Exercise reduced the concentration of an inflammatory makers without modulating the levels of epigenetic marker potentially involved in hypertension: a preliminary study

Abstract

Abstract Epigenetic mechanisms such as histone acetylation status mediated by HAT and HDAC2 enzymes play a central role in the pathophysiology, etiology, and progression of hypertension. The anti-inflammatory effects of physical exercise may be related to the modulation of histone acetylation status, which may alter the epigenome, providing therapeutic benefits for hypertensive individuals. To investigate the effects of an exercise training protocol on epigenetic parameters (HAT activities and HDAC2 concentrations), inflammatory markers (interleukin (IL)-10, tumour necrosis factor (TNF)-α, and C-reactive protein (CRP)), and cardiopulmonary fitness parameters (VO2peak, ambulatory blood pressure, NOx, endothelin 1 (ET-1), flow-mediated dilation, high density lipoprotein (HDL), and triacylglycerol levels) in treated hypertensive patients. Nine hypertensive patients aged 30-59 years underwent 12 weeks of strength or aerobic exercise 3 times a week. Physical fitness, 24-h blood pressure (systolic and diastolic), flow-mediated vasodilation, blood lipid profile analysis, and biomarkers were assessed before and after the intervention. No alterations were found in epigenetic parameters since HAT activities and HDAC2 concentrations remained unchanged after the intervention. Significant increases were found in VO2peak (pre: 29.1±6.3 and post: 31.5±6.3, P=0.021) and HDL (pre: 41.4±9 and post: 46.8±9.5, P=0.003). Furthermore, a significant reduction was seen in 24-h systolic and diastolic blood pressure, respectively: (pre: 119.1±5.6 and post: 114.4±4.5, P=0.6; pre: 73.9±4.1 and post: 70.5±4.2, P=0.4) and in CRP (pre: 2.4±1.4; post: 1.2±0.7*, P=0.03). Lastly, no alterations were found in IL-10 and TNF-α. In treated hypertensive individuals undergoing 12 weeks of exercise training VO2peak, 24 h blood pressure, HDL, and CRP improved. However, changes were not found in concentrations and the activity of HDAC2 and HAT, respectively.