期刊
MUSCLE & NERVE
卷 43, 期 1, 页码 65-75出版社
WILEY
DOI: 10.1002/mus.21831
关键词
actin; atrophy; hypertrophy; myosin; myostatin
资金
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [R01HD062507] Funding Source: NIH RePORTER
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [R01HD039445] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NURSING RESEARCH [R01NR010285] Funding Source: NIH RePORTER
- NICHD NIH HHS [R01-HD-39445, R01 HD039445-04, R01 HD062507, R01 HD062507-01A1, R01 HD039445] Funding Source: Medline
- NINR NIH HHS [R01-NR-010285-08, R01 NR010285, R01 NR010285-09] Funding Source: Medline
In humans, spinal cord injury (SCI) induces deleterious changes in skeletal muscle that may be prevented or reversed by electrical stimulation muscle training. The molecular mechanisms underlying muscle stimulation training remain unknown. We studied two unique SCI subjects whose right soleus received >6 years of training (30 minutes/day, 5 days/week). Training preserved torque, fatigue index, contractile speed, and cross-sectional area in the trained leg, but not the untrained leg. Training decreased 10 mRNAs required for fast-twitch contractions and mRNA that encodes for myostatin, an autocrine/paracrine hormone that inhibits muscle growth. Conversely, training increased 69 mRNAs that mediate the slow-twitch, oxidative phenotype, including PGC-1 alpha, a transcriptional coactivator that inhibits muscle atrophy. When we discontinued right soleus training, training-induced effects diminished slowly, with some persisting for >6 months. Training of paralyzed muscle induces localized and long-lasting changes in skeletal muscle mRNA expression that improve muscle mass and function. Muscle Nerve 43: 65-75, 2011
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据