著者

Shohei Dobashi Chinatsu Aiba Daisuke Ando Masataka Kiuchi Mitsuya Yamakita Katsuhiro Koyama

出版者

The Japanese Society of Physical Fitness and Sports Medicine

雑誌

The Journal of Physical Fitness and Sports Medicine (ISSN:21868131)

巻号頁・発行日

vol.7, no.4, pp.239-245, 2018-07-25 (Released:2018-07-18)

参考文献数

40

被引用文献数

2 2

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Both exercise training and chronic caloric restriction contribute to brain health through enhanced expression of brain-derived neurotrophic factor (BDNF). This study investigated the synergistic effects between 12-week low-intensity exercise training and caloric restriction on hippocampal BDNF expression with redox status in rats. Twenty-six, 7-week-old male Wistar rats were randomly divided into the following 4 groups: (1) sedentary control (Con, n = 7), (2) exercise (Ex, n = 6), (3) caloric restriction (CR, n = 7), and (4) caloric restriction and exercise training (ExCR, n = 6). Although Con and Ex rats were fed ad libitum over time, CR and ExCR rats consumed 40% less food compared to Con rats. Ex and ExCR rats underwent low-intensity treadmill running (30 min/day, 5 days/week). Forty-eight hours after the termination of the 12-week intervention, rats were sacrificed and the hippocampus was quickly dissected for measuring BDNF expression and markers of oxidative stress, including 4-hydroxy-2-nonenal (4-HNE). Hippocampal BDNF expression was significantly increased in Ex compared to Con rats (p = 0.007), whereas the exercise-induced increase in BDNF was completely suppressed by a combination with caloric restriction. Furthermore, we observed a significant relationship between hippocampal BDNF and 4-HNE expression (r = 0.725, p < 0.001). Our findings indicate that exercise training combined with caloric restriction might not have a synergistic effect on hippocampal BDNF expression in young rats. Moreover, exercise-induced oxidative stress can trigger BDNF expression in the hippocampus.

著者

Ryo Fujita Yoshinori Tanaka Yasuhiro Saihara Mitsuya Yamakita Daisuke Ando Katsuhiro Koyama

出版者

日本生理人類学会

雑誌

Journal of PHYSIOLOGICAL ANTHROPOLOGY (ISSN:18806791)

巻号頁・発行日

vol.30, no.5, pp.195-201, 2011-09-30 (Released:2011-10-01)

参考文献数

29

被引用文献数

8 21

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The objectives of this paper were to determine the level of oxidative stress in atrophied gastrocnemius, and to verify the effect of molecular hydrogen (H2) saturated alkaline electrolyzed water (HSW) on gastrocnemius atrophy by modifying the redox status, indicated by 8-hydroxy-2′-deoxyguanosine (8-OHdG), malondialdehyde (MDA), and superoxide dismutase (SOD)-like activity. Female Wistar rats were divided into four groups: (1) the control (CONT); (2) the Hindlimb unloading (HU, for 3 weeks) given purified normal water (HU-NW); (3) the HU given alkaline electrolyzed reduced water (HU-AEW); and (4) the HU given HSW (HU-HSW). We showed that 8-OHdG, but not MDA, significantly increased by 149% and 145% in HU-NW and HU-AEW, respectively, when compared with CONT. In contrast, there was a trend toward suppression in 8-OHdG levels (increased by 95% compared with CONT) by treatment of HSW, though this effect was not prominent. Additionally, SOD-like activity significantly increased in both HU-NW (184%) and HU-AEW (199%) when compared with CONT. This result suggests the elevation of O2−· in the atrophied gastrocnemius. However, upregulation of SOD-like activity in the HU-HSW was increased by only 169% compared with CONT, though this difference is too small to detect statistical significance. HU led to 13% and 15% reduction of gastrocnemius wet weights in HU-NW and HU-AEW, respectively, compared with CONT. And the reduction of gastrocnemius wet weights in HU-HSW was attenuated by 7% compared with CONT. The gastrocnemius wet weights in the HU-HSW group were significantly greater than those in the HU-AEW, but not statistically significant with HU-NW. These results indicate that HU causes an increase in oxidative stress, but, in this experimental protocol, continuous consumption of HSW during HU does not demonstrate successful attenuation of oxidative stress and HU-mediated gastrocnemius atrophy.