Acute effects of thixotropy conditioning of inspiratory muscles on end-expiratory chest wall and lung volumes in normal humans

Acute effects of thixotropy conditioning of inspiratory muscles on end-expiratory chest wall and lung volumes in normal humans
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DOI:
10.1152/japplphysiol.01598.2005
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发表时间:
2006-07-01
影响因子:
3.3
通讯作者:
Homma, Ikuo
Homma, Ikuo
中科院分区:
医学2区
文献类型:
--
作者:
Izumizaki, Masahiko;Iwase, Michiko;Homma, Ikuo

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吸气肌触变调节对正常人呼气末胸壁和肺容量的急性影响。应用生理学杂志101:298-306,2006。2006年3月30日首次出版;DOI:10.1152/japplPhysio1.01598.2005。-在正常人中,吸气肌的触变性条件作用包括在充气的肺容量下进行最大吸气努力,随后是胸腔呼气末位置的增加。当在放气的肺容量下进行条件反射时,紧随其后的是呼气末位置的降低。本研究旨在确定触变调节后呼气末胸壁和肺容量是否发生变化。我们首先使用呼吸感应体积描记术(n=8)检测了在随后的五个呼吸周期中,条件反射对胸壁容量的急性影响。呼气末胸壁体积在充气肺容量调节后增加(P<0.05),这主要是通过肋骨运动获得的。在肺容量减少的条件下,呼气末胸壁体积减少,这可以用胸腔和腹部体积的变化来解释(P<0.05)。充气和收缩肺容量条件处理后,呼气末食道压力分别降低和升高(n=3)。这些呼气末容量和食道压力的变化在条件化后的第一次呼吸中最大。我们还发现肺活量测定吸气量的增加(n=13)在收缩肺容量条件下持续3分钟,而在充气肺容量条件下条件作用1分钟后减少。氦稀释呼气末肺容量在充气和放气条件下分别增加和减少(P<0.05;n=11)。这些结果表明,在正常人中,触变性调节改变了胸壁和肺的呼气末容量。
Acute effects of thixotropy conditioning of inspiratory muscles on end-expiratory chest wall and lung volumes in normal humans. J Appl Physiol 101: 298-306, 2006. First published March 30, 2006; doi: 10.1152/japplphysio1.01598.2005. -Thixotropy conditioning of inspiratory muscles consisting of maximal inspiratory effort performed at an inflated lung volume is followed by an increase in end-expiratory position of the rib cage in normal human subjects. When performed at a deflated lung volume, conditioning is followed by a reduction in end-expiratory position. The present study was performed to determine whether changes in end-expiratory chest wall and lung volumes occur after thixotropy conditioning. We first examined the acute effects of conditioning on chest wall volume during subsequent five-breath cycles using respiratory inductive plethysmography (n = 8). End-expiratory chest wall volume increased after conditioning at an inflated lung volume (P < 0.05), which was attained mainly by rib cage movements. Conditioning at a deflated lung volume was followed by reductions in end-expiratory chest wall volume, which was explained by rib cage and abdominal volume changes (P < 0.05). End-expiratory esophageal pressure decreased and increased after conditioning at inflated and deflated lung volumes, respectively (n = 3). These changes in end-expiratory volumes and esophageal pressure were greatest for the first breath after conditioning. We also found that an increase in spirometrically determined inspiratory capacity (n = 13) was maintained for 3 min after conditioning at a deflated lung volume, and a decrease for 1 min after conditioning at an inflated lung volume. Helium-dilution end-expiratory lung volume increased and decreased after conditioning at inflated and deflated lung volumes, respectively (both P < 0.05; n = 11). These results suggest that thixotropy conditioning changes end-expiratory volume of the chest wall and lung in normal human subjects.