2017年5月
Effects of milk product intake on thigh muscle strength and NFKB gene methylation during home-based interval walking training in older women: A randomized, controlled pilot study
PLOS ONE
- ,
- ,
- ,
- ,
- ,
- ,
- ,
- ,
- 巻
- 12
- 号
- 5
- 開始ページ
- e0176757
- 終了ページ
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1371/journal.pone.0176757
- 出版者・発行元
- PUBLIC LIBRARY SCIENCE
Background
Muscle atrophy with aging is closely associated with chronic systemic inflammation and life-style-related diseases. In the present study, we assessed whether post-exercise milk product intake during 5-month interval walking training (IWT) enhanced the increase in thigh muscle strength and ameliorated susceptibility to inflammation in older women.
Methods
Subjects [n = 37, 66 +/- 5 (standard deviation) yrs] who had been performing IWT for >6 months participated in this study. They were randomly divided into the following 3 groups: IWT alone (CNT, n = 12), IWT + low-dose post-exercise milk product intake (LD, n = 12; 4 g protein and 3 g carbohydrate) or IWT + a 3-times higher dose of milk product intake than the LD group (HD, n = 13). They were instructed to repeat >= 5 sets of fast and slow walking for 3 min each at >= 70% and 40% peak aerobic capacity for walking, respectively, per day for >= 4 days/week.
Results
After IWT, thigh muscle strength increased in the HD group (8 +/- 2%) more than in the CNT group (-2 +/- 3%, P = 0.022), despite similar IWT achievements between the groups (P>0.15). Pyrosequencing analysis using whole blood showed that methylation of NFKB1 and NFKB2, master genes of inflammation, was enhanced in the HD group (29 +/- 7% and 44 +/- 11%, respectively) more than in the CNT group (-20 +/- 6% and -10 +/- 6%, respectively; P<0.001). Moreover, the genome-wide DNA methylation analysis showed that several inflammation-related genes were hyper-methylated in the HD group compared with that in the CNT group, suggesting greater pro-inflammatory cytokine gene suppression in the HD group.
Conclusion
HD milk product intake after exercise produced a greater percent increase in thigh muscle strength and NFKB1 and NFKB2 gene methylation during IWT in physically active older women.
Muscle atrophy with aging is closely associated with chronic systemic inflammation and life-style-related diseases. In the present study, we assessed whether post-exercise milk product intake during 5-month interval walking training (IWT) enhanced the increase in thigh muscle strength and ameliorated susceptibility to inflammation in older women.
Methods
Subjects [n = 37, 66 +/- 5 (standard deviation) yrs] who had been performing IWT for >6 months participated in this study. They were randomly divided into the following 3 groups: IWT alone (CNT, n = 12), IWT + low-dose post-exercise milk product intake (LD, n = 12; 4 g protein and 3 g carbohydrate) or IWT + a 3-times higher dose of milk product intake than the LD group (HD, n = 13). They were instructed to repeat >= 5 sets of fast and slow walking for 3 min each at >= 70% and 40% peak aerobic capacity for walking, respectively, per day for >= 4 days/week.
Results
After IWT, thigh muscle strength increased in the HD group (8 +/- 2%) more than in the CNT group (-2 +/- 3%, P = 0.022), despite similar IWT achievements between the groups (P>0.15). Pyrosequencing analysis using whole blood showed that methylation of NFKB1 and NFKB2, master genes of inflammation, was enhanced in the HD group (29 +/- 7% and 44 +/- 11%, respectively) more than in the CNT group (-20 +/- 6% and -10 +/- 6%, respectively; P<0.001). Moreover, the genome-wide DNA methylation analysis showed that several inflammation-related genes were hyper-methylated in the HD group compared with that in the CNT group, suggesting greater pro-inflammatory cytokine gene suppression in the HD group.
Conclusion
HD milk product intake after exercise produced a greater percent increase in thigh muscle strength and NFKB1 and NFKB2 gene methylation during IWT in physically active older women.
- リンク情報
- ID情報
-
- DOI : 10.1371/journal.pone.0176757
- ISSN : 1932-6203
- PubMed ID : 28520754
- Web of Science ID : WOS:000401487700028