Bergamot Polyphenolic Fraction supplementation improves metabolic balance, endothelial function and maximal oxygen uptake in athletes

Background: The study aimed to evaluate the effects of a 4-week Bergamot Polyphenolic Fraction (BPF Gold; Bergamet Sport) supplementation on serum nitric oxide (NO), asymmetric dimethyl-arginine (ADMA), Endopat indices of endothelial function and maximal oxygen uptake (V_ O2max) of athletes. Methods: The effects of dietary supplementation (BPF Gold, 650 mg twice a day for 4 weeks) and placebo administration on flow-mediated dilatation (via Endopat measurements), serum markers (NO, ADMA), lipid profile, and V_ O2max were analysed in 30 athletes both before and after dietary protocols. Results: Significant differences between pre- and post-intervention baseline NO levels were observed after BPF Gold dietary protocol. Higher post-intervention baseline NO level was observed after BPF Gold diet compared with placebo. Moreover BPF Gold Sport increased baseline NO concentration (ΔNO). The positive correlation was observed between baseline post-intervention NO concentration and maximal oxygen uptale and also between ΔNO and ΔVO2max in response to BPF Gold supplementation. There was an association between a higher Edopat values of endothelial function and higher V O2max after Bergamet Sport diet compared with lower values of placebo. Conclusions: These findings suggest that an increase in NO release in response to BPF Gold Sport supplementation may play a central role in cardiovascular adaptive mechanisms and enhanced exercise performance in athletes

Modulation of Nitric Oxide Synthases by Oxidized LDLs: Role in Vascular Inflammation and Atherosclerosis Development

The maintenance of physiological levels of nitric oxide (NO) produced by eNOS represents a key element for vascular endothelial homeostasis. On the other hand, NO overproduction, due to the activation of iNOS under different stress conditions, leads to endothelial dysfunction and, in the late stages, to the development of atherosclerosis. Oxidized LDLs (oxLDLs) represent the major candidates to trigger biomolecular processes accompanying endothelial dysfunction and vascular inflammation leading to atherosclerosis, though the pathophysiological mechanism still remains to be elucidated. Here, we summarize recent evidence suggesting that oxLDLs produce significant impairment in the modulation of the eNOS/iNOS machinery, downregulating eNOS via the HMGB1-TLR4-Caveolin-1 pathway. On the other hand, increased oxLDLs lead to sustained activation of the scavenger receptor LOX-1 and, subsequently, to NFkB activation, which, in turn, increases iNOS, leading to EC oxidative stress. Finally, these events are associated with reduced protective autophagic response and accelerated apoptotic EC death, which activates atherosclerotic development. Taken together, this information sheds new light on the pathophysiological mechanisms of oxLDL-related impairment of EC functionality and opens new perspectives in atherothrombosis prevention