Petrie Michael A, Kimball Amy L, McHenry Colleen L, Suneja Manish, Yen Chu-Ling, Sharma Arpit, Shields Richard K
Department of Physical Therapy and Rehabilitation Science, Carver College of Medicine, The University of Iowa, Iowa City, Iowa, United States of America.
Department of Internal Medicine, Carver College of Medicine, The University of Iowa, Iowa City, Iowa, United States of America.
PLoS One. 2016 Aug 3;11(8):e0160594. doi: 10.1371/journal.pone.0160594. eCollection 2016.
Skeletal muscle exercise regulates several important metabolic genes in humans. We know little about the effects of environmental stress (heat) and mechanical stress (vibration) on skeletal muscle. Passive mechanical stress or systemic heat stress are often used in combination with many active exercise programs. We designed a method to deliver a vibration stress and systemic heat stress to compare the effects with active skeletal muscle contraction.
The purpose of this study is to examine whether active mechanical stress (muscle contraction), passive mechanical stress (vibration), or systemic whole body heat stress regulates key gene signatures associated with muscle metabolism, hypertrophy/atrophy, and inflammation/repair.
Eleven subjects, six able-bodied and five with chronic spinal cord injury (SCI) participated in the study. The six able-bodied subjects sat in a heat stress chamber for 30 minutes. Five subjects with SCI received a single dose of limb-segment vibration or a dose of repetitive electrically induced muscle contractions. Three hours after the completion of each stress, we performed a muscle biopsy (vastus lateralis or soleus) to analyze mRNA gene expression.
We discovered repetitive active muscle contractions up regulated metabolic transcription factors NR4A3 (12.45 fold), PGC-1α (5.46 fold), and ABRA (5.98 fold); and repressed MSTN (0.56 fold). Heat stress repressed PGC-1α (0.74 fold change; p < 0.05); while vibration induced FOXK2 (2.36 fold change; p < 0.05). Vibration similarly caused a down regulation of MSTN (0.74 fold change; p < 0.05), but to a lesser extent than active muscle contraction. Vibration induced FOXK2 (p < 0.05) while heat stress repressed PGC-1α (0.74 fold) and ANKRD1 genes (0.51 fold; p < 0.05).
These findings support a distinct gene regulation in response to heat stress, vibration, and muscle contractions. Understanding these responses may assist in developing regenerative rehabilitation interventions to improve muscle cell development, growth, and repair.
骨骼肌运动可调节人体中的几个重要代谢基因。我们对环境应激(热)和机械应激(振动)对骨骼肌的影响知之甚少。被动机械应激或全身性热应激常与许多主动运动方案联合使用。我们设计了一种施加振动应激和全身性热应激的方法,以比较其与主动骨骼肌收缩的效果。
本研究的目的是检验主动机械应激(肌肉收缩)、被动机械应激(振动)或全身性全身热应激是否能调节与肌肉代谢、肥大/萎缩以及炎症/修复相关的关键基因特征。
11名受试者参与了本研究,其中6名身体健全,5名患有慢性脊髓损伤(SCI)。6名身体健全的受试者在热应激室中坐30分钟。5名患有SCI的受试者接受单次肢体节段振动或一次重复性电诱导肌肉收缩。在每种应激结束3小时后,我们进行肌肉活检(股外侧肌或比目鱼肌)以分析mRNA基因表达。
我们发现重复性主动肌肉收缩上调了代谢转录因子NR4A3(12.45倍)、PGC-1α(5.46倍)和ABRA(5.98倍);并抑制了MSTN(0.56倍)。热应激抑制了PGC-1α(0.74倍变化;p<0.05);而振动诱导了FOXK2(2.36倍变化;p<0.05)。振动同样导致MSTN下调(0.74倍变化;p<0.05),但程度小于主动肌肉收缩。振动诱导了FOXK2(p<0.05),而热应激抑制了PGC-1α(0.74倍)和ANKRD1基因(0.51倍;p<0.05)。
这些发现支持了热应激、振动和肌肉收缩所引发的独特基因调控。了解这些反应可能有助于开发再生康复干预措施,以改善肌肉细胞的发育、生长和修复。