Department of Pneumology, University Hospital Freiburg, Killianstrasse 5 D, 79106, Germany.
Respir Physiol Neurobiol. 2011 May 31;176(3):90-7. doi: 10.1016/j.resp.2011.01.011. Epub 2011 Feb 2.
Imposing load on respiratory muscles results in a loss of diaphragmatic contractility that develops early, is independent of task failure, and levels off following the initial decrease. This study assessed the progression of diaphragmatic contractility during sustained normocapnic hyperpnea and applied a biometric approximation (hypothesis: non-linear decay). Ten healthy subjects performed three consecutive hyperpnea bouts (I:6 min warm up/II:9 min/III:task failure 28.6 ± 11.5 min; mean ± SD) at maximal voluntary ventilation fractions (I:30-60%/II:70%/III:70%), followed by recovery periods (I:18 min/II:6 min/III:30 min). Twitch transdiaphragmatic pressure (TwPdi) was assessed throughout the protocol. Bouts II and III induced diaphragmatic fatigue (TwPdi baseline vs. Recovery -19 ± 17% and -30 ± 16%, both p < 0.05 RM-ANOVA) while bout I did not. During sustained hyperpnea (II/III), TwPdi followed an exponential decay (r(2) = 0.91). The reduction in diaphragmatic contractility closely follows a non-linear function with an early loss in diaphragmatic contractility during sustained hyperpnea, levels off thereafter, and is independent of task failure. Thus, reasons other than diaphragmatic fatigue are likely to be responsible for task failure during sustained hyperpnea.
施加于呼吸肌的负荷可导致膈肌无力的丧失，这种丧失发生得较早，与任务失败无关，并在初始下降后趋于平稳。本研究评估了在持续的常压高碳酸血症通气过程中膈肌无力的进展，并应用了生物计量逼近（假设：非线性衰减）。10 名健康受试者在最大自主通气分数下进行了三个连续的高碳酸血症通气回合（I：6 分钟预热/II：9 分钟/III：任务失败 28.6 ± 11.5 分钟；平均值 ± 标准差）（I：30-60%/II：70%/III：70%），随后是恢复期（I：18 分钟/II：6 分钟/III：30 分钟）。在整个方案中评估了膈肌抽搐跨膈压（TwPdi）。回合 II 和 III 引起膈肌无力（TwPdi 基线与恢复 -19 ± 17%和 -30 ± 16%，均 p < 0.05 RM-ANOVA），而回合 I 则没有。在持续的高碳酸血症通气期间（II/III），TwPdi 遵循指数衰减（r(2) = 0.91）。膈肌无力的降低与非线性函数密切相关，在持续的高碳酸血症通气期间，膈肌无力早期丧失，随后趋于平稳，与任务失败无关。因此，在持续的高碳酸血症通气期间，任务失败的原因可能不仅仅是膈肌无力疲劳。
