School of Human Movement and Nutrition Sciences, University of Queensland, Brisbane, Queensland, Australia.
RDC Clinical, Brisbane, Queensland, Australia.
J Appl Physiol (1985). 2020 Jul 1;129(1):185-193. doi: 10.1152/japplphysiol.00091.2020. Epub 2020 Jun 18.
We questioned whether the respiratory muscles of humans contribute to systemic oxidative stress following inspiratory flow-resistive breathing, whether the amount of oxidative stress is influenced by the level of resistive load, and whether the amount of oxidative stress is related to the degree of diaphragm fatigue incurred. Eight young and healthy participants attended the laboratory for four visits on separate days. During the first visit, height, body mass, lung function, and maximal inspiratory mouth and transdiaphragmatic pressure (P) were assessed. During , participants undertook inspiratory flow-resistive breathing with either no resistance (control) or resistive loads equivalent to 50 and 70% of their P (P50% and P70%) for 30 min. Participants undertook one resistive load per visit, and the order in which they undertook the loads was randomized. Inspiratory muscle pressures were higher ( < 0.05) during the 5th and Final min of P50% and P70% compared with control. Plasma F-isoprostanes increased ( < 0.05) following inspiratory flow-resistive breathing at P70%. There were no increases in plasma protein carbonyls or total antioxidant capacity. Furthermore, although we evidenced small reductions in transdiapragmaic twitch pressures (P) after inspiratory flow-resistive breathing at P50% and P70%, this was not related to the increase in plasma F-isoprostanes. Our novel data suggest that it is only when sufficiently strenuous that inspiratory flow-resistive breathing in humans elicits systemic oxidative stress evidenced by elevated plasma F-isoprostanes, and based on our data, this is not related to a reduction in P. We examined whether the respiratory muscles of humans contribute to systemic oxidative stress following inspiratory flow-resistive breathing, whether the amount of oxidative stress is influenced by the level of resistive load, and whether the amount of oxidative stress is related to the degree of diaphragm fatigue incurred. It is only when sufficiently strenuous that inspiratory flow-resistive breathing elevates plasma F-isoprostanes, and our novel data show that this is not related to a reduction in transdiaphragmatic twitch pressure.
在吸气阻力呼吸后，人体呼吸肌是否会导致全身氧化应激；氧化应激的程度是否受阻力负荷水平的影响；氧化应激的程度是否与膈肌疲劳的程度有关。八名年轻健康的参与者分别在四天的四个不同时间到实验室参加实验。在第一次访问中，评估了身高、体重、肺功能以及最大口腔吸气压力和膈神经电刺激跨膈压（Pdi）。在 中，参与者在 30 分钟内分别进行无阻力（对照）或相当于 50%和 70%最大吸气压力（P50%和 P70%）的吸气阻力呼吸。参与者每次访问进行一种阻力负荷，且负荷的顺序是随机的。与对照相比，在 P50%和 P70%的第 5 分钟和最后 1 分钟，吸气肌压力更高（<0.05）。在 P70%的吸气阻力呼吸后，血浆 F-异前列烷增加（<0.05）。血浆蛋白羰基和总抗氧化能力没有增加。此外，尽管我们在 P50%和 P70%的吸气阻力呼吸后观察到膈神经电刺激 twitch 压力（Pdi）略有降低，但这与血浆 F-异前列烷的增加无关。我们的新数据表明，只有当吸气阻力呼吸足够剧烈时，才会在人体中引起全身氧化应激，表现为血浆 F-异前列烷升高，并且根据我们的数据，这与 Pdi 的降低无关。我们研究了在吸气阻力呼吸后，人体呼吸肌是否会导致全身氧化应激，氧化应激的程度是否受阻力负荷水平的影响，以及氧化应激的程度是否与膈肌疲劳的程度有关。只有当吸气阻力呼吸足够剧烈时，才会引起血浆 F-异前列烷升高，而我们的新数据表明，这与膈神经电刺激 twitch 压力的降低无关。
