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Mechanisms of hypoxia (in)tolerance in prematurely born adults: PhD thesis (PhD Academy Award)
British Journal of Sports Medicine ( IF 11.6 ) Pub Date : 2024-10-03 , DOI: 10.1136/bjsports-2024-108881 Giorgio Manferdelli
British Journal of Sports Medicine ( IF 11.6 ) Pub Date : 2024-10-03 , DOI: 10.1136/bjsports-2024-108881 Giorgio Manferdelli
The primary aim of my PhD thesis was to investigate the long-term impact of premature birth, defined as any birth occurring before the 37th week of gestation, on the acute physiological responses and adaptation to high-altitude exposure, at rest and during exercise. Specifically, my work aimed to elucidate the mechanisms underlying the specific cardiovascular, cerebrovascular, respiratory, muscular and haematological responses to hypoxia in prematurely born, but otherwise healthy, adults compared with term born healthy peers. Based on previous evidence,1 2 we hypothesised that premature birth would induce adverse physiological responses to hypoxia, impair altitude acclimatisation, therefore predisposing these individuals to an increased risk of high-altitude diseases. Premature birth represents a growing global concern as it affects over 10% of all live births worldwide. In particular, those occurring ‘very’ preterm (≤32 weeks gestation) are often associated with significant respiratory, cardiac and vascular impairments which likely persist into adulthood.3 Increasing evidence demonstrates underdeveloped and/or compromised respiratory and cardiovascular function, as well as low exercise capacity in preterm born adults.3 Interestingly, although it might seem counterintuitive, limited evidence suggests pulmonary vascular, cardiac and possibly skeletal muscle functions in preterm born individuals to be primed for a more resilient response to hypoxic events later in life.4 Identification of the compensatory mechanisms of prematurity-associated responses to hypoxia might be of substantial clinical interest, as …
中文翻译:
早产儿缺氧(不)耐受的机制:博士论文(博士学院奖)
我的博士论文的主要目的是研究早产(定义为妊娠 37 周之前发生的任何分娩)对急性生理反应和对高海拔暴露、休息和运动期间的适应的长期影响。具体来说,我的工作旨在阐明与足月出生的健康同龄人相比,早产但其他方面健康的成年人对缺氧的特定心血管、脑血管、呼吸、肌肉和血液学反应的潜在机制。根据先前的证据,1 2 我们假设早产会引起对缺氧的不良生理反应,损害高原适应,因此使这些个体更容易患高原疾病的风险增加。早产是一个日益受到全球关注的问题,因为它影响了全球超过 10% 的活产婴儿。特别是,那些发生在“极”早产儿(妊娠 ≤32 周)的早产儿通常与严重的呼吸、心脏和血管损伤有关,这些损害可能会持续到成年期。3 越来越多的证据表明,早产儿的呼吸和心血管功能发育不全和/或受损,以及运动能力低下。有趣的是,尽管这似乎有悖常理,但有限的证据表明肺血管、 早产儿个体的心脏和可能的骨骼肌功能为以后的生活对缺氧事件做出更具弹性的反应做好准备.4 确定早产儿对缺氧相关反应的代偿机制可能具有重大的临床意义,因为......
更新日期:2024-10-04
中文翻译:
早产儿缺氧(不)耐受的机制:博士论文(博士学院奖)
我的博士论文的主要目的是研究早产(定义为妊娠 37 周之前发生的任何分娩)对急性生理反应和对高海拔暴露、休息和运动期间的适应的长期影响。具体来说,我的工作旨在阐明与足月出生的健康同龄人相比,早产但其他方面健康的成年人对缺氧的特定心血管、脑血管、呼吸、肌肉和血液学反应的潜在机制。根据先前的证据,1 2 我们假设早产会引起对缺氧的不良生理反应,损害高原适应,因此使这些个体更容易患高原疾病的风险增加。早产是一个日益受到全球关注的问题,因为它影响了全球超过 10% 的活产婴儿。特别是,那些发生在“极”早产儿(妊娠 ≤32 周)的早产儿通常与严重的呼吸、心脏和血管损伤有关,这些损害可能会持续到成年期。3 越来越多的证据表明,早产儿的呼吸和心血管功能发育不全和/或受损,以及运动能力低下。有趣的是,尽管这似乎有悖常理,但有限的证据表明肺血管、 早产儿个体的心脏和可能的骨骼肌功能为以后的生活对缺氧事件做出更具弹性的反应做好准备.4 确定早产儿对缺氧相关反应的代偿机制可能具有重大的临床意义,因为......