• 운동영양학회지
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• 제25권1호
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• pp.16-22
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• 2021

[Purpose] Aerobic exercise training (AT) reverses aging-induced deterioration of arterial stiffness via increased arterial nitric oxide (NO) production. Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NO synthase, was decreased by AT. However, whether AT-induced changes in ADMA levels are related to changes in nitrite/nitrate (NOx) levels remains unclear. Accordingly, we aimed to clarify whether the relationship between plasma ADMA and NOx levels afected the AT-induced reduction of arterial stifness in middle-aged and older adults. [Methods] Thirty-one healthy middle-aged and older male and female subjects (66.4 ± 1.3 years) were randomly divided into two groups: exercise intervention and sedentary controls. Subjects in the training group completed an 8-week AT (60%-70% peak oxygen uptake [${\dot{V}}O_{2peak}$] for 45 min, 3 days/week). [Results] AT signifcantly increased ${\dot{V}}O_{2peak}$ (P < 0.05) and decreased carotid β-stifness (P < 0.01). Moreover, plasma ADMA levels were significantly decreased while plasma NOx levels and NOx/ADMA ratio were significantly increased by AT (P < 0.01). Additionally, no sex diferences in AT-induced changes of circulating ADMA and NOx levels, NOx/ADMA ratio, and carotid β-stifness were observed. Furthermore, the AT-induced increase in circulating ADMA levels was negatively correlated with an increase in circulating NOx levels (r = -0.414, P < 0.05), and the AT-induced increase in NOx/ADMA ratio was negatively correlated with a decrease in carotid β-stifness (r = -0.514, P < 0.01). [Conclusion] These results suggest that the increase in circulating NOx with reduction of ADMA elicited by AT is associated with a decrease in arterial stiffness regardless of sex in middle-aged and older adults.

• Yonsei Medical Journal
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• 제59권9호
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• pp.1138-1142
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• 2018

This study aimed to analyze the impact of sleep deprivation (SD) on cardiac, hemodynamic, and endothelial parameters and to determine whether these are sustained with increased periods of SD. The study included 60 healthy men (mean: age $31.2{\pm}6.3years$; body mass index $24.6{\pm}2.6kg/m^2$). Hemodynamic parameters, parameters of myocardial contractility, spectral analysis of heart rate (HR) and blood pressure (BP) variability, and the sensitivity of arterial baroreflex function were evaluated. Biochemical tests were performed to assess L-arginine (L-Arg) and asymmetric dimethylarginine (ADMA) levels in reflection of endothelial nitric oxide synthase ability. Measurements of cardiovascular system parameters were obtained at 9 a.m. (baseline) on the first day of the study and 9 a.m. (24-h SD), 1 p.m. (28-h SD), and 5 p.m. (32-h SD) on the second day. Blood samples for evaluating biochemical parameters were obtained at baseline and after 24-h SD. ANOVA Friedman's test revealed a significant effect for time in relation to HR (${\chi}^2=26.04$, df=5, p=0.000), systolic BP (${\chi}^2=35.98$, df=5, p=0.000), diastolic BP (${\chi}^2=18.01$, df=5, p=0.003), and mean BP (${\chi}^2=28.32$, df=5, p=0.000). L-Arg and ADMA levels changed from $78.2{\pm}12.9$ and $0.3{\pm}0.1$ at baseline to $68.8{\pm}10.2$ and $0.4{\pm}0.1$ after 24-hr SD, respectively (p=0.001, p=0.004). SD in healthy men is associated with increases in BP, which appear to occur after 24 hours of SD and are maintained over increasing periods of SD. The observed hemodynamic changes may have resulted due to disordered vascular endothelial function, as reflected in alterations in L-Arg and ADMA levels.