LaRosa Domenic A, Ellery Stacey J, Parkington Helena C, Snow Rod J, Walker David W, Dickinson Hayley
Ritchie Centre, Hudson Institute of Medical Research and Department of Obstetrics and Gynaecology, Monash University, Clayton, Victoria, Australia.
Department of Physiology, Monash University, Clayton, Victoria, Australia.
PLoS One. 2016 Mar 1;11(3):e0149840. doi: 10.1371/journal.pone.0149840. eCollection 2016.
Using a model of birth asphyxia, we previously reported significant structural and functional deficits in the diaphragm muscle in spiny mice, deficits that are prevented by supplementing the maternal diet with 5% creatine from mid-pregnancy. The long-term effects of this exposure are unknown. Pregnant spiny mice were fed control or 5% creatine-supplemented diet for the second half of pregnancy, and fetuses were delivered by caesarean section with or without 7.5 min of in-utero asphyxia. Surviving pups were raised by a cross-foster dam until 33±2 days of age when they were euthanized to obtain the diaphragm muscle for ex-vivo study of twitch tension and muscle fatigue, and for structural and enzymatic analyses. Functional analysis of the diaphragm revealed no differences in single twitch contractile parameters between any groups. However, muscle fatigue, induced by stimulation of diaphragm strips with a train of pulses (330 ms train/sec, 40 Hz) for 300 sec, was significantly greater for asphyxia pups compared with controls (p<0.05), and this did not occur in diaphragms of creatine + asphyxia pups. Birth asphyxia resulted in a significant increase in the proportion of glycolytic, fast-twitch fibres and a reduction in oxidative capacity of Type I and IIb fibres in male offspring, as well as reduced cross-sectional area of all muscle fibre types (Type I, IIa, IIb/d) in both males and females at 33 days of age. None of these changes were observed in creatine + asphyxia animals. Thus, the changes in diaphragm fatigue and structure induced by birth asphyxia persist long-term but are prevented by maternal creatine supplementation.
利用出生窒息模型,我们之前报道了刺毛鼠膈肌存在显著的结构和功能缺陷,而在妊娠中期给母鼠饮食补充5%的肌酸可预防这些缺陷。这种暴露的长期影响尚不清楚。妊娠后期,给怀孕的刺毛鼠喂食对照饮食或补充5%肌酸的饮食,通过剖腹产分娩胎儿,部分胎儿伴有或不伴有7.5分钟的宫内窒息。存活的幼崽由代孕母鼠抚养至33±2日龄,然后实施安乐死以获取膈肌,用于离体研究抽搐张力和肌肉疲劳,并进行结构和酶分析。膈肌的功能分析显示,各组之间的单次抽搐收缩参数没有差异。然而,用一串脉冲(330毫秒串/秒,40赫兹)刺激膈肌条300秒诱导的肌肉疲劳,窒息幼崽比对照组明显更严重(p<0.05),而在肌酸+窒息幼崽的膈肌中未出现这种情况。出生窒息导致雄性后代中糖酵解型快肌纤维比例显著增加,I型和IIb型纤维的氧化能力降低,并且在33日龄时,雄性和雌性的所有肌纤维类型(I型、IIa型、IIb/d型)的横截面积均减小。在肌酸+窒息的动物中未观察到这些变化。因此,出生窒息引起的膈肌疲劳和结构变化会长期持续,但可通过母体补充肌酸来预防。