Effects of Blood Flow Restriction Training on Blood Perfusion and Work Ability of Muscles in Elite Para-alpine Skiers.

PURPOSE: The effects of short-term blood flow restriction (BFR) exercise on muscle blood flow perfusion and performance during high-intensity exercise were determined in elite para-alpine standing skiers to assess whether this would be an effective training regimen for elite athletes with disabilities. METHODS: Nine national-level para-alpine standing skiers (mean age, 20.67 ± 1.34 yr; four women) were recruited. Nondominant lower limbs were trained with BFR (eight in final analyses), and dominant lower limbs were trained without BFR (seven in final analyses). The 2-wk protocol included high-load resistance, local muscle endurance (circuit resistance training), and aerobic endurance (stationary cycling) training performed 4 times a week, with BFR during local muscle endurance and aerobic endurance sessions. Muscle strength was measured by maximal voluntary isometric contraction (MVIC) in the knee extensors; microcirculatory blood perfusion (MBP), by laser Doppler blood flow; and muscle strength and endurance, by the total amount of work (TW) performed during high-intensity centrifugal and concentric contractions. RESULTS: BFR significantly increased absolute and relative MVIC (P < 0.001, P = 0.001), MBP (P = 0.011, P = 0.008), and TW (P = 0.006, P = 0.007) from pretraining values, whereas only absolute MVIC increased without BFR (P = 0.047). However, the MVIC increase with BFR exercise (35.88 ± 14.83 N·m) was significantly greater (P = 0.040) than without BFR exercise (16.71 ± 17.79 N·m). CONCLUSIONS: Short-term BFR exercise significantly increased strength endurance, muscle strength, and MBP in national-level para-alpine standing skiers. Our study provides new evidence that BFR exercise can improve local muscle blood perfusion during high-intensity exercise and informs BFR exercise strategies for athletes with disabilities.

Fenofibrate inhibits the expression of VEGFC and VEGFR-3 in retinal pigmental epithelial cells exposed to hypoxia.

The aim of the present study was to examine the mechanisms through which fenofibrate inhibits the ability of human retinal pigment epithelial cells (RPE cells) exposed to hypoxia to stimulate the proliferation and migration of human umbilical vein endothelial cells (HUVECs). For this purpose, RPE cells and HUVECs were divided into the following groups: RPE-normoxia, RPE + fenofibrate, RPE-hypoxia, RPE hypoxia + fenofibrate; HUVECs normal culture and HUVECs + RPE-hypoxia culture supernatant. RPE cell hypoxia was induced by cobalt(II) chloride (CoCl2). A superoxide anion probe was used to measure the production of superoxide anion, which is indicative of hypoxic conditions. Cell proliferation was assessed by MTT assay, and the expression of vascular endothelial growth factor C (VEGFC) and vascular endothelial growth factor receptor-3 (VEGFR-3) in the RPE cell culture supernatant was measured by enzyme-linked immunosorbent assay (ELISA). The migration ability of the HUVECs was determined by scratch-wound assay, and the angiogenic ability of the HUVECs was examined by measuring cell lumen formation. The mRNA and protein expression levels of VEGFC and VEGFR-3 in the RPE cells were measured by RT-qPCR and western blot analysis, respectively. Our results revealed that fenofibrate inhibited the increase in the expression and release of VEGFC and VEGFR-3 into the RPE cell culture supernatant induced by exposure to hypoxia. The culture of HUVECs in medium supernatant of RPE cells epxosed to hypoxia enhanced the viability and migration ability of the HUVECs and promoted lumen formation; these effects were inhibited by fenofibrate. In conclusion, our data demonstrated that the exposure of RPE cells to hypoxia induced the expression and release of VEGFC and VEGFR-3 into the cell culture supernatant. The culture of HUVECs in conditioned medium from RPE cells exposed to hypoxia increased VEGFC and VEGFR-3 expression, and promoted the proliferation and migration of the HUVECs, as well as capillary tube formation, suggesting that RPE cells play an important role in the formation of choroidal neovascularization resulting from hypoxia. Fenofibrate inhibited the upregulation of VEGFC and VEGFR-3 in the RPE cells exposed to hypoxia, and thus reduced the ability of HUVECs to form new blood vessels.