著者

Kazuhiko Tanabe Akiko Yamamoto Noriyuki Suzuki Naohiko Osada Yasuhiro Yokoyama Hisanori Samejima Atsushi Seki Misa Oya Taizo Murabayashi Masaru Nakayama Masanobu Yamamoto Kazuto Omiya Haruki Itoh Masahiro Murayama

出版者

The Japanese Circulation Society

雑誌

JAPANESE CIRCULATION JOURNAL (ISSN:00471828)

巻号頁・発行日

vol.62, no.5, pp.341-346, 1998 (Released:2001-11-25)

参考文献数

20

被引用文献数

8 10

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We have previously reported that chronic sleep deprivation causes a deficiency of intracellular magnesium (Mg) and decreased exercise tolerance. The aim of this study was to clarify whether oral administration of Mg could be effective in restoring the exercise tolerance that is decreased by chronic sleep deprivation. A bicycle ergometer cardiopulmonary exercise test was performed by 16 healthy volunteers (mean age 21.9 years). They were divided into 2 groups: 8 received doses of 100 mg of Mg orally per day for 1 month (Mg group) and the remaining 8 received no Mg and served as the control group. The study conditions were designed as follows: (1) the usual state (good sleep); and (2) the sleep-deprived state (sleeping time up to 60% Iess than the usual state for 1 month). The ratio of intracellular Mg content of the sleep-deprived state to the usual sleep state was significantly higher in the Mg group (p <0.05) than the untreated control group. There was no difference between the sleep-deprived state and the usual state with regard to anaerobic threshold and peak oxygen uptake in the Mg group, whereas both of these decreased in the sleep-deprived state in the control group. These results indicate that decreased exercise tolerance observed in the sleep-deprived state could be improved by oral Mg administration. (Jpn Circ J 1998; 62: 341-346)

著者

Tsuguya SAKAMOTO Chuwa TEI Masahiro MURAYAMA Hirofumi ICHIYASU Yoshiyuki HADA Terumi HAYASHI Keiko AMANO

出版者

International Heart Journal Association

雑誌

Japanese Heart Journal (ISSN:00214868)

巻号頁・発行日

vol.17, no.5, pp.611-629, 1976 (Released:2008-12-09)

参考文献数

20

被引用文献数

214 244

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Left ventricular scanning by echocardiography and ultrasono-cardiotomography was performed to search the possible muscular abnormality in 9 cases with giant T wave inversion without documented cause. The deeply inverted T wave was more than 1.2mV (average was 1.63mV) in the left precordial leads. All the cases had electrocardiographic left ventricular hypertrophy of obscure origin and ischemic episode was absent. Conventional echo beam direction to measure the short axis of the left ventricle disclosed almost normal thickness and movement of both interventricular septum (IVS) and the posterior wall (PW), so that the report of these cases is frequently within normal limits. However, ultrasono-cardiotomography (sector B scan) disclosed the fairly localized hypertrophy near the left ventricular apex, and conventional echocardiography also revealed the same area of either IVS or PW or both below the insertion of the papillary muscles, when the scanning towards the apex was performed (asymmetrical apical hypertrophy: AAH).Control study of 9 cases with IHSS showed asymmetrical septal hypertrophy (ASH) with almost equally hypertrophied IVS from base to apex. All cases had inverted T waves, but these were of lesser degree. Three cases had relatively deep T wave compatible with those of AAH, and these cases also had the apical hypertrophy of considerable degree (unusual type of IHSS, i.e., intermediate type between AAH and ASH).The close relationship between the depth of the inverted T waves and the Apex/Mid wall thickness ratios suggests that the altered recovery process of the hypertrophied apical musculature is responsible for the giant T wave inversion of heretofore unsolved origin. Until the connective link of AAH to the other forms of hypertrophic cardiomyopathy is disclosed, the cases with such a T wave and the apical hypertrophy may be designated as asymmetrical apical hypertrophy (AAH).