnage lifted (repetitions × sets × intensity load) or weekly sets per muscle group for only 4 of the 15 studies, with RT volume being highly dependent on the examined muscle group as well as weekly training frequency per muscle group. Studies involving high RT volume programs (≥ 10 weekly sets per muscle group) revealed low-to-no (mostly female) lean mass loss. Additionally, studies increasing RT volume during CR over time appeared to demonstrate no-to-low lean mass loss when compared to studies reducing RT volume. Since data regarding RT variables applied were incomplete in most of the included studies, evidence is insufficient to conclude that a higher RT volume is better suited to spare lean mass during CR, although data seem to favor higher volumes in female athletes during CR. Moreover, the data appear to suggest that increasing RT volume during CR over time might be more effective in ameliorating CR-induced atrophy in both male and female resistance-trained athletes when compared to studies reducing RT volume. The effects of CR on lean mass sparing seem to be mediated by training experience, pre-diet volume, and energy deficit, with, on average, women tending to spare more lean mass than men. Potential explanatory mechanisms for enhanced lean mass sparing include a preserved endocrine milieu as well as heightened anabolic signaling.
Chronic inflammation is characterized by persisting leukocyte infiltration of the affected tissue, which is enabled by activated endothelial cells (ECs). Chronic inflammatory diseases remain a major pharmacotherapeutic challenge, and thus the search for novel drugs and drug targets is an ongoing demand. We have identified the natural product vioprolide A (vioA) to exert anti-inflammatory actions in vivo and in ECs in vitro through inhibition of its cellular target nucleolar protein 14 (NOP14). VioA attenuated the infiltration of microglia and macrophages during laser-induced murine choroidal neovascularization and the leukocyte trafficking through the vascular endothelium in the murine cremaster muscle. Mechanistic studies revealed that vioA downregulates EC adhesion molecules and the tumor necrosis factor receptor (TNFR) 1 by decreasing the de novo protein synthesis in ECs. Most importantly, we found that inhibition of importin-dependent NF-ĸB p65 nuclear translocation is a crucial part of the action of vioA leading to reduced NF-ĸB promotor activity and inflammatory gene expression. Knockdown experiments revealed a causal link between the cellular target NOP14 and the anti-inflammatory action of vioA, classifying the natural product as unique drug lead for anti-inflammatory therapeutics.