The Effects of Static Stretching On Dynamic Postural Control During Maximum Forward Leaning Task.

The purpose of this study was to determine how the application of static stretching to ankle plantar flexors affects postural control during maximum forward leaning. Twenty-six volunteer males (age 21.4 ± 1.2 years) were randomly assigned to stretching and control conditions. Participants conducted 5-min stretching on a stretch board for the stretching condition and were kept standing for 6-min for the control condition. Before and after intervention, the range of motion (ROM) at ankle dorsiflexion and the center of pressure (COP) excursion during maximal forward leaning were determined. Mean anteroposterior COP position, COP velocity and COP areas were calculated to compare the change in postural control. After stretching, ROM was significantly increased. During maximal forward leaning after stretching, both COP position and velocity showed significant increases compared to before stretching. Moreover, COP position and velocity in the stretching condition were significantly higher than in the control condition after stretching. No significant differences were found in COP area before and after stretching. Five-minute stretching increased not only ROM but also the anterior limit of stability while maintaining posture and led to faster COP shift than before stretching. These results indicate that static stretching would improve dynamic postural control as well.

Cytochrome P450-dependent metabolism of vitamin E isoforms is a critical determinant of their tissue concentrations in rats.

The aim of this study was to clarify the contribution of cytochrome P450 (CYP)-dependent metabolism of vitamin E isoforms to their tissue concentrations. We studied the effect of ketoconazole, a potent inhibitor of CYP-dependent vitamin E metabolism in cultured cells, on vitamin E concentration in rats. Vitamin E-deficient rats fed a vitamin E-free diet for 4 weeks were administered by oral gavage a vitamin E-free emulsion, an emulsion containing alpha-tocopherol, gamma-tocopherol or a tocotrienol mixture with or without ketoconazole. Alpha-tocopherol was detected in the serum and various tissues of the vitamin E-deficient rats, but gamma-tocopherol, alpha- and gamma-tocotrienol were not detected. Ketoconazole decreased urinary excretion of 2,5,7,8-tetramethyl-2(2'-carboxyethyl)-6-hydroxychroman after alpha-tocopherol or a tocotrienol mixture administration, and that of 2,7,8-trimethyl-2(2'-carboxyethyl)-6-hydroxychroman (gamma-CEHC) after gamma-tocopherol or a tocotrienol mixture administration. The gamma-tocopherol, alpha- and gamma-tocotrienol concentrations in the serum and various tissues at 24 h after their administration were elevated by ketoconazole, while the alpha-tocopherol concentration was not affected. The gamma-tocopherol or gamma-tocotrienol concentration in the jejunum at 3 h after each administration was also elevated by ketoconazole. In addition, significant amount of gamma-CEHC was in the jejunum at 3 h after gamma-tocopherol or gamma-tocotrienol administration, and ketoconazole inhibited gamma-tocopherol metabolism to gamma-CEHC in the jejunum. These results showed that CYP-dependent metabolism of gamma-tocopherol and tocotrienol is a critical determinant of their concentrations in the serum and tissues. The data also suggest that some amount of dietary vitamin E isoform is metabolized by a CYP-mediated pathway in the intestine during absorption.