Walk-run training improves the anti-inflammation properties of high-density lipoprotein in patients with metabolic syndrome.

CONTEXT Metabolic syndrome (MetS) is a constellation of cardiovascular risk factors, including central obesity, dysglycemia, hypertension, and dyslipidemia. The anti-inflammatory properties of high density lipoprotein (HDL) can be compromised in MetS. Exercise is recognized as an important factor in the prevention and treatment of MetS. OBJECTIVE This study was designed to investigate whether walk/run training without any specific diet could enhance anti-inflammation capacity of HDL from MetS patients. DESIGN This was a case control study. SETTING The study was conducted in a Zhoudian community, Taian. PATIENTS Thirty nine patients with MetS were recruited and divided into a control group (n = 12) remaining in an untrained state and exercise group (n = 27) performing a 10-week walk/run training program. MAIN OUTCOME MEASURES The anti-inflammation capacities of HDL3 (HDL subfractions) from MetS patients with or without exercise were investigated by co-incubating with TNF- α-injured endothelial cells in vitro. RESULTS The training did not influence serum lipoprotein level in MetS patients and cholesterol efflux capacity of circulating HDL. However, walk/run training increased paraoxonase-1 (PON1) activity and decreased the levels of malondialdehyde in either serum or isolated HDL from MetS patients prominently. More importantly, HDL3 isolated from MetS patients with 10 weeks training protected endothelial cells against tumor necrosis factor-a (TNF-a) -induced injury, decreased monocyte chemotactic protein-1 levels in media and vascular cell adhesion molecule-1 expression markedly. Furthermore, HDL3 isolated from MetS patients with walk/run training inhibited the TNF-á-induced monocyte adhesion to endothelial cells and obviously increased nitric oxide production by activating endothelial nitric oxide synthase. CONCLUSION Walk/run training leads to a significant improvement in HDL anti-inflammation capacity in subjects with MetS without restricted diet, the mechanism underlying which at least partially is due to increased PON1 activity in HDL, NO production, and eNOS expression in endothelial cells.